Obesity - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

OBESITY A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES

J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS

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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2003 by ICON Group International, Inc. Copyright 2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1

Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Obesity: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83663-9 1. Obesity-Popular works. I. Title.

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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.

Copyright Notice If a physician wishes to copy limited passages from this book for patient use, this right is automatically granted without written permission from ICON Group International, Inc. (ICON Group). However, all of ICON Group publications have copyrights. With exception to the above, copying our publications in whole or in part, for whatever reason, is a violation of copyright laws and can lead to penalties and fines. Should you want to copy tables, graphs, or other materials, please contact us to request permission (E-mail: [email protected]). ICON Group often grants permission for very limited reproduction of our publications for internal use, press releases, and academic research. Such reproduction requires confirmed permission from ICON Group International Inc. The disclaimer above must accompany all reproductions, in whole or in part, of this book.

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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on obesity. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.

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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.

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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes & Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health

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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON OBESITY ..................................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Obesity ........................................................................................ 15 E-Journals: PubMed Central ....................................................................................................... 71 The National Library of Medicine: PubMed ................................................................................ 79 CHAPTER 2. NUTRITION AND OBESITY ......................................................................................... 167 Overview.................................................................................................................................... 167 Finding Nutrition Studies on Obesity....................................................................................... 167 Federal Resources on Nutrition ................................................................................................. 175 Additional Web Resources ......................................................................................................... 176 CHAPTER 3. ALTERNATIVE MEDICINE AND OBESITY ................................................................... 179 Overview.................................................................................................................................... 179 The Combined Health Information Database............................................................................. 179 National Center for Complementary and Alternative Medicine................................................ 180 Additional Web Resources ......................................................................................................... 192 General References ..................................................................................................................... 202 CHAPTER 4. DISSERTATIONS ON OBESITY..................................................................................... 203 Overview.................................................................................................................................... 203 Dissertations on Obesity............................................................................................................ 203 Keeping Current ........................................................................................................................ 216 CHAPTER 5. CLINICAL TRIALS AND OBESITY ............................................................................... 217 Overview.................................................................................................................................... 217 Recent Trials on Obesity............................................................................................................ 217 Keeping Current on Clinical Trials ........................................................................................... 238 CHAPTER 6. PATENTS ON OBESITY ............................................................................................... 241 Overview.................................................................................................................................... 241 Patents on Obesity ..................................................................................................................... 241 Patent Applications on Obesity ................................................................................................. 335 Keeping Current ........................................................................................................................ 393 CHAPTER 7. BOOKS ON OBESITY ................................................................................................... 395 Overview.................................................................................................................................... 395 Book Summaries: Federal Agencies............................................................................................ 395 Book Summaries: Online Booksellers......................................................................................... 400 The National Library of Medicine Book Index ........................................................................... 415 Chapters on Obesity................................................................................................................... 416 Directories.................................................................................................................................. 425 CHAPTER 8. MULTIMEDIA ON OBESITY ........................................................................................ 427 Overview.................................................................................................................................... 427 Video Recordings ....................................................................................................................... 427 Audio Recordings....................................................................................................................... 432 Bibliography: Multimedia on Obesity........................................................................................ 433 CHAPTER 9. PERIODICALS AND NEWS ON OBESITY ..................................................................... 435 Overview.................................................................................................................................... 435 News Services and Press Releases.............................................................................................. 435 Newsletters on Obesity .............................................................................................................. 441 Newsletter Articles .................................................................................................................... 442 Academic Periodicals covering Obesity ..................................................................................... 454 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 457 Overview.................................................................................................................................... 457

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Contents NIH Guidelines.......................................................................................................................... 457 NIH Databases........................................................................................................................... 459 Other Commercial Databases..................................................................................................... 467 The Genome Project and Obesity............................................................................................... 467 APPENDIX B. PATIENT RESOURCES ............................................................................................... 473 Overview.................................................................................................................................... 473 Patient Guideline Sources.......................................................................................................... 473 Associations and Obesity ........................................................................................................... 494 Finding Associations.................................................................................................................. 497 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 499 Overview.................................................................................................................................... 499 Preparation................................................................................................................................. 499 Finding a Local Medical Library................................................................................................ 499 Medical Libraries in the U.S. and Canada ................................................................................. 499

ONLINE GLOSSARIES................................................................................................................ 505 Online Dictionary Directories ................................................................................................... 508 OBESITY DICTIONARY.............................................................................................................. 509 INDEX .............................................................................................................................................. 605

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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with obesity is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about obesity, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to obesity, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on obesity. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to obesity, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on obesity. The Editors

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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.

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CHAPTER 1. STUDIES ON OBESITY Overview In this chapter, we will show you how to locate peer-reviewed references and studies on obesity.

The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and obesity, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “obesity” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •

The Association of Obesity with Osteoarthritis of the Hand and Knee in Women: A Twin Study Source: Journal of Rheumatology. 23(7):1221-26; 1996. Summary: This study examines the association of obesity and osteoarthritis (OA) at various sites in middle aged women and estimates the magnitude of the weight difference associated with OA. Researchers performed a co-twin control study within a population of women aged 48 to 70 years. OA was defined radiologically using site specific features and a standard atlas. Twin pairs discordant for OA disease traits were analyzed. Findings reveal the mean weight differences within twin pairs discordant for different OA traits were: tibiofemoral osteophytes 3.75 kg; patellofemoral osteophytes 3.05 kg; and carpometacarpal (CMC) osteophytes 3.06 kg. There was no significant difference in weight within twin pairs discordant for osteophytes at the distal

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interphalangeal or proximal interphalangeal joints or for joint space narrowing at all sites examined except the patellofemoral joint, 4.73 kg. For each kg increase in weight the increased likelihood of developing different OA traits was: tibiofemoral osteophytes 1.14, patellofemoral osteophytes 1.32, patellofemoral narrowing 1.15, and CMC 1.09. The authors suggest obesity is an important risk factor for development of OA at the tibiofemoral and patellofemoral joints of the knee and CMC joints of the hands, with significant increases of 9 to 13 percent in risk of OA per kg increase in body weight. This emphasizes the potential importance of even minor weight reduction as a preventive health measure for OA. 26 references, 6 tables. (AA-M). •

Self-reported Functional Status in Osteoarthritis of the Knee in a Rural Southern Community: The Role of Sociodemographic Factors, Obesity, and Knee Pain Source: Arthritis Care and Research. 9(4):273-278; August 1996. Summary: This journal article for health professionals describes a study that examined the role of Sociodemographic factors, such as age, race, gender, education, and marital status; obesity; severity of radiographic knee osteoarthritis (OA); and severity of knee pain in self-reported disability from OA. The sample included 1,272 African- Americans and Caucasians, aged 45 years or older, from the Johnston County Osteoarthritis Project. Analysis of variance was used to assess variation in mean Health Assessment Questionnaire (HAQ) scores by the above variables. Results indicate that mean HAQ scores differed by severity of radiographic knee OA and knee pain, obesity, and all demographic factors, except race. Only age, female sex, obesity, and knee pain severity were independent effects. Disability associated with knee pain varied by both radiographic knee OA severity and obesity. Findings suggest that knee pain severity was more important than radiographic knee OA severity in determining disability and that obesity compounded disability from knee pain. The article recommendations that future studies of disability in knee OA should include assessment of obesity, severity of radiographic knee OA, and severity of knee pain, as well as their interactions. 30 references and 4 tables. (AA-M).

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Can Obesity Explain the Racial Difference in Stage of Breast Cancer at Diagnosis Between Black and White Women? Source: Journal of Women's Health and Gender-based Medicine. 11(6):527-536, JulyAugust 2002. Summary: Researchers identified 966 incident cases of breast cancer between 1991 and 1997 from Baltimore, Maryland, hospitals to assess to what extent the racial difference in stage at diagnosis can be explained by racial differences in obesity. They reviewed hospital medical records to gather data on (1) age, (2) race, (3) weight, (4) height, (5) cancer detection methods, (6) treatment procedures, and (7) pathology reports. Of the participants, (1) 585 (60 percent) were white; (2) 381 (40 percent) were black; and (3) black women were less educated, resided in an area with a lower median income, were more likely to be uninsured or on Medicaid, and were more likely to be unmarried. Results showed that (1) black women had significantly higher body mass index (BMI) than white women; (2) about 48 percent of black women were obese compared with 26 percent of white women; (3) after adjusting for age, black women had 3.85 times the odds of being obese compared with white women; (4) black women had more advanced breast cancer than white women at diagnosis; (5) high BMI was associated with an advanced stage of breast cancer at diagnosis; and (6) adjustment for the higher prevalence of obesity in black women reduced the risk estimate of more advanced stage of breast cancer at diagnosis in black women compared with white women by about 30

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percent. The researchers conclude that the higher prevalence of obesity among black women explains part but not all of their relative disadvantage in stage at diagnosis of breast cancer. 4 tables, 87 references. •

Screening for Cervical and Breast Cancer: Is Obesity an Unrecognized Barrier to Preventive Care? Source: Annals of Internal Medicine. 132(9):697-704, May 2, 2000. Summary: Researchers examined the relationship between obesity and screening for cervical and breast cancer with Papanicolaou (Pap) smears and mammography. Investigators extracted data from the Year 2000 Supplement of the 1994 National Health Interview Survey. The responses on Pap smears and mammography screening were related to the body mass index (BMI). Obesity was divided into three classes: (1) Class I, BMI 30 to less than 35 kg/m2; (2) class II, BMI 35 to less than 40 kg/m2; and (3) class III, BMI 40 kg/m2 or greater. Women who were underweight made up approximately 3 percent of the sample and were included in all analyses, but their results are not reported. The following sociodemographic factors were included in the analysis as potential confounders: (1) Age, (2) ethnicity/race, (3) marital status, (4) education, (5) annual income, (6) type of health insurance coverage, and (7) region of the United States. Adjustments were made for illness burden using surrogate markers such as (1) selfreported health status, (2) number of days hospitalized in the past year, (3) number of days spent in bed, and (4) number of visits to a physician in the past year. Factors related to the provider, such as specialty of the usual provider and usual place where medical care was received, were also incorporated in the analysis. Of 8,394 women in the survey who were eligible for Pap smear analysis (age 18 to 75 who had not undergone a hysterectomy), 7,857 had complete data on height, weight, and performance of Pap smears. More than 50 percent of these women had normal BMI's. Overweight and obese women reported significantly lower Pap smear screening rates in the past 3 years than did normal weight women, 78 and 78 percent versus 84 percent, respectively. Heavier women were usually older, were less likely to be white or to have private health insurance, and had lower socioeconomic status. They reported a greater illness burden and were more likely to receive their usual health care from general internists and family practitioners than from gynecologists. After adjustment for sociodemographic factors, insurance, and access to health care, Pap smear screening rate differences were still seen between overweight and obese women compared to normalweight women. Of 3,397 women eligible for mammography analysis (age 50 to 75) who had complete information on weight and height, more than half of these were considered overweight or obese. Overall, the unadjusted rate of mammography use during the past 2 years was 65 percent. Overweight and obese women were significantly less likely to report previous mammography in the past 2 years compared to normalweight women. After adjustment for sociodemographics, insurance, and access to health care, mammography screening rate differences between overweight and obese women were also statistically significant compared to normal-weight women. The researchers concluded that overweight and obese women were found less likely to be screened for cervical and breast cancer with Pap smears and mammography than normal-weight women, even after adjusting for other known barriers. Because overweight and obese women have higher mortality rates for cervical and breast cancer, they should be targeted for increased screening. 4 tables, 35 references.

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Effect of Obesity on Screening Mammography: Outcomes Analysis of 88,346 Consecutive Examinations Source: American Journal of Roentgenology. 174(5):1251-1255, May 2000. Summary: Researchers examined the effects of obesity on screening mammography outcome. They performed a retrospective review of 88,346 consecutive screening examinations performed at the Department of Radiology, University of California San Francisco Medical Center (SFMC) between April 1985 and August 1997. They correlated self-reported weights of the patients with their self-reported heights and normalized these to their ideal weight using standard height/weight tables. Based on this, researchers divided patients into adiposity cohorts: (1) Underweight by at least 11 percent, (2) within 10 percent of ideal weight, (3) overweight by 11 to 24 percent, (4) overweight by 25 to 39 percent, and (5) overweight by more than 40 percent. The rates of recall, biopsy, and breast cancer detection of the patients were determined by contacting each woman's personal physician and searching the SFMC's radiology and pathology databases. Mammography screening of the 88,346 women resulted in 4,484 recalls, 1,228 biopsies performed, and 425 cases of screening-detected breast cancer. Differences between the adiposity cohorts for rates of recall, biopsy, and cancer detection were statistically reliable and meaningful. The recall rate increased with progressively increasing adiposity, from 3.88 percent of women who were underweight to 5.55 percent for those who overweight by more than 40 percent. Similar progressive increases in the rate of biopsy and cancer detection per 1,000 women screened with increasing adiposity were also seen, from 0.98 to 1.65 percent and from 3.74 to 6.04 percent. Increasing adiposity also could be correlated with increasing median tumor size and with a more advanced disease stage at diagnosis. Researchers conclude that increasing adiposity correlates with progressive increases in the rates of recall, biopsy, and cancer detection in women undergoing screening mammography. Increasing adiposity also correlates with increased cancer size and stage. These findings provide additional support for the view that obesity is a risk factor for breast cancer. 8 tables, 34 references.

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Is Obesity a Barrier to Physician Screening for Cervical Cancer? Source: American Journal of Medicine. 98(5):491-496, May 1995. Summary: Researchers examined whether obesity affects adherence to recommended guidelines for the performance of Papanicolaou (Pap) smears. Researchers collected data prospectively from May through October of 1989 at the Regenstrief Health Center's General Medicine Practice in Indianapolis, Indiana. This practice provides primary care to a low-income, inner-city population. Researchers gathered data during a clinical trial from 92 randomly-selected physicians who received reminders that required a response as to whether they had performed the Pap smear, and the reason for the action or inaction. Researchers also collected data from questionnaires completed during the first study visit by 970 patients. Patient-specific data came from the health center's medical record system. Researchers defined a body weight greater than 130 percent of ideal as obesity, and a body weight greater than 200 percent of ideal as morbid obesity. To examine the relationship of obesity to the reasons physicians noted for not performing a Pap smear, researchers grouped physician responses into five categories: (1) Patient's psychological concerns; (2) lack of patient time; (3) physician's belief that the patient was terminally ill or too old; (4) patient's physiological reason (acute illness, vaginitis, or menstruation); and (5) lack of physician time. Results showed no significant demographic differences between nonobese and all other women, except for age; obese and morbidly-obese women were younger than nonobese women. According to physician responses, 200 (21 percent) of the women received Pap smears, 136 (14

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percent) were not truly eligible, 143 (15 percent) refused Pap smears, and 491 (51 percent) had their Pap smears rescheduled. All three weight categories had low Pap smear performance, but differences between groups were neither clinically- nor statistically-significant. Comparisons of the odds ratios for obese and morbidly-obese women demonstrated a significant dose-response effect of weight on the proportion of women whose physicians reported not performing a Pap smear due to acute illness, vaginitis, or menstruation. Overall, results did not demonstrate an association between obesity and a reduction in Pap smear performance. 1 figure, 4 tables, 26 references. •

Smell and Taste in Children with Simple Obesity Source: International Journal of Pediatric Otorhinolaryngology. 55(3): 191-196. October 16, 2000. Contact: Available from Elsevier Science. P.O. Box 945, New York, NY 10159-0945. (888) 437-4636. Fax (212) 633-3680. E-mail: [email protected]. Summary: This article reports on a study of 30 children, aged 10 to 16 years and suffering from simple obesity, in whom significantly lowered odor detection thresholds were noted. The thresholds were lower than the average for a given age group in around 20 percent of obese children in cases of odors that stimulated the olfactory nerve and in approximately 57 percent in cases of substances that stimulated both olfactory and trigeminal nerves. Odor identification thresholds were similarly affected, with identification of olfactory nerve plus trigeminal nerve stimulating odors affected more than twice as frequently. In 77 percent of cases, the electrogustometric thresholds were found below the normal range values when anode was used as the stimulating electrode. The authors hypothesize that the detected alterations may be linked to metabolic disturbances, which accompany simple obesity. 3 figures. 1 table. 18 references.

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Obesity: Effects on the Liver and Gastrointestinal System Source: Current Opinion in Gastroenterology. 15(2): 154-158. March 1999. Contact: Available from Lippincott Williams and Wilkins Publishers. 12107 Insurance Way, Hagerstown, MD 21740. (800) 637-3030. Fax (301) 824-7390. Summary: Obesity, determined by a body mass index (BMI) greater than 30, has assumed epidemic proportions in the U.S. More than a cosmetic issue, obesity is associated with many comorbidities that contribute to multiple organ dysfunction, illness, and shortened life span. This review article covers new and emerging information on the relationship between obesity and common and debilitating hepatic and gastrointestinal disorders, including nonalcoholic steatohepatitis, gastroesophageal reflux, gallstones, and colon and esophageal cancer. Because these complications can be prevented or treated by optimizing body weight, it is important that the practicing gastroenterologist include the evaluation and treatment of obesity as part of the general approach to the patient. Calculation of BMI is the most reliable and predictive tool for assessing obesity and effective weight reduction. Multiple, often unsatisfactory, medical strategies exist for weight reduction, each optimally requiring the ancillary services of a professional dietitian. Compelling evidence points to the surgical approach to the severely obese. The author concludes that understanding the role of obesity in these disorders should lead to new insights into the pathogenesis of common liver and gastrointestinal diseases and to new treatment strategies for the practicing gastroenterologist. 41 references (21 annotated).

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Leptin, Obesity, and Liver Disease Source: Gastroenterology. 115(4): 997-1001. October 1998. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 19106-3399. (800) 654-2452 or (407) 345-4000. Summary: This review article summarizes emerging information about relationships among obesity, liver disease, and leptin, a cytokine intimately involved in regulating weight and energy metabolism. Obesity is a multisystem disease that results from a failure of normal homeostatic mechanisms regulating food intake, fat storage, and energy utilization. Common gastrointestinal sequelae of obesity are gastroesophageal reflux disease, gallstones, hepatic steatosis, and nonalcoholic steatohepatitis. The regulation of body weight and fat stores is a complex process involving multiple neural, endocrine, and paracrine regulatory pathways; tight regulation of energy metabolism is one of the critical homeostatic functions of the hypothalamus. Leptin is a circulating cytokine discovered through its role in regulating body weight and energy metabolism. Accumulating evidence suggests that, like other cytokines, leptin has diverse and complex metabolic effects. In the liver, these effects may include a role in regulating fat deposition, fibrogenesis, and inflammation. Obesity in humans, like diet-induced obesity in rodents, is associated with elevated levels of circulating leptin and hypothalamic insensitivity to this protein. Because leptin is an important regulator of both insulin secretion and hepatic responsiveness to insulin action, altered leptin signaling in obese people may contribute to hepatic steatosis. Additional study on the nature and magnitude of leptin's activities in the liver and digestive tract is needed. 1 figure. 34 references.

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Obesity and Gastro-Oesophageal Reflux: Is There a Relationship? Source: European Journal of Gastroenterology and Hepatology. 8(7): 625-626. July 1996. Summary: In this article, the author considers the relationship between obesity and gastroesophageal reflux disease (GERD). The author reviews some of the information that might support or refute even the hypothetical possibility that obesity is a cause of excessive acid reflux. The author concludes that obesity per se should not be considered an etiologic factor in GERD. However, the relationship of GERD symptoms to weight gain and loss cannot go unnoticed. The author hypothesizes that common clinical observations linking GERD symptoms to acute changes in weight are related to changes in the quantity of fat ingested and the volume of the meals. 9 references.

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Obesity and Its Health Risks Source: Current Opinion in Gastroenterology. 12(2): 204-209. March 1996. Contact: Available from Rapid Science Publishers. 400 Market Street, Suite 700, Philadelphia, PA 19106. (215) 574-2266. Fax (215) 574-2292. Summary: This article reviews obesity and its health risks, focusing on the following gastrointestinal complications: increased risk of gallstones (especially during weight reduction); pancreatitis related to gallstones or hyperlipidemia with worse clinical outcome; nonalcoholic steatohepatitis; and increased risks of adenocarcinoma of the esophagus, colorectal adenoma, and cancer. The authors also discuss new studies that define abnormalities in the genetic regulation of appetite and energy metabolism. Treatment options continue to evolve, with improved pharmacologic approaches to appetite and strong support for gastric bypass surgery as the most effective treatment of severely obese patients. 39 references (20 annotated). (AA-M).

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Risk of Symptomatic Gallstones in Women with Severe Obesity Source: American Journal of Clinical Nutrition. 55(3): 652-658. March 1992. Summary: This article reports on a study that investigated the risk of symptomatic gallstones in women with severe obesity. Among 90,302 women aged 34-59 at baseline followed from 1980 to 1988, 2,122 cases of newly diagnosed symptomatic gallstones occurred. From 1980 to 1986, 488 cases of newly diagnosed unremoved gallstones were documented. The authors note a striking increase in gallstone disease risk with obesity. Recent weight loss was associated with a modestly increased risk after adjustment for body mass index (BMI) before weight loss. Current smoking was an independent risk factor for gallstones. 5 tables. 33 references. (AA-M).

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Obesity Surgery Regaining Favor Source: Medical World News. 32(5): 37. May 1991. Summary: This article discusses the recent interest and partial approval by the medical community of gastrointestinal sugery for severe obesity. After a definition of the situations in which such surgery may be appropriate, the author details the complications that might be encountered. Investigators reported sustained weight loss in 50 to 60 percent of patients after five to ten years of follow-up, results clearly surpassing the generally dismal track record of a multitude of special diets and behavior modification programs in treating severely obese patients. The author also considers costs of the surgery, insurance coverage, and the issue of primary care physicians not being interested in managing severely obese patients through nonsurgical strategies.

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Hormone Replacement Therapy, Insulin Sensitivity, and Abdominal Obesity in Postmenopausal Women Source: Diabetes Care. 25(1): 127-133. January 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to determine whether insulin sensitivity differs between postmenopausal women taking estradiol, women on estrogen plus progesterone hormone replacement therapy (HRT), and women not on HRT and whether differences are explained by the differences in total or abdominal adiposity and fat deposition in the muscle. The authors studied 28 obese, sedentary postmenopausal Caucasian women. Women taking oral estrogen (n = 6) were matched for age, weight, and body mass index (BMI) with women not on HRT (n = 6). Eight women taking oral estrogen plus progesterone were matched with eight different women not on HRT for age, weight, and BMI. Maximal aerobic capacity, percentage of fat, total body fat mass, and fat-free mass (FFM) were similar between groups. Visceral fat, subcutaneous abdominal fat, sagittal diameter, and mid thigh low density lean tissue (intramuscular fat) did not differ by hormone status. Basal carbohydrate and fat utilization was not different among groups. Fasting plasma glucose and insulin did not differ by hormone use. Glucose utilization (M) was measured; postmenopausal women taking oral estrogen had a 31 percent lower M than women not on HRT. M was 26 percent lower in women taking estrogen plus progesterone than women not on HRT. M per I, the amount of glucose metabolized per unit of plasma insulin (I), an index of insulin sensitivity, was 36 percent lower in women taking estrogen compared with matched women not on HRT and 28 percent lower in women taking estrogen plus progesterone compared with matched women not on HRT. The authors conclude that

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postmenopausal women taking oral estrogen or those taking a combination of estrogen and HRT are more insulin-resistant than women not on HRT, even when women are of comparable total and abdominal adiposity. 1 figure. 3 tables. 49 references. •

New Insights in Obesity Source: Diabetes Care. 25(4): 789-795. April 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: Next to tobacco use, low levels of physical activity and poor dietary habits are the major factors in the United States leading to increases in mortality. This article is the sixth in a series of reports on the American Diabetes Association (ADA) 61st Scientific Sessions held in Philadelphia, Pennsylvania in June 2001; this article covers topics related to the treatment of type 2 diabetes, primarily obesity. Topics include childhood obesity, clinical studies of obesity, obesity treatment, adipocyte secretory products, and obesity and the brain. In each area, the author summarizes research presented during the conference. 5 references.

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Surgery for Obesity Source: Diabetes Forecast. 55(4): 81-86. April 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article, one in a series of six articles on healthy weight loss, describes the use of surgery for obesity. Written for people with diabetes, the article first defines morbid obesity, which includes being at least 100 pounds over ideal body weight, having a body mass index (BMI) of 35 or more, and having 25 percent or more body fat. The authors then note that indications for surgery for morbid obesity include BMI greater than 40 or BMI greater than 35 in patients with medical problems that would improve with weight loss. The authors discuss the different procedures that can be used (restrictive, malabsorptive, or combination procedures), patient selection, common complications, weight loss potential, reversal of type 2 diabetes, and the long term results for patients who have undergone this type of surgery. The authors conclude with a brief section reviewing the decision making process that accompanies any consideration of surgery for obesity. 3 figures. 2 tables.

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Prevention of Overweight and Obesity in Children: Influences on the Food Environment Source: Diabetes Educator. 28(3): 415-423. May-June 2002. Contact: Available from American Association of Diabetes Educators. 100 West Monroe Street, 4th Floor, Chicago, IL 60603-1901. (312) 424-2426. Summary: There is an epidemic of pediatric overweight and obesity leading to type 2 diabetes in youth. This review article describes the multiple paths of influence on the food environment of youth and identifies diabetes education strategies that are focused on the early prevention of overweight and obesity. The authors conducted a review of relevant professional literature. Their results show that models of obesity prevention in youth need to address genetic factors that influence the development of food preferences in the young child, parenting influences on eating pattern development, and access to and availability of foods in the physical environment of the child. Early

Studies 11

intervention with parents of young children is required to prevent the development of eating patterns that lead to pediatric obesity and type 2 diabetes in youth. Diabetes educators need to be able to inform parents of the multiple paths of influence on the food environment of the child and to suggest strategies to encourage the development of positive food preferences and intake. 1 figure. 1 table. 52 references. •

Diabetes Contributes to Cholesterol Metabolism Regardless of Obesity Source: Diabetes Care. 25(9): 1511-1513. September 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to investigate cholesterol metabolism in obesity with and without diabetes. The authors performed cross-sectional metabolic studies in individuals with and without type 2 diabetes. The study included 16 obese subjects with diabetes (mean age 52 years, plus or minus 2 years) and 16 nondiabetic control subjects of similar age and weight. Serum total cholesterol did not differ between the groups, but LDL and HDL cholesterol were significantly lower and VLDL cholesterol and serum total and CLDL triglycerides were higher in the diabetes group compared to the control group. Cholesterol synthesis was higher and neutral sterol and bile acid excretion and cholesterol turnover tended to be higher in the diabetes group than in the control group. In addition, blood glucose was significantly positively related to fecal neutral sterol excretion in both groups. Cholesterol absorption efficiency was lower and cholesterol synthesis was higher in obese subjects with diabetes than in those without diabetes, suggesting that diabetes modulates cholesterol metabolism more than obesity alone. 1 figure. 3 tables. 32 references.

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Prospective Study of Obesity and Risk of Coronary Heart Disease Among Diabetic Women Source: Diabetes Care. 25(7): 1142-1148. July 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to examine the relationship of obesity, measured as BMI, and weight change to incidence of coronary heart disease (CHD) among women with diabetes. The authors followed 5,897 women with type 2 diabetes in the Nurses' Health Study for up to 20 years. Women were aged 40 to 74 years and had no history of cardiovascular disease or cancer at the beginning of the follow up period. During follow up, the authors document 418 incident cases of CHD (236 of nonfatal myocardial infarction and 182 of fatal CHD). After adjustment for age, smoking, and other coronary risk factors, current BMI (body mass index) was strongly associated with increased risk of CHD among women with diabetes. Increasing BMI values from age 18 years to 1976, before diagnosis of diabetes, were also positively associated with risk of CHD. Weight gain before the diagnosis of diabetes was related to increased risk of CHD. In contrast, weight change after diagnosis of diabetes was not associated with risk of CHD. The authors conclude that these findings provide strong evidence that obesity and weight gain before diagnosis of diabetes are associated with future risk of CHD among women with type 2 diabetes. 1 figure. 2 tables. 34 references.

12 Obesity

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Behavioral Science Research in Diabetes: Lifestyle Changes Related to Obesity, Eating Behavior, and Physical Activity Source: Diabetes Care. 24(1): 117-123. January 2001. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This review article, which grew out of a National Institute of Diabetes and Digestive and Kidney Diseases conference on behavioral science research in diabetes, focuses on lifestyle changes related to obesity, eating behavior, and physical activity. Lifestyle factors related to obesity, eating behavior, and physical activity play a major role in the prevention and treatment of type 2 diabetes. In recent years, there has been progress in the development of behavioral strategies to modify these lifestyle behaviors. Further research, however, is clearly needed because the rates of obesity in the United States are escalating and changing behavior for the long term has proven to be very difficult. The article identifies four key topics related to obesity and physical activity that should be given high priority in future research efforts. These topics are environmental factors related to obesity, eating, and physical activity; adoption and maintenance of healthful eating, physical activity, and weight; the etiology of eating and physical activity; and multiple behavior changes. The article discusses the significance of each of these four topics, reviews prior research in each area, identifies barriers to progress, and makes specific research recommendations. The article concludes that, given the strong association between lifestyle behaviors and the prevention and treatment of type 2 diabetes, it is important that greater research attention be directed at issues related to the development of healthful eating and physical activity habits and strategies for modifying unhealthy behaviors. 81 references. (AA-M).

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Obesity, Type 2 Diabetes and Physical Activity: What's the Connection? Source: Diabetes Self-Management. 18(3): 39-51. May-June 2001. Contact: Available from R.A. Rapaport Publishing, Inc. 150 West 22nd Street, New York, NY 10011. (800) 234-0923. Website: www.diabetes-self-mgmt.com. Summary: This article discusses the connection between obesity, type 2 diabetes, and physical activity. Obesity and type 2 diabetes are strongly related. Both obesity and type 2 diabetes are on the rise at a time when physical inactivity is common. People who are physically inactive tend to be heavier than people who are active, and they tend to develop diabetes more often. The risk of developing diabetes increases as body mass index (BMI) increases. Overweight people tend to get type 2 diabetes at a higher rate than lean people probably because their body is resistant to insulin. Overweight refers to an excess of body weight from muscle, body, fat, or body fluid compared with standards set by the National Institutes of Health and the National Heart, Lung, and Blood Institute, whereas obesity refers specifically to having an abnormally high proportion of body fat. Calculating BMI is the most up to date method of assessing whether a person is overweight or obese. BMI is determined by dividing body weight in kilograms by height in meters squared. Although BMI is simple to calculate, it may misclassify people who are muscular. The health risks of being overweight or obese include type 2 diabetes, cardiovascular and gastrointestinal diseases, various cancers, and other problems. Deep abdominal fat that surrounds the organs is the fat most likely to cause the health risks of obesity. Obesity is caused by an interaction of genetics, physiology, metabolism, and lifestyle. Although there is no cure for obesity, ways of treating and managing it include dietary changes, increased physical activity, behavior therapy, and medication. Research indicates that regular physical activity can improve

Studies 13

insulin sensitivity by 20 percent to 30 percent by building muscle and reducing body fat. The article suggests ways people can be more active during the day and lists additional resources on healthy weight loss. 1 table. •

Acarbose Improves Glycemic Control in Overweight Type 2 Diabetic Patients Insufficiently Treated with Metformin Source: Diabetes Care. 26(2): 269-273. February 2003. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to investigate the efficacy and safety of acarbose as add-on therapy in overweight patients with type 2 diabetes inadequately controlled by metformin. After a 4 week placebo run-in period, subjects were randomized to either acarbose or placebo. The primary efficacy variable was the change in HbA1c (glycosylated hemoglobin, a measure of blood glucose over time) from baseline to the end of the 24 week treatment period. The intention to treat analysis from baseline to week 24 (81 patients for HbA1c and 82 for fasting blood glucose) showed statistically significant differences between acarbose and placebo treatment in HbA1c and fasting blood glucose. In all, 18 patients (47 percent) in the acarbose group were classified as responders with a greater than 5 percent reduction in HbA1c (relative to baseline) at the end point compared to 6 (14 percent) in the placebo group. The safety profiles were similar for both treatment groups except for the higher incidence of gastrointestinal side effects during acarbose therapy. The authors conclude that the addition of acarbose to metformin monotherapy provides an efficacious and safe alternative for glycemic improvement in overweight type 2 patients inadequately controlled by metformin alone. 1 figure. 2 tables. 27 references.

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Effect of Orlistat in Overweight and Obese Patients with Type 2 Diabetes Treated with Metformin Source: Diabetes Care. 25(7): 1123-1128. July 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study of the effect of orlistat, a gastrointestinal lipase inhibitor, on body weight, glycemic control, and cardiovascular risk factors in metformin-treated patients with type 2 diabetes. The 1 year, multicenter, randomized, double blind, placebo controlled trial of 120 milligrams orlistat (n = 249) or placebo (n = 254) combined with a reduced calorie diet was conducted in overweight and obese patients with suboptimal control of type 2 diabetes. After 1 year of treatment, mean weight loss was greater in the orlistat than in the placebo group (minus 4.6 percent of baseline weight versus minus 1.7 percent of baseline weight, respectively). Orlistat treatment caused a greater improvement in glycemic control than placebo, as evidenced by a greater reduction in serum HbA1c (glycosylated hemoglobin, a measure of blood glucose over time), adjusted for changes in metformin and sulfonylurea therapy. Compared with the placebo group, patients treated with orlistat also had greater decreases in total cholesterol, LDL cholesterol, and systolic blood pressure. Although more subjects treated with orlistat experienced gastrointestinal side effects than placebo, more subjects in the placebo group withdrew prematurely from the study than in the orlistat group (44 percent versus 35 percent). The authors conclude that orlistat is a useful adjunctive treatment for producing weight loss and improving glycemic control,

14 Obesity

serum lipid levels, and blood pressure in obese patients with type 2 diabetes who are being treated with metformin. 1 figure. 2 tables. 31 references. •

Evaluation of the Insulin Resistance Syndrome in 5-to 10-Year-Old OverweightObese African-American Children Source: Diabetes Care. 24(8): 1359-1364. August 2001. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This review article describes a study that characterized the insulin sensitivity of overweight and obese 5 to 10 year old African American children screened for participation in a diabetes prevention study and identified the association of insulin sensitivity with obesity, hyperlipidemia, and hypertension. Measures of insulin resistance and insulin sensitivity were calculated from a 2 hour oral glucose tolerance test in 137 African American children. Measures of low density lipoprotein (LDL), high density lipoprotein (HDL), total cholesterol, triglycerides, blood pressure, and body composition were obtained for a subset of the children. The study found that, in response to a glucose challenge, girls and older and heavier children produced significantly more insulin. As body mass index increased, there was a statistically significant decrease in insulin sensitivity, particularly in girls. Insulin sensitivity was inversely correlated with increases in blood pressure, triglycerides, subcutaneous fat, the percentage of total body fat, and Tanner stage, but it was not correlated with LDL and HDL. Total cholesterol was inversely related to whole body insulin sensitivity. These associations suggest that a clustering of risk factors is present in these children. Results provide evidence that overweight African American children should be monitored for insulin resistance and cardiovascular risk factors early in life and that this monitoring should occur as part of their ongoing medical care. 2 figures. 1 table. 32 references. (AA-M).

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Type 2 Diabetes and Metabolic Syndrome in Filipina-American Women: A High-Risk Nonobese Population Source: Diabetes Care. 25(3): 494-499. March 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to compare the prevalence of type 2 diabetes and features of the metabolic syndrome among Filipina and Caucasian women in San Diego County, California. Data on several chronic diseases were collected between 1992 and 1999 from community dwelling Filipina (n = 294) and Caucasian (n = 379) women aged 50 to 69 years. Filipina and Caucasian women did not differ in mean age, body mass index (BMI), percentage of body fat, or waist to hip ratio, although Filipinas had larger waist circumferences and higher percentages of truncal fat. Compared with Caucasians, Filipinas were less likely to be obese, and less likely to smoke, consume alcohol, or take postmenopausal estrogen; Filipinas also had lower levels of HDL cholesterol. Compared with Caucasians, Filipinas had higher prevalence of type 2 diabetes by oral glucose tolerance test criteria and the metabolic syndrome. These differences persisted after adjusting for age, body size, fat distribution, percentage of body fat, smoking, alcohol consumption, exercise, and estrogen therapy. A total of 10 percent of Filipinas with diabetes were obese, compared with one-third of Caucasians with diabetes. The finding of a high prevalence of diabetes in an unstudied nonobese ethnic group reinforces the importance of expanding the study of diabetes to diverse

Studies 15

populations. The authors caution that the high prevalence of diabetes in populations who are not of Northern European ancestry may be missed when they are not obese by Western standards. 1 figure. 3 tables. 32 references. •

Effects of an Energy-Restrictive Diet with or Without Exercise on Abdominal Fat, Intermuscular Fat, and Metabolic Risk Factors in Obese Women Source: Diabetes Care. 25(3): 431-438. March 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to examine whether the combination of diet and aerobic exercise (DA) or diet and resistance exercise (DR) is associated with greater improvements in metabolic risk factors by comparison to diet only (DO) in obese women. A second objective considered whether reductions in metabolic risk factors are related to concurrent changes in abdominal or intermuscular fat distribution. The study included a total of 38 premenopausal obese women who were randomly assigned to one of three 16 week treatments: DO (n = 13), DR (n = 11), or DR (n = 14). Plasma glucose (sugar), insulin, and lipid (fats) levels were measured in a fasting state and after a 75 gram oral glucose challenge. Total, abdominal subcutaneous, visceral, and intermuscular fat were measured by magnetic resonance imaging (MRI). Significant reductions in body weight and in total, abdominal subcutaneous, visceral, and intermuscular fat were observed within each group. Fasting and OGTT insulin, total cholesterol, LDL cholesterol, and apoliprotein B also decreased within each group. The changes in the body fat and metabolic variables were not different across treatment. Visceral fat alone was related to the metabolic risk factors both before and after the treatment. Weight loss was associated with reductions in metabolic risk factors in obese women. The improvement in the metabolic profile was not enhanced by the addition of aerobic or resistance exercise. The findings reinforce the importance of diminished visceral fat in the treatment of insulin resistance. 2 tables. 66 references.

Federally Funded Research on Obesity The U.S. Government supports a variety of research studies relating to obesity. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to obesity. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore obesity. The following is typical of the type of information found when searching the CRISP database for obesity: 2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).

16 Obesity

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Project Title: ALTERED GLUCOSE AND LIPID METABOLISM IN OBESITY AND CVD Principal Investigator & Institution: Charron, Maureen J.; Professor of Biochemistry; Biochemistry; Yeshiva University 500 W 185Th St New York, NY 10033 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Obesity is associated with metabolic abnormalities that increase the risk of type 2 diabetes and cardiovascular disease (CVD). Obese patients with a substantial accumulation of visceral adipose tissue are characterized by higher insulinemic and glycemic responses during an oral glucose challenge and a deteriorated plasma lipoprotein-lipid profile compared to normal body weight or obese individuals with low level visceral adiposity. We will use a mouse model with a primary impairment in insulin-mediated glucose flux into adipocytes to define the molecular mechanisms underlying the pathogenesis of obesity associated CVD. Male mice carrying only one functional copy of the insulin-stimulatable GLUT4 transporter (GLUT4) first display reduced GLUT4 expression specifically in white adipose tissue (WAT). Reduced GLUT4 in WAT leads to visceral obesity, progressive impairment in insulin sensitivity, altered lipid metabolism, and eventually to type 2 diabetes with associated CVD. As such, male GLUT4 mice represent an excellent model to study pathophysiological changes associated with visceral obesity in humans. Interestingly, changes in adipose cell secretory proteins, such as the adipocyte-specific Acrp30, precede the onset of measurable changes in other metabolic parameters in GLUT4 mice. We and others have demonstrated profound effects of Acrp30 on insulin resistance in liver and muscle through specific effects on carbohydrate and lipid metabolism. The objectives of this proposal are I) to understand the molecular mechanisms underlying the metabolic changes that specifically affect male, but not female GLUT4 mice or GLUT4 mice that overexpress GLUT4 in muscle; lI) to test genetically whether correction of Acrp30 downregulation in male GLUT4 will prevent or delay the onset of insulin resistance, visceral obesity and/or CVD. Additionally, we will test whether complete lack of circulating Acrp30 in Acrp30-/-mice will provoke metabolic disturbance in female GLUT4 and exacerbate disease in male GLUT4 mice; III) to assess the effects of high fat diet-induced changes in disease progression in GLUT4 compared to C57BL/6J mice; and IV) to determine transcripitional and translational changes in WAT associated with visceral obesity and alterations following treatment with thiazolidinedione insulin sensitizers in hope of identifying novel therapeutic targets. Combined, this approach will provide a comprehensive systematic characterization of a mouse model of obesity associated CVD derived from early impairment of insulinmediated glucose flux into WAT, and directly address for the first time whether alterations in Acrp30 influence disease progression. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: AN OBESITY LOCUS ON MOUSE CHROMOSOME 7 Principal Investigator & Institution: West, David B.; Visiting Scientist; Division of Life Sciences; University of Calif-Lawrenc Berkeley Lab Lawrence Berkeley National Laboratory Berkeley, CA 94720 Timing: Fiscal Year 2001; Project Start 20-FEB-1998; Project End 31-JAN-2004 Summary: Obesity results in significant morbidity and mortality in the North American population and effective long-term treatments are not available. The etiology of obesity is complex with both genetic predisposition and environmental factors playing a role. One approach to further our understanding of the causal factors responsible for obesity

Studies 17

is to identify the genes and characterize the genetic mechanisms contributing to the disease. An understanding of the genetic mechanisms contributing to obesity may lead to new therapeutic developments and will help us to understand the relevant environmental factors causing obesity. Although finding genes contributing to a complex disease in human populations is possible, appropriate mouse models offer many advantages including the availability of inbred strains and rich genetic resources. It is likely that the same pathways involved in energy metabolism in mouse models will be involved in human disease. There is now significant evidence from a number of different studies in independent laboratories that a genetic locus on proximal mouse chromosome 7 is contributing to variation of body fat in the mouse. We have preliminary data using radiation deletion mutants in the mouse indicating that this gene is having a significant effect on body fat content, is paternally imprinted, and we have localized it to a narrow region just distal to the pink eyed dilution locus on mouse chromosome 7. In this application we propose to further narrow the critical region containing the gene using a panel of additional deletion mutants. We will physically map the critical region, develop a gene expression map for this area and evaluate the role of candidate genes which are located in this physical map. At the end of this project we will have identified a gene contributing to the regulation of body fat in the mouse. Follow-up studies in subsequent funding periods will be dir ected at characterizing the mechanism of action of this gene and determining if it is involved in human obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ANGIOTENSIN: A LINK BETWEEN OBESITY AND HYPERTENSION Principal Investigator & Institution: Cassis, Lisa A.; Professor; Pharmaceutical Sciences; University of Kentucky 109 Kinkead Hall Lexington, KY 40506 Timing: Fiscal Year 2003; Project Start 03-JUN-2003; Project End 31-MAY-2008 Summary: (provided by applicant): The proposed studies are in response to RFA-HL-02016 and will address the working hypothesis that a moderately high fat diet (MHF) stimulates the adipose renin-angiotensin system, contributing to obesity-related elevations in blood pressure. Preliminary data demonstrates that rats fed a MHF diet segregate into obesity prone (OP) versus obesity-resistant (OR) populations. In OP rats, blood pressure was increased coincident with activation of the systemic and adipose renin-angiotensin system. The first hypothesis is that a MHF diet activates the adipose renin-angiotensin system, resulting in an increase in circulating angiotensin peptides and blood pressure. Time-dependent regulation of adipose versus non-adipose components of the renin-angiotensin system will be examined in control, OR and OP rats and compared to the time course for elevations in blood pressure. The contribution of various circulating angiotensin peptides to blood pressure elevations in control, OR and OP rats will be determined. The second hypothesis is that adipocytes from OP rats exhibit a redistribution of free cholesterol from the plasma membrane to intracellular triglyceride pools, thereby increasing the activity of sterol regulatory binding protein-2 and stimulating angiotensinogen (Ao) mRNA expression. This would provide an adipocyte-specific mechanism for regulation of Ao gene expression in response to the MHF diet. The intracellular localization of free cholesterol in adipocytes prepared from control, OR and OP rats will be determined and compared to the level of Ao mRNA expression. The effect of depletion of intracellular free cholesterol pools on adipocyte Ao mRNA expression will be determined. The third hypothesis is that elevations in circulating angiotensin peptides increase blood pressure in OP rats by stimulating sympathetic drive. The responsiveness of the baroreceptor reflex and the blood pressure response to ganglionic blockade will be determined in control, OR and OP rats. A

18 Obesity

second approach will determine the effect of neonatal sympathectomy on blood pressure elevations in diet-induced obesity. In hypothesis 4 a novel animal model will be developed to determine the effect of targeted deficiency of Ao in adipose tissue on blood pressure regulation in diet-induced obesity. The goals of this research are to definitively determine the role of adipose-derived angiotensins and the systemic reninangiotensin system in blood pressure elevations in diet-induced obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BEHAVIORAL PHYSIOLOGY OF BODY WEIGHT REGULATION Principal Investigator & Institution: Lattemann, Dianne F.; Research Professor; Psychology; University of Washington Seattle, WA 98195 Timing: Fiscal Year 2001; Project Start 01-SEP-1988; Project End 31-MAR-2004 Summary: Diet composition plays a significant role in the development of human obesity. A genetic propensity towards dietary obesity has been identified in rodents, and obese individuals demonstrate differences in food preferences from lean individuals. In rodent models, dietary-induced obesity is associated with decreased sensitivity to exogenous administration of the candidate adiposity signal insulin. This suggests that some difference-metabolic, neurochemical, or both-as a consequence of eating a highly palatable, high energy diet is present, resulting in a change in the physiological regulation of body adiposity. Activation of the CNS mesolimbic dopamine (DA) neurons is implicated in the reinforcing or rewarding aspects of several classes of stimuli, including food. We have obtained preliminary evidence that insulin can downregulate the activity of these DA neurons, both at the level of the synapse and at the level of behavior. In this proposal, we pursue the hypothesis that activity of these neurons is altered in association with dietary obesity, and that there is a loss of insulininduced downregulation of DA neuronal activity. To test this hypothesis, we will evaluate performance in two behavioral tasks in which DA has been implicated: lick rates of sweet and fat solutions, and the conditioned place preference (CPP) paradigm; release of DA from the mesolimbic DA neurons by in vivo microdialysis; and the cellular mechanisms underlying altered DA release, using our established methodologies. All studies will utilize normal weight and dietary obese rats (both outbred rats, and the inbred dietary-induced obese (DIO)/dietary obese-resistant (DR) rats, which are genotypically distinct in their propensity to develop dietary obesity), infused with intraventricular (IVT) vehicle or insulin. Together, these studies will evaluate the ability of a candidate adiposity signal to interact with brain pathways associated with reward; and the influence of palatable high energy diets on the function and regulation of the mesolimbic DA neurons. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: OBESITY

BETA-ADRENOCEPTOR

GENETIC

POLYMORPHISMS

AND

Principal Investigator & Institution: Johnson, Julie A.; Professor of Pharmacy Practice & Medicin; Pharmacy Practice; University of Florida Gainesville, FL 32611 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2003 Summary: (Provided by Applicant) Obesity is increasing in prevalence in Western societies, and it represents a major health concern because it increases the risk of cardiovascular disease, metabolic disorders and some forms of cancer. It is estimated that 40% to 70% of the variability in body weight is genetically mediated. A number of genes have been studied as candidate genes for obesity. In the proposed analysis of the

Studies 19

Women's Ischemic Syndrome Evaluation Study (WISE) database, we will test the hypothesis that the beta- adrenergic receptor (betaAR) genes and certain G protein genes are associated obesity. Specifically, we will be studying the association between obesity and genes of the beta1AR (ADRB1), the beta2AR (ADRB2), the beta3AR (ADRB3), the Gs protein alpha subunit (GNAS1) (all three betaARs couple with Gs) and the G protein beta3 subunit (GNB3) (a component of Gi, to which beta3ARs couple). We will also examine the multivariate contributions to obesity of genotype, demographic (e.g., age, region) and environmental (e.g., exercise, childbirth history) factors and their possible interactions. Data for the proposed analysis will derive from the database of the WISE study, a four center NHLBI-funded study of ischemic heart disease in women. Genotypes will be assessed by a high through-put genetic bit analysis method. Analyses on approximately 590 white women and 130 black women will be performed separately, and will include multiple regression analysis to test for impact of the various genes, and various demographic and behavioral factors on body mass index. The proposed analyses are important and novel because they will: a) provide the first information on the relationship between ADRB1 and GNAS1 and obesity, b) provide the first information on the ADRB2 and obesity when assessed by haplotype, c) provide information on potential additive or synergistic effects of the genes under study with respect to obesity, d) for some of the genes, provide the first data on the gene-obesity associations in blacks, e) assess the gene-obesity association with respect to certain environmental/behavioral factors such as physical activity and previous childbirth, and f) utilize a state-of-the-art high throughput method for genetic analysis. The information generated from this study should help identify candidate genes that are worthy of further, extensive investigation. Knowledge about genes that are associated with obesity is important as this information may aid in the drug discovery process for anti-obesity drugs. Additionally, genotyping individuals early in age may help to identify those at increased risk of obesity prior to them becoming obese so that they may take appropriate preventive measures. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BODY FAT AND HORMONES IN ADOLESCENT OBESITY TREATMENT Principal Investigator & Institution: Saelens, Brian; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, OH 45229 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: (provided by applicant) This K23 application will establish the candidate's independent research career in patient-oriented research in adolescent obesity treatment. The candidate, Brian E. Saelens, Ph.D., is a recently appointed Assistant Professor of Pediatrics at Children's Hospital Medical Center (CHMC) in Cincinnati. This K23 proposal combines mentoring in biological and behavioral factors that influence adolescent obesity. The proposed career development plan will provide the candidate necessary training in body fat distribution measurement, weight-affecting hormones, weight-related behaviors, and pubertal maturation. This training will lead to the development of more efficacious intervention for adolescent weight control, specifically to target the reduction of intra-abdominal fat mass accumulation, as this type of fat accretion is most highly related to the negative health consequences of obesity. The candidate's career plan capitalizes on the biologic obesity-related resources and expertise at CHMC and the University of Cincinnati to augment prior and planned training in the behavioral aspects of pediatric obesity. The proposed research plan consists of a targeted prospective (Study 1) and pilot intervention study (Study 2). Study

20 Obesity

1 aims include examining the time course of total body fat and intra-abdominal fat accretion through early puberty among already overweight youth. Study 1 will identify specific periods of relatively high and low intra-abdominal fat accretion. This prospective study also examines potential hormonal and behavioral precursors of changing body fat distribution. Based on Study 1 findings, Study 2 will investigate the differential impact of providing similar behavioral weight control intervention to overweight youth at different time periods of intra-abdominal fat mass accumulation. Intervention efficacy will be examined among overweight youth either 1) timingmatched by intervention during high intra-abdominal fat accumulation or 2) timingmismatched by intervention during low intra-abdominal fat accumulation. Study 2 will also examine baseline hormonal, body composition, and behavioral correlates of weight control treatment success. These studies will provide exceptional training in the biological aspects of obesity, while also having the potential to begin identifying the timing of behavioral intervention that will optimize health benefit of behavioral weight control programs for the increasing population of overweight youth. The combined skill set and experience garnered from the candidate's career development and research plan will provide the necessary early career support for the candidate to establish a successful independent research career in the important area of pediatric obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: BOSTON OBESITY NUTRITION RESEARCH CENTER Principal Investigator & Institution: Corkey, Barbara E.; Professor; Boston Medical Center Gambro Bldg, 2Nd Fl, 660 Harrison Ave, Ste a Boston, MA 02118 Timing: Fiscal Year 2001; Project Start 30-SEP-1992; Project End 31-MAR-2003 Summary: This application represents the competing renewal of the Boston Obesity/Nutrition Research Center. The Boston Obesity/Nutrition Research Center represents a collaboration of four major institutions representing three major universities in Boston, all located within a 1.5 mile radius of each other. The Boston Obesity Center includes the New England Medical Center, the Beth Israel Deaconess Medical Center, the Harvard School of Public Health, and Boston Medical Center. The institutions represent respectively Tufts University, Harvard University, and Boston University. The Boston Obesity/Nutrition Research Center consists of five Core Laboratories. These includes an Epidemiology Core, directed by Dr. Graham Colditz at the Harvard School of Public Health, a Clinical/Metabolic Core, directed by Dr. George Blackburn at the Beth Israel Deaconess Medical Center, a Body Composition/Energy Expenditure Core, directed b Dr. William Dietz at the New England Medical Center, an Adipocyte Core, initially designed as a Cellular Biochemistry Signal Transduction Core, at Boston Medical Center, now directed by Dr. James Kirkland, and a Transgenic Core at the Beth Israel Deaconess Medical Center directed by Dr. Jeffrey Flier. The Obesity Center offers multiple opportunities for education and training in obesity research to fellows on training grants held by Obesity Center investigators in each of the collaborating universities. The investigators represented in this application hold 65 funded R0-1 grants, approximately 45 which are directed at the study of obesity, energy metabolism or other nutritional disease. In the past four years, Boston Obesity Center investigators have published 135 papers with Center support. Twenty percent of the Obesity Center budget provide support for pilot and feasibility studies. Pilot and feasibility award recipients have published almost 50 papers and received a total of 7 grants from NIH or other funding agencies based on the data obtained from their Center funded investigations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CENTRAL OOBESITY SYNDROME IN A SUBSET OF TYPE 1 DIABETES Principal Investigator & Institution: Brunzell, John D.; Prpfessor of Medicine; University of Washington Seattle, WA 98195 Timing: Fiscal Year 2002; Project Start 01-SEP-1976; Project End 31-MAR-2007 Summary: (provided by applicant): Project 2 started as an ancillary study of lipoprotein metabolism to the NIH sponsored clinical trial of intensive diabetes therapy in type 1 diabetics to prevent microvascular disease called the Diabetes Control and Complication Trial (DCCT). The Epidemiology of Diabetes Intervention and Complications (EDIC) is a ten year non-interventional follow-up of DCCT to evaluate the natural history of macrovascular and nephropathy complications in type 1 diabetes. In DCCT, we found that atherogenic small dense LDL were increased with hyperglycemia, microalbuminuria and were increased in that subset of subjects who gained excess weight as a complication of intensive diabetes therapy during DCCT. Those who gained weight with intensive diabetes therapy were centrally obese, insulin resistant, hypertensive, dyslipidemic and had type 2 diabetic parents. This suggests they had inherited the metabolic-central obesity syndrome in addition to type 1 diabetes. This new proposal will use the phenotypes of 1) excessive weight gain with intensive diabetes therapy and 2) the presence of small dense LDL particles as markers of the central obesity-insulin resistance metabolic syndrome that occurred in this subset of type 1 subjects during intensive diabetes therapy. These markers of the central obesity syndrome will be used to predict the occurrence of cardiovascular events and the development or progression of microalbuminuria during the course of EDIC. Candidate genes for development of the central obesity syndrome and for the interaction of excess weight gain with the development of hypertension will be examined. Intraabdominal fat by CT scan and postheparin plasma hepatic lipase will be measured to further develop the phenotype associated with the excessive weight gain with intensive therapy and with development of nephropathy in the Seattle cohort and three Minnesota cohorts of EDIC. The development of the central obesity syndrome with intensive diabetes therapy in type 1 diabetic patients may predispose them to increased risk of cardiovascular disease and nephropathy. If so, modifications of clinical therapy will need to be made in this subset of individuals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CLINICAL AND EXPERIMENTAL STUDY OF HUMAN OBESITY Principal Investigator & Institution: Stunkard, Albert J.; Professor Emeritus of Psychiatry; Psychiatry; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2001; Project Start 01-APR-1997; Project End 31-MAR-2003 Summary: (Applicant's Abstract): We propose to continue the most complete, prospective, longitudinal study of growth and development yet undertaken of children at high risk of obesity. The study of 78 children, now 32 to 53 months of age, selected on the basis of maternal obesity or leanness, has already achieved its initial goal: it has disconfirmed, the results of an influential study and the associated, widely held belief that a low total energy expenditure (TEE) and maternal obesity predict body size and composition at 1 year of age. Instead, it has found, unexpectedly, that the two independent measures of energy intake at 3 months of age predict body size and composition at 1 year of age. We now propose to search further for the risk factors for obesity in this large, carefully studied cohort as it enters the early childhood years. After

22 Obesity

24 months in which there was minimal evidence of genetic influence, our high risk strategy has begun to bear fruit: at 30 months 14% of our sample now exceeds the 95th percentile of weight for height. As at 3 and 24 months, and now at 48 months, we will assess, at 6 and at 8 years, the influence of maternal and paternal body mass index (BMI = kg/m2), subject's body weight, TEE and resting metabolic rate. In addition, to identify behaviors that might be modified in programs of obesity prevention, we will continue to measure food intake (both 3-day records and test meals), taste (especially fat) preferences and psychosocial factors that have been implicated in the development of obesity. These efforts will be greatly enhanced by the ability (for the first time) to assess the environmental factors in a cohort that has been defined genetically as being at high risk for obesity and where metabolic status is known. Our ultimate objective is to identify behaviors that contribute to adiposity and that might be modified in programs of prevention and treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CNS ACTION OF APPETITE SUPPRESSANT AMINOSTEROL Principal Investigator & Institution: Ahima, Rexford S.; Assistant Professor; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2002; Project Start 15-JUL-2002; Project End 31-MAY-2005 Summary: (provided by applicant): The prevalence of obesity in the United States has reached epidemic proportions and poses enormous public health challenges, as obesity is a major risk factor for type 2 diabetes, hypertension, cardiovascular disease and cancer, as well as an independent risk factor for mortality. Although diet and exercise are essential to weight management, it has become increasingly clear that a large proportion of patients would require drug treatment to decrease and maintain body weight. The goal of this grant is to understand the action of a novel cholesterol derivative with potent anti-obesity and anti-diabetic properties. MSI- 1436 is an aminosterol which we have found to cause reversible suppression of food intake, increased energy expenditure and normalization of glucose levels when administered by peripheral and more potently intracerebroventricular injection to rodents. Unlike other anorectics, a single injection of MSI-1436 produces a prolonged effect lasting several days. MSI- 1436 is effective in ob/ob and db/db mice, fa/fa rats, and dietinduced obese mice, suggesting that leptin signaling is not critical to its action. By contrast, MSI-1436 effect is blunted in agouti (Ay/a) mice, suggesting that its central action may involve the melanocortin pathway. Although acute MSI1436 administration strongly induces Fos-immunoreactivity in the paraventricular nucleus and to a lesser extent in the arcuate, ventromedial and pre-mammillary nuclei, the neuronal circuitry mediating the anti-obesity vs anti-diabetic effects of MSI-1436 is not known. We hypothesize that MSI-1436 enters the braii via a specific transport mechanism and engages hypothalamic neuronal targets to regulate energy balance and glucose homeostasis. Specific Aim 1 involves the injection of MSI-1436 into specific hypothalamic nuclei to determine which sites mediate the effects on feeding, body weight and glucose levels. Specific Aim 2 will analyze the distribution of MSI-1436 binding sites and determine the chemical phenotypes 01 MSI-1436 responsive neurons. Specific Aim 3 will determine the contribution of the central melanocortin system by analyzing MSI-1436 response in melanocortin receptor (MCR)-3 and 4 knockout mice. Finally, Specific Aim 4 will utilize GeneChip microarray to determine whether MSI-1436 regulates novel hypothalamic genes. Putative MS-1436 targets will be validated in multiple mouse models. Together these studies will provide insights into the mechanisms underlying MSI-1436 action in the brain. Understanding the basis for the

Studies 23

novel effects of MSI-1436 on feeding behavior, body weight and glucose will greatly enhance the field of obesity and metabolism. New pathways affected by MSI-1436 may elucidate novel cellular targets for the treatment of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: CORE--EPIDEMIOLOGY Principal Investigator & Institution: Colditz, Graham A.; Professor of Medicine and Epidemiology; Boston Medical Center Gambro Bldg, 2Nd Fl, 660 Harrison Ave, Ste a Boston, MA 02118 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Objectives of the Epidemiology Core 1. To provide statistical and epidemiologic support to ongoing or planned obesity studies in the Boston area, which will, in turn, expand the nucleus of expertise and familiarity with design and analysis issues unique to obesity research. 2. To continue to support the development and maintenance of data sets amenable to secondary epidemiologic analyses regarding obesity and nutrition issues, as well as to develop and refine measures of obesity. 3. To interface epidemiology, basic sciences, and clinical medicine so that hypotheses generated by these areas can be tested in ongoing epidemiologic studies. 4. To train young investigators in epidemiologic and statistical techniques used for the study of obesity in populations. 5. To disseminate methods/approaches to data analysis to a broad audience, as Core members gain experience in applying and refining quantitative methods. Obesity research presents unique analytic challenges, solutions to which are of great interest. 6. To help identify groups at high and low risk of the development of obesity, and population characteristics for obesity clinical trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: CULTURAL ASPECTS OF LATINO EARLY CHILDHOOD OBESITY Principal Investigator & Institution: Clark, Lauren; Associate Professor; None; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2005 Summary: (provided by applicant): Childhood obesity in the U.S. has reached a 20-25% prevalence. Latinos have higher rates of obesity across the lifespan, contributing to an ethnic disparity in rates of obesity-related morbidity and mortality. Obesity in childhood tracks into adulthood, making early childhood a key developmental time period for prevention. This study will use qualitative focus group methodology and freelisting to: (1) describe the characteristics Latino mothers use to identify and categorize infants as "obese" and "overweight;" (2) assess the kinds of behaviors, foods, feeding patterns, and other risks believed by Latino family members to contribute to early childhood obesity; (3) ascertain what Latino mothers and father would consider appropriate interventions for young children considered "obese" or "overweight" by health care professionals; (4) identify whom Latinos would consider appropriate persons to intervene in nutrition and activity issues for children; and (5) explore various program characteristics preferred by Latino families for a future obesity prevention program; and (6) identify differences among less- and more-acculturated Latino families regarding early childhood obesity issues, food and feeding practices, and intervention preferences. The study is a qualitatively-driven exploration of cultural dimensions of childhood obesity, cultural knowledge about what constitutes "obesity" and "overweight," and the kinds of feeding and nutrition knowledge parents share about

24 Obesity

young children. Analysis of focus group data will identify cultural models of childhood obesity, cultural knowledge about feeding practices and other factors that contribute to childhood obesity, beliefs about healthful feeding practices, and avenues for intervention congruent with Latino families' preferences. Based on this pilot work, a culturally competent primary prevention program will be designed to prevent Latino early childhood obesity and overweight, and promote healthful nutrition and feeding. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DIET AND PHYSICAL ACTIVITY INTERACTIONS IN OBESITY Principal Investigator & Institution: Hill, James O.; Professor; Pediatrics; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 01-MAY-1990; Project End 31-JUL-2003 Summary: The current epidemic of obesity has occurred despite the existence of a body weight regulatory system which, for most of mankind's history, has matched energy intake with energy expenditure sufficiently to avoid obesity. This suggests that the primary cause of the current obesity epidemic is not genetic, but may be due to an environment in which the energy balance regulatory system cannot function with sufficient precision to keep the population lean. In this application, we propose research aimed at understanding how factors in the environment, namely high fat/energy dense diets and physical inactivity, can promote obesity by affecting the precision of regulation of energy and fat balance. It is our intent to identify dietary and physical activity patterns that are associated with increased precision of energy balance regulation and which can prevent development of obesity. Laboratory data suggest that high fat diets promote obesity by increasing the probability of overconsumption of total energy. Our first aim is to systematically examine the relationship between dietary fat and energy intake across a range of diet compositions in sedentary subjects. While this has been done for diets with extreme variation in dietary fat (i.e., less than or equal to 20 percent vs greater than or equal to 40-60 percent) it has not been done for dietary fat content within the range of usual consumption of U.S. adults (i.e. 20-40 percent fat diets). We hypothesize that this relationship will not be linear and that there will be a threshold level or a range of dietary fat associated with a low probability of increased energy intake and positive energy balance. This information will be useful in developing dietary guidelines for obesity prevention. Our second aim is to determine how level of physical activity interacts with dietary fat content to affect the likelihood of developing positive energy balance. We hypothesize that the optimum level of dietary fat to minimize the probability of positive energy balance will depend on level of physical activity and the optimum level of physical activity to minimize the likelihood of positive energy balance will vary with dietary fat content. This work will be among the first to study the interaction of dietary and physical activity patterns in promotion and prevention of obesity. The results will help identify the changes required in current dietary and physical activity patterns if we are going to be successful in preventing the development of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: DIETARY OBESITY Principal Investigator & Institution: Bray, George A.; Director; None; Lsu Pennington Biomedical Research Ctr 6400 Perkins Rd Baton Rouge, LA 70808 Timing: Fiscal Year 2001; Project Start 01-AUG-1982; Project End 31-JUL-2003

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Summary: The objective of this research grant is to characterize the mechanisms for the differences between two strains of rats which differ in their susceptibility to obesity when eating a high fat diet. The Osborne- Mendel rat (OM) rapidly becomes obese when maintained on a high fat diet while the S5B/PI (S5B) rat remains lean when eating the same diet. We have recently demonstrated that the OM rat increases its intake of a high fat diet after administration of the 5-HT1A agonist, 8-hydroxy-2- (di-nproplyamino)tetralin, which inhibits serotonin synthesis and release. S5B rats do not increase food intake after this treatment. In addition, fenfluramine treatment prevents high fat diet-induced obesity in the OM rat. This proposal focuses on the mechanisms underlying two aspects of this dietary-induced obesity. Our first aim will be to elucidate the central nervous system neurotransmitter signals that mediate fat preference by examining the serotonin system in these two rat strains. We will test the hypothesis that the serotonergic system is more active in the S5B rat than the OM rat. The first three experiments in this aim will investigate the effects on food intake in OM and S5B rats by altering serotonin levels in the paraventricular nucleus. The next five experiments will determine the contribution of the dorsal raphe nucleus to the serotonin systems in OM and S5B rats. The last two experiments will examine the hypothesis that opioids in the hindbrain may modulate the serotonergic signals from the paraventricular nucleus. We will utilize the novel technique of central antisense oligonucleotide application in two critical experiments to test these systems. The second aim will examine the difference in peripheral signaling systems that responds to nutrient infusion in these two rat strains. We will test the hypothesis that fatty acids in the GI tract activate vagal mechanisms more effectively int the S5B rat. We have already demonstrated that S5B rats are much more sensitive to the satiating effects of intraintestinal fat infusions. There are seven experiments proposed which will examine the involvement of the vagus nerve, cholecystokinin, glutamate, c-fos activated neurons and serotonin in the differential responsiveness to nutrient infusion in OM and S5B rats. Our laboratory has made significant advances toward understanding dietary-induced obesity. We now propose these well founded, important and exciting studies which will provide critical new insights into anatomical, physiological and molecular mechanisms by which high levels of dietary fat induce obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DRUG TARGET DISCOVERY IN OBESITY NEURONS Principal Investigator & Institution: Rao, Donald D.; Nt Two 5000 Gullen Mall, Rm 407 Detroit, MI 48202 Timing: Fiscal Year 2002; Project Start 15-JUN-2002; Project End 31-MAR-2004 Summary: Key advances in obesity research over the last decade have established the prominence of the central nervous system (CNS) in body weight regulation. The goal of the proposed research is to develop a target discovery approach that will mine neurons in the CNS known to express important obesity genes. This goal will be accomplished using recently-developed state-of-the-art techniques to genetically tag and then isolate, from the intact brain, specific neuronal subtypes already known to be important for body weight regulation. We will then catalog the transcriptome of these "obesity neurons" and determine gene expression profiles of these neurons under conditions designed to reveal gene function. The identification of genes selectively expressed in specific neuronal subtypes will provide the molecular raw material for the next generation of anti-obesity drug targets. The proposed approach for CNS target discovery combines three core technologies: (1) genetic tagging of neuronal subpopulations with modified bacterial artificial chromosome (BAC) transgenes, (2)

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harvesting of tagged "obesity neurons" and (3) RNA expression profiling analysis of the captured "obesity neurons" under conditions designed to reveal gene function. The ultimate commercial aim is to sell or license validated CNS anti-obesity drug targets, target-specific high through-put assays, and chemical leads for these targets. PROPOSED COMMERCIAL APPLICATION: The optimized drug discovery platform derived from this research will serve as a standardized method for identifying various CNS drug targets, not only those involved in obesity. The commercial value of the platform will be realized through the quality of targets and by the potential chemical leads developed against these targets. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: EARLY SOCIOECONOMIC & PSYCHOSOCIAL RISK FOR OBESITY Principal Investigator & Institution: Gahagan, Sheila; Pediatrics & Communicable Dis; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, MI 481091274 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-MAY-2006 Summary: (Adapted from applicant's description): The goal of this K23 proposal is to provide research training related to childhood obesity. The applicant is an academic pediatrician who has worked in settings serving children in poverty since 1983. She has worked with African American, American Indian and Hispanic American populations. The epidemic of obesity is more severe in underrepresented minority groups in the US and increasingly in some developing countries. Children from disadvantaged backgrounds are put at increased risk for obesity by a variety of factors. This proposal relies on five ongoing longitudinal US and international samples with rich growth, demographic and psychological data on the subjects and their families. The samples include: 260 preschool children from southeast Michigan; two cohorts (100 each) from an American Indian population showing recent rapid increases in birthweight and obesity; 150 Costa Rican children studied from 1 year, who are now age 19; 1000 Chileans who are currently 5 years old and studied since 4 months; and 3,400 Finnish men and women with high rates of cardiovascular disease. The research training and research plans proposed in this project are closely linked to activities involving these 5 longitudinal projects. These ongoing research projects will be the framework for continued data collection, new data analysis, and comparative study. Dr. Betsy Lozoff, Director of the Center for Human Growth and Development and Professor of Pediatrics is the project mentor. An outstanding committee composed of leaders in child nutrition, behavior, development, obesity, biostatistics and health disparities will direct the training and advise the research. Dr. Gahagan proposes to explore the behavioral and psychological factors that cause additive risk for obesity in young children. While not ignoring the importance of genetics, nutrition, and physical activity, this work will promote understanding the role of poverty in childhood obesity. The hypothesis that children are put at risk for obesity and its consequent health problems by biologic and social factors including poverty, parental mental health, and parental-decision making about childhood nutrition and activity will be examined in depth in five different populations at risk. If obesity is to be prevented, it is critical to understand the precursors on multiple levels and target those factors that are modifiable for intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ENERGY BALANCE IN THE OBESE CCK A RECEPTOR DEFICIENT RAT Principal Investigator & Institution: Moran, Timothy H.; Professor; Psychiatry and Behavioral Scis; Johns Hopkins University 3400 N Charles St Baltimore, MD 21218 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2006 Summary: Obesity has reached epidemic proportions in the United States, and both genetic and environmental contributions to the development and maintenance of obesity have been identified in human studies and animal models. Recent rodent models of genetic obesity have hypothalamic signaling pathways related to the overall control of metabolism and energy balance. Unlike these strains, the obese Otsuka LongEvans Tokushima Fatty (OLETF) rat is a unique genetic model of obesity with an identified deficit in a peripheral gut-brain peptide signaling pathway critical to the within meal control of food intake. OLETF rats spontaneously lack the promoter region for the gene that encodes for the cholecystokinin (CCK) A receptor, the subtype that mediates the satiety actions of this meal-elicited peptide. OLETF rats are obese and hyperphagic, and we have shown that their hyperphagia is characterized by increased meal size, consistent with the lack of a meal related signal important in the negative feedback control of food intake. In this proposal, we hypothesize that OLETF hyperphagia and obesity: 1) depends upon their genetically determined inability to detect meal-related CCK negative feedback signals critical in the control of meal size, and 2) is not dependent on altered central nervous system processing of other metabolic and hypothalamic signals important in the overall control of energy balance. Experiments in this proposal are designed to address multiple aspects of this hypothesis. Specifically, we will: 1) identify the roles of increased meal size and hyperphagia in the development of obesity in OLETF rats, 2) characterize metabolic profiles and patterns of hypothalamic gene expression in ad lib and pair fed OLETF rats, 3) identify potential interactions between exercise and disordered patterns of food intake in OLETF rats, 4) characterize OLETF feeding and metabolic responses to high fat and macronutrient selection diets and 5) compare the OLETF rat to a newly available CCK-A knockout mouse that does not develop obesity. Together, results from these studies will: 1) identify and characterize the ways in which a unique genetic deficit in a peripheral satiety signaling pathway interacts with a range of environmental factors (exercise, dietary restriction, diet composition) to modulate the development and maintenance of obesity, and 2) identify how such a satiety deficit interacts with central hypothalamic pathways mediating the control of energy balance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ENERGY EXPENDITURE AND THE INCIDENCE OF OBESITY Principal Investigator & Institution: Bandini, Linda G.; New England Medical Center Hospitals 750 Washington St Boston, MA 021111533 Timing: Fiscal Year 2001; Project Start 01-MAY-1989; Project End 31-OCT-2003 Summary: Adolescence in girls is a critical period for the development of obesity. Reduced energy expenditure represents a strong risk factor. We are continuing to follow annually a cohort (originally 197 pre- menarcheal girls) who were enrolled (1990-1993) in a longitudinal study of energy expenditure and its relationship to the development of obesity. One hundred and fifty-nine girls (80.7%) remain active in the study. Of these 159 subjects, 59 have completed the study and the other 100 continue to seen annually. A baseline measures of body composition, resting metabolic rate, total daily energy expenditure, and VO2 max were completed. Measures of diet and activity were

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obtained from a 7-day food record, a 7-day activity record, and activity questionnaires. Since enrollment, girls are seen annually until 4 years after menarche when they exit the study. At their annual visit, measures of diet, activity, growth and body composition by anthropometric measures are obtained. Blood is drawn for the measurement of sex hormones and insulin. At the end of this proposed grant period, all but five girls will be 4 years post menarcheal and will exit the study. At that time we will have determined whether reductions in energy expenditure at baseline (total daily energy expenditures, resting energy expenditure, percent non- resting energy expenditure or VO2 max) are associated with increases in body fat as girls mature. We will also determine whether differences in ethnicity, or parental obesity contribute to the changes in body fat in a subcohort of girls, visceral fat was previously measured at menarche by MRI. At the time of the MRI, measures of body composition and anthropometry were repeated, blood was drawn for the measurement of sex hormones, and questionnaires were completed rating to diet, activity and behaviors such as smoking and alcohol abuse. We will repeat these measures in these girls at their exit visit. This study will allow us to determine what factors contribute to visceral fat deposition in girls during puberty. These studies will clarify the role of energy expenditure in the development of obesity and identify factors that contribute to the deposition of visceral fat. Identification of factors which contribute to the development of obesity and central fat distribution will aid in the development of programs designed to reduce the incidence and morbidity associated with adolescent obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ENHANCED INTERNET BEHAVIOR THERAPY FOR TREATING OBESITY Principal Investigator & Institution: Tate, Deborah F.; Assistant Professor; Miriam Hospital Providence, RI 02906 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Given the increasing prevalence of obesity and fact that many adults have a strong preference to lose weight without attending weekly treatment meetings, there is need to develop effective alternatives to behavioral lifestyle interventions requiring less face-to-face contact. The Internet offers exciting opportunities to deliver behavior change interventions that minimize face-to-face interaction. We have recently developed and tested an Internet behavioral weight loss program compared with an Internet educational program in a randomized trial and found the behavioral program produced significantly better weight losses (4.1 kg) at 6 months. Our study clearly establishes the potential for using the Internet to deliver alternative treatment programs; however, treatment efficacy research is needed to further develop an Internet approach that will promote longer-term weight loss. The objectives of the proposed study are I) to enhance our Internet program to develop a state of the art Internet Cognitive-Behavior Therapy (I-CBT) program for obesity treatment; and 2) to conduct a randomized trial comparing the enhanced program with a Minimal CBT program also delivered via the Internet. We propose to recruit 100 overweight adults and randomly assign them to Enhanced Internet CBT or Minimal Internet CBT programs. The Minimal I-CBT condition will be given links to weight loss websites, weekly structured cognitive-behavioral lessons for weight loss, weekly prompting, and an on-line bulletin board. The Enhanced I-CBT program will have these same features plus weekly on-line group therapy sessions, computer-aided selfmonitoring diaries, and weekly individual e-mail feedback from a therapist. The primary outcome is weight loss from 0-12 months. Secondary outcomes will examine

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patterns of weight change and changes in waist, diet, physical activity, and social support. The proposed research has significant implications for expanding the audience served by obesity treatment program by using the Internet. This study utilizes an innovative approach and extends our programmatic research on the development of a cognitive-behavioral Internet treatment for obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: ENVIRONMENTAL TEMPERATURE, SNS DEVELOPMENT AND OBESITY Principal Investigator & Institution: Young, James B.; Medicine; Northwestern University Office of Sponsored Programs Chicago, IL 60611 Timing: Fiscal Year 2001; Project Start 01-JUL-1977; Project End 31-MAR-2006 Summary: (Scanned from the Applicant's Description): The long-term goal of this project is to determine how environmental exposures during development contribute to the acquisition of obese or hypertensive traits in the adult. If successful, it may be possible to devise strategies for early intervention which might prevent or at least forestall the development of these disorders. The studies proposed in this application address the lasting influence of several environmental factors during fetal and neonatal life (environmental temperature, maternal diet and prenatal exposure to glucocorticoids) on an animal's susceptibility to become obese as an adult. It is the contention of the applicants that these three exposures induce different obesity-prone phenotypes by altering specific aspects of sympathoadrenal function, along with possible increases in food intake. The applicants propose that early exposure to cool environmental temperatures will predispose animals to develop obesity without features of the so-called 'metabolic syndrome', while maternal ingestion of a synthetic diet will predispose similar animals to develop obesity along with the 'metabolic syndrome'. The applicants also predict that prenatal exposure to glucocorticoids will exacerbate any other tendencies in the offspring to develop the 'metabolic syndrome' in conjunction with obesity. Furthermore, since these exposures are not mutually exclusive of one another, the applicants propose that maternal exposure both to glucocorticoids and to a synthetic diet will interact synergistically to exaggerate tendencies in the offspring toward obesity and the 'metabolic syndrome'. In addition, since the brainstem locus for sympathetic premotoneurons to brown fat in raphe pallidus (RPa) may also contribute to regulation of glucose metabolism, it is hypothesized that activation or inhibition of RPa will produce corresponding changes in glucose disposal. The applicants propose to use techniques of norepinephrine (NE) turnover and urine catecholamine levels to assess sympathetic and adrenal medullary function, respectively, in unanesthetized animals and to utilize neurophysiological studies of impulse traffic in sympathetic fibers of anesthetized rats to examine the importance of RPa in mediating SNS activation by specific stimuli, such as insulin and leptin. The potential impact of changes in sympathetic activity regulated by RPa for glucose and energy metabolism will also be examined. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: FAMILY-BASED TREATMENT OF SEVERE PEDIATRIC OBESITY Principal Investigator & Institution: Marcus, Marsha D.; Professor; Psychiatry; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, PA 15260 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 31-MAY-2005

30 Obesity

Summary: (adapted from investigator's abstract) The prevalence of pediatric obesity has increased significantly and approximately 11 percent of American children and adolescents are obese. Of particular concern, the greatest increase in prevalence has occurred among the heaviest medical and psychosocial morbidity than milder obesity is. Moreover, severely obese children are likelier than less severely obese children are to be become obese adults and suffer the long term health consequences of obesity. Although the efficacy of family based behavioral weight control programs in the treatment of moderate pediatric obesity is well established, few studies have focused on the treatment of severe obesity. Thus in this application, we propose a randomized controlled trial to evaluate the efficacy of a family-based behavioral weight control program in the management of severe pediatric obesity. Two hundred children aged 812 will be randomized to a 6-month family-based program or usual care, and will complete assessments at pre- and post-treatment and 6 month and 12 month follow-ups. It is hypothesized that: Children who participate in the family based program, when compared to children who receive usual care, will report symptoms. A secondary aim of the proposed investigation is to examine the relationships among gender, race, compliance to diet and exercise, level of parent adherence and treatment outcome. The proposed investigation will gather data about a serious public health problem and establish a foundation for programmatic research to develop effective treatments for an underserved population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FINE LOCALIZATION OF GENES FOR HUMAN OBESITY Principal Investigator & Institution: Price, R Arlen.; Professor; Psychiatry; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: (Adapted from Investigator's Abstract) The long-term goal of this study is to identify genes for common forms of obesity. To this end, the investigators previously have completed studies of the epidemiology, heritability and mode of inheritance of obesity. They have developed a cohort of families having both extreme obesity and thinness, and they have used this sample to examine candidate genes and regions, and, more recently, in a genome scan searching for linkage to obesity phenotypes. In a first stage scan they identified several genomic regions of interest, particularly a 15 cM interval of 20ql3 which may contain one or more obesity related genes. They have separate support to expand their linkage sample and conduct another genome scan, which should refine existing linkages and identify additional candidate regions for the fine mapping studies proposed in this application. However, it is doubtful that linkage methods alone will permit a resolution finer than two to five cM, an interval too large for positional cloning. The investigators note that there is a need for a cohort of triads which can be used to fine map genes for obesity, including those identified through their own linkage studies as well as through reported linkage and association studies conducted by others. In the current application, the investigators propose to develop another cohort of families consisting of extremely obese individuals and their parents for family based linkage disequilibrium studies. Specifically, the investigators propose to do the following: 1) develop a sample of 600 triads (160 from currently supported studies and 440 newly collected triads) having extremely obese female probands (BMI >= 40 kg/m2) and two parents assessed for obesity phenotypes (one or more parents will be of normal weight with maximum lifetime BMI<27); 2) genotype triads for markers and candidate genes in regions of interest; 3) conduct family based transmission disequilibrium studies to fine map obesity related genes to within as few

Studies 31

as 50 kb (0.05 cM). Although no support is requested for further aims, later studies will examine genes and expressed sequences in the identified regions using single strand conformational analysis and sequencing. Candidate sequences then will be tested for effects on obesity phenotypes through functional assays. The investigators note that obesity is an increasingly prevalent condition having serious consequences for health and quality of life. They further note that the identification of genes for common forms of obesity should lead to more individualized therapies and more effective prevention strategies. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FOOD PREVENTION

SUBSTITUTION

FOR

CHILD

NUTRITION/OBESITY

Principal Investigator & Institution: Faith, Myles S.; Psychiatry; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Childhood obesity is increasing nationwide, is associated with serious health complications, and tracks into adulthood. However, controlled obesity prevention studies remain scarce. Behavioral-economics theory offers a novel framework for conceptualizing and designing such interventions. To this end, we propose a randomized controlled trial that tests the effects of a "Family-Based Food Substitutions" intervention - with and without a Home-Food-Provisions component - on long-term weight change in children at risk for obesity. Based on behavioral-economics theory, we predict that increasing fruit and vegetable intake will substitute for the intake of untargeted energy dense foods and thereby reduce weight gain in children at-risk for obesity. This effect is predicted to be enhanced among families provided home provisions of targeted fruits and vegetables. Participants will be 180 families of diverse ethnic background, with the target child being 4 to 6 years old and "at-risk" for obesity. Families will be randomized to one of the following three treatment groups: (1) Minimal Intervention Control; (2) Family-Based Food Substitutions (FBFS); or (3) FBFS with Home-Food Provisions. There will be 60 families per condition. Families assigned to the control group will receive nutrition education. Those assigned to the FBFS group will be trained in behavioral strategies that target increased child fruit and vegetable intake (e.g., role modeling and contingency management training for parents). Families assigned to the FBFS with Home-Food-Provisions group will receive the aforementioned package plus supplies of targeted fruits and vegetables to enhance their home accessibility. The primary outcome measure will be short-term and 2-year changes in the children's body composition. Secondary outcomes will include measures of dietary intake, parental food preparation skills, and fruit and vegetable accessibility. Mediator analyses will elucidate the mechanisms by which the intervention exerts its effect on changes in body composition. This investigation is designed to provide new insights into environmental manipulations that will induce food substitutions compatible with obesity prevention, while advancing behavioral-economics theory. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FOUR-CORNERS BREAST AND ENDOMETRIAL CANCER STUDY Principal Investigator & Institution: Giuliano, Anna R.; Associate Professor; None; University of Arizona P O Box 3308 Tucson, AZ 857223308 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-JUL-2004

32 Obesity

Summary: (Adapted from Applicant's Abstract) The incidence of breast and endometrial cancers varies almost three-fold between non-Hispanic white populations and Native American and Hispanic populations living in the 4-Corners area of the United States (Arizona, New Mexico, Colorado, and Utah). Interestingly, although American Indian and Hispanic women have higher prevalences of many risk factors for breast and endometrial cancer identified in non-Hispanic white women (e.g., obesity, low levels of vigorous physical activity, low intakes of fruits and vegetables, high rates of insulin resistance) they have lower cancer incidence rates. In this study the investigators focus on the metabolic factors of obesity/weight changes and indicators of insulin status as they relate to breast and endometrial cancers. Obesity is associated both with estrogen and insulin by two interrelated disease pathways. Insulin may influence cancer risk directly through its effects on insulin-like growth factor (IGF) and its binding proteins (IGFBPs) and well as indirectly through its effect on estrogen levels. The investigators propose focusing on the insulin pathway because of the high levels of insulin pathway dysfunction in this population. A multi-center case-control study is proposed that targets women living in the 4-Corners area; the study will consist of a 2.5 hour in-person interview and a blood draw. Over a three-year case ascertainment period, the study will enroll 3000 breast cancer cases, 450 endometrial cancer cases and 3000 controls, half of whom will be Hispanic/Native American and half of whom will be non-Hispanic white women between the ages of 25 and 79. Molecular variants of genes that influence obesity and insulin (androgen receptor gene (AR), vitamin D receptor gene(VDR), insulin receptor (ADRB3)) will be examined both independently and in conjunction with metabolic factors to determine differences in genetic susceptibility in the population. Because of the diverse population (Hispanics, Native American, and non-Hispanic white women), the investigators propose to evaluate ethnic background and genetic admixture in relationship to gene markers, environmental factors, and breast and endometrial cancer risk. Genetic admixture (Ameridian to European genetic mixture) is a novel and innovative way to study the continuum of ethnic diversity. C-peptide, glycosylated hemoglobin, IGF-1, and IGFBP3 will be evaluated with respect to breast and endometrial cancer in a subset of women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FOUR-CORNERS BREAST CANCER STUDY Principal Investigator & Institution: Byers, Tim E.; Professor of Preventive Medicine; Preventive Med and Biometrics; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-JUL-2004 Summary: (Adapted from Applicant's Abstract) The incidence of breast and endometrial cancers varies almost three-fold between non-Hispanic white populations and Native American and Hispanic populations living in the 4-Corners area of the United States (Arizona, New Mexico, Colorado, and Utah). Interestingly, although American Indian and Hispanic women have higher prevalences of many risk factors for breast and endometrial cancer identified in non-Hispanic white women (e.g., obesity, low levels of vigorous physical activity, low intakes of fruits and vegetables, high rates of insulin resistance) they have lower cancer incidence rates. In this study the investigators focus on the metabolic factors of obesity/weight changes and indicators of insulin status as they relate to breast and endometrial cancers. Obesity is associated both with estrogen and insulin by two interrelated disease pathways. Insulin may influence cancer risk directly through its effects on insulin-like growth factor (IGF) and its binding proteins (IGFBPs) and well as indirectly through its effect on estrogen levels. The investigators

Studies 33

propose focusing on the insulin pathway because of the high levels of insulin pathway dysfunction in this population. A multi-center case-control study is proposed that targets women living in the 4-Corners area; the study will consist of a 2.5 hour in-person interview and a blood draw. Over a three-year case ascertainment period, the study will enroll 3000 breast cancer cases, 450 endometrial cancer cases and 3000 controls, half of whom will be Hispanic/Native American and half of whom will be non-Hispanic white women between the ages of 25 and 79. Molecular variants of genes that influence obesity and insulin (androgen receptor gene (AR), vitamin D receptor gene(VDR), insulin receptor (ADRB3)) will be examined both independently and in conjunction with metabolic factors to determine differences in genetic susceptibility in the population. Because of the diverse population (Hispanics, Native American, and non-Hispanic white women), the investigators propose to evaluate ethnic background and genetic admixture in relationship to gene markers, environmental factors, and breast and endometrial cancer risk. Genetic admixture (Ameridian to European genetic mixture) is a novel and innovative way to study the continuum of ethnic diversity. C-peptide, glycosylated hemoglobin, IGF-1, and IGFBP3 will be evaluated with respect to breast and endometrial cancer in a subset of women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FOXA2 IN METABOLISM Principal Investigator & Institution: Stoffel, Markus; Professor; Lab/Metabolic Diseases; Rockefeller University New York, NY 100216399 Timing: Fiscal Year 2003; Project Start 30-SEP-1998; Project End 31-JUL-2008 Summary: (provided by applicant): Obesity results from a massive expansion of white adipose tissue and recruitment of adipocyte precursor cells and is a common cause of insulin resistance and diabetes. Obesity may arise from increased fat cell size due to lipid accumulation or increased number of adipocytes arising from differentiation of preadipocyes to mature adipocytes. The processes that control adipogenesis include the coordinated expression of a complicated transcription factor network and numerous cellular and hormonal signals. We have recently identified the winged-helix forkhead transcription factor Foxa2 (Hnf-3_) to be expressed de novo in visceral and subcutaneous fat of genetic mouse models of obesity and diet-induced obesity. In these insulin resistant mice, the expression of Foxa2 correlates with serum insulin concentrations. Expression of Foxa2 in preadipocytes blocks adipocyte differentiation by directly activating the gene encoding adipocyte differentiation factor-1 (Pref-1). In addition, Foxa2 is a potent transcriptional activator of "insulin sensitizing" genes. We hypothesize that Foxa2 is a counter regulatory factor in the development of obesity and may be a "biomarker" of insulin resistance. To test this hypothesis we are proposing a series of molecular and genetic studies to elucidate the role of Foxa2 in adipocytes in vitro and in vivo. In aim 1 we will examine the role of Foxa2 in adipocyte differentiation and gene expression in vitro. In aim 2 we will generate and characterize animal models that either lack Foxa2 expression or overexpress Foxa2 in adipocytes. In aim 3 we are proposing to study two functional domains of Foxa2 that are important for its transcriptional activity. In aim 4 we will generate and characterize tissue-specific mutant "knock-in" mice that express a constitutive active form of Foxa2 in pancreatic islets, adipose tissue and liver, due to the loss of a putative Akt-dependent phosphorylation site. Lastly, we will perform a feasibility study to test if FOXA2 expression in adipose tissue of humans correlates with insulin resistance and therefore may be useful as a biomarker (aim 5). Together, this proposal will 1.) Help to establish the role of Foxa2 in adipocyte differentiation and obesity, 2.) Elucidate novel, posttranscriptional

34 Obesity

mechanisms that are important for Foxa2 activity, 3.) Investigate the link between FOXA2 adipocyte expression and obesity/insulin resistance in humans and 4) contribute to our basic understanding of transcriptional pathways that are regulated by insulin. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: FREE-LIVING PHYSICAL ACTIVITY AND ENERGY EXPENDITURE Principal Investigator & Institution: Boozer, Carol N.; Assistant Professor; St. Luke'sRoosevelt Inst for Hlth Scis Health Sciences New York, NY 10019 Timing: Fiscal Year 2002; Project Start 15-AUG-2002; Project End 31-JUL-2004 Summary: (provided by applicant): The current epidemic of obesity in the United States and much of the rest of the world may be related to the decreased physical activity (PA) characteristic of modem life. Definition of the specific relationship of PA and obesity has been hampered by inadequate PA assessment methodology. We have recently validated a newly available PA measurement device (IDEEA) and found it to detect type, duration and intensity of many types of PA at better than 98% accuracy. We propose to use this device to describe specific PA of adolescent girls. But prior to beginning that study, we will further evaluate IDEEA to determine if it can also be used to accurately assess energy expenditure (EE). We will do this by validating it against the gold standards for EE measurement - respirometry indirect calorimetry and doubly labeled water. Specifically, we will compare IDEEA-derived estimates for EE, with: 1) EE measured for specific PA by hood respirometry, 2) EE measured by 24-hour chamber respirometry, and 3) free-living EE assessed by doubly labeled water. We will then use IDEEA to collect cross-sectional data on free-living PA and EE in adolescent girls. We choose this group because adolescence is a critical period for development of obesity, particularly in females. Adolescent obesity tracks not only with adult obesity, but also with other risk factors independent of adult weight. This is also the period of racial divergence in adiposity. We will therefore use this device to assess type, duration and intensity of PA and EE in free-living Caucasian and African-American girls, ages 11-16. Body composition (fat mass and fat-free mass) will then be modeled as a function of age, ethnicity, sexual maturation (Tanner stage) and specific free-living physical activities and associated EE. Findings from these studies will provide critical validation of this important new PA measurement device to the research community. They will also provide a far more complete description of PA in adolescent girls than has ever been possible before. Finally, data from these studies will provide the basis for a future application to conduct a longitudinal, PA intervention study in this population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

•

Project Title: GENE THERAPY, OBESITY AND HYPOTHALAMIC SIGNALING Principal Investigator & Institution: Kalra, Satya P.; Professor; Neuroscience; University of Florida Gainesville, FL 32611 Timing: Fiscal Year 2001; Project Start 01-JUN-1986; Project End 31-MAY-2006 Summary: (Scanned from the Applicant's Description): With one out of every two adult Americans rated as medically obese, obesity is the number one health problem in the United States. Since it is a major risk factor for heart disease, diabetes, stroke, hypertension, and morbidity, the treatment of obesity and associated diseases entails enormous medical costs. The major objective of this proposal is (1) to examine whether viral vector mediated delivery of weight-reducing signals, such as leptin, is a viable therapy (gene therapy), alternative to the pharmacologic approach, to control body

Studies 35

weight (BW) gain for extended periods in normal male and female rats and in rodents with obesity due to environmental (diet-induced) and genetic factors. We believe that leptin acts by (1) augmenting energy expenditure (thermogenesis) and/or curbing appetite and (2) that the beneficial effects of leptin gene therapy are manifest at sites that enhance energy expenditure and modify hypothalamic appetite regulating signals such as the orexigenic signals, NPY, AgrP and GABA, and the anorexigenic melanocortin signal alpha-MSH, and intracellular signal transduction sequalae involving STAT3 and SOCS-3. We have successfully generated a recombinant adeno-associated virus (rAAV) vector to efficiently transfer the naturally occurring body weight reducing peptide, leptin (rAAV-lep). Aim 1: Examine the long-term (one-year) efficacy of rAAV-lep to reduce BW gain when delivered intracerebroventricular (icv) or systemically in out-bred Sprague-Dawley (SD) rats and obese rats maintained on a high-energy (HE) diet. Aim 2: Evaluate the efficacy of icv and peripheral rAAV-lep in those genetic models of obesity that (1) lack leptin (ob/ob mice) and (2) display resistance to peripheral and not central leptin (New Zealand obese mice); and (3) lack NPY (-/-) and display obesity when maintained on HE diet. Finally, we will also characterize the underlying mechanism(s) if excessive ectopic leptin itself induces leptin ineffectiveness (resistance) in these experiments. The causal mechanisms responsible for phenotype changes will be identified by evaluation of hypothalamic leptin expression and signaling through analysis of gene expression, and peptide levels, signal transduction sequalae (p-STAT3 and SOCS-3) and metabolic indices (body temperature, 24h urinary NE activity, oxygen consumption, UCP1 mRNA, and blood leptin, insulin glucose, and corticosterone levels). The outcome of these investigations will provide fundamental information on the broader potential of using gene delivery of naturally occurring anorectic molecules for BW control and their mechanism of action. This new knowledge will be applied to the ultimate goal of site-directed gene delivery aimed at the newly identified vulnerable loci in hypothalamic signaling to curb overeating and abnormal weight gain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETIC FACTORS IN PHYSICAL ACTIVITY AND OBESITY Principal Investigator & Institution: Bray, Molly M.; Assistant Professor; Human Genetics Center; University of Texas Hlth Sci Ctr Houston Box 20036 Houston, TX 77225 Timing: Fiscal Year 2003; Project Start 15-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Currently, more than half the adults in the U.S. are considered to be overweight, and almost one quarter of these adults meet or surpass the criteria for obesity (BMI>30 kg/m2). Numerous studies of related and unrelated individuals have provided support for the role of genes in the determination of body size and mass. This is particularly true in the case of morbidly obese young adults, in whom a genetic susceptibility for obesity very likely precedes or exacerbates the effects of overeating or lack of physical activity often found in these individuals. Prevention programs designed to reduce the risk of obesity commonly focus on modifiable environments and behaviors such as physical activity and diet, with varied results among individuals. This heterogeneity in response to obesity interventions is also at least in part of genetic origin. Nevertheless, little is known about how genetic variation in genes related to the regulation of body mass/fat and obesity may alter or influence one's response to exercise or diet intervention. Though the number of genetic factors that may be related to obesity is substantial, at least four mechanisms may contribute to an individual's body composition response to exercise intervention: 1) predisposition for the formation and growth of adipose tissue, 2) propensity for muscle cell growth or maintenance, 3) sensitivity to factors that influence satiety, and/or 4) alterations in

36 Obesity

energy metabolism. Thus, the purpose of this study is to investigate the association between genetic variation within genes related to adipogenesis, myocyte differentiation and growth, satiety, and energy metabolism and response to a well-established 30-week exercise training protocol, as determined by changes in body composition and blood lipids, in a multi-racial cohort of college-age men and women. In addition, we will investigate levels of gene expression in adipose and muscle tissue samples both pre- and post-training in order to identify additional genes related to body composition and/or responsivity to exercise. We have selected a powerful sample of males and females from multiple racial groups (N=1,536) designed to maximize our likelihood of detecting genetic differences related to body composition change. Results of this study will be invaluable not only in understanding the processes of exercise response and body composition change but also in improving intervention programs designed to reduce or prevent obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENETICS OF OBESITY AND DIABETES Principal Investigator & Institution: Attie, Alan D.; Professor; Biochemistry; University of Wisconsin Madison 750 University Ave Madison, WI 53706 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-MAY-2006 Summary: (Scanned from the Applicant's Description): The majority of persons with non-insulin-dependent diabetes mellitus (NIDDM) are obese. Nevertheless, although most obese people have insulin resistance, the great majority never develop NIDDM. There are essentially no biochemical clues that allow us to predict which obese individuals will develop diabetes, much less why they develop diabetes. In addition, there is limited mechanistic information to help us understand why obesity is so intimately related to diabetes. The objective of this project is to identify genes that link obesity and diabetes in mice. We have mapped two gene loci that determine whether or not an obese mouse will develop Type 2 diabetes. We have also mapped two loci that strongly affect body weight in a population of obese hyperphagic mice. The aims of this project are to: 1) Create interval-specific congenic strains for each mapped locus. 2) Refine the obesity and diabetes phenotypes. 3) Use a positional candidate strategy to identify the genes responsible for the mapped traits. Identification of obesity and diabetes susceptibility genes will provide clues to novel pathways and biochemical mechanisms underlying complex disease problems. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: GENETICS OF OBESITY RELATED SUBPHENOTYPES Principal Investigator & Institution: Sonnenberg, Gabriele E.; Professor of Medicine; Medicine; Medical College of Wisconsin Po Box26509 Milwaukee, WI 532264801 Timing: Fiscal Year 2001; Project Start 01-JUN-1998; Project End 31-MAY-2003 Summary: The investigators propose the development of a new and extensive gene database directed at questions relating to obesity. This database can be seen as complimenting similar databases already being developed for African-American and Latin groups in other parts of the country as well as the Ottawa family study in Canada. The investigators propose analyzing genetic variance at a variety of genomic sites as well as general genomic screen with respect to potential correlation with six specific phenotypic variables associated with obesity: Total body fat mass by dual energy x-ray absorptiometry, visceral fat size by CT, insulin sensitivity by minimal model, LDL density size distribution by gradient gel electrophoresis, left ventricular hypertrophy by

Studies 37

echo, and acute insulin response to IV glucose bolus. The rationale for the selection of these variables relates to the development of adverse effects associated with obesity particularly, more so than to obesity as a general phenomenon. The sample group will consist of 880 individuals drawn from a database consisting of 1,465 individuals belonging to 304 families and specifically having 326 concordant and 596 discordant sibpairs. Data, including DNA samples and baseline anthropometric measures have been already acquired on this database. The investigators propose measurement of the specific variables indicated above and correlation of those with genomic variance through either sib-pair linkage analysis or the more recently proposed variance components linkage analysis from the San Antonio group. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: GENOME SCAN FOR OBESITY IN A MULTI-ETHNIC SAMPLE Principal Investigator & Institution: Zhu, Xiaofeng; Prev Medicine and Epidemiology; Loyola University Medical Center Lewis Towers, 13Th Fl Chicago, IL 60611 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2003 Summary: (Provided by Applicant) In this project we propose to use the considerable resources generated by the 4 cooperating networks in the "Family Blood Pressure Program" (FBPP) to conduct a genome-wide scan data for obesity. In the FBPP microsatellite markers were typed at a density of -10cM by the Mammalian Genotyping Service (MGS) in Marshfield, WI. The complete data set will include 9,940 individuals representing 4 ethnic groups (white, black, Hispanic and Asian). Obesity will be characterized as a weight/height ratio (body mass index) and waist/hip ratio. This data set will be larger than any prior genome scan for obesity, and the inclusion of multiple ethnic groups will make it possible to examine genetic heterogeneity. The specific aims of the grant are to conduct linkage and association analyses to localize regions influencing obesity. Investigators at the applicant institution will work closely with the FBPP Coordinating Center (Washington University, St. Louis) and investigators from each of the 4 FBPP networks. Evidence will be sought for consistency between results obtained from analyses of the genome scan performed by each of the individuals, and results summarized from the literature, with those found in meta-analysis. Despite intensive efforts the genetic basis of obesity has been difficult to establish. Linkage analysis using a genome-wide scan can potentially identify genomic regions not previously thought to be associated with susceptibility to obesity and provides a comprehensive test of the consistency of previous studies. The enormous data repository created by this project presents an important opportunity to make use of this technique. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: IMPROVING THE EFFECTIVENESS OF OBESITY MANAGEMENT Principal Investigator & Institution: Wadden, Thomas A.; Professor; Psychiatry; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2003; Project Start 20-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): This is an application for a Midcareer Investigator Award in Patient-Oriented Research (K24) for Improving the Effectiveness of Obesity Management. The award will provide the candidate 40% effort for each of the next 5 years to increase his mentoring of postdoctoral fellows and junior faculty and to continue his research to improve the treatment of obesity. Postdoctoral fellows will be provided both clinical and research training and will have the opportunity to collaborate

38 Obesity

on the candidate's current NIH-funded studies. These include two randomized clinical trials to improve the maintenance of weight loss. The first encourages obese individuals to increase their daily lifestyle activity (Lifestyle Activity for Weight Management, DK56114), while the second combines behavior modification with the long-term use of weight loss medication (Behavior Modification and Pharmacotherapy for Obesity, DK56124). A third trial is the Look AHEAD study that is assessing the long-term health consequences of intentional weight loss and increased physical activity in overweight individuals with type 2 diabetes (U01-DK57135). The candidate will assist postdoctoral fellows in initiating their own investigations and mentor them through the stages from formulating a suitable question to publishing their results. He will similarly facilitate the research of junior faculty who are supported by Mentored Patient-Oriented Research Awards (K23) and similar mechanisms. The present award will support the candidate's efforts to improve the treatment of obesity in primary care practice. Working with faculty in the Department of Family Practice and Community Medicine, he will develop a brief physician-delivered intervention for weight management. The success of this intervention will be assessed in a controlled pilot study conducted in the Department's outpatient practice. Thus, this award will help the candidate move beyond the customary efficacy trials of obesity therapies (conducted in research clinics such as his own) to examine the effectiveness of a weight management intervention delivered in the more challenging arena of primary care practice. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INFANT CARE, FEEDING, AND RISK OF OBESITY Principal Investigator & Institution: Bentley, Margaret E.; Associate Dean; Nutrition; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, NC 27599 Timing: Fiscal Year 2002; Project Start 05-APR-2002; Project End 31-MAR-2007 Summary: (provided by applicant): Overweight and obesity are increasing rapidly in the U.S., particularly among low-income minority populations. While genetic factors no doubt play an important role, environmental and behavioral factors must surely be driving the epidemic given its rapid increase in the past decade. Recent research suggests that care and feeding styles during childhood may be related to subsequent risk of obesity yet little is known about the period when infants make the transition through the weaning period to a family diet or how specific parenting styles or environments may influence the development of obesity in very young children. The obesity literature has focused primarily on children during the adiposity rebound period or older, and few studies describe risk factors in the first 2 years of life, when patterns first develop and are under parental or caregiver control. This research will examine: 1) household factors that influence parenting and infant feeding patterns; 2) relationship of feeding styles to infant diet; and 3) relationship of dietary intake to infant fatness. We will conduct the study among African American mothers and infants in North Carolina, a group at high risk for the development of obesity. In Phase I, we will conduct in-depth ethnographic research that defines culture-specific features of parenting and feeding and to identify household and contextual factors that may either prevent or promote infant obesity development in this population. This is a critical part of the research because it will allow us to define specific indicators related to our ecological model. We will also adapt an existing instrument, the Child Feeding Questionnaire (CFQ) to be culturally and age-appropriate for administration among mothers of African-Americans infants during the longitudinal study. In Phase II, we will conduct a longitudinal, observational study of 200 mother-infant African-American

Studies 39

dyads, followed from 3-18 months of age. The study is designed to identify the constellation of household, caregiver, and child characteristics associated with the risk of obesity. Infants will be followed at 3, 6, 9, 12, and 18 months through assessments in their home environments. We will assess relationships among feeding styles, dietary intake, and infant fatness, while taking into account the role of activity, maternal BMI, and other risk factors. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INTERLEUKIN-6 EXPRESSION AND FUNCTION IN ADIPOSE CELLS Principal Investigator & Institution: Harp, Joyce B.; Associate Professor; Nutrition; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, NC 27599 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: Elevated interleukin-6 (IL-6) is associated with fat wasting in systemic infection and cancer cachexia. However, important new data indicates that circulating IL-6 is also elevated in human obesity, and adipose tissue is the principal source of this elevation. Because obesity is among the most prevalent public health challenges in the United States, it is important to understand IL-6 expression and function in adipose tissue, and to determine whether dysregulated expression of adipose tissue IL-6 is involved in the development of obesity and obesity-related co-morbidities. IL-6 traditionally signals through STAT3 activation, but in differentiating preadipocytes, IL-6 inhibits and STAT3 appears to be necessary for adipocyte formation. In this proposal we propose the following Specific Aims.. Aim 1: To determine mechanisms involved in IL6-induced inhibition of adipogenesis. We hypothesize that greater than or equal to 10 ng/ml IL-6 inhibits the preadipocyte to adipocyte conversion by altering normal cell cycle progression and subsequent adipogenic transcription factor expression. We will determine in 3T3-L1 preadipocytes the effect of IL-6 on cell cycle progression and differentiation. Using chimeric GM-CSF- gp130 receptor transfections, the signaling mechanisms involved to transduce IL-6 effects will be explored. To explore the physiological relevance of IL-6 in adipose tissue, we will determine whether IL-6 knockout mice have altered adipose tissue growth, glucose, and lipid metabolism on normal and high fat diets. Aim 2: To characterize adipose tissue IL-6 expression in animal models of obesity. We find IL-6 mRNA is expressed in adipose tissue of lean mice, but it has been reported that obese db/db mice do not express IL-6 mRNA in adipose tissue. Since glucocorticoids repress IL-6 expression, we hypothesize that IL-6 expression is depressed in adipose tissue of ob/ob and db/db mice by high systemic corticosterone levels that are characteristic of these models of obesity. We also predict that IL-6 expression is elevated in adipose tissue of diet-induced obese (DIO) mice, similarly to obese humans. DIO mice retain normal corticosterone levels with the development of obesity. We will characterize IL- 6 expression in adipose tissue of lean control, DIO, ob/ob, and db/db all on a C57BL/6J background at baseline and in response to glucocorticoid agonists and antagonists, and thiazolidinediones. Aim 3: To identify the differentiation-induced STAT3 activating ligand. Our new pilot data indicate that IL-6 is not the autocrine factor responsible for MDI-induced STAT3 activation, but that the heparin binding ligand midkine (MK) is. In this Aim, we will confirm our preliminary studies, and determine whether midkine is the sole STAT3 activating ligand released upon MDI stimulation of 3T3-LI cells. Aim 4: To determine the role of STAT3 activation in adipogenesis. We hypothesize that activation of STAT3 is necessary for adipogenesis. We will block MDI-induced STAT3 activation by

40 Obesity

overexpression of PIAS3. Alternately, we will mimic STAT3 activation by overexpression of a constitutively active STAT3 to determine whether STAT3 activation alone is necessary and sufficient to induce adipogenesis. The role of STAT3 in fat pad formation will be investigated by implantation into the subcutaneous space of nude mice human preadipocytes that express vector, PIAS3, or constitutively active STAT3. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: INTRA-ABDOMINAL ADOLESCENTS

FAT

AND

RISK

OF

DISEASE

IN

Principal Investigator & Institution: Goran, Michael I.; Associate Director and Professor; Preventive Medicine; University of Southern California 2250 Alcazar Street, Csc-219 Los Angeles, CA 90033 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-MAY-2002 Summary: There are distinct gaps in our understanding of the link between obesity and/or fat distribution and increased disease risk in adolescent children. We propose a 5-year longitudinal study to examine the temporal relationships between changes in body fat, body fat pattern, insulin sensitivity, lipd profile, physical activity, and sex hormones during adolescent growth. We will use state-of-the-art techniques for measuring total body fat (4-compartment model), body fat pattern (dual energy X-ray absorptiometry, computed tomography), physical activity (combination of doubly labeled water and indirect calorimetry), and whole-body insulin sensitivity (Bergman Minimal model). We will examine blood pressure and circulation lipid and lipoprotein levels as risk factors for cardiovascular disease, and fasting indulin and insulin sensitivity as risk factors for non-insulin dependent diabetes mellitus. We propose to study Caucasian and African American adolescents because these groups are at increased risk of obesity and related diseases and have not been thoroughly examined. Preliminary data and recent publications from other investigators support the concept that accumulation of body fat in the intra- abdominal region begins to occur before and during adolescence. Moreover, these data provide evidence that the relationship between obesity and disease risk in adolescents may be explained by accumulation of intra-abdominal adipose tissue (IAAT). Thus, we propose to examine the following hypotheses: 1) The relationship between obesity and disease risk in Caucasian and African American adolescents is due specifically to the accumulation of IAAT; 2) Physical inactivity, total body fat, and sex hormone levels contribute to the development of IAAT during adolescence, which leads to the development of insulin resistance which in turn leads to the development of dyslipidemia. The strength of these cause and effect relationships will not be significantly influenced by ethnicity, or gender; and ,3) IAAT can be accurately predicted from anthropometry, and more accurate equations can be developed by inclusion of total abdominal fat by dual energy X-ray absorptiometry. Our unifying hypothesis is that the development of IAAT during adolescence is the specific cause of increased risk of disease resulting from obesity. This longitudinal study will add to our understanding of the etiology of obesity and the emergence of different body fat patterns during adolescent development. The study will yield substantial information of the mechanism(s) relating obesity to increased disease risk in Caucasian and African American adolescents, and this information will be useful for the design of prevention and intervention programs aimed at reducing long term risk of disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: LEPTIN AND VENTILATORY CONTROL DURING SLEEP Principal Investigator & Institution: O'donnell, Christopher P.; Associate Professor of Medicine; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, MD 21218 Timing: Fiscal Year 2001; Project Start 10-JUL-2000; Project End 31-MAY-2004 Summary: The prevalence of obesity is increasing dramatically in western society, especially in the U.S. where 22% of the population have a body mass index greater than 30 kg/m2. As weight is gained, individuals can develop elevated, resting levels of PaCO2 and depressed hypercapnic ventilatory responses (Obesity Hypoventilation Syndrome; OHS). The mechanisms that link obesity and respiratory depression are unclear. The premise of this proposal is that the recently cloned metabolic hormone, leptin, can prevent respiratory depression in obesity. Our findings indicate that obese ob/ob mice, which lack circulating leptin, exhibit the major clinical features of OHS, and that leptin replacement reverses respiratory depression independent of weight. The current application is designed to explore influences of leptin on ventilatory control, and the pathways and factors which modulate its effect. Various transgenic mice and novel techniques are employed to measure ventilation, sleep wake/state and arterial blood gases in chronically instrumented mice. Insights gained from murine experiments will be applied in humans to define the relationship between leptin and ventilation in obesity. Specific Aim l, examines whether leptin can increase the gain of central chemoreceptors, and whether an acute 10% reduction in body fat in obese mice affects ventilatory control. Specific Aim 2 examines whether leptin acts through hypothalamic and peripheral chemoreceptor pathways to alter respiratory control. Specific Aim 3, examines whether leptin is upregulated as a compensatory response to chronic hypoxia. In Specific Aim 4, the mechanistic animal studies will be extended to determine how leptin levels in the CNS relate to PaCO2 in severely obese humans. Finally, the role of gender and sleep/wake state will be explored across Specific Aims 1-4. These studies will enhance understanding of the pathogenesis of respiratory failure in obesity, provide insight into the role of leptin in patients with ventilatory insufficiency of other causes, and offer the possibility of specific therapeutic intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: LEPTIN IN VASCULAR DISEASE Principal Investigator & Institution: Eitzman, Daniel T.; Assistant Professor of Internal Medicine; Internal Medicine; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, MI 481091274 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: Obesity, is epidemic in the United States and is emerging as a strong independent risk factor for complications of atherosclerotic vascular disease such as myocardial infarction and stroke. Since thrombosis overlying an atherosclerotic plaque is the immediate cause of myocardial infarction and stroke, the obese state may promote the development of thrombosis at sites of vascular disease. Leptin, a hormone produced by the adipocyte, increases with obesity and may be one of the mediators responsible for the increased cardiovascular risk associated with obesity. We have recently demonstrated that leptin or leptin receptor deficiency is protective against thrombosis in a mouse model of arterial injury. Furthermore, this protective effect of leptin deficiency on thrombosis is reversed with leptin replacement. Consistent with a prothrombotic effect of leptin in humans, a recent clinical trial has demonstrated that elevated plasma leptin is an independent risk factor for cardiovascular events. The goals of this proposal are to characterize the impact of varying elevations of ieptin on thrombosis and

42 Obesity

atherosclerosis using established mouse models. In addition, mice with plateiet and endothelial leptin receptor deficiency will be generated using the Cre-loxP system to determine the relevant target tissues involved in mediating the adverse vascular effects of leptin. These studies will determine the functional in vivo significance of leptin and various leptin receptor pools in vascular disease and have important implications for understanding the effects of obesity on cardiovascular complications. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LEPTIN INDUCED REVERSAL ON INSULIN RESISTANCE IN OBESITY Principal Investigator & Institution: O'doherty, Robert M.; Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, PA 15260 Timing: Fiscal Year 2001; Project Start 15-FEB-2001; Project End 31-JAN-2005 Summary: (Adapted from the applicant's abstract) Skeletal muscle resistance is a major contributor to the hyperglycemia, hyperinsulinemia and dyslipidemia associated with type II diabetes and obesity. Recent work has implicated leptin, the adipocyte-derived hormone, in improving insulin sensitivity. Thus, leptin administration to leptin-deficient ob/ob mice corrects hyperglycemia and hyperinsulinemia, while elevating leptin in normal rats increases insulin sensitivity. Based on these observations the effects of leptin on the metabolic abnormalities of the high-fat fed rat, a model of diet-induced obesity that more closely resembles human obesity than monogenetic obesity models, were investigated. These studies, performed by the P.I. and discussed in this proposal, demonstrate that a gene therapy intervention that elevates plasma leptin levels reverses the skeletal muscle insulin resistance and other metabolic abnormalities associated with diet-induced obesity. However, the mechanisms underlying these effects are unknown. This proposal, therefore, focuses on identification of the mechanisms underlying leptininduced reversal of skeletal muscle insulin resistance in diet-induced obesity. Three specific aims will test the hypotheses that skeletal muscle insulin resistance by leptin. These variables have been implicated in the pathogenesis of insulin resistance and the determination of muscle insulin sensitivity, and are altered by leptin. Identification of the mechanisms mediating leptin-induced reversal of muscle insulin resistance may serve as a platform for the rational design of pharmaceutical or genetic therapy of insulin resistance in human obesity and type II diabetes. Specific Aims: 1. To determine the role of altered lipid metabolism in mediating leptin-induced improvements in insulin sensitivity. 2. To determine the role of altered activity of the insulin signaling pathway in mediating leptin-induced improvements in insulin sensitivity. 3. To determine the role of altered metabolic gene expression in mediating leptin-induced improvements in insulin sensitivity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: LEPTIN RECEPTOR AND THE OBESITY/DIABETES SYNDROME Principal Investigator & Institution: Chua, Streamson C,.; Associate Professor of Pediatrics; Pediatrics; Columbia University Health Sciences New York, NY 10032 Timing: Fiscal Year 2001; Project Start 01-JUN-2000; Project End 31-MAY-2005 Summary: This project is designed to determine the role of leptin receptor expression in neurons and adipocytes to the control of energy balance. The lack of leptin receptor (Lepr) results in a syndrome of obesity and diabetes. Investigations with leptin in humans and rodents suggest that the major weight-regulating action of leptin occurs in the hypothalamus. Specific neuronal populations, defined by their neuropeptide content

Studies 43

such as NPY/AGRP and POMC/CART, are important mediators of leptin action. However, leptin has actions on adipocytes, such as the regulation of lipolysis, that may contribute to the obese phenotype. The goals of this proposal are: A) Evaluate the obesity-reducing effects of the expressing LeprB in neurons only, in adipocytes only, and in neurons and adipocytes; B) Evaluate the obesity-producing effects of abrogating leptin receptor expression in neurons only, in adipocytes only, and in neurons and adipocytes; C) Determine the obesity- and diabetes-reducing effects of expressing LeprB in POMC/CART neurons, in AGRP/NPY neurons, and in POMC/CART neurons and AGRP/NPY neurons. For A, transgenes with cell type-specific promoter/enhancers will be used to drive LeprB expression. The transgenes will be combined with the db-3J mutation, a 17bp deletion of coding exon 12 that prevents the synthesis of all membrane-bound LEPR isoforms. For B, the cre-lox system will be used to obtain tissuespecific lot deletion of coding exon 17 of Lepr. Homologous recombination in embryonal stem cells will be used to introduce two loxP sites that flank coding exon 17. The manipulated ES cells containing the floxed Lepr allele will be used to generate mice that carry Lepr-flox. Transgenes that express cre recombinase in a tissue- specific manner, neurons only or adipocytes only, will be bred with Lepr flox mice to obtain animals with tissue-specific deletion of Lepr expression. A gene knock-in method (C) will be used to identify specific neuronal populations that mediate the effects of leptin on obesity and diabetes. Expression of LeprB in chemically defined neurons will be achieved by the insertion of an IRES- LeprB/IRES-beta-Galactosidase cDNA cassette (internal ribosomal entry site) in the 3' untranslated regions of the Pomc and Agrp genes, generating a tricistronic mRNA. Thus, the effect of expression of LeprB in AGRP/NPY neurons and/or POMC/CART neurons on the obese/diabetic phenotype can be evaluated in db3J/db-3J mice. These experiments will provide data regarding the role of leptin receptor signaling in AGRP/NPY neurons and POMC/CART neurons to the obesity/diabetes syndrome. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LIPID BINDING PROTEINS IN OBESITY/DIABETES SYNDROMES Principal Investigator & Institution: Bernlohr, David A.; Professor and Head; Biochem/Mole Biol/Biophysics; University of Minnesota Twin Cities 200 Oak Street Se Minneapolis, MN 554552070 Timing: Fiscal Year 2001; Project Start 12-AUG-1998; Project End 31-JUL-2002 Summary: The PI has a long-standing interest in fatty acid binding proteins. The present proposal hinges on studies of two such proteins, aP2 and KLBP. The hypothesis of this proposal is that aP2, but not KLBP, stimulates gene transcription by delivering lipid ligands to the lipid activated transcription factor PPAR gamma 2. Since aP2 knock-out mice develop obesity only on a high fat diet, and such obesity is uncoupled from insulin resistance and TNF alpha production, the PI hypothesizes that aP2 affects the development of obesity by trafficking hydrophobic ligand to nuclear transcription factors, thereby regulating the expression of genes whose products are involved in the development of insulin resistance and NIDDM. The PI proposes the following set of experiments to test the hypothesis: A. To express wild-type and lipid binding proteins in aP2 and KLBP null mice, and to assess the expression of TNF alpha and the development of insulin resistance in these mice under different dietary conditions; B. To characterize the interactions between aP2 and PPAR gamma 1 and 2 in response to thiazolidinediones and polyunsaturated fatty acids; and C to examine lipid trafficking in adipocytes derived from KLBP and ap2 null mice using retroviral expression techniques.

44 Obesity

Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: LIPID METABOLISM IN OBESITY, WEIGHT LOSS AND EXERCISE Principal Investigator & Institution: Houmard, Joseph A.; Professor and Director; Human Performance Laboratory; East Carolina University 1000 E 5Th St Greenville, NC 27858 Timing: Fiscal Year 2001; Project Start 15-AUG-2000; Project End 31-JUL-2005 Summary: (Adapted from the applicant's abstract):The long-term objective of this research is to better understand defects in human skeletal muscle that contribute to the morbidity and mortality evident with obesity. There is evidence that lipid metabolism in the skeletal muscle of obese individuals is altered in a manner favoring lipid storage. For example, some data indicate that obese skeletal muscle has a reduced capacity to oxidize lipid. There is also evidence that muscle-associated triglyceride concentration increases with obesity. These are important observations as the accumulation of lipid in skeletal muscle is associated with insulin resistance. The storage of lipid in skeletal muscle may thus predispose obese individuals toward insulin resistance and the many conditions linked with insulin resistance (hypertension, coronary artery disease, diabetes mellitus). Despite these important implications, the cellular mechanism that promotes lipid accretion in obese skeletal muscle is not evident. In the current application experiments are proposed that will determine the mechanism(s) responsible for promoting lipid storage in skeletal muscle with obesity and if intervention compensates or corrects the initial defect(s). The primary hypothesis is that postabsorptive (fasting) lipid metabolism in skeletal muscle is altered with obesity in a manner that promotes lipid accumulation in this tissue. This hypothesis is based upon preliminary work, where it was observed that lipid oxidation is depressed in the muscle of obese individuals in conjunction with reductions in oxidative enzyme activities. These preliminary data form the basis for the working hypothesis that lipid oxidation is depressed in skeletal muscle with obesity which promotes lipid storage. The secondary hypothesis is that weight loss does not enhance lipid oxidation, but reduces muscle triglyceride stores by an alternative mechanism. The tertiary hypothesis is that exercise training reverses the initial decrement in lipid oxidation evident with obesity, promoting lipid utilization. To test these hypotheses it will be determined: Specific Aim I - if postabsorptive lipid metabolism is impaired in skeletal muscle from obese individuals in a manner that promotes the accumulation of lipid; Specific Aim II - if the impairment in postabsorptive lipid metabolism in the skeletal muscle of obese individuals is corrected or compensated for with weight loss and; Specific Aim III - if exercise training enhances postabsorptive lipid metabolism in obese individuals and the cellular mechanisms responsible. Findings will be important as little is known concerning the mechanisms responsible for the defects in lipid metabolism with obesity and the impact of intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: MECHANISMS OF CARDIOVASCULAR DISEASE IN OBESITY Principal Investigator & Institution: Loskutoff, David J.; Professor; Scripps Research Institute 10550 N Torrey Pines Rd La Jolla, CA 920371000 Timing: Fiscal Year 2001; Project Start 01-JUN-1999; Project End 31-MAY-2003 Summary: Little information is available about the molecular mechanisms that promote the hypercoagulable state and increased risk for cardiovascular disease in human obesity. Although plasminogen activator inhibitor 1 (PAI-1) is consistently and

Studies 45

significantly elevated in the plasma of obese humans and is a known risk factor for atherothrombolic disease, the origin and regulatory mechanism(s) that control its expression in obesity remain to be defined. Our studies of obese mice and cultured adipocytes suggest that elevated plasma PAI-1 results from increased synthesis by adipocytes in response to tumor necrosis factor-alpha and insulin, and that the adipocyte may play a central and previously unrecognized role in hemostatic gene expression in human obesity. The following observations provide additional novel insights into adipocytes and PAI-1 biosynthesis in obesity and form the basis of this application: (1) transforming growth factor beta (TGF-beta) mRNA is chronically elevated in adipose tissue of obese mice and is a powerful inducer of PAI-1 in adipocytes; (2) the adipocyte is the primary insulin-responsive cell in terms of PAI-1; and (3) insulin continues to induce PAI-1 in metabolically insulin-resistant adipocytes and mice. We hypothesize that the increased TGF-beta and hyperinsulinemia in obesity alters the biosynthetic activity of adipocytes and promotes the cardiovascular risk associated with this condition. In Aim 1, we will investigate the regulation and consequences of TGF-beta expression in obesity and during adipogenesis. The possibility that TGF-beta alters preadipocyte growth and differentiation as well as adipocyte gene expression, glucose homeostasis, and insulin-resistance will be explored in vivo and in vitro using specific inhibitors of TGF-beta. In Aim 2, we will examine additional models of murine obesity to determine the generality and tissue specificity of the effects of insulin on PAI-1. We will also employ inhibitors of insulin-signaling to define the pathways that control PAI-1 gene expression, and to test the hypothesis that in adipocytes, glucose homeostasis and PAI-1 gene expression are regulated by different pathways. These studies should provide novel information about TGF-beta and insulin and their respective roles in the regulation of PAI-1 in adipocytes in health and disease. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: METABOLIC CONTROL OF FEEDING BEHAVIOR Principal Investigator & Institution: Friedman, Mark I.; Associate Director; Monell Chemical Senses Center 3500 Market St Philadelphia, PA 19104 Timing: Fiscal Year 2003; Project Start 01-AUG-1993; Project End 31-MAR-2006 Summary: (provided by applicant): Postabsorptive fuel metabolism is an important factor in the control of food intake. Sensors in brain and liver that are sensitive to various metabolic parameters have been implicated in this control. In liver, considerable evidence indicates that changes in energy metabolism produce a stimulus or stimuli that are transduced into a neural signal that carries this metabolic information to the central nervous system for use in controlling food intake. In particular, changes in hepatic ATP content, or some closely related change in liver energy status, generate signals that initiate or terminate feeding behavior under various conditions, such as fastingrefeeding, type I diabetes, and treatment with metabolic inhibitors. Recent studies in this laboratory have revealed that three different animal models of obesity (genetic, dietary and neurological) show reduced hepatic energy status, suggesting that changes in liver energy status are also involved in overeating and the development of obesity. The overall goal of this project is to assess whether and how altered hepatic energy metabolism is a contributing cause of hyperphagia (overeating) that leads to obesity. Some rats overeat and become obese when fed a diet high in fat content (obesity-prone), whereas others of the same strain do not (obesity-resistant). The proposed research will use this diet-induced animal model of obesity because it appears most comparable to the obesity commonly seen in humans. We hypothesize that, during the development of obesity, hyperphagia may be driven at least in part by decreased liver energy status,

46 Obesity

which is secondary to the redirection of fuels into storage and away from oxidative pathways. Overeating could result from a faster decline in hepatic energy status between meals or a slower recovery in hepatic energy status during and after a meal. The project has three specific aims: (1) Determine whether overeating in obesity prone rats is due to an enhanced susceptibility to reductions in liver energy status. (2) Determine whether overeating in obesity prone rats is due to a slow restoration of liver energy status. (3) Determine whether calcium signaling during metabolic stimulus transduction differs in hepatocytes from lean and obese rats. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NIDDM SUSCEPTIBILITY GENES IN A BIRACIAL COHORT Principal Investigator & Institution: Brancati, Frederick L.; Associate Professor; Medicine; Johns Hopkins University 3400 N Charles St Baltimore, MD 21218 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-JUL-2004 Summary: (Adapted from the Investigator's Abstract) Type 2 diabetes mellitus and its atherosclerotic complications impose a substantial burden on health of Americans in general and on African Americans in particular. Recent discoveries in molecular genetics have lead to the identification of functional variations in several candidate genes for susceptibility to obesity, insulin resistance, and/or diabetes. These include genes which code for beta-2and beta-3 adrenergic receptors, insulin receptor substrate 1, fatty acid binding protein 2, frataxin, and leptin receptor. If their role as novel susceptibility factors is confirmed, these variants promise to illuminate the pathophysiologic basis of diabetes and diabetes related cardiovascular diseases, accelerate the development of chemopreventive agents, and facilitate the conduct of prevention trials by marking individuals at high risk. Unfortunately many previous association studies of these mutations in human populations have been limited by small, selected study samples; by limited cross-sectional data on behavioral factors and on cardiovascular risk phenotype; and by paucity of data on African Americans. The investigators, therefore, propose to conduct an epidemiologic study of functional variants in 10 candidate genes for susceptibility to type 2 diabetes, obesity, and insulin resistance. The main objective will be to detect modest effects consistent with polygenic nature of diabetes but with better sensitivity and precision than previous association and linkage studies. The study sample will a community based cohort of 3,250 African Americans and 3,250 Whites aged 45 to 64 who are participants in the ongoing Atherosclerosis Risk in Communities (ARIC) study. Supported by NHLBI the ARIC study has assembled an extensive data base including behavioral assessment (e.g. diet and physical activity), anthropometry, laboratory blood tests (e.g. oral glucose tolerance test and serum lipids), and carotid ultrasonography as well as clinical events and mortality. Using race specific case-control, cross-sectional, and longitudinal analyses the investigators will determine if these putative diabetes alleles are associated with incident and prevalent diabetes, with obesity and weight gain, with hyperinsulinemia in non-diabetic individuals with the presence of an adverse cardiovascular risk factor profile, and with atherosclerosis progression and cardiovascular disease incidence over 12 years of follow up. The investigators will assess how behavioral and environmental factors such as obesity, diet, and physical activity, influence the expression of genetically conferred risk. Strength of this proposal include the close collaboration between clinical, epidemiologic, and laboratory researchers, a wealth of prospectively collected data from an NIH sponsored study, and a sample size large enough to detect modest gene effects and to investigate gene-gene and gene-environmental interactions. Most important, this study will provide unique information on the expression of

Studies 47

diabetes susceptibility genes in the general population and possibly suggest genetic explanations for the excess prevalence of type 2 diabetes and obesity in African Americans. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: NOVEL NON-PEPTIDE AGONISTS OF THE MELANOCORTIN RECEPTOR Principal Investigator & Institution: Struthers, Scott; Neurocrine Biosciences, Inc. 10555 Science Center Dr San Diego, CA 921211100 Timing: Fiscal Year 2002; Project Start 01-FEB-2002; Project End 31-JUL-2003 Summary: (Scanned from the Applicant's Abstract): Obesity is the most common contributing factor to illness worldwide, including such diseases as Type II diabetes, coronary heart disease and cancer. Although the molecular basis for obesity is still unknown, recent research has provided evidence which demonstrated that melanocortins play a prominent role in regulating energy balance. Results from murine genetic experiments, in which the melanocortin-3 receptor gene has been disrupted, suggests that this receptor may play a unique regulatory role in overall energy metabolism of these animals. Thus, we propose to initiate a series of studies to explore the pharmacology of this receptor and its role in obesity. Initially, we will use a MC3-R selective peptide modulator, gamma-melanocyte stimulating hormone, to test its effect on energy balance in obese mice. In parallel, we also propose to initiate a focused highthroughput combinatorial chemistry approach to identify small organic molecules designed to stimulate the MC3 receptor, as well as selective antagonists, in order to provide better pharmacologic tools. If our results confirm that activation of MC3-R does not effect appetite, but rather influences energy partitioning and metabolism, the small molecule agonists identified in Phase I of this study could serve as chemical leads for a novel class of anti-obesity therapeutics. PROPOSED COMMERCIAL APPLICATION: We are proposing to develop a small molecule agonist of the melanocortin-3 receptor. This receptor has been shown to play a key role in regulating the amount of body fat and energy balance. Thus, an MO receptor agonist may be a novel approach toward preventing obesity and its co-morbidities, and could provide an important novel class of human therapeutic agents. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: NOVEL MELANOCORTINS

REGULATION

OF

ADIPOGENESIS:

AGOUTI

&

Principal Investigator & Institution: Mynatt, Randall L.; None; Lsu Pennington Biomedical Research Ctr 6400 Perkins Rd Baton Rouge, LA 70808 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Over the past 10 years the agouti/melanocortin system has become recognized as a major regulator of bodyweight homeostasis. For example, a greater number of mutations in the agouti/melanocortin signaling pathway are linked to obesity in humans than any other pathway. The basic paradigm is that melanocortins bind to a family of receptors and reduce bodyweight. Agouti and agouti related protein (AGRP) are endogenous antagonists of melanocortin receptor binding. Moreover, the chronic antagonism of melanocortin receptors by agouti/AGRP leads to obesity. Our preliminary data clearly demonstrate that humans express and regulate agouti in adipose tissue. Therefore, it is important to determine the impact of agouti/melanocortin signaling in fat on obesity and diabetes. The focus of ongoing

48 Obesity

studies in my laboratory is to understand the function of agouti/melanocortin signaling in adipose tissue and evaluate its contribution to obesity and diabetes. Data collected from transgenic mice that overexpress agouti in adipose tissue and studies in cultured adipocytes have led us to propose that agouti/melanocortins are part of a communication circuit between the brain and adipose tissue which conveys centrallymediated signals (ACTH and alpha-MSH) and modulates adipocytes responsiveness to these signals (agouti). The overall hypothesis is that Agouti/melanocortins regulate adipogenesis and adipocyte metabolism at several levels. First, we hypothesize that agouti increases the proliferation of preadipocytes. Our second hypothesis is that agouti promotes the differentiation of preadipocytes into mature adipocytes. Third, we predict that agouti alters cAMP-dependent signaling pathways in the mature adipocyte such that it is more resistant to lipolysis and more efficient at storing triglycerides. The focus of this proposal is to understand both the mechanisms of agouti/melanocortin action on preadipocytes and adipocytes and the basis for how these effects on adipocyte function contribute to obesity. The preliminary data in this proposal demonstrate that the agouti/melanocortin system is potentially one of the major regulators of adipocyte function, just as it is a major regulator of bodyweight homeostasis, This makes a strong case for studying agouti/melanocortin signaling in adipose tissue and its relevance in understanding the underlying mechanisms of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OBESITY AND CARDIAC RISK IN AMERICAN INDIAN CHILDREN Principal Investigator & Institution: Adams, Alexandra K.; Family Medicine; University of Wisconsin Madison 750 University Ave Madison, WI 53706 Timing: Fiscal Year 2002; Project Start 12-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Background: Childhood obesity is a significant risk factor for the development of adult obesity, cardiovascular disease (CVD), and diabetes. Recent studies suggest very high rates of obesity in American Indian (AI) children. Candidate: This K23 award will facilitate Dr. Alexandra Adams' development as a patient-oriented scientist with a long-term goal of becoming a high-quality, independent academic investigator who develops intervention strategies for prevention of obesity, CVD and diabetes in Al populations. Qualifications: Dr. Adams' unique qualifications for this K23 award include her medical training and a Ph.D. in nutritional science. Since joining the University of Wisconsin (UW) Family Medicine (DFM) clinical and research faculty in 1999, she has established a strong working relationship with Al communities in Wisconsin and has initiated a number of important collaborative studies with tribal communities. Environment: The DFM and Medical School are committed to Dr Adams' development as a patient-oriented scientist. This is reflected in strong support letters, senior research mentors involved with the project, written commitment from her Chair, GCRC support, and collaborative opportunities with other UW research teams in one of the strongest research environments in the US. Training: Dr. Adams will develop her career in patient-oriented research by obtaining advanced training in clinical research design, blostatistics, participatory research, ethics, writing skills, and advanced body composition techniques. As part of her K-23 plan, She will complete the UW Clinical Investigator Preparatory Pathway (CIPP K30 grant) as well as participate in courses, seminars and training activities. She will receive extensive group and one-on-one mentoring from a number of LTW senior NIH-funded scientists and Dr. Ann Macaulay, Director of the Kahnawake Schools Diabetes Prevention Program at McGill University. Research: Dr Adams is working on a three phase collaborative participatory research project with two WI tribal communities who have asked her to partner with them to

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reduce the disease burden in their communities by decreasing obesity and CVD risk factors in their children. She hypothesizes that the high prevalence of obesity in WI Al children, which places them at high risk for adult CVD and diabetes, begins early in childhood. Thus, obesity prevention efforts must be targeted early in childhood. The project will 1) assess obesity prevalence and cardiac risk factors in Al children ages 0-7, 2) conduct growth modeling of the familial and environmental determinants of obesity, and 3) work in partnership with the communities to design community-based early intervention strategies to prevent childhood obesity. Significance: With the assistance of the K23 award, Dr. Adams will develop and test interventions to prevent obesity in Al children and its sequelae; CVD and diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OBESITY AND NEGATIVE AFFECT-INDUCED EATING Principal Investigator & Institution: Pagoto, Sherry L.; Psychology; University of Illinois at Chicago 1737 West Polk Street Chicago, IL 60612 Timing: Fiscal Year 2003; Project Start 05-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): This proposal describes a 5-year training program that will enable Dr. Sherry Pagoto to develop expertise in the research of behavioral mechanisms of positive energy balance in obesity. In the past four years, Dr. Pagoto has completed her training in clinical psychology, with a specialization in cardiovascular risk reduction via behavior change (e.g., weight management, stress reduction, smoking cessation). Dr. Pagoto will work closely with her sponsor Dr. Bonnie Spring, as well as her co-mentors, Drs. Audrey Ruderman and Donald Hedeker at the University of Illinois at Chicago, Dr. Marian Fitzgibbon at Northwestern University in Chicago, and Dr. Karina Davidson at Mt. Sinai School of Medicine in New York. Dr. Pagoto's short term goals are to enhance the theoretical, methodological, and statistical skills needed to study the behavioral mechanisms of unhealthy eating patterns that lead to weight gain and obesity. Her long-term goals are to develop an independent laboratory and a network of collaborators devoted to the understanding of risk factors and treatments for obesity and other outcomes that contribute to cardiovascular risk. Two studies are proposed. Study 1 aims to compare the calorie intake of obese and nonobese males and females during anxious, angry, and neutral mood states. The hypothesis is that both anxiety and anger compared to neutral mood, trigger disproportionately increased eating among both obese males and females compared to normal controls. Anger may be more potent than anxiety in triggering disproportionately increased eating in obese individuals. Study 2 addresses a potential behavioral mechanism of negative affectinduced eating. The aim is to examine the effect of food intake on anxious and angry mood states in obese and nonobese males and females, testing the hypothesis that the negative affect dispelling consequences of eating are greater for obese individuals than for normal weight controls. This is the first study to systematically investigate the effects of eating on different mood states using comparable methodology. Results should increase the understanding of obesity and be used to enhance weight loss interventions. The University of Illinois at Chicago provides an ideal setting for training behavioral scientists and the mentoring team will provide a sound training experience for the PI from which an academic career can be launched. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

50 Obesity

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Project Title: OBESITY PREV AMONG PREPUBERTAL AFRICAN AMERICAN GIRLS Principal Investigator & Institution: Baranowski, Thomas; Professor; Pediatrics; Baylor College of Medicine 1 Baylor Plaza Houston, TX 77030 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-MAY-2002 Summary: Obesity is a risk factor for several adult chronic diseases. Obesity is more prevalent among African-Americans (AA) than other ethnic groups, especially AA females. Obesity tracks from childhood into the adult years. Children above the 50th percentile (50 percent tile) and/or who have one or two obese parents are more likely to become obese than others. Thus, intervening just before and early in puberty among those at high risk may prevent obesity among those not already obese, and prevent or minimize further weight gain among those already overweight and lower chronic disease burden. We hypothesize that participation in 60 min or more per day of moderate to vigorous physical activity, eating 5 or more servings of fruit, juice and vegetables (FJ and V) per day, and decreasing dietary fat intake will minimize weight gain over a two year period among prepubertal 8-year-old (yo) AA girls in the upper 50 percent tile of BMI or who have one or more obese parents. Behavioral objectives will be achieved through a 2-year intervention consisting of a four-week summer day camp and a 23 month child-parent weekly interactive Fun, Food and Fitness web site to learn about healthy eating and physical activity. This study will employ a randomized two group (treatment-control) design with four annual repeated measures at baseline, mid program (+12 mo), post program (+24 mo), and a year after the program(+36 mo) starting with 336 girls. The primary intervention outcomes will be body weight and fat gain as measured by DEXA; secondary outcomes include cardiovascular disease risk factors, energy expenditure measured by doubly labeled water, dietary practices and psychosocial variables. Candidate gene polymorphisms and resting metabolic rate will be examined for association with obesity related phenotypes and response to intervention. Prior to the Intervention (Phase I) we will initiate three studies: 1) test of the validity of two alternative approaches to self-report of physical activity (24-hour physical activity recall vs. week activity recall); 2) assessment of family and personal factors that influence physical activity among these girls; and 3) development and pilot testing of a culturally sensitive month-long summer camp and two month world wide web program to help 8yo AA girls change their dietary and physical activity practices. This will be the first obesity prevention project to employ a month-long summer camp, web technology, and sophisticated biological measures to assess factors predictive of body composition change. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: OBESITY SCHOOLCHILDREN

PREVENTION

IN

AFRICAN

AMERICAN

Principal Investigator & Institution: Wang, Youfa; Human Nutrition and Dietetics; University of Illinois at Chicago 1737 West Polk Street Chicago, IL 60612 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2005 Summary: (provided by applicant): Obesity is the second leading preventable cause of disease and death in the United States. Low socioeconomic status (SES) and minorities are disproportionately affected. Obesity prevention among children and adolescents is a public health priority. Schools have been identified as key settings for obesity prevention; however, most health education interventions have had only a moderate effect on body weight. We propose a randomized intervention trial (pilot study) to test

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the feasibility and effectiveness of a school-based, environmental obesity prevention program in urban Iow-SES African American students. Schools, students and their families, and local communities will be involved to promote healthy eating and physical activity (HEPA) for prevention of childhood obesity. Six Chicago public schools will be randomly assigned as intervention (4 schools) and controls (2 schools). Focus group studies will assess needs and barriers for promotion of HEPA and guide the intervention. The intervention group will receive a School Environment Enrichment (SEE) program to modify the school physical and social environment, targeting food service, recess, physical education (PE) and school climate, and a Community Support & Environment Modification (CSEM) program, involving local corner and chain grocery stores to promote healthy eating among students and their families. Family involvement will be included for 5th and 6th graders, who will be followed for two years, to test ways to modify family environment. To assess the intervention effectiveness, multilevel data will be collected from schools (eg, food service, recess and PE), students (eg, body weight, eating and physical activity), parents (eg, family food purchasing practices) and communities (eg, available choices of snack foods in local stores). In addition, process evaluation data will be collected to assess the feasibility and acceptance (participation and satisfaction) of various intervention components by the target audience. The primary outcome variable is change in students' body weight status; secondary outcomes include changes in students' eating behavior and physical activity and changes in target environmental factors. In addition, cost-effectiveness of the intervention will be determined. If the intervention proves effective, a full-scale study will be developed. Findings from this study will provide insights into the prevention of obesity among Iow-SES and minority students. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: DYSFUNCTION

OBESITY,

ADIPOCYTOKINES,

AND

ENDOTHELIAL

Principal Investigator & Institution: Gokce, Noyan; Boston Medical Center Gambro Bldg, 2Nd Fl, 660 Harrison Ave, Ste a Boston, MA 02118 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The obesity epidemic has become a major public health problem in this country with unprecedented exposure of individuals to cardiovascular risk. There is growing urgency to understand mechanisms of obesityrelated cardiovascular disease and the beneficial effects of weight modification. The overall objective is to investigate the relationships between obesity, vascular endothelial dysfunction, adipocyte metabolism, and oxidative stress, and the effect of weight loss on these parameters. The vascular endothelium regulates vasomotor tone, platelet activity, and inflammation through the synthesis and elaboration of paracrine factors such as endothelium-derived nitric oxide (EDNO). Endothelium-dependent vasodilation and platelet inhibition are impaired in atherosclerosis and associated risk factors, possibly due to increased vascular oxidative stress and reduced NO bioactivity. Loss of normal vascular endothelial function supports a local vasospastic, prothrombotic, and proinflammatory milieu, and is linked to the pathophysiology of cardiovascular events including myocardial infarction, stroke, and unstable angina. There is growing recogition that metabolic activity of adipose tissue, through release of proatherogenic factors, may play a pathophysiologic role in mechanisms of vascular dysfunction and cardiovascular disease. No prior study has examined the effect of obesity and weight loss interventions on adipocyte and vascular endothelial function. This project proposes in specific aim 1: to characterize the relationship between overweight or obesity and

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vascular endothelial dysfunction, in specific aim 2: to determine whether weight reduction and risk factor modification improves vascular endothelial function and markers of oxidative stress and inflammation, and in specific aim 3: to examine the metabolic role of adipose tissue for vascular dysfunction, and investigate the effects of weight loss on adipocyte expression of proatherogenic factors. The proposed studies have the potential to provide important insights into mechanisms of obesity -associated cardiovascular disease and examine whether weight loss mediates its cardioprotective action via phenotypic modification of adipocyte and vascular endothelial function. The proposed project takes advantage of Boston Medical Center's NIH funded Center for Obesity Research (C.O.R.E) and a tightly integrated Nutrition and Weight Loss Center. In addition, the investigators bring a unique combination of expertise that will greatly enhance the project's ability to address these important clinical questions. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OBESITY, LEPTIN AND GALLSTONE PATHOGENESIS Principal Investigator & Institution: Pitt, Henry A.; Surgery; Medical College of Wisconsin Po Box26509 Milwaukee, WI 532264801 Timing: Fiscal Year 2001; Project Start 15-JUL-1992; Project End 31-MAR-2006 Summary: (Verbatim from Applicant's Abstract): Approximately 30,000,000 Americans have gallstones, and the vast majority are overweight. This laboratory's long-term objective is to understand the pathogenesis of cholesterol gallstone formation. Gallstone pathogenesis is related to alterations in 1) hepatic lipid metabolism, 2) cholesterol crystal nucleation, and/or 3) biliary motility. Gallstones occur most commonly in obese, middle-aged, multiparous women. Recent studies have clarified the role of gender, iron deficiency, and female hormones in gallstone pathogenesis. Similarly, the role of leptin and malformation of its receptor in the pathogenesis of obesity has been elucidated in the last few years. However, the connections between obesity, leptin and gallstone formation remain obscure. Recent data from this laboratory is congenitally obese ob/ob mice suggest that they have alterations in biliary lipids, enhanced cholesterol crystal formation and increased gallbladder volume. Leptin receptors also have been demonstrated in the liver and biliary tree of both mice and humans. Therefore, the hypothesis of this proposal is that leptin or malfunction of its receptor contribute to the increased incidence of gallstone formation in obesity by altering hepatic lipid metabolism, cholesterol crystal nucleation and biliary motility. Two related specific aims will be 1) to determine whether obesity, leptin, or leptin receptor malfunction alters a) hepatic lipid metabolism, b) cholesterol crystal nucleation, and/or c) biliary motility and 2) determine whether genetic alteration in leptin and its receptor on gallstone formation are additive. Preliminary studies in female, leptin deficient ob/ob mice suggest that these animals are prone to cholesterol gallstone formation. A series of studies in ob/ob, ob+/- (heterozygote), db/db (leptin receptor malfunction, and AY (Agouti yellow) mice as well genetically crossed ob/ob and db/db mice are proposed to dissect which pathogenic mechanisms link obesity, leptin and gallstones. Similarly, bile serum and tissue from lean and obese humans undergoing cholecystectomy will be systematically studied to establish clinical relevance. These studies should lead to unique strategies for gallstone prevention, which is the ultimate goal of this research. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: OBESITY, NITRIC OXIDE, OXIDATIVE STRESS, NA SENSITIVITY Principal Investigator & Institution: Flack, John M.; Professor; Wayne State University 656 W. Kirby Detroit, MI 48202

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Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: We propose a 39-week clinical study in healthy, normotensive, overweight (BMI equal to or more than 25 kg/m[2]) African American men and women aged 45 years and older that, after an initial screening and eligibility period (4 weeks), will be conducted in three phases. Phase 1 (9 weeks) begins the isocaloric 100 mmol dietary sodium diet phase. After the initial 3 weeks, a six-week period of 100 mmol/d sodium supplementation will be administered to determine salt sensitivity. Phase 2 (8 weeks) will maintain the 100 mmol sodium dietary intake and will additionally add a weight loss component to attain weight loss of about 1.5 - 2 pounds/week. Phase 3 (18 weeks) will consist of a two-period crossover trial consisting of randomization to the treatment sequence of dietary sodium supplementation of 100 mmol/d (6 weeks) followed by placebo (6 weeks) or vice versa. A 6-week placebo washout period will separate the two active periods. The 100 mmol sodium/weight loss diet from phase 2 will be maintained during this treatment phase. The difference in BP between the end of the sodium and placebo periods will determine salt sensitivty after weight loss. The overarching study hypothesis is that obesity-related salt sensitivity is attributable, in large degree, to oxidative-stress mediated reductions in nitric oxide [NO] availability. The destruction of NO is linked to obesity-related elevations of non-esterified fatty acids, leptin, and reninangiotensin-aldosterone system activity - all of which are known to increase oxidative stress. Genetic variation in the angiotensin converting enzyme, specifically homozygosity for the insertion [I] polymorphism, will predict higher levels of salt sensitivity, oxidative stress, and lesser NO production. Environmental stressors interact with obesity to augment salt sensitivity. We further hypothesize that the degree of reversibility of salt sensitivity will closely parallel weight loss-induced reductions in oxidative stress. The primary specific aim of the study is to determine the main and interactive effects of stressors, obesity, and genetic variation of the ACE and endothelial nitric oxide synthase (eNOS) genotypes on oxidative stress and salt sensitivity and, after weight loss, to re-examine these effects as well as to link changes in oxidative stress to persistence of salt sensitivity between study phases 2 and 3. This study will provide important new insights into the pathophysiology of salt sensitivity in African Americans who are at high risk for development of hypertension and related cardiovascular diseases. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: OBESITY/NUTRITION RESEARCH CENTER Principal Investigator & Institution: Kelley, David E.; Professor; Medicine; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, PA 15260 Timing: Fiscal Year 2003; Project Start 30-SEP-1992; Project End 31-MAR-2008 Summary: (provided by applicant): The University of Pittsburgh is seeking to renew funding of the Obesity and Nutrition Research Center for its third five-year period. Established in 1992, the initial focus of the Pittsburgh Center was on behavioral interventions. During the current funding cycle, under its new leadership, the Center has retained its focus on clinical investigation, but has substantially expanded its scope to include involvement with metabolic, epidemiological, body composition, genetic and laboratory investigations of obesity and nutrition. At the same time the Center has built upon the prior strength in behavioral interventions for obesity by expanding these endeavors into eating disorders and additional aspects of physical activity and nutrition. Collectively, the goal of the Pittsburgh ONRC is to facilitate and promote research, especially collaborative and multi-disciplinary efforts, to develop more effective interventions for the prevention and treatment of obesity and to gain a more complete

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understanding of the causes and complications of obesity and other nutritional disorders. This goal is of major public health significance because a majority of adults in this country are overweight or obese, this prevalence is increasing, and the prevalence of obesity in children has increased dramatically during the past two decades. Two of the major complications of obesity are cardiovascular disease and diabetes mellitus, and the research base in these areas is very strong at the University of Pittsburgh. During the past funding cycle, several of the cores have grown significantly. There is now a robust program of body composition, bio-imaging and metabolic research in children and adults, and numerous large epidemiological trials entailing nutritional and activity interventions with vascular disease outcomes. The program and core support for behavioral interventions has also grown substantially, from a few senior investigators into a group of interactive, strongly funded investigators with complementary expertise for whom the presence of the ONRC core facilities has been pivotal. There are several key new initiatives underway including multi-disciplinary programs in childhood obesity and bariatric surgery. Bolstered by strong institutional support, a more diverse scientific base, new facilities, and new partnerships with the adult and pediatric GCRCs, the Pittsburgh ONRC is prepared to continue its important leadership role in clinical research for obesity and nutritional disorders. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PHOTOPERIODIC CONTROL OF OBESITY Principal Investigator & Institution: Bartness, Timothy J.; Professor; Biology; Georgia State University University Plaza Atlanta, GA 30303 Timing: Fiscal Year 2001; Project Start 01-SEP-1984; Project End 31-JUL-2004 Summary: (applicant's abstract): Obesity is a disease of literally and figuratively enormous proportions. A model of naturally occurring obesity, photoperiod-induced seasonal obesity in Siberian hamsters, was chosen for study. Siberian hamsters are naturally obese when housed in long "summer-like" days. This obesity gradually develops and is expressed fully when the animals are adults. When Siberian hamsters are exposed to short days, as in fall/winter, they lose body fat. With subsequent increasing day lengths, as occurs in spring/summer, they regain their body fat; thus, the obesity is reversible, unlike most of the animal models of human obesity. It seems that a better understanding of the fundamental processes involved in the development and reversal of obesity might result from studying this natural cycle of body fat because, in these animals, it is seasonally advantageous for them to be obese at one time of year and lean at another time of the year. Two aspects of the control of fatness are the focus of this grant proposal: 1) the connections of the brain to body fat by the sympathetic nervous system, and 2) the regulation of total body fat as revealed by the compensatory increases in fat that are triggered after surgically-produced decreases in fatness (lipectomy). Attempts will be made to identify a brain controller of the number of fat cells in the body, including the chemical means by which the brain communicates with fat depots to increase or decrease fat cell number. Further attempts will be made to identify how the brain "knows" when body fat is decreased after we remove some of it experimentally (lipectomy). Tests will be done directly to one brain area, the paraventricular nucleus, to determine whether it is involved in the control of the short-day-induced decreases in fatness, as seems to be suggested by the neural circuitry connecting this brain area to body fat. Finally, a new strategy/tactic will be used to identify the chemicals in the brain that are part of the neural circuit connecting the brain to fat and that may be involved in the reversal from obese to the lean state. This multidisciplinary approach should provide new information about the importance of the control of body fat by the brain. In

Studies 55

addition, these findings should provide insight into the fundamental processes involved in the development, maintenance, and especially the reversal of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PHYSIOLOGY OF MELANIN CONCENTRATING HORMONE IN OBESITY Principal Investigator & Institution: Ludwig, David S.; Assistant Professor of Pediatrics; Children's Hospital (Boston) Boston, MA 021155737 Timing: Fiscal Year 2001; Project Start 15-APR-1997; Project End 31-MAR-2002 Summary: (Taken from the applicant's abstract) The prevalence of obesity in the U.S. ranges from 25% overall to greater than 50% in some minority groups. Obesity may constitute the most common health problem in America, with associated morbidity and mortality rates equal to that of cancer. However, therapeutic options remain largely ineffectual. Thus, research into the pathophysiology and treatment of obesity assumes great significance to national health. Recent studies have demonstrated the importance of the brain, and specifically hypothalamus, to the regulation of body weight. Several hypothalamic substances have been identified which dramatically alter appetite and metabolic rate. In the present study, we have chosen to investigate the role of one particularly interesting hypothalamic neuropeptide, melanin concentrating hormone (MCH). Toward this end, transgenic mouse strains overexpressing the MCH gene will be produced. These strains should provide information regarding the physiologic actions of MCH in body weight regulation. In addition, the transgenic mice may constitute useful models for examining the actions of potential anti-obesity treatments. As an alternative approach, the effects of MCH administration by direct intracerebral injection will be studied. Dr. Ludwig's main research area is the neuroendocrine control of appetite and metabolism. In particular, he is interested in understanding how abnormal structure and function of the hypothalamus may underlie body weight disorders. The project will be conducted in the Division of Endocrinology and Metabolism of Beth Israel Hospital, Boston, under the supervision of Dr. Jeffrey Flier (Division Chief). Obesity and diabetes comprise the predominant research focus of the Division. Specific projects involve studies of insulin signal transduction, brown adipose tissue function, and leptin. The research environment contains state-of-the-art molecular biology, animal research, and transgenic facilities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: POLYMORPHISMS OF B1 AND B2 RECEPTOR GENES AND OBESITY Principal Investigator & Institution: Lima, John J.; Professor; Nemours Children's Clinic 807 Children's Way Jacksonville, FL 322078482 Timing: Fiscal Year 2001; Project Start 15-JUN-2001; Project End 31-MAY-2003 Summary: Obesity has been associated with insulin resistance, hyperinsulinemia, noninsulin-dependent diabetes mellitus, hypertension and a higher risk of cardiovascular disease and death. Genetic, metabolic and environmental factors are known to contribute to obesity. Genes that are involved in the regulation of catecholamine function may be important because of the role catecholamines play in energy expenditure and lipolysis. Ninety percent of fat in the body is stored in white adipose tissue as triglycerides, which are broken to free fatty acids and glycerol through the action of hormone-sensitive lipase. Lipolysis is stimulated by beta1, beta2 and beta3 adrenergic receptors in human adipocytes, with the beta1 and beta2 adrenergic

56 Obesity

receptors (beta1 and beta2 AR) being the most dominant subtypes. Catecholaminestimulated lipolysis is reduced in obesity, which is thought to be due to defects in the beta2 AR-signaling pathway. Mis-sense mutations in the beta1 AR gene results in polymorphisms at nucleic acid 145 (A->G), which results in a substitution of Ser for Gly at position 49, and at nucleic acid 1165 (G- >C, which results in a substitution of Gly for Arg and position 389. Beta1 AR polymorphisms have functional significance; whether or not they associate with obesity is unknown. Mutations in the 5' leader and coding regions of the human beta2 AR gene give rise to several polymorphisms, which can after receptor density and function. The working hypotheses of this submission are that polymorphisms at position 389 and haplotypes of beta2 AR polymorphisms in the 5' leader and coding regions associate with obesity. Specific Aim #1: to compare the beta1 AR allele frequencies and genotypes in healthy obese and non- obese subjects. The hypothesis driving this specific aim is that obesity associates with the Gly 389 beta1 AR allele. Specific Aims #2: to compare the distribution of beta2 AR haplotypes in healthy obese (Body Mass Indexes > 30) and non-obese (BMI < 25) subjects. Beta2 AR haplotypes will be determined by PCR and direct sequencing. The thesis driving this specific aim is that obesity associates with the Arg19-Gly16- Glu27 beta2 AR haplotype. The distribution of beta2 AR haplotypes in 118 non-obese and 118 otherwise healthy obese subjects will be compared. The results of this study will determine whether polymorphisms in beta1 and beta2 AR allels associate with obesity. The information obtained from our studies are important in designing clinical trials of interventions designed to reduce body weight. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PREVENTION OF OBESITY BY ALTERATION OF DIETARY FAT Principal Investigator & Institution: Donnelly, Joseph E.; Professor and Director; Educ Psychology and Research; University of Kansas Lawrence Lawrence, KS 66045 Timing: Fiscal Year 2001; Project Start 15-FEB-2001; Project End 31-JAN-2006 Summary: Treatment for obesity has proven difficult as most reduced obese individuals regain the weight which had been lost. The lack of success in treating obesity argues for strategies to prevent obesity or weight re-gain. The PIs propose to use 3 clinically appropriate levels of fat intake in a population at-risk for weight gain in a long-term study where energy intake and macronutrient composition is verified by multi-method techniques. Primary Aim-Prevention of weight gain. The PI will determine the effects of 3 levels of verified dietary fat intake on body weight and body composition in college students at-risk for weight gain. We hypothesize that ad libitum diets which contain greater than 35 percent fat will promote weight gain compared to subjects who ingest ad libitum diets which contain 28 to 32 percent fat or 25 percent fat or less. Specifically, the PI expects a dose response for the level of fat in the diet for body weight and fat mass. Secondary aims will may contribute to our understanding of how various levels of fat intake may prevent or promote obesity and may provide explanation for the anticipated differences in individual responses with the groups. Association of fat intake to total energy intake. The PI expects that subjects consuming diets with higher amounts of fat to have greater total energy intakes and will therefore show weight gain in a dose response fashion. Specifically, the PI will hypothesize that subjects consuming ad libitum diets with 35 percent fat or greater will show an increase in total energy intake compared to subjects consuming a 28 to 32 percent fat diet or subjects consuming a diet of 25 percent fat or less. Individual response - the PI expects subjects with greater body fat to gain more weight and fat mass compared to leaner subjects and expect subjects who are restrained eaters to gain less weight than those who exhibit disinhibited eating.

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Although the PI expects increase energy intake for the groups that receive high fat intakes, they do not expect all subjects within each group to respond in similar fashion. The long-term results expect to show those subjects who gained the least amount of weight during the intervention will have the lowest weights 1,2 and 3 years post intervention. The results of this study should advance our understanding of the role of dietary fat in the prevention of obesity and weight re-gain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: PSYCHOSOCIAL DETERMINANTS OF NUTRIENT INTAKE IN GIRLS Principal Investigator & Institution: Striegel-Moore, Ruth H.; Professor; Psychology; Wesleyan University Middletown, CT 06459 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2005 Summary: (provided by applicant): Studies have documented the importance of eating behavior as a modifiable risk factor for the development of obesity and cardiovascular disease (CVD). The burden of obesity and CVD is not equally distributed in the population; women from ethnic minority populations are particularly likely to be obese and to have higher rates of CVD and stroke than white women. Thus, the broad, longterm goal of this research is to better understand the determinants of nutrient intake in black and white adolescent girls and to examine the effects of nutrient intake and eating behaviors on obesity, a significant risk factor for CVD. Overall we wish to determine the extent to which psychological and familial factors contribute to nutrient intake in black and white girls, beyond the well-established effects of ethnicity and socioeconomic factors. Specifically, the aims of the project are the following: 1) to provide a detailed developmental description of eating behaviors and nutrient intake in black and white girls and to examine the "clustering" of certain eating behaviors (e.g., skipping meals and snacking) into eating patterns; 2) to determine the clinical significance of eating behaviors and eating patterns by examining their contribution to nutrient intake and the development of obesity; 3) to examine the role of psychological and familial factors as determinants of eating behaviors, eating patterns, nutrient intake, and obesity in black and white girls. Capitalizing upon the availability of extensive data collected prospectively among an exceptionally well-maintained cohort of 2,379 black and white females over a 12-year period (from ages 9-10 to ages 21-23), we propose to apply innovative analytic procedures to further the scientific understanding of the determinants of nutrient intake and eating behaviors in adolescent girls. Participants were assessed annually for ten years as part of the National Heart, Lung and Blood Institute Growth and Health Study (NGHS) with measurements of anthropometry, food intake, eating and weight related attitudes and behaviors and family cohesion. Parents also provided information about weight, eating, and family environment at two assessments. In a subsequent study with the same sample, structured clinical interviews were conducted to determine history of psychiatric disorders and risk factors for eating disorders. Adult weight was also measured. Results from our secondary analyses will be useful for interventions aimed at improving nutritional health. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: RACE, LIPOPROTEIN LIPASE AND OBESITY AFTER MENOPAUSE Principal Investigator & Institution: Goldberg, Andrew P.; Professor; Medicine; University of Maryland Balt Prof School Baltimore, MD 21201 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008

58 Obesity

Summary: (provided by applicant): This study is designed to determine the cellular mechanisms underlying the paradoxical association of insulin resistance with decreased visceral adiposity and circulating triglyceride (TG) levels in African-American (AA) compared to Caucasian (CAU) postmenopausal women. This will provide insight into mechanisms underlying racial differences in obesity and its associated metabolic dysfunction (insulin resistance, type 2 diabetes, dyslipidemia, hypertension). The hypothesis is that postmenopausal AA women have a higher skeletal muscle lipoprotein lipase (SM-LPL) and a lower adipose tissue LPL (AT-LPL) activity that leads to the preferential accumulation of TG in muscle (SM-TG), while the converse exists in CAU women. We also postulate that a weight loss (WL) intervention, by preferentially decreasing SM-LPL activity in AA and AT-LPL activity in CAU, will promote reductions of SM-TG in AA and of visceral adiposity in CAU to improve lipoprotein lipid profiles and insulin sensitivity. Specific aims determine whether: 1) decreased visceral (omental and mesenteric) and subcutaneous abdominal (SAT) AT-LPL activity and increased skeletal muscle LPL activity in rectus abdominis and vastus lateralis are the cellular mechanisms underlying racial differences in visceral obesity and SM-TG accumulation in AA compared to CAU postmenopausal women using tissue obtained during elective abdominal surgery and by needle biopsy, and 2) WL, by reducing SM (vastus lateralis - and SAT-LPL activity, is associated with a decrease in SM and visceral fat accumulation to increase in vivo insulin action (hyperinsulinemic euglycemic clamp) and the in vitro antilipolytic response to insulin in a homogeneous population of healthy obese AA and CAU postmenopausal women. We will study healthy, obese (BMI = 30-40 kg/m2), sedentary 50-65 year old postmenopausal women not on hormone-replacement therapy. We will measure AT- and SM-LPL activity, SM-TG content, visceral fat and mid-thigh low density lean tissue area (CT scans) insulin sensitivity in abdominal adipocytes as insulin suppression of lipolysis and in whole body estimated by hyperinsulinemic euglycemic clamps and using the Homeostasis Model Assessment of Insulin Resistance (HOMA IR), total body fat (DXA), lipoprotein lipids, oral glucose tolerance and obesity-related hormones (leptin, insulin, SHBG, free testosterone). Collectively, these results will determine whether racial differences in the tissue-specific LPL activity, the key enzyme for hydrolysis and the ensuing storage of circulating TGs, establish a metabolic setting in obese AA of increased SM-TG (due to increased SM-LPL and decreased visceral fat) and in obese CAU of increased visceral fat (due to increased AT-LPL) that predisposes them to insulin resistance and risk for type 2 diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REDUCING TELEVISION VIEWING TO PREVENT CHILDHOOD OBESITY Principal Investigator & Institution: Robinson, Thomas N.; Assistant Professor Of; Medicine; Stanford University Stanford, CA 94305 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-MAR-2003 Summary: We propose to test the efficacy of reducing television, videotape and videotape and video game use to prevent obesity among third grade children, in a randomized controlled school-based trial. The United States has experienced dramatic increases in obesity among both children and adults. There is a pressing need for innovative interventions to prevent obesity. There has been widespread speculation that television viewing might be one of the most easily modifiable causes of obesity among children. This hypothesis has broad appeal, but has been difficult to validate. We propose an innovative experimental model. In the current environment, in which

Studies 59

television viewing is already so prevalent, the question of greatest clinical, practical and policy importance is: Will reducing television, videotape and video game use prevent childhood obesity? As a foundation for this proposal, we have completed two pilot studies that demonstrate the feasibility and potential promise of the proposed study. We propose a school-based randomized controlled trial involving 12 ethnically-diverse elementary schools and approximately 900 third graders. Six schools will be randomly assigned to receive an intervention to reduce television, videotape and video game use and the other six schools will receive an attention-placebo control intervention. The intervention model is derived from principles of Bandura's social cognitive theory and includes a classroom curriculum and parent newsletters. The primary intervention will be delivered throughout the third grade school year. Survey and physical assessments of all children will occur at baseline, at the end of 3rd grade (post- test) and at the beginning and end of 4th grade (4 month and one year follow-ups, respectively). A subsample of children will also complete 4 days of activity monitoring and three 24-hour dietary recalls. Parents will be interviewed by phone at baseline, post-test and one-year follow up. We hypothesize that, compared to controls, third grade children exposed to a school-based intervention to reduce time spent watching television and videotapes and playing video games, will significantly reduce their prevalence of obesity over a single school year. The primary outcome measure will be body mass index. We will also test maintenance of the primary outcome over the follow-up period and effects of the intervention on hypothesized mediating variables; amount of television, videotape and video game use, physical activity, cardiorespiratory fitness, dietary fat and calorie intake and eating while watching television. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: REGULATORY RESPONSES TO POSITIVE ENERGY BALANCE Principal Investigator & Institution: Seeley, Randy J.; Professor; Psychiatry; University of Cincinnati 2624 Clifton Ave Cincinnati, OH 45221 Timing: Fiscal Year 2002; Project Start 30-SEP-1997; Project End 31-JAN-2007 Summary: (provided by applicant): The incidence of obesity has reached epidemic proportions, is a major health burden, and costs the U.S. billions of dollars in health care and lost productivity. Failure to develop effective treatments for obesity is in large part due to a lack of clear understanding as to how food intake and energy balance are regulated by the CNS. Thus, research to determine the processes by which food intake and energy balance are controlled is likely to have a major impact on public health, but the research to date has been imbalanced. For whereas considerable effort has been devoted to understanding the neurochemical response to negative energy balance, relatively little attention has been devoted to the inverse situation of positive energy balance. This oversight is significant since obesity is necessarily associated with periods of positive energy balance and therefore can be considered as a failure of the body weight regulatory system to respond appropriately to positive energy balance. Thus studying the responses to positive energy balance may provide valuable clues concerning the etiology of obesity. Moreover, the regulatory responses to positive energy balance represent the recruitment of endogenous systems that produce reduced food intake, increased energy expenditure and significant weight loss. Finding potential ways to mimic or trigger these endogenous regulatory response systems could provide unique insights and therapeutic strategies for the treatment of obesity. The current proposal seeks to identify critical aspects of this response system. When animals are force-fed calories in excess of caloric need (involuntary overfeeding), their spontaneous food intake drops to near zero and they gain body weight. Additionally, for some time

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after the overfeeding regimen is terminated, spontaneous food intake remains low until body weight has returned to control levels. Our data indicate that this regulatory response to positive energy balance is mediated by the CNS melanocortin system. We propose assessing several hypotheses concerning how the CNS melanocortin system orchestrates the response to positive energy balance. First, we will determine the critical population of melanocortin receptors that mediate the reduced food intake and increased energy expenditure that follow a period of positive energy balance. Second, we will determine the critical inputs into the melanocortin system that signal positive energy balance. Finally, we will evaluate the unique effects of an endogenous melanocortin receptor antagonist that counteracts the normal response to positive energy balance. The information from this proposal will be critical to a complete picture of how energy balance is regulated and how disorders of energy balance such as obesity may be treated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: RESEARCH IN PRADER-WILLI SYNDROME AND OBESITY Principal Investigator & Institution: Driscoll, Daniel J.; Hayward Professorship in Genetics Resear; Pediatrics; University of Florida Gainesville, FL 32611 Timing: Fiscal Year 2001; Project Start 07-JUN-2000; Project End 31-MAY-2005 Summary: (Adapted from the candidate's description) The goals of this translational research project are to genetically and clinically dissert the imprinted genes underlying each component of Prader-Willi syndrome (especially the gene causing obesity), and to explore the potential role of early childhood morbid obesity plays in mental retardation. This will be accomplished by screening for mutations in candidate genes for various phenotypic components of PWS; performing psychometric testing on children with early onset morbid obesity and their families; and correlating hormonal and neurotransmitter levels from blood and CSF with the psychometric and mutation analyses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: RESISTANCE TRAINING FOR THE PREVENTION OF OBESITY Principal Investigator & Institution: Washburn, Richard A.; Associate Professor; Energy Balance Laboratory; University of Kansas Lawrence Lawrence, KS 66045 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-MAY-2005 Summary: (provided by applicant): Obesity is associated with numerous co-morbidities, including cardiovascular disease, diabetes, hypertension and some cancers. Weight loss is difficult; therefore interventions to prevent the development of obesity are warranted. In this project we will evaluate the potential of resistance training (RT) to prevent the development of obesity in healthy, sedentary, overweight, young (18-25 yrs) college men and women, an accessible group at high risk for becoming obese. RT offers an innovative approach to obesity prevention that differs in concept from. Unlike aerobic exercise, RT results in a minimal increase in energy expenditure during exercise, but may result in significant increases in total daily energy expenditure resulting from increased resting metabolic rate (RMR) mainly as a result of increased fat-free mass (FFM). The efficacy of the RT protocols recommended as part of adult fitness programs to alter FFM and RMR is unknown. Therefore; this research project will determine the level of RT necessary to induce increases in muscle mass and RMR, which may, in turn be associated with weight maintenance or loss. All RT will be supervised and verified by the research team. We will compare changes in FFM and RMR elicited by 24 weeks of

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RT conducted as recommended by ACSM (1 set, 3 d/wk, resistance 8-12 repetitions maximum (RM), 9 exercises) with a higher intensity RT program (1 set, 3 d/wk, resistance 3-6 RM, 9 exercises) in a volunteer sample of 108 young adults (36 men, 72 women) matched on muscle mass and randomly assigned to the RT protocols or a nonexercise control condition within gender. Fat-free and muscle mass (DEXA), RMR (indirect calorimetry), and muscular strength (1-RM) will be assessed at baseline, and at 12 and 24 weeks. Dietary intake (24hr. recall) will be assessed monthly. If our pilot project proves successful, i.e., our RT program results in clinically significant increases in RMR, we will propose a larger and longer (18 m) randomized trial to assess the efficacy of RT for weight loss or prevention of weight gain. This trial will employ a complete energy balance model including detailed assessments of total energy intake and expenditure using state-of-the-science techniques (doublylabeled water, wholeroom calorimetry, visual plate waste), and will investigate potential mechanisms, such as changes in protein turnover and sympathetic nervous system activity, that may be associated with increased RMR resulting from RT. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: RESISTIN'S ROLE IN OBESITY RELATED INSULIN RESISTANCE Principal Investigator & Institution: Steppan, Claire M.; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2004 Summary: (provided by applicant) This proposed research plan describes a 3 year training program for the development of an academic career. The candidate has completed four years of post-doctoral fellowship training and will expand her training during this time period to progress to an academic position. This proposal will define the role of resistin in obesity-related insulin resistance. Mitchell A. Lazar, M.D., Ph.D. will mentor the applicant's scientific development. Dr. Lazar is a recognized leader in the field of nuclear receptors and adipogenesis. Dr. Lazar is the Chief of Endocrinology, Metabolism and Diabetes and the Director of the Penn Diabetes Center. To enhance the training, the applicant will enlist the expertise of Morris Birnbaum, M.D., Ph.D., Howard Hughes Professor and Rexford Ahima, M.D., Ph.D., assistant professor and Director of the Physiology Core of the Penn Diabetes Center. In addition to performing research, the Principal Investigator will benefit from lectures, seminars, and advisory committee meetings. The proposed research will focus on a newly identified hormone that is secreted from adipocytes and which has been shown to antagonize the effects of insulin. The proposed experiments will entail analyzing components in the insulin signaling cascade downstream of insulin binding to determine the mechanism of antagonism of insulin action by resistin (Specific Aim 1). In order to address the role of resistin in insulin resistance associated with obesity (Specific Aim 2), we will study the in vivo regulation of resistin in several different animal models of obesity. We plan to study obesity models in which leptin signaling is impaired (ob/ob, db/db) and intact (Agouti, Cpe-fat). The proposed research plan will reveal detailed information about resistin's role in obesity and diabetes. The scientific environment of the University of Pennsylvania provides the ideal opportunity for the candidate to develop her career by executing the proposed research while utilizing the expertise and resources of Dr. Mitchell A. Lazar. Such an environment should allow the candidate to maximize her potential to establish herself as an independent investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: ROLE OF THE LOWER GUT IN THE CONTROL OF ENERGY BALANCE Principal Investigator & Institution: Koopmans, Henry S.; University of Calgary 2500 University Dr Nw Calgary, Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2006 Summary: Surgery has been the most successful treatment for morbid obesity. The main objective of this grant proposal is to determine why lower gut signals generated in bypass surgery have been so successful in causing reduced food intake and body weight loss. We recently discovered that lower gut signals also cause a 10-25 percent increase in energy expenditure. One objective of this grant proposal is to determine how stimulation of different lengths of the ileum, caecum and colon affect energy balance and the plasma levels of the lower gut hormones: neurotensin; PYY and GLP1. Another objective is to determine the role of the extrinsic nerves to the ileum in altering food intake, energy expenditure and body weight by doing ileal transplantation surgery or denervation of the superior mesenteric nerves. A time course of the changes in energy expenditure, upper gut tissue growth and plasma lower gut hormone levels resulting from ileal transposition will be investigated in preparation for a later peptide infusion study. The role of the various macronutrients in changing energy balance and lowering body weight will be assessed by feeding various diets to rats with a 20 cm segment of ileum moved up to the mid-duodenum. The short-term objective of this research is to understand the internal control of daily intake and energy expenditure. The long-term objective is to find a medical treatment (drug or hormone analog) for obesity. In Western societies, obesity is a major medical problem that causes a great deal of human suffering. Obesity is associated with such chronic and debilitating conditions as diabetes, cancer (breast, endometrial, prostate and colon), hypertension, hyperlipidemia, stroke and heart disease. An effective medical treatment for obesity would improve the quality of life for millions of people and would reduce the cost of long-term health care. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: RURAL COMMUNITY PARTNERSHIP TO PROMOTE FITNESS BY AGE 5 Principal Investigator & Institution: Dennison, Brbara A.; Mary Imogene Bassett Hospital Cooperstown, NY 13326 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2005 Summary: (provided by applicant): This proposal, Rural Community Partnership to Promote Fitness by Age 5, focuses on preventing the development of obesity among young, preschool-age children, by targeting the environment where children are increasingly spending time prior to the start of kindergarten-childcare centers (daycare, preschools, and Head Start centers). The theoretical frameworks of "Diffusion of Innovation" and "Social Marketing" will guide the development of this intervention by researchers and childcare center directors and staff. Support from community, medical, and educational organizations and collaboration with the local McDonald's restaurant, Price Chopper grocery stores, and SUNY-Cobleskill Culinary Institute will facilitate consistency of message. We propose to assess food and physical activity policies and environments at childcare centers, and then collaboratively develop innovative policy and environmental changes to promote healthy eating (especially snacking), decrease behaviors that encourage overeating, increase physical activity, and decrease TV/video viewing at these centers. We propose to develop and provide training sessions for staff at childcare centers that promote these policy changes and environmental innovations.

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As the primary outcome, we will evaluate the difference in the prevalence of child obesity at age 5, i.e., at the time of kindergarten entrance, between the intervention and the control communities. At the conclusion of this research project, a childcare centerbased environmental approach to prevent the development of child obesity will have been developed, implemented, and evaluated. This obesity prevention program will be transferable to other childcare centers to improve the health of America's children. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: SELF-MONITORED MANAGEMENT

PHYSICAL

ACTIVITY

FOR

WEIGHT

Principal Investigator & Institution: Walker, Karen E.; Temple University 406 Usb, 08345 Philadelphia, PA 19122 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2006 Summary: (provided by applicant): This application for a Mentored Research Scientist Development Award (K01) is a re-submission by a new investigator. The goal of the award is to provide the investigator further training in the fields of obesity and community health nursing. As part of this training, the investigator will receive mentoring and pursue academic study in the following areas: 1) etiology and complications of obesity; 2) behavioral treatment of obesity; 3) community health nursing; 4) conduct of clinical trials; 5) exercise physiology; 6) biostatistics; and 7) nutrition. The proposal builds on a background in cardiovascular research, clinical study of weight loss maintenance, and community-based activities. Recent data show that 61% of US adults are overweight or obese. As a result, there is an epidemic of obesity-related health problems such as diabetes, coronary artery disease, and high blood pressure. Losses of only 5% to 10% of body weight significantly improve health, and individuals in programs that modify diet and lifestyle typically achieve weight losses of this magnitude. Unfortunately, the great majority of people cannot maintain the loss. Regular exercise is crucial to the maintenance of weight loss, but most individuals have problems with adherence due to a variety of barriers to exercise. Typical barriers are lack of time, lack of childcare, and lack of access to facilities. The goal of the proposed research is to improve the maintenance of weight loss by increasing physical activity in a low-income, primarily African American population that participates in a community-based behavioral weight loss program. All participants (n=152) will be treated with a 20-week weight reduction program followed by 52 weeks of maintenance. At the outset of the study, subjects will be randomized to one of two physical activity conditions. The research has two specific aims: The first is to compare at week 72 the maintenance of weight loss and physical activity adherence in individuals who are prescribed a standard structured exercise program of walking (Condition 1) versus a lifestyle activity intervention self-monitored via pedometer (Condition 2). Adherence will be determined by obtaining a common measure of physical activity across both conditions using accelerometers. The second aim is to compare short- (week 20) and long-term (week 72) differences between the two conditions in measures of physical (serum lipids, glucose/insulin ratio, interleukin-6, Creactive protein, resting blood pressure, cardiorespiratory fitness) and psychosocial health (mood, quality of life). This study has been selected to further develop the investigator's knowledge of the treatment of obesity using principles of community health nursing, and the training has been designed to facilitate the investigator's development as an independent clinical scientist studying innovative ways of reducing cardiovascular risks within urban communities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: SOCIAL DETERMINANTS OF OBESITY AND RISK OF STROKE Principal Investigator & Institution: Dubowitz, Tamara; Maternal and Child Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, MA 02460 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2006 Summary: (provided by applicant): Stroke is the third leading cause of death in the United States, and a leading cause of long-term disability. The risk for stroke varies by race/ethnicity; stroke incidence is greater among African Americans at younger ages, contributing to a mortality rate 80 percent greater than that of Caucasians (Keppel et al 2002; DHHS 2000; Stroke Progress Review Group, NINDS 2002). Limited understanding exists concerning the etiology and variations of subtypes of stroke incidence in different populations and geographic locations over time (Stroke Progress Review Group, NINDS 2002). Obesity, which results in part from a complex pathway of numerous lifestyle precursors, is a strong predictor of cerebrovascular disease such as stroke and other cardiovascular disease (WHO, 2000). Moreover, dietary intake and physical activity contribute to energy imbalances that result in obesity and independently predict stroke (AICR 1997; USDA/USDHHS 2000; USDHHS 1996; 2000; Krebs-Smith SM. 2001). Few studies consider both biological and social determinants of intermediate outcomes of cerebrovascular disease from a multileveled perspective. This application considers longitudinal measures of social and biological variables to investigate the independent effect of social disparities to the development of obesity among low-income multi-ethnic postpartum women at increased risk of stroke and other comorbidities. As women face particular biological and social transition during the postpartum period, the proposed research seeks to measure social determinants of pregnancy-related weight gain over time, adjusting for diet, physical and biological predictors of obesity and stroke. Research findings from the proposed work can inform the design of future interventions to reduce risk of stroke in women of reproductive age in low income, racial/ethnic subpopulations at highest risk of obesity and its sequelae. Specific aims include examination of: (1) individual and household social determinants pregnancy-related weight change and obesity; (2) social disparity in dietary intake and nutritional status and its relation to pregnancy-related weight change and obesity; and (3) neighborhood characteristics that influence the development of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: THE 4 CORNERS BREAST AND ENDOMETRIAL CANCER STUDY Principal Investigator & Institution: Baumgartner, Kathy B.; Phd; Internal Medicine; University of New Mexico Albuquerque Controller's Office Albuquerque, NM 87131 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-JUL-2004 Summary: (Adapted from Applicant's Abstract) The incidence of breast and endometrial cancers varies almost three-fold between non-Hispanic white populations and Native American and Hispanic populations living in the 4-Corners area of the United States (Arizona, New Mexico, Colorado, and Utah). Interestingly, although American Indian and Hispanic women have higher prevalences of many risk factors for breast and endometrial cancer identified in non-Hispanic white women (e.g., obesity, low levels of vigorous physical activity, low intakes of fruits and vegetables, high rates of insulin resistance) they have lower cancer incidence rates. In this study the investigators focus on the metabolic factors of obesity/weight changes and indicators of insulin status as they relate to breast and endometrial cancers. Obesity is associated both with estrogen and insulin by two interrelated disease pathways. Insulin may influence cancer risk directly through its effects on insulin-like growth factor (IGF) and its binding proteins

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(IGFBPs) and well as indirectly through its effect on estrogen levels. The investigators propose focusing on the insulin pathway because of the high levels of insulin pathway dysfunction in this population. A multi-center case-control study is proposed that targets women living in the 4-Corners area; the study will consist of a 2.5 hour in-person interview and a blood draw. Over a three-year case ascertainment period, the study will enroll 3000 breast cancer cases, 450 endometrial cancer cases and 3000 controls, half of whom will be Hispanic/Native American and half of whom will be non-Hispanic white women between the ages of 25 and 79. Molecular variants of genes that influence obesity and insulin (androgen receptor gene (AR), vitamin D receptor gene(VDR), insulin receptor (ADRB3)) will be examined both independently and in conjunction with metabolic factors to determine differences in genetic susceptibility in the population. Because of the diverse population (Hispanics, Native American, and non-Hispanic white women), the investigators propose to evaluate ethnic background and genetic admixture in relationship to gene markers, environmental factors, and breast and endometrial cancer risk. Genetic admixture (Ameridian to European genetic mixture) is a novel and innovative way to study the continuum of ethnic diversity. C-peptide, glycosylated hemoglobin, IGF-1, and IGFBP3 will be evaluated with respect to breast and endometrial cancer in a subset of women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: THE EPIDEMIOLOGY OF BODY MASS INDEX REBOUND Principal Investigator & Institution: Daniels, Stephen R.; Professor of Pediatrics and Environment; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, OH 45229 Timing: Fiscal Year 2001; Project Start 17-AUG-2000; Project End 31-JUL-2005 Summary: (Adapted from the Investigator's Abstract) Obesity is the most obesity which are present prior to the onset of excess weight gain has been problematic. Recently, it has been shown that the timing of body mass index (BMI) rebound may be a predictor of future obesity. BMI increases during the first year of life. It then declines until it reaches a minimum value during childhood and subsequently increases into adolescence and adulthood. The nadir of BMI is called BMI rebound. Studies have shown that BMI rebound at a younger age is associated with increased risk of obesity later in life. Currently, very little is known about the epidemiology of BMI rebound. The purpose of the proposed investigation is to precisely determine the age of BMI rebound and evaluate the body composition changes which occur during this time to determine if BMI rebound corresponds to a rebound in adiposity. In addition, determinants of the changes in body composition, such as diet and physical activity, will be investigated. Finally, the relationship of the timing of BMI rebound to body composition and cardiovascular risk factor status will be studied. The proposed investigation is a cohort study designed to follow 320 children from age three age seven years. Subjects will be evaluated every four months during the period of the study. Data will be collected on height, weight, body composition, diet and physical activity. At age seven years, the level of adiposity, the distribution of body fat, and cardiovascular risk factors will be studied. The investigators note that better understanding of the epidemiology of BMI rebound could lead to improved identification of children at high risk of future obesity prior to excess weight gain. They further note that elucidation of the determinants of the timing of BMI rebound could lead to the development of clinical and public health strategies to prevent the development of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TREATMENT FOR OBESITY AND BINGE EATING DISORDER Principal Investigator & Institution: Grilo, Carlos M.; Associate Professor; Psychiatry; Yale University 47 College Street, Suite 203 New Haven, CT 065208047 Timing: Fiscal Year 2002; Project Start 01-AUG-1996; Project End 31-JUL-2007 Summary: (provided by applicant): This application seeks funds to conduct a study of cognitive behavioral and behavioral weight loss treatments for obese patients with binge eating disorder (BED). The proposed study builds directly upon the findings of the initial project that examined the efficacy of fluoxetine treatment and cognitive behavioral therapy (CBT) and the relative efficacy of the treatments alone and in combination for patients with BED (balanced 2 x 2 factorial design). CBT produced significant and clinically meaningful improvements in the behavioral (binge eating), cognitive (attitudinal features of eating disorders), and associated psychological (depression) features of BED, but not for the physical problem of obesity. In the 2 x 2 factorial design: (1) CBT was superior to treatment without CBT, treatment with fluoxetine was not superior to treatment without fluoxetine, and no interaction between treatments occurred; (2) Specific comparisons among specifc treatments revealed that fluoxetine was not superior to placebo, CBT + Placebo and CBT + Fluoxetine were similar, and CBT + Placebo and CBT + Fluoxetine were superior to Fluoxetine-only and Placebo-only. Findings suggest that CBT has efficacy for the behavioral, cognitive, associated psychological features of BED. The strong association between BED and obesity, and the major health risks associated with obesity highlight the need for developing interventions that also reduce weight. It remains uncertain whether behavioral weight loss (BWL) has efficacy for producing weight loss in BED or for reducing binge eating and its associated features. The proposed study involves a comparison of three treatment conditions: (1) CBT; (2) BWL, and (3) a sequential (twopart) treatment consisting of CBT followed by BWL. Assessments will occur at baseline, bimonthly during treatment, and 6-and 12-months post-treatment. The primary specific aim is to test the relative efficacy of CBT, BWL, and a sequential treatment consisting of CBT followed by BWL. Secondary aims are to (1) explore predictors and processes of change during the acute treatment and follow-up period, and (2) examine whether (a) BWL ("dieting") after the CBT produces weight loss, and (b) weight regain (if it occurs following BWL) is accompanied/followed by reoccurrence of binge eating, attitudinal features of eating disorders, psychological distress, or psychiatric disturbances. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: TREATMENT OF OBESITY IN UNDERSERVED RURAL SETTINGSTOURS Principal Investigator & Institution: Perri, Michael G.; Professor; Medicine; University of Florida Gainesville, FL 32611 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2007 Summary: (provided by applicant): Higher rates of obesity, sedentary lifestyle, and coronary heart disease are observed in rural than non-rural areas of the U.S., yet the treatment of obesity in the rural population has received little research attention. Efficacy studies, typically conducted in urban settings, show that lifestyle interventions produce clinically significant weight reductions, but a regaining of lost weight commonly follows the conclusion of treatment. Recent studies have demonstrated that clinic-based, extended-care programs can improve the maintenance of lost weight. Thus, the next logical steps in this line of research are (a) to extend these studies to community settings with underserved populations and (b) to test alternative and potentially more

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efficient methods of providing extended care, such as through the use of telephonebased rather than clinic-based maintenance programs. The primary objective of TOURS is to test the effectiveness of weight-loss maintenance programs in a randomized controlled trial, conducted in medically underserved rural settings. Obese women (N=300), ages 50-75 years, from six medically underserved rural counties will be randomly assigned to one of three 18- months long obesity treatment programs. Each treatment condition will include an initial 6-month lifestyle intervention followed by one of three 12-month follow-up programs: (A) an Office-based Maintenance Program, (B) a Telephone-Based Maintenance Program, or (C) an Education Control Condition. Dependent variables to be assessed at baseline, 6 months, and 18 months will include body weight, as well as a selected Array of health-related indicators and quality of life measures. It is hypothesized that participants assigned to either of the experimental programs will exhibit better maintenance of lost weight compared with those assigned to the control condition. Potential mediators and moderators of the intervention program-weight change relationship will be examined, and exploratory analyses of the costs and cost effectiveness of the interventions will be conducted. This trial will contribute important public health information regarding methods for improving obesity management in an underserved population at high risk for weight-related chronic diseases and disability. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: UAB CLINICAL NUTRITION RESEARCH UNIT Principal Investigator & Institution: Allison, David B.; Professor; Nutrition Sciences; University of Alabama at Birmingham Uab Station Birmingham, AL 35294 Timing: Fiscal Year 2003; Project Start 01-JUN-2000; Project End 31-MAY-2005 Summary: (adapted from the application) The proposed UAB Clinical Nutrition Research Unit (CNRU) will foster a multidisciplinary approach to basic, clinical and translational research with an emphasis on understanding the metabolic factors, environmental influences, and associated genetic traits underlying nutrition and obesity-related health problems. The University of Alabama at Birmingham (UAB) provides an ideal academic environment for interdisciplinary research centers. With a 50-year history of pioneering research, the Department of Nutrition Sciences currently includes 18 primary research faculty and $8.3 million in total direct cost funding (80% federal). In addition, the Department coordinates all of the extensive nutrition training and service programs at UAB. To complement its well-established nutrition research program, in 1990, the Department initiated a campus-wide effort to strengthen obesity research. Institutional support of $1.96 million enabled development of the Energy Metabolism Research Laboratory and recruitment of an outstanding team of scientists. The result was rapid growth in new/peer-reviewed funding and interdisciplinary collaborations, such that in 1996 UAB established an intramurally-funded UniversityWide Obesity Nutrition Research Center which, with NIH funding, will evolve into the proposed CNRU. The CNRU research base comprises 60 investigators from 18 academic units, with total direct funding of $44 million for nutrition/obesity research (88% federal; 11 R01s). Of the 77 funded nutrition/obesity studies and approved P/F projects, 65 (84%) will use CNRU Cores. The Energy Metabolism/Body Composition Core will support metabolic studies in humans and small animals; Genetics Core will focus on research related to gene expression, polymorphism detection, and genetic animal models; Nutrient Analysis Core will provide an array of nutrient analyses and new methods development; and the Biostatistics Core will support study design and data analysis. The CNRU will also support three P/F studies, a New Investigator, and an

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Enrichment Program. With exceptional institutional support and an ideal academic infrastructure, UAB has established a strong base of obesity/nutrition research and is now poised to greatly expand this effort through creation of a CNRU. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: UCLA TRAINING PROGRAM IN NUTRITION AND OBESITY Principal Investigator & Institution: Heber, David; Professor/Chief; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, CA 90024 Timing: Fiscal Year 2003; Project Start 30-SEP-1992; Project End 31-MAR-2008 Summary: This proposal requests renewed support for the UCLA Nutrition and Obesity Training Program in order to continue to train diverse and highly trained clinical and basic scientists in nutrition and obesity research. Through stipends and educational support of four postdoctoral M.D. or Ph.D. trainees, this program seeks to develop a new generation of scientists and physician-scientists capable of translating advances in the understanding of gene-nutrient interactions relevant to obesity and obesity-related diseases to clinical medicine and community health both nationally and internationally. Obesity-related diseases account for 300,000 deaths per year and one of 9 health care dollars are spent on over 30 obesity-related diseases. This program was established in 1992, and has since developed a cadre of dedicated faculty, a clear record of accomplishment among nutrition fellows who have advanced their careers to become competitively funded investigators in nutrition and obesity-related research areas. Since the last renewal, the UCLA Center for Human Nutrition has grown considerably with the funding in 1999 of the UCLA P50 Center for Dietary Supplements Research:Botanicals (CDSRB), and the NCI -funded P30 Clinical Nutrition Research (CNRU) which was competitively renewed for five years in 2002. All of these programs are housed in the Center for Human Nutrition which also is the site of successful clinical programs integrated into the research training of both basic and clinical scientists including the University Obesity Center, the Surgical Obesity Program, the Primary Care Network, and Community Outreach Programs in the Venice Family Clinic and Martin Luther King Medical Center. The Administrative Unit of the Center will administer the training program and foster the growth of the trainees. The training program will be directed by a Steering Committee including Principal Training Faculty from six broad areas: 1 ) The Genetics of Obesity; 2) Adipocyte and Lipid Metabolism; 3) Neuroregulation and Satiety; 4) Eating Disorders and Behavioral Medicine; 5) Clinical Research and Biostatistics; and 6) Minority and International Nutrition Research. The UCLA Center for Human Nutrition including the Nutrition Research Laboratories and the Scientific Core Laboratories of the CNRU and the CDSRB will provide laboratory resources and faculty expertise. Trainees in basic and clinical sciences training side by side will be prepared for the research agenda mandated by the growing epidemic of obesity through the acquisition of skills in molecular biology, genetics and neurosciences while critically understanding their translation to the clinical and public health challenges of the epidemic of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: VALIDATION OF HMGI-C AS A DRUG TARGET IN OBESITY Principal Investigator & Institution: Chouinard, Roland A.; Hmgene, Inc. 1308 Centennial Ave, #140 Piscataway, NJ 08854 Timing: Fiscal Year 2001; Project Start 15-AUG-1999; Project End 31-JUL-2003

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Summary: The unique, novel approach of HMGene to obesity treatment is to develop drugs that act directly on adipose tissue. The goal of Phase II will be to further validate HMGI-C, an architectural transcription factor which regulates gene expression in adipogenesis, as a drug target in obesity. In Phase I, it was shown that inactivation of HMGI-C reverses the obesity induced by leptin deficiency. Phase II will extend those studies to show that the same holds true for diet induced obesity which is a more physiological model and more closely parallels the human disease. As HMGI-C is a transcriptional regulator and sits at the apex of a genomic cascade, DNA microarray and RNA differential display technology will be used to identify genes in the HMGI-C genomic pathway which will provide novel drug targets. Finally, as the ultimate goal is to develop a safe, effective therapeutic for the treatment of obesity, both biochemical and cellular based assays will be developed in order to screen for small molecule inhibitors of HMGI-C which may be useful in the treatment of obesity. PROPOSED COMMERCIAL APPLICATIONS: Successful completion of this project would open up new prospects of the discovery of effective, clinically valuable anti-obesity drugs, which would have an enormous commercial potential. It is estimated that the U.S. mark for a prescription anti-obesity drug is approximately $ 1 billion in annual sales. For an overthe-counter drug, potential market is believed to be $10 billion. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: VISCREAL ADIPOSITY: GENETIC AND ENVIRONMENTAL INFLUENCES Principal Investigator & Institution: Demerath, Ellen W.; Assistant Professor; Community Health; Wright State University Colonel Glenn Hwy Dayton, OH 45435 Timing: Fiscal Year 2003; Project Start 20-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The goal of the proposed study is to understand the genetic architecture underlying visceral obesity and its associated physiological components. Accumulation of fat deep within the abdomen (i.e., visceral adipose tissue) is known to play a pivotal role in the development of non-insulin dependent diabetes mellitus and cardiovascular disease (CVD). In our proposed study, we aim to disentangle the genetic and environmental factors that explain human variation in visceral adiposity by viewing it as a component of a phenotypic complex that also includes insulin resistance, vascular inflammation, and hormonal variations (the "visceral obesity complex"). The proposed study is built upon an existing study of 1,000 individuals in five large multi-generational kindreds, in which whole-genome genotyping and disease risk factor phenotyping are already underway. The proposed study has three specific aims. In Specific Aim 1 we will phenotype the study population using MRI and dual energy x-ray absorptiometry to measure the amount and distribution of visceral and subcutaneous adipose tissue, using ELISA to assay concentration of adipocyte-derived hormones, and using a repeated 24-hour dietary recall protocol to characterize current energy and macronutrient intake. In Specific Aim 2 we will use variance components-based quantitative genetic methods for extended pedigrees to estimate the heritability of the independent components of the visceral obesity complex, identify key environmental variables and covariates (i.e., sex, age, diet, physical activity, hormone usage, smoking and alcohol consumption) that influence the visceral obesity complex alone or in interaction with genetic factors, and examine the extent to which common genetic factors underlie this complex of closely related traits. In Specific Aim 3, we will use variance components-based linkage methods to identify quantitative trait loci (QTL) harboring genes that influence variation in constituent components of the visceral obesity complex. We also will examine gene-by-

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environment, gene-by-sex, and gene-by-age interactions in these traits. Fine mapping procedures will be used further localize QTL that are identified. At the conclusion of the proposed study, we will have identified particular genetic loci that influence the visceral obesity complex, and will better understand how particular genotypes may, when confronted with particular environments, predispose individuals to the accumulation of visceral adipose tissue, thereby putting them at increased future risk for developing diabetes and CVD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •

Project Title: WEIGHT GAIN IN AFRICAN-AMERICAN GIRLS Principal Investigator & Institution: Rochon, James; Research Professor; Statistics; George Washington University 2121 I St Nw Washington, DC 20052 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-MAY-2002 Summary: According to NHANES data, the prevalence of obesity in the U.S. population has increased from 25 percent to 33 percent over the past 10 years. Obesity is well accepted as a risk factor for coronary heart disease and type 2 diabetes, and it exacerbates many chronic conditions such as hypertension and dyslipidemia. Not surprisingly, the economic costs of obesity are staggering and amount to approximately 100 billion dollars annually. The prevalence of obesity appears to be proportionately greater in certain minority populations. Almost twice as many African-American women are overweight compared to Caucasians. Moreover, the disproportionate levels of obesity in African-American women may have their origins in childhood and adolescence. Approximately 30 percent of African-American girls between the ages of 6 and 17 years are overweight, compared to only 22 percent for all other youth as a whole. Large prevention trials, most notably, the Child and Adolescent Trial for Cardiovascular Health (CATCH) and the Dietary Intervention Study in Children (DISC), have been largely unsuccessful in producing reductions in dietary fat, body weight or BMI. Thus, the NHLBI has proposed a research program to develop and test interventions to prevent weight gain in preadolescent African-American girls. The Biostatistics Center of the George Washington University proposes to serve as the Coordinating Center for this project. In this role, we will attend to the following functions. (1) Study Coordination and Planning: We will help establish an efficient organizational structure to ensure that all activities advance in a coordinated fashion. (2) Data Management Activities: We will apply our Distributed Data Entry system for on-going data collection and generate periodic reports summarizing the execution of the trial. (3) Statistical Analysis: We will provide statistical leadership in the design of the study, and perform interim and final analyses in an expeditious and timely manner. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

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Project Title: WISE MIND: ENVIRONMENTAL APPROACH FOR OBESITY PREVENTION Principal Investigator & Institution: Williamson, Donald A.; Professor; None; Lsu Pennington Biomedical Research Ctr 6400 Perkins Rd Baton Rouge, LA 70808 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2005 Summary: (provided by applicant): In this pilot study, we propose a two-arm primary prevention trial to test the efficacy of an environmental approach for the prevention of obesity in children who are in the second through sixth grades. An attention-placebo control group will receive an environmental approach for the prevention of alcohol drug tobacco use and abuse. This test of an environmental approach targets a school system

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for change. Four schools with a total of approximately 1,040 students will be the participants in the study. The four schools will be randomly assigned to one of the two treatment arms. The prevention study will be conducted across two consecutive academic years. The primary endpoint will be body mass index. The primary aim of the study is to test the efficacy of the obesity program for the prevention of weight gain in children. Changes in dietary intake and physical activity will be tested as mediators of changes in body mass index. Also, age of the child, initial body mass index, and gender will be tested as factors that are associated with differential outcomes related to the prevention of weight gain. Secondary endpoints include: body composition, waist circumference, physical activity, dietary intake, body image, mood, and self-esteem. The environmental program for the prevention of obesity will have multiple components that are designed to alter automatic/habitual decision making by students. The results of this pilot study will guide the development of full-scale investigations in a larger set of schools. The findings of the study will have significant impact upon public health policy regarding prevention of obesity. Several innovations are utilized in the study, including novel applications of the internet to provide environmental prompts to parents and families, and the use of a new method, called digital photography of foods, for measurement of the food selections and food intake of individual students, in school cafeterias. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen

E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “obesity” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for obesity in the PubMed Central database: •

11[beta]-Hydroxysteroid dehydrogenase type 1 knockout mice show attenuated glucocorticoid-inducible responses and resist hyperglycemia on obesity or stress. by Kotelevtsev Y, Holmes MC, Burchell A, Houston PM, Schmoll D, Jamieson P, Best R, Brown R, Edwards CR, Seckl JR, Mullins JJ. 1997 Dec 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=25139

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A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors. by Ste. Marie L, Miura GI, Marsh DJ, Yagaloff K, Palmiter RD. 2000 Oct 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17343

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A new class of obesity genes encodes leukocyte adhesion receptors. by Dong ZM, Gutierrez-Ramos JC, Coxon A, Mayadas TN, Wagner DD. 1997 Jul 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23855

3 4

Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.

With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.

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Abnormal regulation of the leptin gene in the pathogenesis of obesity. by Ioffe E, Moon B, Connolly E, Friedman JM. 1998 Sep 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21729

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Adrenalectomy stimulates hypothalamic proopiomelanocortin expression but does not correct diet-induced obesity. by Makimura H, Mizuno TM, Beasley J, Silverstein JH, Mobbs CV. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165436

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Alteration of the Leptin Network in Late Morbid Obesity Induced in Mice by Brain Infection with Canine Distemper Virus. by Bernard A, Cohen R, Khuth ST, Vedrine B, Verlaeten O, Akaoka H, Giraudon P, Belin MF. 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=104257

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An agouti mutation lacking the basic domain induces yellow pigmentation but not obesity in transgenic mice. by Miltenberger RJ, Mynatt RL, Bruce BD, Wilkison WO, Woychik RP, Michaud EJ. 1999 Jul 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17559

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Aromatase-deficient (ArKO) mice have a phenotype of increased adiposity. by Jones ME, Thorburn AW, Britt KL, Hewitt KN, Wreford NG, Proietto J, Oz OK, Leury BJ, Robertson KM, Yao S, Simpson ER. 2000 Nov 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18833

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Association between postnatal catch-up growth and obesity in childhood: prospective cohort study. by Ong KK, Ahmed ML, Emmett PM, Preece MA, Dunger DB. 2000 Apr 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27335

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Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency. by Farooqi IS, Matarese G, Lord GM, Keogh JM, Lawrence E, Agwu C, Sanna V, Jebb SA, Perna F, Fontana S, Lechler RI, DePaoli AM, O'Rahilly S. 2002 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150795

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Breast feeding and obesity: cross sectional study. by von Kries R, Koletzko B, Sauerwald T, von Mutius E, Barnert D, Grunert V, von Voss H. 1999 Jul 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28161

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Breast is best for avoiding obesity. by Kerr C. 2002 Aug 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=117486

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C75 increases peripheral energy utilization and fatty acid oxidation in diet-induced obesity. by Thupari JN, Landree LE, Ronnett GV, Kuhajda FP. 2002 Jul 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123169

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Central overweight and obesity in British youth aged 11-16 years: cross sectional surveys of waist circumference. by McCarthy HD, Ellis SM, Cole TJ. 2003 Mar 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151972

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Ciliary neurotrophic factor activates leptin-like pathways and reduces body fat, without cachexia or rebound weight gain, even in leptin-resistant obesity. by Lambert PD, Anderson KD, Sleeman MW, Wong V, Tan J, Hijarunguru A, Corcoran TL, Murray JD, Thabet KE, Yancopoulos GD, Wiegand SJ. 2001 Apr 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=31889

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Ciliary neurotrophic factor corrects obesity and diabetes associated with leptin deficiency and resistance. by Gloaguen I, Costa P, Demartis A, Lazzaro D, Di Marco A, Graziani R, Paonessa G, Chen F, Rosenblum CI, Van der Ploeg LH, Cortese R, Ciliberto G, Laufer R. 1997 Jun 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21071

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Combined effects of insulin treatment and adipose tissue-specific agouti expression on the development of obesity. by Mynatt RL, Miltenberger RJ, Klebig ML, Zemel MB, Wilkinson JE, Wilkison WO, Woychik RP. 1997 Feb 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19614

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Correction of obesity and diabetes in genetically obese mice by leptin gene therapy. by Muzzin P, Eisensmith RC, Copeland KC, Woo SL. 1996 Dec 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26217

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Corticotropin-releasing factor-binding protein ligand inhibitor blunts excessive weight gain in genetically obese Zucker rats and rats during nicotine withdrawal. by Heinrichs SC, Lapsansky J, Behan DP, Chan RK, Sawchenko PE, Lorang M, Ling N, Vale WW, De Souza EB. 1996 Dec 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26429

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Decreased Food Intake does not Completely Account for Adiposity Reduction after ob Protein Infusion. by Levin N, Nelson C, Gurney A, Vandlen R, Sauvage FD. 1996 Feb 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40010

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Diet-induced changes in uncoupling proteins in obesity-prone and obesity-resistant strains of mice. by Surwit RS, Wang S, Petro AE, Sanchis D, Raimbault S, Ricquier D, Collins S. 1998 Mar 31; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19963

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Differential effects of a centrally acting fatty acid synthase inhibitor in lean and obese mice. by Kumar MV, Shimokawa T, Nagy TR, Lane MD. 2002 Feb 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122295

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Do Plants Have a One-Way Ticket to Genomic Obesity? by Bennetzen JL, Kellogg EA. 1997 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=157029

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Ectopic Expression of the Agouti Gene in Transgenic Mice Causes Obesity, Features of Type II Diabetes, and Yellow Fur. by Klebig ML, Wilkinson JE, Geisler JG, Woychik RP. 1995 May 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41780

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Effects of Greek orthodox christian church fasting on serum lipids and obesity. by Sarri KO, Tzanakis NE, Linardakis MK, Mamalakis GD, Kafatos AG. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=156653

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Effects of peroxisome proliferator-activated receptor [delta] on placentation, adiposity, and colorectal cancer. by Barak Y, Liao D, He W, Ong ES, Nelson MC, Olefsky JM, Boland R, Evans RM. 2002 Jan 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=117556

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Establishing a standard definition for child overweight and obesity worldwide: international survey. by Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. 2000 May 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27365

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Evaluation of implementation and effect of primary school based intervention to reduce risk factors for obesity. by Sahota P, Rudolf MC, Dixey R, Hill AJ, Barth JH, Cade J. 2001 Nov 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59380

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Evaluation of indices of obesity in men: descriptive study. by Pounder D, Carson D, Davison M, Orihara Y. 1998 May 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28542

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Fatty acid-induced [beta] cell apoptosis: A link between obesity and diabetes. by Shimabukuro M, Zhou YT, Levi M, Unger RH. 1998 Mar 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19389

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High penetrance, overweight, and glucocorticoid receptor variant: case-control study. by Lin RC, Wang WY, Morris BJ. 1999 Nov 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28280

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Hormone replacement therapy use dramatically increases breast oestrogen receptor expression in obese postmenopausal women. by Lawson JS, Field AS, Tran DD, Houssami N. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=57804

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Hypothalamic growth hormone secretagogue receptor regulates growth hormone secretion, feeding, and adiposity. by Shuto Y, Shibasaki T, Otagiri A, Kuriyama H, Ohata H, Tamura H, Kamegai J, Sugihara H, Oikawa S, Wakabayashi I. 2002 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150991

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Identification of the Promoter of the Mouse Obese Gene. by Brousse FC, Shan B, Chen J. 1996 Apr 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39493

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Immediate and long term effects of weight reduction in obese people with asthma: randomised controlled study. by Stenius-Aarniala B, Poussa T, Kvarnstrom J, Gronlund EL, Ylikahri M, Mustajoki P. 2000 Mar 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27319

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Impact of obesity on glucose and lipid profiles in adolescents at different age groups in relation to adulthood. by Plourde G. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=134463

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Implications of childhood obesity for adult health: findings from thousand families cohort study. by Wright CM, Parker L, Lamont D, Craft AW. 2001 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=60301

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Increased Energy Expenditure, Decreased Adiposity, and Tissue-Specific Insulin Sensitivity in Protein-Tyrosine Phosphatase 1B-Deficient Mice. by Klaman LD, Boss O, Peroni OD, Kim JK, Martino JL, Zabolotny JM, Moghal N, Lubkin M, Kim YB, Sharpe AH, Stricker-Krongrad A, Shulman GI, Neel BG, Kahn BB. 2000 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85999

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Increasing prevalence of obesity in primary school children: cohort study. by Rudolf MC, Sahota P, Barth JH, Walker J. 2001 May 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=31260

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Insulin depletion leads to adipose-specific cell death in obese but not lean mice. by Loftus TM, Kuhajda FP, Lane MD. 1998 Nov 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24345

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Lipotoxic heart disease in obese rats: Implications for human obesity. by Zhou YT, Grayburn P, Karim A, Shimabukuro M, Higa M, Baetens D, Orci L, Unger RH. 2000 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26513

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Long-term correction of obesity and diabetes in genetically obese mice by a single intramuscular injection of recombinant adeno-associated virus encoding mouse leptin. by Murphy JE, Zhou S, Giese K, Williams LT, Escobedo JA, Dwarki VJ. 1997 Dec 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28408

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Loss of stearoyl --CoA desaturase-1 function protects mice against adiposity. by Ntambi JM, Miyazaki M, Stoehr JP, Lan H, Kendziorski CM, Yandell BS, Song Y, Cohen P, Friedman JM, Attie AD. 2002 Aug 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123282

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Major histocompatibility complex class I-restricted T cells are required for all but the end stages of diabetes development in nonobese diabetic mice and use a prevalent T cell receptor [alpha] chain gene rearrangement. by DiLorenzo TP, Graser RT, Ono T, Christianson GJ, Chapman HD, Roopenian DC, Nathenson SG, Serreze DV. 1998 Oct 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22866

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Mice Lacking Paternally Expressed Pref-1/Dlk1 Display Growth Retardation and Accelerated Adiposity. by Moon YS, Smas CM, Lee K, Villena JA, Kim KH, Yun EJ, Sul HS. 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=133956

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Muscle-specific PPAR[gamma]-deficient mice develop increased adiposity and insulin resistance but respond to thiazolidinediones. by Norris AW, Chen L, Fisher SJ, Szanto I, Ristow M, Jozsi AC, Hirshman MF, Rosen ED, Goodyear LJ, Gonzalez FJ, Spiegelman BM, Kahn CR. 2003 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=171387

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Mutations in the small heterodimer partner gene are associated with mild obesity in Japanese subjects. by Nishigori H, Tomura H, Tonooka N, Kanamori M, Yamada S, Sho K, Inoue I, Kikuchi N, Onigata K, Kojima I, Kohama T, Yamagata K, Yang Q, Matsuzawa Y, Miki T, Seino S, Kim MY, Choi HS, Lee YK, Moore DD, Takeda J. 2001 Jan 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=14629

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Obese gene expression at in vivo levels by fat pads derived from s.c. implanted 3T3F442A preadipocytes. by Mandrup S, Loftus TM, MacDougald OA, Kuhajda FP, Lane MD. 1997 Apr 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20717

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Obese Gene Expression: Reduction by Fasting and Stimulation by Insulin and Glucose in Lean Mice, and Persistent Elevation in Acquired (Diet-Induced) and

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Genetic (Yellow Agouti) Obesity. by Mizuno TM, Bergen H, Funabashi T, Kleopoulos SP, Zhong Y, Bauman WA, Mobbs CV. 1996 Apr 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39626 •

Obesity a heavy burden in Nova Scotia. by Moulton D. 2000 Nov 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80435

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Obesity and hyperleptinemia in metallothionein (-I and -II) null mice. by Beattie JH, Wood AM, Newman AM, Bremner I, Choo KH, Michalska AE, Duncan JS, Trayhurn P. 1998 Jan 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18223

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Obesity and mild hyperinsulinemia found in neuropeptide Y-Y1 receptor-deficient mice. by Kushi A, Sasai H, Koizumi H, Takeda N, Yokoyama M, Nakamura M. 1998 Dec 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28100

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Obesity drug sibutramine (Meridia): hypertension and cardiac arrhythmias. by Wooltorton E. 2002 May 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=111085

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Obesity in Canadian children. by Auer R, Lau D, Reimer R. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81101

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Obesity in Canadian children. by Katzmarzyk PT. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81103

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Obesity in Canadian children. by Finkelstein M. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81102

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Obesity in Canadian children. by Andersen R. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81105

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Obesity in Canadian children. by Tremblay M, Willms JD. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81104

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Obesity increases sensitivity to endotoxin liver injury: Implications for the pathogenesis of steatohepatitis. by Yang SQ, Lin HZ, Lane MD, Clemens M, Diehl AM. 1997 Mar 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20127

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Obesity may soon be leading cause of preventable death in US. by Sibbald B. 2002 Mar 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=99423

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Obesity resistance and enhanced glucose metabolismin mice transplanted with white adipose tissue lackingacyl CoA:diacylglycerol acyltransferase 1. by Chen HC, Jensen DR, Myers HM, Eckel RH, Farese RV Jr. 2003 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=156099

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Overweight and obesity in relation to cardiovascular disease risk factors among medical students in Crete, Greece. by Bertsias G, Mammas I, Linardakis M, Kafatos A. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=140012

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Paradoxical resistance to diet-induced obesity in UCP1-deficient mice. by Liu X, Rossmeisl M, McClaine J, Kozak LP. 2003 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151850

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Perilipin ablation results in a lean mouse with aberrant adipocyte lipolysis, enhanced leptin production, and resistance to diet-induced obesity. by Tansey JT, Sztalryd C, Gruia-Gray J, Roush DL, Zee JV, Gavrilova O, Reitman ML, Deng CX, Li C, Kimmel AR, Londos C. 2001 May 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33496

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Physiological response to long-term peripheral and central leptin infusion in lean and obese mice. by Halaas JL, Boozer C, Blair-West J, Fidahusein N, Denton DA, Friedman JM. 1997 Aug 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23177

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Plasma interleukin 8 concentrations in obese subjects with impaired glucose tolerance.. by Straczkowski M, Kowalska I, Nikolajuk A, Dzienis-Straczkowska S, Szelachowska M, Kinalska I. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=162167

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Prevalence and trends in overweight and obesity in three cross sectional studies of British children, 1974-94. by Chinn S, Rona RJ. 2001 Jan 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26603

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Prevalence of attention deficit/hyperactivity disorder among adults in obesity treatment. by Altfas JR. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130024

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Prevalence of overweight and obese children between 1989 and 1998: population based series of cross sectional studies. by Bundred P, Kitchiner D, Buchan I. 2001 Feb 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26573

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Prevalence of overweight and obesity in British children: cohort study. by Reilly JJ, Dorosty AR, Emmett PM. 1999 Oct 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=32263

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Randomised controlled trial of primary school based intervention to reduce risk factors for obesity. by Sahota P, Rudolf MC, Dixey R, Hill AJ, Barth JH, Cade J. 2001 Nov 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59381

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Rat Obesity Gene Fatty (fa) Maps to Chromosome 5: Evidence for Homology with the Mouse Gene Diabetes (db). by Truett GE, Bahary N, Friedman JM, Leibel RL. 1991 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52392

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Regulated Expression of the Obese Gene Product (Leptin) in White Adipose Tissue and 3T3-L1 Adipocytes. by MacDougald OA, Hwang C, Fan H, Lane MD. 1995 Sep 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40918

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Relation between obesity from childhood to adulthood and the metabolic syndrome: population based study. by Vanhala M, Vanhala P, Kumpusalo E, Halonen P, Takala J. 1998 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28624

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Reversing adipocyte differentiation: Implications for treatment of obesity. by Zhou YT, Wang ZW, Higa M, Newgard CB, Unger RH. 1999 Mar 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26794

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Targeted Deletion of the tub Mouse Obesity Gene Reveals that tubby Is a Loss-ofFunction Mutation. by Stubdal H, Lynch CA, Moriarty A, Fang Q, Chickering T, Deeds JD, Fairchild-Huntress V, Charlat O, Dunmore JH, Kleyn P, Huszar D, Kapeller R. 2000 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85204

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Targeted disruption of H3 receptors results in changes in brain histamine tone leading to an obese phenotype. by Takahashi K, Suwa H, Ishikawa T, Kotani H. 2002 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151650

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Targeted disruption of hormone-sensitive lipase results in male sterility and adipocyte hypertrophy, but not in obesity. by Osuga JI, Ishibashi S, Oka T, Yagyu H, Tozawa R, Fujimoto A, Shionoiri F, Yahagi N, Kraemer FB, Tsutsumi O, Yamada N. 2000 Jan 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15409

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The Canadian obesity epidemic, 1985 --1998. by Katzmarzyk PT. 2002 Apr 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=100878

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The emerging science of body weight regulation and its impact on obesity treatment. by Korner J, Aronne LJ. 2003 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151906

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The expression of adipogenic genes is decreased in obesity and diabetes mellitus. by Nadler ST, Stoehr JP, Schueler KL, Tanimoto G, Yandell BS, Attie AD. 2000 Oct 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17207

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The G-308A variant of the Tumor Necrosis Factor-[alpha] (TNF-[alpha]) gene is not associated with obesity, insulin resistance and body fat distribution. by Romeo S, Sentinelli F, Capici F, Arca M, Berni A, Vecci E, Mario UD, Baroni MG. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=56593

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The relation of menarcheal age to obesity in childhood and adulthood: the Bogalusa heart study. by Freedman DS, Khan LK, Serdula MK, Dietz WH, Srinivasan SR, Berenson GS. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=156622

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The search for new ways to treat obesity. by Hirsch J. 2002 Jul 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123098

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The spread of the childhood obesity epidemic. by Andersen RE. 2000 Nov 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80413

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Tissue factor gene expression in the adipose tissues of obese mice. by Samad F, Pandey M, Loskutoff DJ. 1998 Jun 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22693

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Troglitazone prevents mitochondrial alterations, [beta] cell destruction, and diabetes in obese prediabetic rats. by Higa M, Zhou YT, Ravazzola M, Baetens D, Orci L, Unger RH. 1999 Sep 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18065

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Tsp509I polymorphism in exon 2 of the glucocorticoid receptor gene in relation to obesity and cortisol secretion: cohort study. by Rosmond R, Bouchard C, Bjorntorp P. 2001 Mar 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26546

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Tumor necrosis factor [alpha] is a key component in the obesity-linked elevation of plasminogen activator inhibitor 1. by Samad F, Uysal KT, Wiesbrock SM, Pandey M, Hotamisligil GS, Loskutoff DJ. 1999 Jun 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22014

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Tumor necrosis factor [alpha] mediates apoptosis of brown adipocytes and defective brown adipocyte function in obesity. by Nisoli E, Briscini L, Giordano A, Tonello C, Wiesbrock SM, Uysal KT, Cinti S, Carruba MO, Hotamisligil GS. 2000 Jul 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16665

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Yeast Vps55p, a Functional Homolog of Human Obesity Receptor Gene-related Protein, Is Involved in Late Endosome to Vacuole Trafficking. by Belgareh-Touze N, Avaro S, Rouille Y, Hoflack B, Haguenauer-Tsapis R. 2002 May 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111137

The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with obesity, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “obesity” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for obesity (hyperlinks lead to article summaries): •

A case-control study of the association of diet and obesity with gout in Taiwan. Author(s): Lyu LC, Hsu CY, Yeh CY, Lee MS, Huang SH, Chen CL. Source: The American Journal of Clinical Nutrition. 2003 October; 78(4): 690-701. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14522726&dopt=Abstract

PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.

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A clinical view of the obesity problem. Author(s): Pi-Sunyer X. Source: Science. 2003 February 7; 299(5608): 859-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574620&dopt=Abstract

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A comparison of diet and exercise therapy versus laparoscopic Roux-en-Y gastric bypass surgery for morbid obesity: a decision analysis model. Author(s): Patterson EJ, Urbach DR, Swanstrom LL. Source: Journal of the American College of Surgeons. 2003 March; 196(3): 379-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12648689&dopt=Abstract

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A cost-analysis of adopting a healthful diet in a family-based obesity treatment program. Author(s): Raynor HA, Kilanowski CK, Esterlis I, Epstein LH. Source: Journal of the American Dietetic Association. 2002 May; 102(5): 645-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12008989&dopt=Abstract

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A cross-cultural analysis of 'motivation for eating' as a potential factor in the emergence of global obesity: Japan and the United States. Author(s): Hawks SR, Madanat HN, Merrill RM, Goudy MB, Miyagawa T. Source: Health Promotion International. 2003 June; 18(2): 153-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746387&dopt=Abstract

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A dietary and behavioural programme for the treatment of obesity. A 4-year clinical trial and a long-term posttreatment follow-up. Author(s): Lantz H, Peltonen M, Agren L, Torgerson JS. Source: Journal of Internal Medicine. 2003 September; 254(3): 272-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930237&dopt=Abstract

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A functional variant in the peroxisome proliferator-activated receptor gamma2 promoter is associated with predictors of obesity and type 2 diabetes in Pima Indians. Author(s): Muller YL, Bogardus C, Beamer BA, Shuldiner AR, Baier LJ. Source: Diabetes. 2003 July; 52(7): 1864-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829658&dopt=Abstract

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A lifecourse study of risk for hyperinsulinaemia, dyslipidaemia and obesity (the central metabolic syndrome) at age 49-51 years. Author(s): Parker L, Lamont DW, Unwin N, Pearce MS, Bennett SM, Dickinson HO, White M, Mathers JC, Alberti KG, Craft AW. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 2003 May; 20(5): 406-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752491&dopt=Abstract

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A longitudinal evaluation of adolescent depression and adult obesity. Author(s): Richardson LP, Davis R, Poulton R, McCauley E, Moffitt TE, Caspi A, Connell F. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 739-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912778&dopt=Abstract

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A low-carbohydrate as compared with a low-fat diet in severe obesity. Author(s): Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2074-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761364&dopt=Abstract

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A meta-analysis of obesity and the risk of pancreatic cancer. Author(s): Berrington de Gonzalez A, Sweetland S, Spencer E. Source: British Journal of Cancer. 2003 August 4; 89(3): 519-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888824&dopt=Abstract

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A new treatment for morbid obesity. Author(s): Offutt MR. Source: The Nurse Practitioner. 2003 August; 28(8): 54-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902942&dopt=Abstract

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A perspective on obesity. Author(s): Johnson RW, Broadnax PA. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 69-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856445&dopt=Abstract

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A primer on early childhood obesity and parental influence. Author(s): Hodges EA. Source: Pediatric Nursing. 2003 January-February; 29(1): 13-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630500&dopt=Abstract

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A programme of behaviour modification and nutrition counselling in the treatment of obesity: a randomised 2-y clinical trial. Author(s): Melin I, Karlstrom B, Lappalainen R, Berglund L, Mohsen R, Vessby B. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 September; 27(9): 1127-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917721&dopt=Abstract

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A qualitative study of general practitioners' and practice nurses' attitudes to obesity management in primary care. Author(s): Mercer SW, Tessier S. Source: Health Bull (Edinb). 2001 July; 59(4): 248-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664735&dopt=Abstract

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A randomized trial of a low-carbohydrate diet for obesity. Author(s): Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2082-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761365&dopt=Abstract

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A reduced-glycemic load diet in the treatment of adolescent obesity. Author(s): Ebbeling CB, Leidig MM, Sinclair KB, Hangen JP, Ludwig DS. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 773-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912783&dopt=Abstract

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A war on obesity, not the obese. Author(s): Friedman JM. Source: Science. 2003 February 7; 299(5608): 856-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574619&dopt=Abstract

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Abdominal obesity and risk of ischemic stroke: the Northern Manhattan Stroke Study. Author(s): Suk SH, Sacco RL, Boden-Albala B, Cheun JF, Pittman JG, Elkind MS, Paik MC; Northern Manhattan Stroke Study. Source: Stroke; a Journal of Cerebral Circulation. 2003 July; 34(7): 1586-92. Epub 2003 May 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775882&dopt=Abstract

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Acupuncture for the treatment of obesity: a review of the evidence. Author(s): Lacey JM, Tershakovec AM, Foster GD. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 419-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664074&dopt=Abstract

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Additional insight on childhood obesity article. Author(s): Landry D. Source: Pediatric Nursing. 2003 May-June; 29(3): 253. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837005&dopt=Abstract

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Adiponectin expression from human adipose tissue: relation to obesity, insulin resistance, and tumor necrosis factor-alpha expression. Author(s): Kern PA, Di Gregorio GB, Lu T, Rassouli N, Ranganathan G. Source: Diabetes. 2003 July; 52(7): 1779-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829646&dopt=Abstract

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Adipose tissue is a major source of interleukin-1 receptor antagonist: upregulation in obesity and inflammation. Author(s): Juge-Aubry CE, Somm E, Giusti V, Pernin A, Chicheportiche R, Verdumo C, Rohner-Jeanrenaud F, Burger D, Dayer JM, Meier CA. Source: Diabetes. 2003 May; 52(5): 1104-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716739&dopt=Abstract

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Adolescent obesity, overt and relational peer victimization, and romantic relationships. Author(s): Pearce MJ, Boergers J, Prinstein MJ. Source: Obesity Research. 2002 May; 10(5): 386-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006638&dopt=Abstract

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All obesity is not created equal. Author(s): Rosch PJ. Source: Science. 2003 September 5; 301(5638): 1325. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12958343&dopt=Abstract

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An after-school obesity prevention program for African-American girls: the Minnesota GEMS pilot study. Author(s): Story M, Sherwood NE, Himes JH, Davis M, Jacobs DR Jr, Cartwright Y, Smyth M, Rochon J. Source: Ethn Dis. 2003 Winter; 13(1 Suppl 1): S54-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713211&dopt=Abstract

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An association between body mass index and markers of inflammation: is obesity the proinflammatory state in patients on peritoneal dialysis? Author(s): Stompor T, Sulowicz W, Dembinska-Kiec A, Janda K, Wojcik K, Zdzienicka A. Source: Perit Dial Int. 2003 January-February; 23(1): 79-83. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12691512&dopt=Abstract

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An obesity clinic model. Author(s): Munnelly P, Feehan S. Source: The Proceedings of the Nutrition Society. 2002 February; 61(1): 9-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12002800&dopt=Abstract

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Are physicians equipped to address the obesity epidemic? Knowledge and attitudes of internal medicine residents. Author(s): Block JP, DeSalvo KB, Fisher WP. Source: Preventive Medicine. 2003 June; 36(6): 669-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744909&dopt=Abstract

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Are there long term protective effects of breast feeding against later obesity? Author(s): Koletzko B, von Kries R. Source: Nutr Health. 2001; 15(3-4): 225-36. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12003089&dopt=Abstract

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Associates of obesity and weight dissatisfaction among Finnish adolescents. Author(s): Mikkila V, Lahti-Koski M, Pietinen P, Virtanen SM, Rimpela M. Source: Public Health Nutrition. 2003 February; 6(1): 49-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581465&dopt=Abstract

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Association between eating patterns and obesity in a free-living US adult population. Author(s): Ma Y, Bertone ER, Stanek EJ 3rd, Reed GW, Hebert JR, Cohen NL, Merriam PA, Ockene IS. Source: American Journal of Epidemiology. 2003 July 1; 158(1): 85-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835290&dopt=Abstract

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Association of African genetic admixture with resting metabolic rate and obesity among women. Author(s): Fernandez JR, Shriver MD, Beasley TM, Rafla-Demetrious N, Parra E, Albu J, Nicklas B, Ryan AS, McKeigue PM, Hoggart CL, Weinsier RL, Allison DB. Source: Obesity Research. 2003 July; 11(7): 904-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855761&dopt=Abstract

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Association of maternal obesity and depressive symptoms with television-viewing time in low-income preschool children. Author(s): Burdette HL, Whitaker RC, Kahn RS, Harvey-Berino J. Source: Archives of Pediatrics & Adolescent Medicine. 2003 September; 157(9): 894-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963595&dopt=Abstract

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Association of polymorphisms in GPR10, the gene encoding the prolactin-releasing peptide receptor with blood pressure, but not obesity, in a U.K. Caucasian population. Author(s): Bhattacharyya S, Luan J, Challis B, Schmitz C, Clarkson P, Franks PW, Middelberg R, Keogh J, Farooqi IS, Montague C, Brennand J, Wareham NJ, O'Rahilly S. Source: Diabetes. 2003 May; 52(5): 1296-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716769&dopt=Abstract

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Association of the mitochondrial DNA 15497G/A polymorphism with obesity in a middle-aged and elderly Japanese population. Author(s): Okura T, Koda M, Ando F, Niino N, Tanaka M, Shimokata H. Source: Human Genetics. 2003 October; 113(5): 432-6. Epub 2003 August 02. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905068&dopt=Abstract

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Association of the TNF-alpha -308 G/A promoter polymorphism with insulin resistance in obesity. Author(s): Dalziel B, Gosby AK, Richman RM, Bryson JM, Caterson ID. Source: Obesity Research. 2002 May; 10(5): 401-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006640&dopt=Abstract

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Austronesian-speaking people in Papua New Guinea have susceptibility to obesity and type 2 diabetes. Author(s): Sakaue M, Fuke Y, Katsuyama T, Kawabata M, Taniguchi H. Source: Diabetes Care. 2003 March; 26(3): 955-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610072&dopt=Abstract

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Autonomic dysfunction of the beta-cell and the pathogenesis of obesity. Author(s): Lustig RH. Source: Reviews in Endocrine & Metabolic Disorders. 2003 March; 4(1): 23-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618557&dopt=Abstract

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Bariatric surgery and long-term control of morbid obesity. Author(s): Brolin RE. Source: Jama : the Journal of the American Medical Association. 2002 December 11; 288(22): 2793-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472304&dopt=Abstract

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Bariatric surgery for morbid obesity. Author(s): Duell PB. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1779; Author Reply 1779. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684352&dopt=Abstract

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Bariatric surgery for morbid obesity: why, who, when, how, where, and then what? Author(s): Choban PS, Jackson B, Poplawski S, Bistolarides P. Source: Cleve Clin J Med. 2002 November; 69(11): 897-903. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12430975&dopt=Abstract

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Bariatric surgery for severe obesity. Author(s): Sugerman HJ. Source: J Assoc Acad Minor Phys. 2001 July; 12(3): 129-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11851201&dopt=Abstract

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Behavior therapy and sibutramine for the treatment of adolescent obesity: a randomized controlled trial. Author(s): Berkowitz RI, Wadden TA, Tershakovec AM, Cronquist JL. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1805-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684359&dopt=Abstract

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Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency. Author(s): Farooqi IS, Matarese G, Lord GM, Keogh JM, Lawrence E, Agwu C, Sanna V, Jebb SA, Perna F, Fontana S, Lechler RI, DePaoli AM, O'Rahilly S. Source: The Journal of Clinical Investigation. 2002 October; 110(8): 1093-103. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393845&dopt=Abstract

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Beneficial role of dietary phytoestrogens in obesity and diabetes. Author(s): Bhathena SJ, Velasquez MT. Source: The American Journal of Clinical Nutrition. 2002 December; 76(6): 1191-201. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450882&dopt=Abstract

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Benefits of sustained moderate weight loss in obesity. Author(s): Pasanisi F, Contaldo F, de Simone G, Mancini M. Source: Nutr Metab Cardiovasc Dis. 2001 December; 11(6): 401-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12055705&dopt=Abstract

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Beta(2)-adrenergic receptor mutation and abdominal obesity risk: effect modification by gender and HDL-cholesterol. Author(s): Corbalan MS, Marti A, Forga L, Martinez-Gonzalez MA, Martinez JA. Source: European Journal of Nutrition. 2002 June; 41(3): 114-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12111048&dopt=Abstract

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Beta-Adrenergic receptors, diet-induced thermogenesis, and obesity. Author(s): Lowell BB, Bachman ES. Source: The Journal of Biological Chemistry. 2003 August 8; 278(32): 29385-8. Epub 2003 June 04. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788929&dopt=Abstract

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Binge eating disorder in extreme obesity. Author(s): Hsu LK, Mulliken B, McDonagh B, Krupa Das S, Rand W, Fairburn CG, Rolls B, McCrory MA, Saltzman E, Shikora S, Dwyer J, Roberts S. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 October; 26(10): 1398-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12355338&dopt=Abstract

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Biocultural aspects of obesity in young Mexican schoolchildren. Author(s): Brewis A. Source: American Journal of Human Biology : the Official Journal of the Human Biology Council. 2003 May-June; 15(3): 446-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12704721&dopt=Abstract

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Biological and environmental determinants of childhood obesity. Author(s): Blass EM. Source: Nutrition in Clinical Care : an Official Publication of Tufts University. 2003 January-April; 6(1): 13-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841426&dopt=Abstract

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Biomarkers and functional foods for obesity and diabetes. Author(s): Hill JO, Peters JC. Source: The British Journal of Nutrition. 2002 November; 88 Suppl 2: S213-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495462&dopt=Abstract

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Blood pressure, lipids, and obesity are associated with retinopathy: the hoorn study. Author(s): van Leiden HA, Dekker JM, Moll AC, Nijpels G, Heine RJ, Bouter LM, Stehouwer CD, Polak BC. Source: Diabetes Care. 2002 August; 25(8): 1320-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12145228&dopt=Abstract

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Bodily characteristics and lifestyle of Czech children aged 7.00 to 10.99 years, incidence of childhood obesity. Author(s): Kovarova M, Vignerova J, Blaha P, Osancova K. Source: Cent Eur J Public Health. 2002 December; 10(4): 169-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528392&dopt=Abstract

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Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Author(s): Lavie CJ, Osman AF, Milani RV, Mehra MR. Source: The American Journal of Cardiology. 2003 April 1; 91(7): 891-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12667583&dopt=Abstract

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Body composition assessment in extreme obesity and after massive weight loss induced by gastric bypass surgery. Author(s): Das SK, Roberts SB, Kehayias JJ, Wang J, Hsu LK, Shikora SA, Saltzman E, McCrory MA. Source: American Journal of Physiology. Endocrinology and Metabolism. 2003 June; 284(6): E1080-8. Epub 2003 February 25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604503&dopt=Abstract

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Body fat percentages measured by dual-energy X-ray absorptiometry corresponding to recently recommended body mass index cutoffs for overweight and obesity in children and adolescents aged 3-18 y. Author(s): Taylor RW, Jones IE, Williams SM, Goulding A. Source: The American Journal of Clinical Nutrition. 2002 December; 76(6): 1416-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450911&dopt=Abstract

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Body image disturbance in obese outpatients before and after weight loss in relation to race, gender, binge eating, and age of onset of obesity. Author(s): Sorbara M, Geliebter A. Source: The International Journal of Eating Disorders. 2002 May; 31(4): 416-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11948646&dopt=Abstract

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Body mass and survival in patients with chronic heart failure without cachexia: the importance of obesity. Author(s): Davos CH, Doehner W, Rauchhaus M, Cicoira M, Francis DP, Coats AJ, Clark AL, Anker SD. Source: Journal of Cardiac Failure. 2003 February; 9(1): 29-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12612870&dopt=Abstract

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Body mass index and mortality in asian populations: implications for obesity cutpoints. Author(s): Stevens J, Nowicki EM. Source: Nutrition Reviews. 2003 March; 61(3): 104-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723643&dopt=Abstract

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Body mass index in 7-9-y-old French children: frequency of obesity, overweight and thinness. Author(s): Rolland-Cachera MF, Castetbon K, Arnault N, Bellisle F, Romano MC, Lehingue Y, Frelut ML, Hercberg S. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 December; 26(12): 1610-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461677&dopt=Abstract

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Body mass index measurements and prevalence of overweight and obesity in schoolchildren living in the province of Belgian Limburg. Author(s): Massa G. Source: European Journal of Pediatrics. 2002 June; 161(6): 343-6. Epub 2002 April 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12029455&dopt=Abstract

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Body mass index, overweight and obesity in married and never married men and women in Poland. Author(s): Lipowicz A, Gronkiewicz S, Malina RM. Source: American Journal of Human Biology : the Official Journal of the Human Biology Council. 2002 July-August; 14(4): 468-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12112568&dopt=Abstract

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Body weight and obesity in adults and self-reported abuse in childhood. Author(s): Williamson DF, Thompson TJ, Anda RF, Dietz WH, Felitti V. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 August; 26(8): 1075-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119573&dopt=Abstract

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Body weight regulation and obesity. Author(s): Kaplan LM. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 443-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763397&dopt=Abstract

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Bombesin and its family of peptides: prospects for the treatment of obesity. Author(s): Yamada K, Wada E, Santo-Yamada Y, Wada K. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 281-90. Review. Erratum In: Eur J Pharmacol. 2002 July 19; 448(2-3): 269. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007542&dopt=Abstract

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Both fasting-induced leptin reduction and GH increase are blunted in Cushing's syndrome and in simple obesity. Author(s): Grottoli S, Gauna C, Tassone F, Aimaretti G, Corneli G, Wu Z, Strasburger CJ, Dieguez C, Casanueva FF, Ghigo E, Maccario M. Source: Clinical Endocrinology. 2003 February; 58(2): 220-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580939&dopt=Abstract

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Both under-nutrition and obesity increase morbidity following liver transplantation. Author(s): Hade AM, Shine AM, Kennedy NP, McCormick PA. Source: Ir Med J. 2003 May; 96(5): 140-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846275&dopt=Abstract

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Breastfeeding and lowering the risk of childhood obesity. Author(s): Armstrong J, Reilly JJ; Child Health Information Team. Source: Lancet. 2002 June 8; 359(9322): 2003-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076560&dopt=Abstract

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Breast-feeding and obesity. Author(s): Gillman MW. Source: The Journal of Pediatrics. 2002 December; 141(6): 749-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461485&dopt=Abstract

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Cardiac autonomic neuropathy in diabetic patients: influence of diabetes duration, obesity, and microangiopathic complications--the French multicenter study. Author(s): Valensi P, Paries J, Attali JR; French Group for Research and Study of Diabetic Neuropathy. Source: Metabolism: Clinical and Experimental. 2003 July; 52(7): 815-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870154&dopt=Abstract

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Cardiac function and obesity. Author(s): Vasan RS. Source: Heart (British Cardiac Society). 2003 October; 89(10): 1127-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975393&dopt=Abstract

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Cardiovascular outcomes for obesity and metabolic syndrome. Author(s): Vega GL. Source: Obesity Research. 2002 November; 10 Suppl 1: 27S-32S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446855&dopt=Abstract

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Cardiovascular risks in obesity. Author(s): Uchegbu EC, Kopelman PG. Source: J Endocrinol Invest. 2002 November; 25(10): 915-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508955&dopt=Abstract

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Cashing in on obesity? Author(s): Victoroff MS. Source: Manag Care. 2002 December; 11(12): 18-20. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12536953&dopt=Abstract

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CCK1R agonists: a promising target for the pharmacological treatment of obesity. Author(s): Szewczyk JR, Laudeman C. Source: Current Topics in Medicinal Chemistry. 2003; 3(8): 837-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678836&dopt=Abstract

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Central overweight and obesity in British youth aged 11-16 years: cross sectional surveys of waist circumference. Author(s): McCarthy HD, Ellis SM, Cole TJ. Source: Bmj (Clinical Research Ed.). 2003 March 22; 326(7390): 624. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649234&dopt=Abstract

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Central pre-proglucagon derived peptides: opportunities for treatment of obesity. Author(s): Larsen PJ, Vrang N, Tang-Christensen M. Source: Current Pharmaceutical Design. 2003; 9(17): 1373-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769729&dopt=Abstract

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Chemical toxins: a hypothesis to explain the global obesity epidemic. Author(s): Baillie-Hamilton PF. Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 April; 8(2): 185-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006126&dopt=Abstract

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Chief medical officer's report on the nation's health: concerted action is needed to fight obesity, says chief medical officer. Author(s): Kmietowicz Z. Source: Bmj (Clinical Research Ed.). 2003 July 12; 327(7406): 69. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855501&dopt=Abstract

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Child to adult socioeconomic conditions and obesity in a national cohort. Author(s): Power C, Manor O, Matthews S. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 September; 27(9): 1081-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917714&dopt=Abstract

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Childhood obesity in Canada: a review of prevalence estimates and risk factors for cardiovascular diseases and type 2 diabetes. Author(s): Ball GD, McCargar LJ. Source: Canadian Journal of Applied Physiology = Revue Canadienne De Physiologie Appliquee. 2003 February; 28(1): 117-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671200&dopt=Abstract

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Childhood obesity in Kuwait--prevalence and trends. Author(s): Sorkhou I, Al-Qallaf K, Al-Shamali N, Hajia A, Al-Qallaf B. Source: Family Medicine. 2003 July-August; 35(7): 463-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861451&dopt=Abstract

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Childhood obesity, a modern plague. A gray-haired pediatrician's perspective. Author(s): Willson CF. Source: N C Med J. 2002 November-December; 63(6): 300-1. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970977&dopt=Abstract

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Childhood obesity: a challenge for the anaesthetist? Author(s): Smith HL, Meldrum DJ, Brennan LJ. Source: Paediatric Anaesthesia. 2002 November; 12(9): 750-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519133&dopt=Abstract

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Childhood obesity: modernity's scourge. Author(s): Waters EB, Baur LA. Source: The Medical Journal of Australia. 2003 May 5; 178(9): 422-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12720504&dopt=Abstract

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Childhood obesity--a public health problem. Author(s): Belfield J. Source: School Nurse News. 2003 January; 20(1): 20, 22, 24. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12616765&dopt=Abstract

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Childhood obesity--why should we be worried? Author(s): Roche EF. Source: Ir Med J. 2003 April; 96(4): 100-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793468&dopt=Abstract

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Childhood social class and adulthood obesity: findings from the Glasgow Alumni Cohort. Author(s): Okasha M, McCarron P, McEwen J, Durnin J, Davey Smith G. Source: Journal of Epidemiology and Community Health. 2003 July; 57(7): 508-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821695&dopt=Abstract

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CHO intake alters obesity risk associated with Pro12Ala polymorphism of PPARgamma gene. Author(s): Marti A, Corbalan MS, Martinez-Gonzalez MA, Forga L, Martinez JA. Source: J Physiol Biochem. 2002 December; 58(4): 219-20. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744304&dopt=Abstract

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Cidea-deficient mice have lean phenotype and are resistant to obesity. Author(s): Zhou Z, Yon Toh S, Chen Z, Guo K, Ng CP, Ponniah S, Lin SC, Hong W, Li P. Source: Nature Genetics. 2003 September; 35(1): 49-56. Epub 2003 August 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910269&dopt=Abstract

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Circumferential abdominoplasty for sequential treatment after morbid obesity. Author(s): Modolin M, Cintra W Jr, Gobbi CI, Ferreira MC. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 95-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630621&dopt=Abstract

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Clinical obesity issues from an internist's perspective. Author(s): Klein S. Source: Obesity Research. 2002 November; 10 Suppl 1: 87S-88S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446867&dopt=Abstract

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Clinical predictors of leak after laparoscopic Roux-en-Y gastric bypass for morbid obesity. Author(s): Hamilton EC, Sims TL, Hamilton TT, Mullican MA, Jones DB, Provost DA. Source: Surgical Endoscopy. 2003 May; 17(5): 679-84. Epub 2003 March 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618940&dopt=Abstract

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Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene. Author(s): Farooqi IS, Keogh JM, Yeo GS, Lank EJ, Cheetham T, O'Rahilly S. Source: The New England Journal of Medicine. 2003 March 20; 348(12): 1085-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12646665&dopt=Abstract

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Coagulation and fibrinolysis abnormalities in obesity. Author(s): De Pergola G, Pannacciulli N. Source: J Endocrinol Invest. 2002 November; 25(10): 899-904. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508953&dopt=Abstract

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Coexistence of social inequalities in undernutrition and obesity in preschool children: population based cross sectional study. Author(s): Armstrong J, Dorosty AR, Reilly JJ, Emmett PM; Child Health Information Team. Source: Archives of Disease in Childhood. 2003 August; 88(8): 671-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12876159&dopt=Abstract

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Cognitive interference due to food cues in childhood obesity. Author(s): Braet C, Crombez G. Source: Journal of Clinical Child and Adolescent Psychology : the Official Journal for the Society of Clinical Child and Adolescent Psychology, American Psychological Association, Division 53. 2003 March; 32(1): 32-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573930&dopt=Abstract

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Cognitive-behavioral approaches in the management of obesity. Author(s): Wisotsky W, Swencionis C. Source: Adolescent Medicine (Philadelphia, Pa.). 2003 February; 14(1): 37-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529189&dopt=Abstract

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Comment on "Obesity and the environment: where do we go from here?". Author(s): Butte NF, Ellis KJ. Source: Science. 2003 August 1; 301(5633): 598; Author Reply 598. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12893926&dopt=Abstract

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Comparison between different methods to assess the prevalence of obesity in a sample of Italian children. Author(s): Valerio G, Scalfi L, De Martino C, Franzese A, Tenore A, Contaldo F. Source: J Pediatr Endocrinol Metab. 2003 February; 16(2): 211-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713259&dopt=Abstract

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Complex haplotypes of IRS2 gene are associated with severe obesity and reveal heterogeneity in the effect of Gly1057Asp mutation. Author(s): Lautier C, El Mkadem SA, Renard E, Brun JF, Gris JC, Bringer J, Grigorescu F. Source: Human Genetics. 2003 July; 113(1): 34-43. Epub 2003 April 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687350&dopt=Abstract

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Confusing food with obesity. Author(s): Lupien JR. Source: Science. 2003 May 16; 300(5622): 1091. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750499&dopt=Abstract

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Consensus view on the role of dietary fat and obesity. Author(s): Foreyt JP, Poston WS. Source: The American Journal of Medicine. 2002 December 30; 113 Suppl 9B: 60S-62S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12566140&dopt=Abstract

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Contemporary surgical management of obesity. Author(s): McNatt SS, Howard-McNatt M. Source: W V Med J. 2002 November-December; 98(6): 273-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645282&dopt=Abstract

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Correlates of overweight and obesity among lesbian and bisexual women. Author(s): Yancey AK, Cochran SD, Corliss HL, Mays VM. Source: Preventive Medicine. 2003 June; 36(6): 676-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744910&dopt=Abstract

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Could elevated C-reactive protein in patients with obstructive sleep apnea be due to obesity per se? Author(s): Cheng TO. Source: Circulation. 2003 January 7; 107(1): E9; Author Reply E9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515763&dopt=Abstract

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C-reactive protein and gestational diabetes: the central role of maternal obesity. Author(s): Retnakaran R, Hanley AJ, Raif N, Connelly PW, Sermer M, Zinman B. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 August; 88(8): 3507-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915627&dopt=Abstract

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Cryptic terminal deletion of chromosome 9q34: a novel cause of syndromic obesity in childhood? Author(s): Cormier-Daire V, Molinari F, Rio M, Raoul O, de Blois MC, Romana S, Vekemans M, Munnich A, Colleaux L. Source: Journal of Medical Genetics. 2003 April; 40(4): 300-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12676904&dopt=Abstract

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Current management strategies for coexisting diabetes mellitus and obesity. Author(s): Scheen AJ. Source: Drugs. 2003; 63(12): 1165-84. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12790691&dopt=Abstract

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DASH diet lowers blood pressure and lipid-induced oxidative stress in obesity. Author(s): Lopes HF, Martin KL, Nashar K, Morrow JD, Goodfriend TL, Egan BM. Source: Hypertension. 2003 March; 41(3): 422-30. Epub 2003 February 03. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623938&dopt=Abstract

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Data management for clinical research in obesity. Author(s): Einbinder JS. Source: Obesity Research. 2002 November; 10 Suppl 1: 6S-9S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446851&dopt=Abstract

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De novo MECP2 frameshift mutation in a boy with moderate mental retardation, obesity and gynaecomastia. Author(s): Kleefstra T, Yntema HG, Oudakker AR, Romein T, Sistermans E, Nillessen W, van Bokhoven H, de Vries BB, Hamel BC. Source: Clinical Genetics. 2002 May; 61(5): 359-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12081720&dopt=Abstract

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Defective melanocortin 4 receptors in hyperphagia and morbid obesity. Author(s): List JF, Habener JF. Source: The New England Journal of Medicine. 2003 March 20; 348(12): 1160-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12646673&dopt=Abstract

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Deficit in the discrimination of nonverbal emotions in children with obesity and their mothers. Author(s): Baldaro B, Rossi N, Caterina R, Codispoti M, Balsamo A, Trombini G. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 February; 27(2): 191-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12586998&dopt=Abstract

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Defining childhood obesity: fiddling whilst Rome burns? Author(s): Poskitt EM. Source: Acta Paediatrica (Oslo, Norway : 1992). 2001 December; 90(12): 1361-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11853327&dopt=Abstract

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Demographics and trends in overweight and obesity in patients at time of kidney transplantation. Author(s): Friedman AN, Miskulin DC, Rosenberg IH, Levey AS. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2003 February; 41(2): 480-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552513&dopt=Abstract

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Depression and obesity treatments are life saving. Author(s): Licinio J, Wong ML. Source: Nature Medicine. 2002 December; 8(12): 1336; Author Reply 1336. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12457157&dopt=Abstract

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Depression and obesity. Author(s): Stunkard AJ, Faith MS, Allison KC. Source: Biological Psychiatry. 2003 August 1; 54(3): 330-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12893108&dopt=Abstract

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Depression in diabetes and obesity: racial/ethnic/gender issues in older adults. Author(s): Blazer DG, Moody-Ayers S, Craft-Morgan J, Burchett B. Source: Journal of Psychosomatic Research. 2002 October; 53(4): 913-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377303&dopt=Abstract

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Dermatological complications of obesity. Author(s): Garcia Hidalgo L. Source: American Journal of Clinical Dermatology. 2002; 3(7): 497-506. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12180897&dopt=Abstract

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Detection of cardiovascular risk factors by indices of obesity obtained from anthropometry and dual-energy X-ray absorptiometry in Japanese individuals. Author(s): Ito H, Nakasuga K, Ohshima A, Maruyama T, Kaji Y, Harada M, Fukunaga M, Jingu S, Sakamoto M. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 February; 27(2): 232-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12587004&dopt=Abstract

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Developing health messages: qualitative studies with children, parents, and teachers help identify communications opportunities for healthful lifestyles and the prevention of obesity. Author(s): Borra ST, Kelly L, Shirreffs MB, Neville K, Geiger CJ. Source: Journal of the American Dietetic Association. 2003 June; 103(6): 721-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12778044&dopt=Abstract

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Development and future of gastroplasties for morbid obesity. Author(s): Mason EE. Source: Archives of Surgery (Chicago, Ill. : 1960). 2003 April; 138(4): 361-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686521&dopt=Abstract

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Development of novel medications for use in the treatment of obesity in children will be directed by delineating controls of energy homeostasis. Author(s): Sherman PM, Zlotkin SH. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 721. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912773&dopt=Abstract

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Diabetes and hypertension in severe obesity and effects of gastric bypass-induced weight loss. Author(s): Sugerman HJ, Wolfe LG, Sica DA, Clore JN. Source: Annals of Surgery. 2003 June; 237(6): 751-6; Discussion 757-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796570&dopt=Abstract

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Diabetes contributes to cholesterol metabolism regardless of obesity. Author(s): Simonen PP, Gylling HK, Miettinen TA. Source: Diabetes Care. 2002 September; 25(9): 1511-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12196419&dopt=Abstract

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Diabetes mellitus and obesity. Author(s): Roth A. Source: Primary Care. 2002 June; 29(2): 279-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391712&dopt=Abstract

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Diabetes, obesity, and Acrp30/adiponectin. Author(s): Hug C, Lodish HF. Source: Biotechniques. 2002 September; 33(3): 654, 656, 658 Passim. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12238775&dopt=Abstract

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Diet and physical activity for obesity: how effective are they? Author(s): Womble LG, Clark VL, Wadden TA. Source: J Endocrinol Invest. 2002 November; 25(10): 922-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508957&dopt=Abstract

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Diet, exercise, and the challenge of combating obesity in primary care. Author(s): McInnis KJ. Source: The Journal of Cardiovascular Nursing. 2003 April-June; 18(2): 93-100; Quiz 1012. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680567&dopt=Abstract

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Diet, obesity and reflux in the etiology of adenocarcinomas of the esophagus and gastric cardia in humans. Author(s): Mayne ST, Navarro SA. Source: The Journal of Nutrition. 2002 November; 132(11 Suppl): 3467S-3470S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12421872&dopt=Abstract

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Diet, obesity, and cardiovascular risk. Author(s): Bonow RO, Eckel RH. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2057-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761363&dopt=Abstract

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Dietary fat is a major player in obesity--but not the only one. Author(s): Astrup A. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 May; 3(2): 57-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12120420&dopt=Abstract

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Dietary fat plays a major role in obesity: no. Author(s): Willett WC. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 May; 3(2): 59-68. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12120421&dopt=Abstract

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Diet-dependent obesity and hypercholesterolemia in the New Zealand obese mouse: identification of a quantitative trait locus for elevated serum cholesterol on the distal mouse chromosome 5. Author(s): Giesen K, Plum L, Kluge R, Ortlepp J, Joost HG. Source: Biochemical and Biophysical Research Communications. 2003 May 16; 304(4): 812-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727230&dopt=Abstract

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Differences in oral temperature and body shape in two populations with different propensities for obesity. Author(s): Vozarova B, Weyer C, Bogardus C, Ravussin E, Tataranni PA. Source: Annals of the New York Academy of Sciences. 2002 June; 967: 516-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079882&dopt=Abstract

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Differences in overweight and obesity among Australian schoolchildren of low and middle/high socioeconomic status. Author(s): O'Dea JA. Source: The Medical Journal of Australia. 2003 July 7; 179(1): 63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831394&dopt=Abstract

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Differences in the relation of obesity to serum triacylglycerol and VLDL subclass concentrations between black and white children: the Bogalusa Heart Study. Author(s): Freedman DS, Bowman BA, Otvos JD, Srinivasan SR, Berenson GS. Source: The American Journal of Clinical Nutrition. 2002 May; 75(5): 827-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11976155&dopt=Abstract

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Differentiation between obesity and insulin resistance in the association with Creactive protein. Author(s): McLaughlin T, Abbasi F, Lamendola C, Liang L, Reaven G, Schaaf P, Reaven P. Source: Circulation. 2002 December 3; 106(23): 2908-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12460870&dopt=Abstract

100 Obesity

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Discovery and optimization of a series of carbazole ureas as NPY5 antagonists for the treatment of obesity. Author(s): Block MH, Boyer S, Brailsford W, Brittain DR, Carroll D, Chapman S, Clarke DS, Donald CS, Foote KM, Godfrey L, Ladner A, Marsham PR, Masters DJ, Mee CD, O'Donovan MR, Pease JE, Pickup AG, Rayner JW, Roberts A, Schofield P, Suleman A, Turnbull AV. Source: Journal of Medicinal Chemistry. 2002 August 1; 45(16): 3509-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12139462&dopt=Abstract

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Disease severity at time of referral for pediatric failure to thrive and obesity: time for a paradigm shift? Author(s): Miller LA, Grunwald GK, Johnson SL, Krebs NF. Source: The Journal of Pediatrics. 2002 July; 141(1): 121-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12091862&dopt=Abstract

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Do stress reactions cause abdominal obesity and comorbidities? Author(s): Bjorntorp P. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 May; 2(2): 73-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119665&dopt=Abstract

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Does metformin provide a new approach to the management of obesity? Author(s): Rivlin RS. Source: Heart Disease. 2001 September-October; 3(5): 283-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11975806&dopt=Abstract

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Dopamine transporter genotype as a risk factor for obesity in African-American smokers. Author(s): Epstein LH, Jaroni JL, Paluch RA, Leddy JJ, Vahue HE, Hawk L, Wileyto EP, Shields PG, Lerman C. Source: Obesity Research. 2002 December; 10(12): 1232-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490667&dopt=Abstract

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Dopamine, hypertension and obesity. Author(s): Contreras F, Fouillioux C, Bolivar A, Simonovis N, Hernandez-Hernandez R, Armas-Hernandez MJ, Velasco M. Source: Journal of Human Hypertension. 2002 March; 16 Suppl 1: S13-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11986886&dopt=Abstract

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Dopaminergic tone and obesity: an insight from prolactinomas treated with bromocriptine. Author(s): Doknic M, Pekic S, Zarkovic M, Medic-Stojanoska M, Dieguez C, Casanueva F, Popovic V. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2002 July; 147(1): 77-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12088923&dopt=Abstract

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Drug strategies for the treatment of obesity. Author(s): Alemany M, Remesar X, Fernandez-Lopez JA. Source: Idrugs. 2003 June; 6(6): 566-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12811679&dopt=Abstract

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Dusting off the epidemiological triad: could it work with obesity? Author(s): Egger G, Swinburn B, Rossner S. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 115-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760446&dopt=Abstract

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Dysfunctional immune-privilege in morbid obesity: implications and effect of gastric bypass surgery. Author(s): Cottam DR, Schaefer PA, Shaftan GW, Angus LD. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 49-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630613&dopt=Abstract

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Early life risk factors in cancer: the relation of birth weight to adult obesity. Author(s): Leong NM, Mignone LI, Newcomb PA, Titus-Ernstoff L, Baron JA, TrenthamDietz A, Stampfer MJ, Willett WC, Egan KM. Source: International Journal of Cancer. Journal International Du Cancer. 2003 March 1; 103(6): 789-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12516100&dopt=Abstract

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Early prevention of obesity and cardiovascular diseases. Author(s): Merker N, Wagner N, Kirch W, Muller MJ. Source: Deutsche Medizinische Wochenschrift. 2002 December 13; 127(50): 2661-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12481235&dopt=Abstract

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Eating disorders and obesity. Author(s): Reslewic S. Source: Science. 2003 May 16; 300(5622): 1091. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750498&dopt=Abstract

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Eating patterns and obesity in children. The Bogalusa Heart Study. Author(s): Nicklas TA, Yang SJ, Baranowski T, Zakeri I, Berenson G. Source: American Journal of Preventive Medicine. 2003 July; 25(1): 9-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818304&dopt=Abstract

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Economic and psychological implications of the obesity epidemic. Author(s): Kottke TE, Wu LA, Hoffman RS. Source: Mayo Clinic Proceedings. 2003 January; 78(1): 92-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528882&dopt=Abstract

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Effect of family history, obesity and exercise on breast cancer risk among postmenopausal women. Author(s): Carpenter CL, Ross RK, Paganini-Hill A, Bernstein L. Source: International Journal of Cancer. Journal International Du Cancer. 2003 August 10; 106(1): 96-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794763&dopt=Abstract

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Effect of obesity and/or sleep apnea on chemosensitivity: differences between men and women. Author(s): Buyse B, Markous N, Cauberghs M, Van Klaveren R, Muls E, Demedts M. Source: Respiratory Physiology & Neurobiology. 2003 February 19; 134(1): 13-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573877&dopt=Abstract

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Effect of obesity on health-related quality of life among Appalachian elderly. Author(s): Goins RT, Spencer SM, Krummel DA. Source: Southern Medical Journal. 2003 June; 96(6): 552-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938781&dopt=Abstract

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Effect of obesity on recombinant follicle-stimulating hormone absorption: subcutaneous versus intramuscular administration. Author(s): Steinkampf MP, Hammond KR, Nichols JE, Slayden SH. Source: Fertility and Sterility. 2003 July; 80(1): 99-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12849809&dopt=Abstract

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Effect of subclinical hypothyroidism and obesity on whole-body and regional bone mineral content. Author(s): Bertoli A, Fusco A, Andreoli A, Magnani A, Tulli A, Lauro D, De Lorenzo A. Source: Hormone Research. 2002; 57(3-4): 79-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006702&dopt=Abstract

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Effect of television viewing on pediatric obesity. Author(s): Ma GS, Li YP, Hu XQ, Ma WJ, Wu J. Source: Biomed Environ Sci. 2002 December; 15(4): 291-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12642985&dopt=Abstract

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Effect of the factor VII R353Q missense mutation on plasma apolipoprotein B levels: impact of visceral obesity. Author(s): Berthier MT, Houde A, Bergeron J, Prud'homme D, Despres JP, Vohl MC. Source: Journal of Human Genetics. 2003; 48(7): 367-73. Epub 2003 July 08. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851844&dopt=Abstract

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Effect of weight loss on VLDL-triglyceride and apoB-100 kinetics in women with abdominal obesity. Author(s): Mittendorfer B, Patterson BW, Klein S. Source: American Journal of Physiology. Endocrinology and Metabolism. 2003 March; 284(3): E549-56. Epub 2002 December 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475754&dopt=Abstract

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Effective management of obesity. Author(s): Shepherd TM. Source: The Journal of Family Practice. 2003 January; 52(1): 34-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540311&dopt=Abstract

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Effects of growth hormone administration in human obesity. Author(s): Shadid S, Jensen MD. Source: Obesity Research. 2003 February; 11(2): 170-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582210&dopt=Abstract

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Effects of hypertension and obesity on endometrial thickness. Author(s): Serdar Serin I, Ozcelik B, Basbug M, Ozsahin O, Yilmazsoy A, Erez R. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 2003 July 1; 109(1): 72-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818448&dopt=Abstract

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Effects of isolated obesity on systolic and diastolic left ventricular function. Author(s): Pascual M, Pascual DA, Soria F, Vicente T, Hernandez AM, Tebar FJ, Valdes M. Source: Heart (British Cardiac Society). 2003 October; 89(10): 1152-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975404&dopt=Abstract

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Effects of obesity and weight loss on soluble CD40L levels. Author(s): Desideri G, Ferri C. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1781-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684355&dopt=Abstract

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Effects of obesity on morbidity in children and adolescents. Author(s): Must A, Anderson SE. Source: Nutrition in Clinical Care : an Official Publication of Tufts University. 2003 January-April; 6(1): 4-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841425&dopt=Abstract

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Enhanced erythrocyte adhesiveness/aggregation in obesity corresponds to low-grade inflammation. Author(s): Samocha-Bonet D, Lichtenberg D, Tomer A, Deutsch V, Mardi T, Goldin Y, Abu-Abeid S, Shenkerman G, Patshornik H, Shapira I, Berliner S. Source: Obesity Research. 2003 March; 11(3): 403-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634437&dopt=Abstract

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Enhanced fat oxidation through physical activity is associated with improvements in insulin sensitivity in obesity. Author(s): Goodpaster BH, Katsiaras A, Kelley DE. Source: Diabetes. 2003 September; 52(9): 2191-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941756&dopt=Abstract

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Epidemic obesity and the metabolic syndrome. Author(s): Haffner S, Taegtmeyer H. Source: Circulation. 2003 September 30; 108(13): 1541-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517149&dopt=Abstract

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Epidemiology and consequences of obesity. Author(s): Stevens J, Truesdale KP. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 438-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763396&dopt=Abstract

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Establishing body composition in obesity. Author(s): Pietrobelli A, Heymsfield SB. Source: J Endocrinol Invest. 2002 November; 25(10): 884-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508951&dopt=Abstract

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Evaluation and treatment of obesity. Author(s): Azar ST, Zantout MS. Source: J Med Liban. 2000 September-October; 48(5): 310-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12489585&dopt=Abstract

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Evidence for distinct genetic effects on obesity and lipid-related CVD risk factors in diabetic compared to nondiabetic American Indians: the Strong Heart Family Study. Author(s): North KE, MacCluer JW, Williams JT, Welty TK, Best LG, Lee ET, Fabsitz RR, Howard BV. Source: Diabetes/Metabolism Research and Reviews. 2003 March-April; 19(2): 140-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673782&dopt=Abstract

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Evolution of operative procedures for the management of morbid obesity 1950-2000. Author(s): Buchwald H, Buchwald JN. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 October; 12(5): 705-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12448398&dopt=Abstract

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Exercise and diet in obesity treatment: an integrative system dynamics perspective. Author(s): Abdel-Hamid TK. Source: Medicine and Science in Sports and Exercise. 2003 March; 35(3): 400-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618569&dopt=Abstract

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Exercise considerations in hypertension, obesity, and dyslipidemia. Author(s): MacKnight JM. Source: Clinics in Sports Medicine. 2003 January; 22(1): 101-21, Vii. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12613089&dopt=Abstract

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Experimental drugs take aim at obesity. Author(s): Vastag B. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1763-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684341&dopt=Abstract

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Exploring the association between body weight, stigma of obesity, and health care avoidance. Author(s): Drury CA, Louis M. Source: Journal of the American Academy of Nurse Practitioners. 2002 December; 14(12): 554-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12567923&dopt=Abstract

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Expression of 11beta-hydroxysteroid dehydrogenase type 1 in adipose tissue is not increased in human obesity. Author(s): Tomlinson JW, Sinha B, Bujalska I, Hewison M, Stewart PM. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 December; 87(12): 5630-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12466364&dopt=Abstract

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Facing the problem of obesity: a call to action. Author(s): Mina WC. Source: Mo Med. 2003 May-June; 100(3): 176-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847860&dopt=Abstract

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Factorial study of the effects of atorvastatin and fish oil on dyslipidaemia in visceral obesity. Author(s): Chan DC, Watts GF, Mori TA, Barrett PH, Beilin LJ, Redgrave TG. Source: European Journal of Clinical Investigation. 2002 June; 32(6): 429-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12059988&dopt=Abstract

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Factors associated with overweight/obesity in economically active South African populations. Author(s): Senekal M, Steyn NP, Nel JH. Source: Ethn Dis. 2003 Winter; 13(1): 109-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723019&dopt=Abstract

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Familial approach to the treatment of childhood obesity: conceptual mode. Author(s): Golan M, Weizman A. Source: Journal of Nutrition Education. 2001 March-April; 33(2): 102-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12031190&dopt=Abstract

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Familial clustering of obesity and the role of nutrition: Tehran Lipid and Glucose Study. Author(s): Mirmiran P, Mirbolooki M, Azizi F. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 December; 26(12): 1617-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461678&dopt=Abstract

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Familial combined hyperlipidemia (FCHL) in children: the significance of early development of hyperapoB lipoproteinemia, obesity and aging. Author(s): Kuromori Y, Okada T, Iwata F, Hara M, Noto N, Harada K. Source: J Atheroscler Thromb. 2002; 9(6): 314-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12560593&dopt=Abstract

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Familial isolated growth hormone deficiency is associated with increased systolic blood pressure, central obesity, and dyslipidemia. Author(s): Barreto-Filho JA, Alcantara MR, Salvatori R, Barreto MA, Sousa AC, Bastos V, Souza AH, Pereira RM, Clayton PE, Gill MS, Aguiar-Oliveira MH. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 May; 87(5): 2018-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11994335&dopt=Abstract

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Family history of prostate cancer and obesity in relation to high-grade disease and extraprostatic extension in young men with prostate cancer. Author(s): Rohrmann S, Roberts WW, Walsh PC, Platz EA. Source: The Prostate. 2003 May 1; 55(2): 140-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12661039&dopt=Abstract

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Family-based interventions for the treatment of childhood obesity. Author(s): St Jeor ST, Perumean-Chaney S, Sigman-Grant M, Williams C, Foreyt J. Source: Journal of the American Dietetic Association. 2002 May; 102(5): 640-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12008987&dopt=Abstract

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Fast food and obesity in China. Author(s): Cheng TO. Source: Journal of the American College of Cardiology. 2003 August 20; 42(4): 773. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932622&dopt=Abstract

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Fasting and daylong triglycerides in obesity with and without type 2 diabetes. Author(s): van Wijk JP, Halkes CJ, Erkelens DW, Castro Cabezas M. Source: Metabolism: Clinical and Experimental. 2003 August; 52(8): 1043-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898471&dopt=Abstract

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Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. Author(s): Seppala-Lindroos A, Vehkavaara S, Hakkinen AM, Goto T, Westerbacka J, Sovijarvi A, Halavaara J, Yki-Jarvinen H. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 July; 87(7): 3023-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12107194&dopt=Abstract

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Fat versus carbohydrate in insulin resistance, obesity, diabetes and cardiovascular disease. Author(s): Hung T, Sievenpiper JL, Marchie A, Kendall CW, Jenkins DJ. Source: Current Opinion in Clinical Nutrition and Metabolic Care. 2003 March; 6(2): 16576. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12589186&dopt=Abstract

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Feeding our children to death: the tragedy of childhood obesity in America. Author(s): Freeman-Fobbs P. Source: Journal of the National Medical Association. 2003 February; 95(2): 119. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760606&dopt=Abstract

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Fetal environment and subsequent obesity: a study of maternal smoking. Author(s): Power C, Jefferis BJ. Source: International Journal of Epidemiology. 2002 April; 31(2): 413-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11980805&dopt=Abstract

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Fibrin glue as a sealant for high-risk anastomosis in surgery for morbid obesity. Author(s): Liu CD, Glantz GJ, Livingston EH. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 45-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630612&dopt=Abstract

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Fighting childhood obesity with university-community partnerships. Author(s): Thompson LS, Grey M. Source: Nurs Leadersh Forum. 2002 Fall; 7(1): 20-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12683028&dopt=Abstract

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Fighting fat. New drugs against obesity in the pipeline. Author(s): Brower V. Source: Embo Reports. 2002 July; 3(7): 601-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12101089&dopt=Abstract

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Five-year results of laparoscopic vertical banded gastroplasty in the treatment of massive obesity. Author(s): Magnusson M, Freedman J, Jonas E, Stockeld D, Granstrom L, Naslund E. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 December; 12(6): 826-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12568189&dopt=Abstract

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Focus issue: the signaling skinny on obesity. Author(s): Chong LD, Adler EM, Ray LB. Source: Science's Stke [electronic Resource] : Signal Transduction Knowledge Environment. 2003 February 11; 2003(169): Eg2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582198&dopt=Abstract

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Food insecurity is associated with increased risk of obesity in California women. Author(s): Adams EJ, Grummer-Strawn L, Chavez G. Source: The Journal of Nutrition. 2003 April; 133(4): 1070-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672921&dopt=Abstract

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Food stamp program participation is positively related to obesity in low income women. Author(s): Gibson D. Source: The Journal of Nutrition. 2003 July; 133(7): 2225-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840184&dopt=Abstract

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For the patient. Are vegetarians at less risk for obesity, diabetes, and hypertension? Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 148. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723025&dopt=Abstract

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For the patient. What lifestyle choices place people at-risk of obesity? Factors associated with overweight/obesity in economically active South African populations. Author(s): Senekal M, Steyn NP, Nel JH. Source: Ethn Dis. 2003 Winter; 13(1): 153. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723030&dopt=Abstract

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Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and beta-cell dysfunction. Author(s): Boden G, Shulman GI. Source: European Journal of Clinical Investigation. 2002 June; 32 Suppl 3: 14-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12028371&dopt=Abstract

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Functional characterization of melanocortin-4 receptor mutations associated with childhood obesity. Author(s): Tao YX, Segaloff DL. Source: Endocrinology. 2003 October; 144(10): 4544-51. Epub 2003 June 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12959994&dopt=Abstract

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Further evidence for the association between obesity-related traits and the apolipoprotein A-IV gene. Author(s): Fiegenbaum M, Hutz MH. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 484-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664082&dopt=Abstract

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Future of obesity and chronic-disease management in health care: the employer perspective. Author(s): Walters GA. Source: Obesity Research. 2002 November; 10 Suppl 1: 84S-86S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446866&dopt=Abstract

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Future of obesity and chronic-disease management in health care: the HMO perspective. Author(s): Hyatt JD. Source: Obesity Research. 2002 November; 10 Suppl 1: 79S-81S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446864&dopt=Abstract

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Future of obesity and disease management in health care: the government perspective. Author(s): Primack A. Source: Obesity Research. 2002 November; 10 Suppl 1: 82S-83S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446865&dopt=Abstract

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Galanin/GALP and galanin receptors: role in central control of feeding, body weight/obesity and reproduction? Author(s): Gundlach AL. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 255-68. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007540&dopt=Abstract

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Gastric bypass for morbid obesity in patients 50 years or older: is laparoscopic technique safer? Author(s): Gonzalez R, Lin E, Mattar SG, Venkatesh KR, Smith CD. Source: The American Surgeon. 2003 July; 69(7): 547-53; Discussion 553-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12889614&dopt=Abstract

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Gastric bypass is an effective treatment for obstructive sleep apnea in patients with clinically significant obesity. Author(s): Rasheid S, Banasiak M, Gallagher SF, Lipska A, Kaba S, Ventimiglia D, Anderson WM, Murr MM. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 58-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630614&dopt=Abstract

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Gastric bypass surgery for obesity. Author(s): Buechner JS. Source: Medicine and Health, Rhode Island. 2003 March; 86(3): 81-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12703143&dopt=Abstract

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Gastric bypass surgery for severe obesity. Author(s): Sugerman HJ. Source: Semin Laparosc Surg. 2002 June; 9(2): 79-85. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12152150&dopt=Abstract

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Gastric dilatation in a girl with former obesity and atypical anorexia nervosa. Author(s): Holtkamp K, Mogharrebi R, Hanisch C, Schumpelick V, Herpertz-Dahlmann B. Source: The International Journal of Eating Disorders. 2002 November; 32(3): 372-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12210653&dopt=Abstract

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Gastric restrictive procedures to treat obesity: reasons for failure and long-term evaluation of the results of operative revision. Author(s): Kaminski DL. Source: International Journal of Surgical Investigation. 2001; 2(5): 413-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678546&dopt=Abstract

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Gastro-oesophageal reflux disease in obesity: pathophysiological and therapeutic considerations. Author(s): Barak N, Ehrenpreis ED, Harrison JR, Sitrin MD. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 February; 3(1): 9-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119661&dopt=Abstract

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Gender, obesity and health. Author(s): Heitmann BL. Source: Sb Lek. 2002; 103(4): 465-70. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688160&dopt=Abstract

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Genetic and environmental contributions to obesity and binge eating. Author(s): Bulik CM, Sullivan PF, Kendler KS. Source: The International Journal of Eating Disorders. 2003 April; 33(3): 293-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12655626&dopt=Abstract

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Genetic predisposition to obesity in bulimia nervosa: a mutation screen of the melanocortin-4 receptor gene. Author(s): Hebebrand J, Fichter M, Gerber G, Gorg T, Hermann H, Geller F, Schafer H, Remschmidt H, Hinney A. Source: Molecular Psychiatry. 2002; 7(6): 647-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12140789&dopt=Abstract

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Genetic variability in responses to caloric restriction in animals and in regulation of metabolism and obesity in humans. Author(s): Allison DB, Miller RA, Austad SN, Bouchard C, Leibel R, Klebanov S, Johnson T, Harrison DE. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2001 March; 56 Spec No 1: 55-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12088213&dopt=Abstract

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Genetic variation in the small heterodimer partner gene and young-onset type 2 diabetes, obesity, and birth weight in U.K. subjects. Author(s): Mitchell SM, Weedon MN, Owen KR, Shields B, Wilkins-Wall B, Walker M, McCarthy MI, Frayling TM, Hattersley AT. Source: Diabetes. 2003 May; 52(5): 1276-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716764&dopt=Abstract

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Genetics and pathophysiology of human obesity. Author(s): Cummings DE, Schwartz MW. Source: Annual Review of Medicine. 2003; 54: 453-71. Epub 2001 December 03. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12414915&dopt=Abstract

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Genetics of obesity and type 2 diabetes: tracking pathogenic traits during the predisease period. Author(s): Bougneres P. Source: Diabetes. 2002 December; 51 Suppl 3: S295-303. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475766&dopt=Abstract

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Genetics of obesity. Author(s): Clement K, Boutin P, Froguel P. Source: American Journal of Pharmacogenomics : Genomics-Related Research in Drug Development and Clinical Practice. 2002; 2(3): 177-87. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12383024&dopt=Abstract

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Genome scan for childhood and adolescent obesity in German families. Author(s): Saar K, Geller F, Ruschendorf F, Reis A, Friedel S, Schauble N, Nurnberg P, Siegfried W, Goldschmidt HP, Schafer H, Ziegler A, Remschmidt H, Hinney A, Hebebrand J. Source: Pediatrics. 2003 February; 111(2): 321-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563058&dopt=Abstract

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Genotype, obesity and cardiovascular disease--has technical and social advancement outstripped evolution? Author(s): Zimmet P, Thomas CR. Source: Journal of Internal Medicine. 2003 August; 254(2): 114-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12859692&dopt=Abstract

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Genotype-by-smoking interaction for leptin levels in the Metabolic Risk Complications of Obesity Genes project. Author(s): Martin LJ, Kissebah AH, Sonnenberg GE, Blangero J, Comuzzie AG; Metabolic Risk Complications of Obesity Genes Project. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 March; 27(3): 334-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629560&dopt=Abstract

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Ghrelin and the hyposomatotropism of obesity. Author(s): Lindeman JH, Pijl H, Van Dielen FM, Lentjes EG, Van Leuven C, Kooistra T. Source: Obesity Research. 2002 November; 10(11): 1161-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12429880&dopt=Abstract

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Ghrelin as a potential anti-obesity target. Author(s): Horvath TL, Castaneda T, Tang-Christensen M, Pagotto U, Tschop MH. Source: Current Pharmaceutical Design. 2003; 9(17): 1383-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769730&dopt=Abstract

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Ghrelin, growth and obesity. Author(s): Ukkola O, Poykko S. Source: Annals of Medicine. 2002; 34(2): 102-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12108573&dopt=Abstract

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Girls health Enrichment Multi-site Studies (GEMS): new approaches to obesity prevention among young African-American girls. Author(s): Obarzanek E, Pratt CA. Source: Ethn Dis. 2003 Winter; 13(1 Suppl 1): S1-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713206&dopt=Abstract

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Glucagon administration elicits blunted GH but exaggerated ACTH response in obesity. Author(s): Tassone F, Grottoli S, Rossetto R, Maccagno B, Gauna C, Giordano R, Ghigo E, Maccario M. Source: J Endocrinol Invest. 2002 June; 25(6): 551-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12109628&dopt=Abstract

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Glucose transport and phosphorylation in skeletal muscle in obesity: insight from a muscle-specific positron emission tomography model. Author(s): Williams KV, Bertoldo A, Mattioni B, Price JC, Cobelli C, Kelley DE. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 March; 88(3): 12719. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629118&dopt=Abstract

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Glucose-dependent insulinotropic polypeptide analogues and their therapeutic potential for the treatment of obesity-diabetes. Author(s): Gault VA, Flatt PR, O'Harte FP. Source: Biochemical and Biophysical Research Communications. 2003 August 22; 308(2): 207-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901855&dopt=Abstract

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Glycemic index and obesity. Author(s): Brand-Miller JC, Holt SH, Pawlak DB, McMillan J. Source: The American Journal of Clinical Nutrition. 2002 July; 76(1): 281S-5S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12081852&dopt=Abstract

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Gourmand savants and environmental determinants of obesity. Author(s): Myslobodsky M. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 121-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760447&dopt=Abstract

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Guidance on surgery for morbid obesity. Author(s): Cooper R. Source: Br J Perioper Nurs. 2002 October; 12(10): 340. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400389&dopt=Abstract

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Guidelines for childhood obesity prevention programs: promoting healthy weight in children. Author(s): Berg F, Buechner J, Parham E; Weight Realities Division of the Society for Nutrition Education. Source: Journal of Nutrition Education and Behavior. 2003 January-February; 35(1): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12596730&dopt=Abstract

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Hand-assisted laparoscopic gastric bypass does not improve outcome and increases costs when compared to open gastric bypass for the surgical treatment of obesity. Author(s): DeMaria EJ, Schweitzer MA, Kellum JM, Meador J, Wolfe L, Sugerman HJ. Source: Surgical Endoscopy. 2002 October; 16(10): 1452-5. Epub 2002 June 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063573&dopt=Abstract

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Harry Potter and obesity. Author(s): Adami GF. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 April; 12(2): 298. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11975235&dopt=Abstract

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Health consequences of obesity in youth: childhood predictors of adult disease. Author(s): Dietz WH. Source: Pediatrics. 1998 March; 101(3 Pt 2): 518-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12224658&dopt=Abstract

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Health consequences of obesity. Author(s): Reilly JJ, Methven E, McDowell ZC, Hacking B, Alexander D, Stewart L, Kelnar CJ. Source: Archives of Disease in Childhood. 2003 September; 88(9): 748-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937090&dopt=Abstract

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Healthy Eating and Activity Together (HEAT): weapons against obesity. Author(s): Gottesman MM. Source: Journal of Pediatric Health Care : Official Publication of National Association of Pediatric Nurse Associates & Practitioners. 2003 July-August; 17(4): 210-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847433&dopt=Abstract

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Herbal simulation of ephedrine and caffeine in treatment of obesity. Author(s): Dulloo AG. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 May; 26(5): 590-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12032740&dopt=Abstract

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High circulating ghrelin: a potential cause for hyperphagia and obesity in praderwilli syndrome. Author(s): DelParigi A, Tschop M, Heiman ML, Salbe AD, Vozarova B, Sell SM, Bunt JC, Tataranni PA. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 December; 87(12): 5461-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12466337&dopt=Abstract

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High prevalence of obesity in asthmatic patients on sick leave. Author(s): Nathell L, Jensen I, Larsson K. Source: Respiratory Medicine. 2002 August; 96(8): 642-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12195847&dopt=Abstract

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High serum concentrations of soluble E-selectin correlate with obesity but not fat distribution in patients with type 2 diabetes mellitus. Author(s): Matsumoto K, Sera Y, Abe Y, Tominaga T, Horikami K, Hirao K, Ueki Y, Miyake S. Source: Metabolism: Clinical and Experimental. 2002 July; 51(7): 932-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12077744&dopt=Abstract

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High-insulinogenic nutrition--an etiologic factor for obesity and the metabolic syndrome? Author(s): Kopp W. Source: Metabolism: Clinical and Experimental. 2003 July; 52(7): 840-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870158&dopt=Abstract

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Highlights from the annual scientific assembly: mechanisms to stop the epidemic of obesity: surgical therapy for obesity. Author(s): Sugerman HJ. Source: Southern Medical Journal. 2002 June; 95(6): 657-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12081225&dopt=Abstract

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Hip-Hop to Health Jr., an obesity prevention program for minority preschool children: baseline characteristics of participants. Author(s): Stolley MR, Fitzgibbon ML, Dyer A, Van Horn L, KauferChristoffel K, Schiffer L. Source: Preventive Medicine. 2003 March; 36(3): 320-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634023&dopt=Abstract

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Histologic findings of gallbladder mucosa in 87 patients with morbid obesity without gallstones compared to 87 control subjects. Author(s): Csendes A, Burdiles P, Smok G, Csendes P, Burgos A, Recio M. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 547-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763414&dopt=Abstract

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Historical perspective: visceral obesity and related comorbidity in Joannes Baptista Morgagni's 'De sedibus et causis morborum per anatomen indagata'. Author(s): Enzi G, Busetto L, Inelmen EM, Coin A, Sergi G. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 534-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664088&dopt=Abstract

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Homocysteine and psychological traits: a study in obesity. Author(s): Marchesini G, Manini R, Bianchi G, Sassi S, Natale S, Chierici S, Visani F, Baraldi L, Forlani G, Melchionda N. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2002 May; 18(5): 403-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11985945&dopt=Abstract

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Hormonal regulation of human adipocytes at the cross-roads between obesity and hypertension. Author(s): Tikhonoff V, Staessen JA. Source: Journal of Hypertension. 2002 May; 20(5): 839-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12011640&dopt=Abstract

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Hormonal regulation of the human adipose-tissue renin-angiotensin system: relationship to obesity and hypertension. Author(s): Gorzelniak K, Engeli S, Janke J, Luft FC, Sharma AM. Source: Journal of Hypertension. 2002 May; 20(5): 965-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12011658&dopt=Abstract

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Human leptin administered intraperitoneally stimulates natriuresis and decreases renal medullary Na+, K+-ATPase activity in the rat -- impaired effect in dietaryinduced obesity. Author(s): Beltowski J, W jcicka G, Gorny D, Marciniak A. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2002 June; 8(6): Br221-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12070427&dopt=Abstract

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Human obesity and type 2 diabetes are associated with alterations in SREBP1 isoform expression that are reproduced ex vivo by tumor necrosis factor-alpha. Author(s): Sewter C, Berger D, Considine RV, Medina G, Rochford J, Ciaraldi T, Henry R, Dohm L, Flier JS, O'Rahilly S, Vidal-Puig AJ. Source: Diabetes. 2002 April; 51(4): 1035-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11916923&dopt=Abstract

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Hunter-gatherers win profit-sharing deal for obesity drug. Author(s): Wise J. Source: Bulletin of the World Health Organization. 2003; 81(5): 382. Epub 2003 July 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856057&dopt=Abstract

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Hyperglycaemic siblings of Type II (non-insulin-dependent) diabetic patients have increased PAI-1, central obesity and insulin resistance compared with their paired normoglycaemic sibling. Author(s): Herlihy OM, Barrow BA, Grant PJ, Levy JC. Source: Diabetologia. 2002 May; 45(5): 635-41. Epub 2002 April 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12107743&dopt=Abstract

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Hyperinsulinemia, dyslipidemia, and obesity as risk factors for hospitalized gallbladder disease. A prospective study. Author(s): Boland LL, Folsom AR, Rosamond WD; Atherosclerosis Risk in Communities (ARIC) Study Investigators. Source: Annals of Epidemiology. 2002 February; 12(2): 131-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11880221&dopt=Abstract

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Hyperinsulinism and overgrowth without obesity. Author(s): Srinivasan S, Waters MJ, Rowland JE, Baxter RC, Verge CF. Source: Archives of Disease in Childhood. 2003 April; 88(4): 332-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12651761&dopt=Abstract

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Hypertension and obesity after the menopause. Author(s): Rappelli A. Source: Journal of Hypertension. 2002 May; 20 Suppl 2: S26-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183846&dopt=Abstract

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Hypertension and obesity. Author(s): Najman DM, Kapoor P, Serrano A, Tckachenko D. Source: Archives of Internal Medicine. 2003 May 12; 163(9): 1114-5; Author Reply 1115-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742816&dopt=Abstract

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Hypertension and obesity. Author(s): Diaz ME. Source: Journal of Human Hypertension. 2002 March; 16 Suppl 1: S18-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11986887&dopt=Abstract

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Hypertension in obesity. Author(s): Redon J. Source: Nutr Metab Cardiovasc Dis. 2001 October; 11(5): 344-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11887431&dopt=Abstract

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Hypertension, obesity, and the renin-angiotensin system: a tale of tight associations. Author(s): Sibley S. Source: Minn Med. 2003 January; 86(1): 46-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12585560&dopt=Abstract

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Hypothalamic growth hormone-releasing hormone (GHRH) cell number is increased in human illness, but is not reduced in Prader-Willi syndrome or obesity. Author(s): Goldstone AP, Unmehopa UA, Swaab DF. Source: Clinical Endocrinology. 2003 June; 58(6): 743-55. Erratum In: Clin Endocrinol (Oxf). 2003 August; 59(2): 266. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780752&dopt=Abstract

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Hypothalamic obesity in humans: what do we know and what can be done? Author(s): Pinkney J, Wilding J, Williams G, MacFarlane I. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 February; 3(1): 27-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119657&dopt=Abstract

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Images in cardiology: Massive epicardial adipose tissue indicating severe visceral obesity. Author(s): Iacobellis G, Leonetti F, Di Mario U. Source: Clin Cardiol. 2003 May; 26(5): 237. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769252&dopt=Abstract

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Immunohistochemical identification of the beta(3)-adrenoceptor in intact human adipocytes and ventricular myocardium: effect of obesity and treatment with ephedrine and caffeine. Author(s): De Matteis R, Arch JR, Petroni ML, Ferrari D, Cinti S, Stock MJ. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 November; 26(11): 1442-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439645&dopt=Abstract

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Impaired glucose tolerance: obesity and inactivity as modifiable risk factors. Author(s): Taylor K. Source: Adv Nurse Pract. 2001 December; 9(12): 59-61. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400355&dopt=Abstract

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Implications of the prevalence of stunting, overweight and obesity amongst South African primary school children: a possible nutritional transition? Author(s): Jinabhai CC, Taylor M, Sullivan KR. Source: European Journal of Clinical Nutrition. 2003 February; 57(2): 358-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571672&dopt=Abstract

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Increased abdominal obesity, insulin and glucose levels in nondiabetic subjects with a T29C polymorphism of the transforming growth factor-beta1 gene. Author(s): Rosmond R, Chagnon M, Bouchard C, Bjorntorp P. Source: Hormone Research. 2003; 59(4): 191-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649573&dopt=Abstract

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Increased adrenal androgen levels in patients with Prader-Willi syndrome are associated with insulin, IGF-I, and leptin, but not with measures of obesity. Author(s): L'Allemand D, Eiholzer U, Rousson V, Girard J, Blum W, Torresani T, Gasser T. Source: Hormone Research. 2002; 58(5): 215-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401940&dopt=Abstract

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Increased oxidative stress and hypozincemia in male obesity. Author(s): Ozata M, Mergen M, Oktenli C, Aydin A, Sanisoglu SY, Bolu E, Yilmaz MI, Sayal A, Isimer A, Ozdemir IC. Source: Clinical Biochemistry. 2002 November; 35(8): 627-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12498997&dopt=Abstract

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Increasing portion sizes in American diets: more calories, more obesity. Author(s): Nestle M. Source: Journal of the American Dietetic Association. 2003 January; 103(1): 39-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525791&dopt=Abstract

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Increasing prevalence of type 2 diabetes mellitus in Thai children and adolescents associated with increasing prevalence of obesity. Author(s): Likitmaskul S, Kiattisathavee P, Chaichanwatanakul K, Punnakanta L, Angsusingha K, Tuchinda C. Source: J Pediatr Endocrinol Metab. 2003 January; 16(1): 71-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12585343&dopt=Abstract

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India sees parallel rise in malnutrition and obesity. Author(s): Chatterjee P. Source: Lancet. 2002 December 14; 360(9349): 1948. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12493270&dopt=Abstract

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Indices of obesity, dyslipidemia, and insulin resistance in apparently healthy Caribbean subjects. Author(s): Ezenwaka CE, Kalloo R. Source: Journal of Clinical Laboratory Analysis. 2003; 17(1): 6-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12526016&dopt=Abstract

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Infant feeding and obesity through the lifecourse. Author(s): Parsons TJ, Power C, Manor O. Source: Archives of Disease in Childhood. 2003 September; 88(9): 793-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937101&dopt=Abstract

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Influence of depressive mood on the association of CRP and obesity in 3205 middle aged healthy men. Author(s): Ladwig KH, Marten-Mittag B, Lowel H, Doring A, Koenig W. Source: Brain, Behavior, and Immunity. 2003 August; 17(4): 268-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831829&dopt=Abstract

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Influencing the childhood behaviors that lead to obesity: role of the pediatrician and health care professional. Author(s): Rivara FP, Whitaker R, Sherman PM, Cuttler L. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 719-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912772&dopt=Abstract

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Insulin resistance in type 2 diabetes: association with truncal obesity, impaired fitness, and atypical malonyl coenzyme A regulation. Author(s): Bavenholm PN, Kuhl J, Pigon J, Saha AK, Ruderman NB, Efendic S. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 January; 88(1): 82-7. Erratum In: J Clin Endocrinol Metab. 2003 May; 88(5): 2036. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519834&dopt=Abstract

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Insulin resistance, impaired postprandial lipid metabolism and abdominal obesity. A deadly triad. Author(s): Frayn KN. Source: Medical Principles and Practice : International Journal of the Kuwait University, Health Science Centre. 2002; 11 Suppl 2: 31-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12444308&dopt=Abstract

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Insulin-stimulated protein kinase C lambda/zeta activity is reduced in skeletal muscle of humans with obesity and type 2 diabetes: reversal with weight reduction. Author(s): Kim YB, Kotani K, Ciaraldi TP, Henry RR, Kahn BB. Source: Diabetes. 2003 August; 52(8): 1935-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882908&dopt=Abstract

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Interacting genetic loci on chromosomes 20 and 10 influence extreme human obesity. Author(s): Dong C, Wang S, Li WD, Li D, Zhao H, Price RA. Source: American Journal of Human Genetics. 2003 January; 72(1): 115-24. Epub 2002 December 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12478478&dopt=Abstract

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Intermediate results following laparoscopic adjustable gastric banding for morbid obesity. Author(s): Victorzon M, Tolonen P. Source: Digestive Surgery. 2002; 19(5): 354-7; Discussion 358. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12435905&dopt=Abstract

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Inter-relationships between lifestyle and diabetes mellitus, overweight/obesity and hypertension in Nigeria. Author(s): Abidoye RO, Izunwa RD, Akinkuade FO, Abidoye GO. Source: Nutr Health. 2002; 16(3): 203-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12418804&dopt=Abstract

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Interventions for treating obesity in children. Author(s): Summerbell CD, Ashton V, Campbell KJ, Edmunds L, Kelly S, Waters E. Source: Cochrane Database Syst Rev. 2003; (3): Cd001872. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917914&dopt=Abstract

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Intra-abdominal obesity and metabolic risk factors: a study of young adults. Author(s): von Eyben FE, Mouritsen E, Holm J, Montvilas P, Dimcevski G, Suciu G, Helleberg I, Kristensen L, von Eyben R. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 941-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861235&dopt=Abstract

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Intracellular retention is a common characteristic of childhood obesity-associated MC4R mutations. Author(s): Lubrano-Berthelier C, Durand E, Dubern B, Shapiro A, Dazin P, Weill J, Ferron C, Froguel P, Vaisse C. Source: Human Molecular Genetics. 2003 January 15; 12(2): 145-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499395&dopt=Abstract

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Is maternal obesity a predictor of shoulder dystocia? Author(s): Robinson H, Tkatch S, Mayes DC, Bott N, Okun N. Source: Obstetrics and Gynecology. 2003 January; 101(1): 24-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12517641&dopt=Abstract

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Is obesity a disease of the blood-brain barrier? Physiological, pathological, and evolutionary considerations. Author(s): Banks WA. Source: Current Pharmaceutical Design. 2003; 9(10): 801-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678879&dopt=Abstract

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Is obesity a risk factor for cirrhosis-related death or hospitalization? A populationbased cohort study. Author(s): Ioannou GN, Weiss NS, Kowdley KV, Dominitz JA. Source: Gastroenterology. 2003 October; 125(4): 1053-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517789&dopt=Abstract

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Is obesity associated with early sexual maturation? A comparison of the association in American boys versus girls. Author(s): Wang Y. Source: Pediatrics. 2002 November; 110(5): 903-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415028&dopt=Abstract

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Is oxidant stress a connection between obesity and atherosclerosis? Author(s): Morrow JD. Source: Arteriosclerosis, Thrombosis, and Vascular Biology. 2003 March 1; 23(3): 368-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12639824&dopt=Abstract

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Is the Canadian childhood obesity epidemic related to physical inactivity? Author(s): Tremblay MS, Willms JD. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 September; 27(9): 1100-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917717&dopt=Abstract

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Is the gender difference in LDL size explained by the metabolic complications of visceral obesity? Author(s): Lemieux I, Pascot A, Lamarche B, Prud'homme D, Nadeau A, Bergeron J, Despres JP. Source: European Journal of Clinical Investigation. 2002 December; 32(12): 909-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534450&dopt=Abstract

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JAMA patient page. Obesity. Author(s): Torpy JM, Lynm C, Glass RM. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1880. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684367&dopt=Abstract

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Jejunoileal bypass in the treatment of morbid obesity: a 25-year follow-up study of 36 patients. Author(s): Vage V, Solhaug JH, Berstad A, Svanes K, Viste A. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 June; 12(3): 312-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12082879&dopt=Abstract

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Laparoscopic adjustable gastric banding for morbid obesity. Author(s): Ferraro DR. Source: Aorn Journal. 2003 May; 77(5): 923-40; Quiz 942-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769325&dopt=Abstract

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Laparoscopic adjustable gastric banding in the treatment of morbid obesity. Author(s): O'Brien PE, Dixon JB. Source: Archives of Surgery (Chicago, Ill. : 1960). 2003 April; 138(4): 376-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686523&dopt=Abstract

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Laparoscopic adjustable gastric banding with duodenal switch for morbid obesity: technique and preliminary results. Author(s): Gagner M, Steffen R, Biertho L, Horber F. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 June; 13(3): 444-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841909&dopt=Abstract

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Laparoscopic era of operations for morbid obesity. Author(s): Cottam DR, Mattar SG, Schauer PR. Source: Archives of Surgery (Chicago, Ill. : 1960). 2003 April; 138(4): 367-75. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686522&dopt=Abstract

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Laparoscopic gastric banding: a minimally invasive surgical treatment for morbid obesity: prospective study of 500 consecutive patients. Author(s): Zinzindohoue F, Chevallier JM, Douard R, Elian N, Ferraz JM, Blanche JP, Berta JL, Altman JJ, Safran D, Cugnenc PH. Source: Annals of Surgery. 2003 January; 237(1): 1-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12496523&dopt=Abstract

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Laparoscopic gastric bypass for morbid obesity with linear gastroenterostomy. Author(s): Korenkov M, Goh P, Yucel N, Troidl H. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 June; 13(3): 360-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841894&dopt=Abstract

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Laparoscopic management of complications following laparoscopic Roux-en-Y gastric bypass for morbid obesity. Author(s): Papasavas PK, Caushaj PF, McCormick JT, Quinlin RF, Hayetian FD, Maurer J, Kelly JJ, Gagne DJ. Source: Surgical Endoscopy. 2003 April; 17(4): 610-4. Epub 2003 February 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582772&dopt=Abstract

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Laser acupuncture and low-calorie diet during visceral obesity therapy after menopause. Author(s): Wozniak P, Stachowiak G, Pieta-Dolinska A, Oszukowski P. Source: Acta Obstetricia Et Gynecologica Scandinavica. 2003 January; 82(1): 69-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580844&dopt=Abstract

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Left atrial size in children with hypertension: the influence of obesity, blood pressure, and left ventricular mass. Author(s): Daniels SR, Witt SA, Glascock B, Khoury PR, Kimball TR. Source: The Journal of Pediatrics. 2002 August; 141(2): 186-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183712&dopt=Abstract

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Legal interest expands from tobacco to obesity. Author(s): Willensky D. Source: Bulletin of the World Health Organization. 2003; 81(4): 309-10. Epub 2003 May 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764502&dopt=Abstract

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Leisure-time activity is an important determinant of long-term weight maintenance after weight loss in the Sibutramine Trial on Obesity Reduction and Maintenance (STORM trial). Author(s): van Baak MA, van Mil E, Astrup AV, Finer N, Van Gaal LF, Hilsted J, Kopelman PG, Rossner S, James WP, Saris WH; STORM Study Group. Source: The American Journal of Clinical Nutrition. 2003 August; 78(2): 209-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885699&dopt=Abstract

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Leptin and the central neural mechanisms of obesity hypertension. Author(s): Rahmouni K, G Haynes W. Source: Drugs Today (Barc). 2002 December; 38(12): 807-17. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582470&dopt=Abstract

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Leptin and the treatment of obesity: its current status. Author(s): Eur J Pharmacol. 2002 Aug 16;450(1):93-109 Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 129-39. Review. /entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12176114

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Leptin: a novel link between obesity, diabetes, cardiovascular risk, and ventricular hypertrophy. Author(s): Sader S, Nian M, Liu P. Source: Circulation. 2003 August 12; 108(6): 644-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912793&dopt=Abstract

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Letting the "Gini" out of the bottle: social causation and the obesity epidemic. Author(s): Goodman E. Source: The Journal of Pediatrics. 2003 March; 142(3): 228-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640364&dopt=Abstract

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Leukocytosis and hyperleptinemia in obesity: is there a link? Author(s): Perfetto F, Mancuso F, Tarquini R. Source: Haematologica. 2002 May; 87(5): Elt25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12010685&dopt=Abstract

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Lifestyle factors, obesity and the risk of chronic kidney disease. Author(s): Stengel B, Tarver-Carr ME, Powe NR, Eberhardt MS, Brancati FL. Source: Epidemiology (Cambridge, Mass.). 2003 July; 14(4): 479-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843775&dopt=Abstract

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Lifestyle modification in the management of obesity. Author(s): Wadden TA, McGuckin BG, Rothman RA, Sargent SL. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 452-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763398&dopt=Abstract

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Linkage and linkage disequilibrium mapping of genes influencing human obesity in chromosome region 7q22.1-7q35. Author(s): Li WD, Li D, Wang S, Zhang S, Zhao H, Price RA. Source: Diabetes. 2003 June; 52(6): 1557-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765970&dopt=Abstract

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Links between body mass index, total body fat, cholesterol, high-density lipoprotein, and insulin sensitivity in patients with obesity related to depression, anger, and anxiety. Author(s): Laederach-Hofmann K, Kupferschmid S, Mussgay L. Source: The International Journal of Eating Disorders. 2002 July; 32(1): 58-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183947&dopt=Abstract

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Liver volume and visceral obesity in women with hepatic steatosis undergoing gastric banding. Author(s): Busetto L, Tregnaghi A, De Marchi F, Segato G, Foletto M, Sergi G, Favretti F, Lise M, Enzi G. Source: Obesity Research. 2002 May; 10(5): 408-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006641&dopt=Abstract

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Local and systemic impact of transcriptional up-regulation of 11beta-hydroxysteroid dehydrogenase type 1 in adipose tissue in human obesity. Author(s): Wake DJ, Rask E, Livingstone DE, Soderberg S, Olsson T, Walker BR. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 August; 88(8): 3983-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915696&dopt=Abstract

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Localized lichen myxoedematosus (papular mucinosis) associated with morbid obesity: report of two cases. Author(s): Saez-Rodriguez M, Garcia-Bustinduy M, Lopez-Alba A, Noda-Cabrera A, Guimera-Martin-Neda F, Dorta-Alom S, Escoda-Garcia M, Fagundo-Gonzalez E, Sanchez-Gonzalez R, Martin-Herrera A, Garcia-Montelongo R. Source: The British Journal of Dermatology. 2003 January; 148(1): 165-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534614&dopt=Abstract

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Longitudinal analysis of changes in indices of obesity from age 8 years to age 18 years. Project HeartBeat! Author(s): Dai S, Labarthe DR, Grunbaum JA, Harrist RB, Mueller WH. Source: American Journal of Epidemiology. 2002 October 15; 156(8): 720-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12370160&dopt=Abstract

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Long-term and recent time trends in the prevalence of obesity among Dutch men and women. Author(s): Visscher TL, Kromhout D, Seidell JC. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 September; 26(9): 1218-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12187399&dopt=Abstract

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Long-term data indicate a progressive loss in efficacy of adjustable silicone gastric banding for the surgical treatment of morbid obesity. Author(s): Doherty C, Maher JW, Heitshusen DS. Source: Surgery. 2002 October; 132(4): 724-7; Discussion 727-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12407358&dopt=Abstract

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Long-term results of laparoscopic adjustable gastric banding for the treatment of morbid obesity. Author(s): Belachew M, Belva PH, Desaive C. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 August; 12(4): 564-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12194552&dopt=Abstract

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Low adiponectin levels in adolescent obesity: a marker of increased intramyocellular lipid accumulation. Author(s): Weiss R, Dufour S, Groszmann A, Petersen K, Dziura J, Taksali SE, Shulman G, Caprio S. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 May; 88(5): 2014-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727947&dopt=Abstract

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Low circulating IGF-II concentrations predict weight gain and obesity in humans. Author(s): Sandhu MS, Gibson JM, Heald AH, Dunger DB, Wareham NJ. Source: Diabetes. 2003 June; 52(6): 1403-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765950&dopt=Abstract

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Low plasma antioxidants and normal plasma B vitamins and homocysteine in patients with severe obesity. Author(s): Reitman A, Friedrich I, Ben-Amotz A, Levy Y. Source: Isr Med Assoc J. 2002 August; 4(8): 590-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183861&dopt=Abstract

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Management and treatment of obesity. Author(s): Zizza CA. Source: Southern Medical Journal. 2003 June; 96(6): 537-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938777&dopt=Abstract

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Management of obesity as a chronic disease: nonpharmacologic, pharmacologic, and surgical options. Author(s): Fujioka K. Source: Obesity Research. 2002 December; 10 Suppl 2: 116S-123S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490660&dopt=Abstract

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Managing obesity. Author(s): Rabinowitz E. Source: Healthplan. 2003 January-February; 44(1): 40-2, 44-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12611252&dopt=Abstract

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Managing overweight and obesity in women. Author(s): Klauer J, Aronne LJ. Source: Clinical Obstetrics and Gynecology. 2002 December; 45(4): 1080-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12438886&dopt=Abstract

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Maternal gestational diabetes, birth weight, and adolescent obesity. Author(s): Gillman MW, Rifas-Shiman S, Berkey CS, Field AE, Colditz GA. Source: Pediatrics. 2003 March; 111(3): E221-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12612275&dopt=Abstract

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Maternal obesity and breast-feeding practices. Author(s): Li R, Jewell S, Grummer-Strawn L. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4): 931-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663294&dopt=Abstract

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Maternal obesity and pregnancy outcomes. Author(s): Castro LC, Avina RL. Source: Current Opinion in Obstetrics & Gynecology. 2002 December; 14(6): 601-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12441699&dopt=Abstract

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Maternal obesity and risk for birth defects. Author(s): Watkins ML, Rasmussen SA, Honein MA, Botto LD, Moore CA. Source: Pediatrics. 2003 May; 111(5 Part 2): 1152-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728129&dopt=Abstract

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Measurement of sleep apnea during obesity treatment. Author(s): Billington CJ. Source: Obesity Research. 2002 November; 10 Suppl 1: 38S-41S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446857&dopt=Abstract

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Measuring food intake in studies of obesity. Author(s): Lissner L. Source: Public Health Nutrition. 2002 December; 5(6A): 889-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12638596&dopt=Abstract

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Medical and surgical options in the treatment of severe obesity. Author(s): Fisher BL, Schauer P. Source: American Journal of Surgery. 2002 December; 184(6B): 9S-16S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527344&dopt=Abstract

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Medical management of obesity: a clinical imperative? Author(s): Haynes WG. Source: Curr Diab Rep. 2003 February; 3(1): 1-3. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643140&dopt=Abstract

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Medical management of obesity: present and future therapy. Author(s): Klein S. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 464-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763399&dopt=Abstract

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Melanocortin-3-receptor gene variants in morbid obesity. Author(s): Schalin-Jantti C, Valli-Jaakola K, Oksanen L, Martelin E, Laitinen K, Krusius T, Mustajoki P, Heikinheimo M, Kontula K. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 January; 27(1): 70-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532156&dopt=Abstract

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Melanocortin-4 receptor gene: case-control study and transmission disequilibrium test confirm that functionally relevant mutations are compatible with a major gene effect for extreme obesity. Author(s): Hinney A, Hohmann S, Geller F, Vogel C, Hess C, Wermter AK, Brokamp B, Goldschmidt H, Siegfried W, Remschmidt H, Schafer H, Gudermann T, Hebebrand J. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 September; 88(9): 4258-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970296&dopt=Abstract

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Metabolic disturbances in obesity versus sleep apnoea: the importance of visceral obesity and insulin resistance. Author(s): Vgontzas AN, Bixler EO, Chrousos GP. Source: Journal of Internal Medicine. 2003 July; 254(1): 32-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823641&dopt=Abstract

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Metabolic effects of the Gly1057Asp polymorphism in IRS-2 and interactions with obesity. Author(s): Stefan N, Kovacs P, Stumvoll M, Hanson RL, Lehn-Stefan A, Permana PA, Baier LJ, Tataranni PA, Silver K, Bogardus C. Source: Diabetes. 2003 June; 52(6): 1544-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765968&dopt=Abstract

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Metabolic syndrome & obesity: co-epidemics could overwhelm home health care. Author(s): Pearce LC. Source: Caring. 2003 June; 22(6): 24-8, 30, 32-3; Quiz 34-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905569&dopt=Abstract

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Methods of estimating years of life lost due to obesity. Author(s): Peeters A, Bonneux L, Barendregt J, Nusselder W. Source: Jama : the Journal of the American Medical Association. 2003 June 11; 289(22): 2941; Author Reply 2941-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12799399&dopt=Abstract

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Midface hypoplasia, obesity, developmental delay and neonatal hypotonia in two brothers. Author(s): Rozendaal L, Del Canho H, Waterham HR, Hennekam RC. Source: Clinical Dysmorphology. 2003 January; 12(1): 9-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12514359&dopt=Abstract

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Minireview: From anorexia to obesity--the yin and yang of body weight control. Author(s): Zigman JM, Elmquist JK. Source: Endocrinology. 2003 September; 144(9): 3749-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12933644&dopt=Abstract

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Minireview: human obesity-lessons from monogenic disorders. Author(s): O'Rahilly S, Farooqi IS, Yeo GS, Challis BG. Source: Endocrinology. 2003 September; 144(9): 3757-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12933645&dopt=Abstract

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Modifications of blood pressure and IGF-I levels after weight loss in obesity. Author(s): Dall'Aglio E, Salimbeni I, Rocci A, Mazzoni S, Corradi F, Cattadori E, Visioli S, Banchini A, Valenti G, Ceda GP. Source: J Endocrinol Invest. 2002; 25(10 Suppl): 107-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508940&dopt=Abstract

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Molecular and genetic mechanisms of obesity: implications for future management. Author(s): Liu YJ, Araujo S, Recker RR, Deng HW. Source: Current Molecular Medicine. 2003 June; 3(4): 325-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776988&dopt=Abstract

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Molecular genetics of human obesity-associated MC4R mutations. Author(s): Lubrano-Berthelier C, Cavazos M, Dubern B, Shapiro A, Stunff CL, Zhang S, Picart F, Govaerts C, Froguel P, Bougneres P, Clement K, Vaisse C. Source: Annals of the New York Academy of Sciences. 2003 June; 994: 49-57. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851297&dopt=Abstract

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Morbid obesity and hypersomnolence in several members of an ancient royal family. Author(s): Michalopoulos A, Tzelepis G, Geroulanos S. Source: Thorax. 2003 March; 58(3): 281-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12612315&dopt=Abstract

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Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Author(s): Eichenberger A, Proietti S, Wicky S, Frascarolo P, Suter M, Spahn DR, Magnusson L. Source: Anesthesia and Analgesia. 2002 December; 95(6): 1788-92, Table of Contents. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12456460&dopt=Abstract

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Morbid obesity: the disease and comorbidities. Author(s): Owens TM. Source: Critical Care Nursing Quarterly. 2003 April-June; 26(2): 162-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744597&dopt=Abstract

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Muscle fiber type is associated with obesity and weight loss. Author(s): Tanner CJ, Barakat HA, Dohm GL, Pories WJ, MacDonald KG, Cunningham PR, Swanson MS, Houmard JA. Source: American Journal of Physiology. Endocrinology and Metabolism. 2002 June; 282(6): E1191-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006347&dopt=Abstract

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Musculoskeletal pain in the obese: a comparison with a general population and longterm changes after conventional and surgical obesity treatment. Author(s): Peltonen M, Lindroos AK, Torgerson JS. Source: Pain. 2003 August; 104(3): 549-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12927627&dopt=Abstract

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Nasal continuous positive airway pressure improves quality of life in obesity hypoventilation syndrome. Author(s): Hida W, Okabe S, Tatsumi K, Kimura H, Akasiba T, Chin K, Ohi M, Nakayama H, Satoh M, Kuriyama T. Source: Sleep & Breathing = Schlaf & Atmung. 2003 March; 7(1): 3-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712392&dopt=Abstract

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National and international strategies to prevent obesity and diabetes. Author(s): Reeder BA. Source: Advances in Experimental Medicine and Biology. 2001; 498: 393-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11900397&dopt=Abstract

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National Cholesterol Education Program Adult Treatment Panel III guidelines and obesity: implications for Canada. Author(s): Ardern CI, Katzmarzyk PT. Source: The Canadian Journal of Cardiology. 2003 September; 19(10): 1171-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14532943&dopt=Abstract

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Neonatal nutrition: metabolic programming of pancreatic islets and obesity. Author(s): Srinivasan M, Laychock SG, Hill DJ, Patel MS. Source: Experimental Biology and Medicine (Maywood, N.J.). 2003 January; 228(1): 1523. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12524468&dopt=Abstract

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Neuroendocrine and metabolic determinants of the adaptation of GH/IGF-I axis to obesity. Author(s): Maccario M, Tassone F, Grottoli S, Rossetto R, Gauna C, Ghigo E. Source: Annales D'endocrinologie. 2002 April; 63(2 Pt 1): 140-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11994678&dopt=Abstract

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Neuroendocrine and peripheral activities of ghrelin: implications in metabolism and obesity. Author(s): Muccioli G, Tschop M, Papotti M, Deghenghi R, Heiman M, Ghigo E. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 235-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007539&dopt=Abstract

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Neuroimaging and obesity: mapping the brain responses to hunger and satiation in humans using positron emission tomography. Author(s): Del Parigi A, Gautier JF, Chen K, Salbe AD, Ravussin E, Reiman E, Tataranni PA. Source: Annals of the New York Academy of Sciences. 2002 June; 967: 389-97. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079866&dopt=Abstract

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Neuropeptide Y receptors as targets for anti-obesity drug development: perspective and current status. Author(s): Parker E, Van Heek M, Stamford A. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 173-87. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007534&dopt=Abstract

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New criteria for 'obesity disease' in Japan. Author(s): Examination Committee of Criteria for 'Obesity Disease' in Japan; Japan Society for the Study of Obesity. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2002 November; 66(11): 987-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419927&dopt=Abstract

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New insights in obesity. Author(s): Bloomgarden ZT. Source: Diabetes Care. 2002 April; 25(4): 789-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11919138&dopt=Abstract

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New Moves: a school-based obesity prevention program for adolescent girls. Author(s): Neumark-Sztainer D, Story M, Hannan PJ, Rex J. Source: Preventive Medicine. 2003 July; 37(1): 41-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12799128&dopt=Abstract

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New obesity center at WVU offering comprehensive program.. Author(s): Dino GA, Cohen D, Tessaro I, Ducatman A. Source: W V Med J. 2002 November-December; 98(6): 288-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645285&dopt=Abstract

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New pharmacological tools for obesity. Author(s): Nisoli E, Carruba MO. Source: J Endocrinol Invest. 2002 November; 25(10): 905-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508954&dopt=Abstract

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Nicotine, body weight and potential implications in the treatment of obesity. Author(s): Li MD, Kane JK, Konu O. Source: Current Topics in Medicinal Chemistry. 2003; 3(8): 899-919. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678839&dopt=Abstract

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Night eating in obesity: a descriptive study. Author(s): Adami GF, Campostano A, Marinari GM, Ravera G, Scopinaro N. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2002 July-August; 18(7-8): 5879. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12093435&dopt=Abstract

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No association found between the Ala54Thr polymorphism of FABP2 gene and obesity and obesity with dyslipidemia in Japanese schoolchildren. Author(s): Endo K, Yanagi H, Hirano C, Hayakawa Y, Hamaguchi H, Tomura S. Source: J Atheroscler Thromb. 2001; 8(3): 80-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11866034&dopt=Abstract

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No evidence for involvement of the calpain-10 gene 'high-risk' haplotype combination for non-insulin-dependent diabetes mellitus in early onset obesity. Author(s): Hinney A, Antwerpen B, Geller F, Schafer H, Siegfried W, Goldschmidt H, Remschmidt H, Ziegler A, Hebebrand J. Source: Molecular Genetics and Metabolism. 2002 June; 76(2): 152-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12083814&dopt=Abstract

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No influence of obesity on the pharmacokinetics and pharmacodynamics of melagatran, the active form of the oral direct thrombin inhibitor ximelagatran. Author(s): Sarich TC, Teng R, Peters GR, Wollbratt M, Homolka R, Svensson M, Eriksson UG. Source: Clinical Pharmacokinetics. 2003; 42(5): 485-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739986&dopt=Abstract

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No linkage to obesity in candidate regions of chromosome 2 and 10 in a selected sample of Swedish twins. Author(s): Iliadou A, Lichtenstein P, Ahlberg S, Hoffstedt J, Arner P, Schalling M, Pedersen NL, Lavebratt C. Source: Twin Research : the Official Journal of the International Society for Twin Studies. 2003 April; 6(2): 162-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724003&dopt=Abstract

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Non-communicable diseases (diabetes, obesity and hyperlipidaemia) in urban slums. Author(s): Misra A, Pandey RM, Sharma R. Source: Natl Med J India. 2002 July-August; 15(4): 242-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12296484&dopt=Abstract

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Nutrition for health promotion: phytochemicals, functional foods, and alternative approaches to combat obesity. Author(s): Bloch AS. Source: Dent Clin North Am. 2003 April; 47(2): 411-23, Viii-Ix. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699239&dopt=Abstract

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Nutrition, physical activity, and obesity. Author(s): Jacobson MF. Source: Lancet. 2002 October 19; 360(9341): 1250. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401275&dopt=Abstract

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Nutrition, physical activity, and obesity. Author(s): Summers JB, Kaminski JM. Source: Lancet. 2002 October 19; 360(9341): 1249. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401274&dopt=Abstract

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Nutrition, physical activity, and obesity. Author(s): Kerr D, James J. Source: Lancet. 2002 October 19; 360(9341): 1249. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401273&dopt=Abstract

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Nutrition, physical activity, and obesity. Author(s): Das UN, Meguid MM. Source: Lancet. 2002 October 19; 360(9341): 1249-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401272&dopt=Abstract

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Nutritional advice for obesity management and health. Author(s): Hunking P. Source: British Journal of Community Nursing. 2002 May; 7(5): 246-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12048498&dopt=Abstract

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Nutritional risk assessment and obesity in rural older adults: a sex difference. Author(s): Ledikwe JH, Smiciklas-Wright H, Mitchell DC, Jensen GL, Friedmann JM, Still CD. Source: The American Journal of Clinical Nutrition. 2003 March; 77(3): 551-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12600842&dopt=Abstract

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Obesity - a global problem. Author(s): Siddiqui NI. Source: Mymensingh Med J. 2003 July; 12(2): 76-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894035&dopt=Abstract

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Obesity and cancer. Author(s): Abu-Abid S, Szold A, Klausner J. Source: J Med. 2002; 33(1-4): 73-86. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939106&dopt=Abstract

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Obesity and cancer. Author(s): Smith JA. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892104&dopt=Abstract

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Obesity and cancer. Author(s): Gaesser GA. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892103&dopt=Abstract

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Obesity and cancer. Author(s): Frankel PH. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892102&dopt=Abstract

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Obesity and cancer. Author(s): Flegal KM, Williamson DF, Graubard BI. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892101&dopt=Abstract

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Obesity and cancer. Author(s): Deutsch ME. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890851&dopt=Abstract

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Obesity and cardiovascular disease: the hippocrates paradox? Author(s): Lavie CJ, Milani RV. Source: Journal of the American College of Cardiology. 2003 August 20; 42(4): 677-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932600&dopt=Abstract

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Obesity and diabetes in African American women. Author(s): Tilghman J. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 66-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856444&dopt=Abstract

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Obesity and hip osteoarthritis. Author(s): Lievense AM, Reijman M, Pols HA, Bierma-Zeinstra SM. Source: The American Journal of Medicine. 2003 September; 115(4): 329; Author Reply 329-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12967700&dopt=Abstract

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Obesity and its nurturing effect on hepatitis C. Author(s): McCullough AJ. Source: Hepatology (Baltimore, Md.). 2003 September; 38(3): 557-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939581&dopt=Abstract

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Obesity and low back pain. Author(s): Bener A, Alwash R, Gaber T, Lovasz G. Source: Coll Antropol. 2003 June; 27(1): 95-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12974137&dopt=Abstract

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Obesity and overweight among adults in North Carolina. Author(s): Buescher PA. Source: N C Med J. 2002 November-December; 63(6): 287. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970975&dopt=Abstract

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Obesity and pregnancy--the propagation of a viscous cycle? Author(s): Catalano PM. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 August; 88(8): 3505-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915626&dopt=Abstract

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Obesity and the heart: an ever-growing problem. Author(s): Lavie CJ, Milani RV, Messerli FH. Source: Southern Medical Journal. 2003 June; 96(6): 535-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938776&dopt=Abstract

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Obesity and the risk of early and late mortality after coronary artery bypass graft surgery. Author(s): Kim J, Hammar N, Jakobsson K, Luepker RV, McGovern PG, Ivert T. Source: American Heart Journal. 2003 September; 146(3): 555-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947378&dopt=Abstract

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Obesity and the risk of newly diagnosed asthma in school-age children. Author(s): Gilliland FD, Berhane K, Islam T, McConnell R, Gauderman WJ, Gilliland SS, Avol E, Peters JM. Source: American Journal of Epidemiology. 2003 September 1; 158(5): 406-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12936895&dopt=Abstract

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Obesity as a potential risk factor for adenocarcinomas and squamous cell carcinomas of the uterine cervix. Author(s): Lacey JV Jr, Swanson CA, Brinton LA, Altekruse SF, Barnes WA, Gravitt PE, Greenberg MD, Hadjimichael OC, McGowan L, Mortel R, Schwartz PE, Kurman RJ, Hildesheim A. Source: Cancer. 2003 August 15; 98(4): 814-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910527&dopt=Abstract

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Obesity goes global. Author(s): Nash JM. Source: Time. 2003 August 25; 162(8): 53-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12964464&dopt=Abstract

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Obesity in 70-year-old subjects as a risk factor for 15-year coronary heart disease incidence. Author(s): Dey DK, Lissner L. Source: Obesity Research. 2003 July; 11(7): 817-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855750&dopt=Abstract

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Obesity in African American women. Author(s): July FM. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856441&dopt=Abstract

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Obesity in general elective surgery. Author(s): McCarthy R, Leslie T, Williams DJ. Source: Lancet. 2003 August 16; 362(9383): 577; Author Reply 577-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932397&dopt=Abstract

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Obesity in general elective surgery. Author(s): Slim K, Kwiatkowski F, Chipponi J. Source: Lancet. 2003 August 16; 362(9383): 577; Author Reply 577-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932396&dopt=Abstract

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Obesity in general elective surgery. Author(s): Pravinkumar E. Source: Lancet. 2003 August 16; 362(9383): 576-7; Author Reply 577-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932394&dopt=Abstract

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Obesity is associated with impaired platelet-inhibitory effect of acetylsalicylic acid in nondiabetic subjects. Author(s): Tamminen M, Lassila R, Westerbacka J, Vehkavaara S, Yki-Jarvinen H. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 907-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861231&dopt=Abstract

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Obesity prevention in pediatric primary care: four behaviors to target. Author(s): Whitaker RC. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 725-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912775&dopt=Abstract

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Obesity, tamoxifen use, and outcomes in women with estrogen receptor-positive early-stage breast cancer. Author(s): Dignam JJ, Wieand K, Johnson KA, Fisher B, Xu L, Mamounas EP. Source: Journal of the National Cancer Institute. 2003 October 1; 95(19): 1467-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14519753&dopt=Abstract

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Obesity: an epidemic. Author(s): Hamdy RC. Source: Southern Medical Journal. 2003 June; 96(6): 531-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938774&dopt=Abstract

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Obesity: associations with acute mountain sickness. Author(s): Ri-Li G, Chase PJ, Witkowski S, Wyrick BL, Stone JA, Levine BD, Babb TG. Source: Annals of Internal Medicine. 2003 August 19; 139(4): 253-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12965980&dopt=Abstract

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Overweight and obesity prevalence rates among youth in the Carolinas. Author(s): Terrell DF. Source: N C Med J. 2002 November-December; 63(6): 281-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970974&dopt=Abstract

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Pediatric obesity policy: the danger of skepticism. Author(s): Cuttler L, Whittaker JL, Kodish ED. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 722-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912774&dopt=Abstract

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Peroxisome proliferator activated receptors and obesity. Author(s): Kersten S. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 223-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007538&dopt=Abstract

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Perspectives on childhood obesity. Author(s): Strauss R. Source: Current Gastroenterology Reports. 2002 June; 4(3): 244-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12010626&dopt=Abstract

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Pharmacoeconomics of obesity management in childhood and adolescence. Author(s): Kiess W, Bottner A, Bluher S, Raile K, Seidel B, Kapellen T, Keller E, Kratzsch J. Source: Expert Opinion on Pharmacotherapy. 2003 September; 4(9): 1471-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12943476&dopt=Abstract

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Pharmacological therapy of obesity: past, present, and future. Author(s): Weigle DS. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 June; 88(6): 2462-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788841&dopt=Abstract

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Pharmacotherapy of obesity: an update. Author(s): Schurgin S, Siegel RD. Source: Nutrition in Clinical Care : an Official Publication of Tufts University. 2003 January-April; 6(1): 27-37. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841428&dopt=Abstract

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Photo quiz. Obesity and daytime sleepiness. Prader-Willi syndrome. Author(s): Baumgart DC, Gerl H. Source: American Family Physician. 2003 July 1; 68(1): 151-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12887122&dopt=Abstract

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Physical activity, obesity, and the incidence of type 2 diabetes in a high-risk population. Author(s): Kriska AM, Saremi A, Hanson RL, Bennett PH, Kobes S, Williams DE, Knowler WC. Source: American Journal of Epidemiology. 2003 October 1; 158(7): 669-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14507603&dopt=Abstract

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Physical inactivity, energy intake, obesity and the risk of rectal cancer in Canada. Author(s): Mao Y, Pan S, Wen SW, Johnson KC; Canadian Cancer Registries Epidemiology Research Group. Source: International Journal of Cancer. Journal International Du Cancer. 2003 July 20; 105(6): 831-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767070&dopt=Abstract

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Plasmalemmal fatty acid transport is regulated in heart and skeletal muscle by contraction, insulin and leptin, and in obesity and diabetes. Author(s): Bonen A, Benton CR, Campbell SE, Chabowski A, Clarke DC, Han XX, Glatz JF, Luiken JJ. Source: Acta Physiologica Scandinavica. 2003 August; 178(4): 347-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12864739&dopt=Abstract

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Plasminogen activator inhibitor-1, inflammation, obesity, insulin resistance and vascular risk. Author(s): Juhan-Vague I, Alessi MC, Mavri A, Morange PE. Source: Journal of Thrombosis and Haemostasis : Jth. 2003 July; 1(7): 1575-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12871293&dopt=Abstract

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Poor cell surface expression of human melanocortin-4 receptor mutations associated with obesity. Author(s): Nijenhuis WA, Garner KM, van Rozen RJ, Adan RA. Source: The Journal of Biological Chemistry. 2003 June 20; 278(25): 22939-45. Epub 2003 April 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12690102&dopt=Abstract

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Possible lessons from the tobacco experience for obesity control. Author(s): Mercer SL, Green LW, Rosenthal AC, Husten CG, Khan LK, Dietz WH. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4 Suppl): 1073S1082S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663321&dopt=Abstract

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Predicting obesity in early adulthood from childhood and parental obesity. Author(s): Magarey AM, Daniels LA, Boulton TJ, Cockington RA. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 505-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664084&dopt=Abstract

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Prevalence of obesity and dyslipidemia in middle-aged men and women in Tanzania, Africa: relationship with resting energy expenditure and dietary factors. Author(s): Njelekela M, Kuga S, Nara Y, Ntogwisangu J, Masesa Z, Mashalla Y, Ikeda K, Mtabaji J, Yamori Y, Tsuda K. Source: J Nutr Sci Vitaminol (Tokyo). 2002 October; 48(5): 352-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12656207&dopt=Abstract

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Prevalence of obesity and its association with blood pressure, serum lipids and selected lifestyles in a Puerto Rican population of adolescents 12-16 years of age. Author(s): Venegas HL, Perez CM, Suarez EL, Guzman M. Source: P R Health Sci J. 2003 June; 22(2): 137-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12866137&dopt=Abstract

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Prevalence of obesity in children in Alabama and Texas participating in social programs. Author(s): Feese M, Franklin F, Murdock M, Harrington K, Brown-Binns M, Nicklas T, Hughes S, Morales M. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1780-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684354&dopt=Abstract

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Prevalence of overweight and obesity among Costa Rican elementary school children. Author(s): Nunez-Rivas HP, Monge-Rojas R, Leon H, Rosello M. Source: Revista Panamericana De Salud Publica = Pan American Journal of Public Health. 2003 January; 13(1): 24-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744799&dopt=Abstract

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Prevalence of overweight and obesity in affluent adolescent girls in Chennai in 1981 and 1998. Author(s): Subramanyam V, Jayashree R, Rafi M. Source: Indian Pediatrics. 2003 August; 40(8): 775-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12956109&dopt=Abstract

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Prevalence of overweight and obesity in affluent adolescent girls in Chennai in 1981 and 1998. Author(s): Subramanyam V, R J, Rafi M. Source: Indian Pediatrics. 2003 April; 40(4): 332-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736406&dopt=Abstract

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Prevalence of overweight, obesity, and associated diseases among outpatients in a public hospital. Author(s): Huang J, Marin E, Yu H, Carden D, Arnold C, Davis T, Banks D. Source: Southern Medical Journal. 2003 June; 96(6): 558-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938782&dopt=Abstract

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Preventing obesity. Author(s): Kealy MM. Source: Awhonn Lifelines / Association of Women's Health, Obstetric and Neonatal Nurses. 2003 February-March; 7(1): 24-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12674056&dopt=Abstract

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Prevention of childhood obesity: sociocultural and familial factors. Author(s): Bruss MB, Morris J, Dannison L. Source: Journal of the American Dietetic Association. 2003 August; 103(8): 1042-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12891156&dopt=Abstract

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Prevention of obesity in young children: a critical challenge for medical professionals. Author(s): Sothern MS, Gordon ST. Source: Clinical Pediatrics. 2003 March; 42(2): 101-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12659382&dopt=Abstract

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Prevention of pediatric overweight and obesity. Author(s): Krebs NF, Jacobson MS; American Academy of Pediatrics Committee on Nutrition. Source: Pediatrics. 2003 August; 112(2): 424-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12897303&dopt=Abstract

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Principles and practices in the management of obesity. Author(s): Foster GD. Source: American Journal of Respiratory and Critical Care Medicine. 2003 August 1; 168(3): 274-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888610&dopt=Abstract

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Prospective association between obesity and depression: evidence from the Alameda County Study. Author(s): Roberts RE, Deleger S, Strawbridge WJ, Kaplan GA. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 514-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664085&dopt=Abstract

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Prospects for obesity treatment: MCH receptor antagonists. Author(s): Collins CA, Kym PR. Source: Curr Opin Investig Drugs. 2003 April; 4(4): 386-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12808876&dopt=Abstract

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Protein tyrosine phosphatase 1B: a novel target for type 2 diabetes and obesity. Author(s): Ramachandran C, Kennedy BP. Source: Current Topics in Medicinal Chemistry. 2003; 3(7): 749-57. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678842&dopt=Abstract

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Proton magnetic resonance spectroscopy study of soleus muscle in non-obese healthy and Type 2 diabetic Asian Northern Indian males: high intramyocellular lipid content correlates with excess body fat and abdominal obesity. Author(s): Misra A, Sinha S, Kumar M, Jagannathan NR, Pandey RM. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 2003 May; 20(5): 361-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752484&dopt=Abstract

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Quality of life and obesity. Author(s): Kolotkin RL, Meter K, Williams GR. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 November; 2(4): 219-29. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119993&dopt=Abstract

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Quality of life following laparoscopic gastric banding in patients with morbid obesity. Author(s): Freys SM, Tigges H, Heimbucher J, Fuchs KH, Fein M, Thiede A. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2001 July-August; 5(4): 401-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11985982&dopt=Abstract

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Quality of life in obesity hypoventilation syndrome. Author(s): Hida W. Source: Sleep & Breathing = Schlaf & Atmung. 2003 March; 7(1): 1-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712391&dopt=Abstract

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Racial/ethnic differences in weight concerns: protective and risk factors for the development of eating disorders and obesity among adolescent females. Author(s): White MA, Kohlmaier JR, Varnado-Sullivan P, Williamson DA. Source: Eat Weight Disord. 2003 March; 8(1): 20-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12762621&dopt=Abstract

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Randomized controlled trial of the effect of n-3 fatty acid supplementation on the metabolism of apolipoprotein B-100 and chylomicron remnants in men with visceral obesity. Author(s): Chan DC, Watts GF, Mori TA, Barrett PH, Redgrave TG, Beilin LJ. Source: The American Journal of Clinical Nutrition. 2003 February; 77(2): 300-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540386&dopt=Abstract

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Rapid weight gain during infancy and obesity in young adulthood in a cohort of African Americans. Author(s): Stettler N, Kumanyika SK, Katz SH, Zemel BS, Stallings VA. Source: The American Journal of Clinical Nutrition. 2003 June; 77(6): 1374-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791612&dopt=Abstract

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Rapid weight gain during infancy as a predictor of adult obesity. Author(s): Yanovski JA. Source: The American Journal of Clinical Nutrition. 2003 June; 77(6): 1350-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791608&dopt=Abstract

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Recent developments in the treatment of obesity-related hypertension. Author(s): Pischon T, Sharma AM. Source: Current Opinion in Nephrology and Hypertension. 2002 September; 11(5): 497502. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12187313&dopt=Abstract

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Recent tax changes may assist treatment of obesity. Author(s): Fitzner K, Caputo N, Trendell W, French MV, Bondi MA, Jennings C. Source: Manag Care Interface. 2003 January; 16(1): 47-51, 55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12564405&dopt=Abstract

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Recruitment of African-American pre-adolescent girls into an obesity prevention trial: the GEMS pilot studies. Author(s): Story M, Sherwood NE, Obarzanek E, Beech BM, Baranowski JC, Thompson NS, Owens AS, Mitchell M, Rochon J. Source: Ethn Dis. 2003 Winter; 13(1 Suppl 1): S78-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713213&dopt=Abstract

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Redefining type 2 diabetes: 'diabesity' or 'obesity dependent diabetes mellitus'? Author(s): Astrup A, Finer N. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2000 October; 1(2): 57-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119987&dopt=Abstract

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Reduction in obesity and coronary risk factors after high caloric exercise training in overweight coronary patients. Author(s): Savage PD, Brochu M, Poehlman ET, Ades PA. Source: American Heart Journal. 2003 August; 146(2): 317-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12891202&dopt=Abstract

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Regulation of PPARgamma and obesity by agouti/melanocortin signaling in adipocytes. Author(s): Mynatt RL, Stephens JM. Source: Annals of the New York Academy of Sciences. 2003 June; 994: 141-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851309&dopt=Abstract

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Relation between physical activity and obesity. Author(s): Salbe AD, Weyer C, Harper I, Lindsay RS, Ravussin E, Tataranni PA. Source: The American Journal of Clinical Nutrition. 2003 July; 78(1): 193-4; Author Reply 194-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816794&dopt=Abstract

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Relationship between juvenile obesity, dietary energy and fat intake and physical activity. Author(s): Gillis LJ, Kennedy LC, Gillis AM, Bar-Or O. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 April; 26(4): 458-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12075571&dopt=Abstract

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Relationship between obesity and cardiovascular risk factors in elderly Chinese subjects. Author(s): Thomas GN, Zhao HL, Ma YQ, Ys Leung W, Cn Chan J, Tomlinson B, Ajh Critchley J. Source: Chin Med J (Engl). 2002 June; 115(6): 897-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12123561&dopt=Abstract

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Relationship between obesity and health-related quality of life in men. Author(s): Yancy WS Jr, Olsen MK, Westman EC, Bosworth HB, Edelman D. Source: Obesity Research. 2002 October; 10(10): 1057-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12376587&dopt=Abstract

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Relationship between obesity, insulin resistance, and coronary heart disease risk. Author(s): Abbasi F, Brown BW Jr, Lamendola C, McLaughlin T, Reaven GM. Source: Journal of the American College of Cardiology. 2002 September 4; 40(5): 937-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12225719&dopt=Abstract

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Relationship of beta2-adrenergic receptor polymorphism with obesity in type 2 diabetes. Author(s): van Tilburg JH, Wijmenga C, van Bakel H, Rozeman L, Pearson PL, van Haeften TW. Source: Diabetes Care. 2003 January; 26(1): 251-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12502697&dopt=Abstract

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Relationship of internalized racism to abdominal obesity and blood pressure in AfroCaribbean women. Author(s): Tull SE, Wickramasuriya T, Taylor J, Smith-Burns V, Brown M, Champagnie G, Daye K, Donaldson K, Solomon N, Walker S, Fraser H, Jordan OW. Source: Journal of the National Medical Association. 1999 August; 91(8): 447-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12656433&dopt=Abstract

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Relationship of urodynamic parameters and obesity in women with stress urinary incontinence. Author(s): Bai SW, Kang JY, Rha KH, Lee MS, Kim JY, Park KH. Source: J Reprod Med. 2002 July; 47(7): 559-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12170533&dopt=Abstract

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Relationships of the systolic blood pressure response during exercise with insulin resistance, obesity, and endurance fitness in men with type 2 diabetes mellitus. Author(s): Kumagai S, Kai Y, Hanada H, Uezono K, Sasaki H. Source: Metabolism: Clinical and Experimental. 2002 October; 51(10): 1247-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12370842&dopt=Abstract

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Relative impact of insulin resistance and obesity on cardiovascular risk factors in polycystic ovary syndrome. Author(s): Goodarzi MO, Erickson S, Port SC, Jennrich RI, Korenman SG. Source: Metabolism: Clinical and Experimental. 2003 June; 52(6): 713-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12800096&dopt=Abstract

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Relevance of energy expenditure and energy intake to the etiology of obesity. Author(s): Chapelot D, Louis-Sylvestre J. Source: The American Journal of Clinical Nutrition. 2002 August; 76(2): 489; Author Reply 489-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12145028&dopt=Abstract

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Renal and cardiovascular considerations for the nonpharmacological and pharmacological therapies of obesity-hypertension. Author(s): Zhang R, Thakur V, Morse S, Reisin E. Source: Journal of Human Hypertension. 2002 December; 16(12): 819-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522462&dopt=Abstract

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Research agenda for pediatric gastroenterology, hepatology and nutrition: nutrition and obesity. Report of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition for the Children's Digestive Health and Nutrition Foundation. Author(s): Baker SS, Motil KJ, Heyman MB. Source: Journal of Pediatric Gastroenterology and Nutrition. 2002; 35 Suppl 3: S281-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12394366&dopt=Abstract

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Researching new treatments for obesity: from neuroscience to inflammation. Author(s): Donnelly R. Source: Diabetes, Obesity & Metabolism. 2003 January; 5(1): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12542719&dopt=Abstract

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Resistin - a mediator of obesity-associated insulin resistance or an innocent bystander? Author(s): Ukkola O. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2002 November; 147(5): 571-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12444887&dopt=Abstract

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Risk factors for the development of obesity in children surviving brain tumors. Author(s): Lustig RH, Post SR, Srivannaboon K, Rose SR, Danish RK, Burghen GA, Xiong X, Wu S, Merchant TE. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 February; 88(2): 611-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574189&dopt=Abstract

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Risk stratification of obesity as a coronary risk factor. Author(s): Kannel WB, Wilson PW, Nam BH, D'Agostino RB. Source: The American Journal of Cardiology. 2002 October 1; 90(7): 697-701. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12356380&dopt=Abstract

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Role of ghrelin polymorphisms in obesity based on three different studies. Author(s): Ukkola O, Ravussin E, Jacobson P, Perusse L, Rankinen T, Tschop M, Heiman ML, Leon AS, Rao DC, Skinner JS, Wilmore JH, Sjostrom L, Bouchard C. Source: Obesity Research. 2002 August; 10(8): 782-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181387&dopt=Abstract

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Role of obesity and leptin in the pubertal process and pubertal growth--a review. Author(s): Shalitin S, Phillip M. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 869-74. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861226&dopt=Abstract

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Roux-en-Y gastric bypass for morbid obesity. Author(s): Barrow CJ. Source: Aorn Journal. 2002 October; 76(4): 590, 593-604; Quiz 606-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12382465&dopt=Abstract

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School-based obesity prevention: a blueprint for taming the epidemic. Author(s): Baranowski T, Cullen KW, Nicklas T, Thompson D, Baranowski J. Source: American Journal of Health Behavior. 2002 November-December; 26(6): 486-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12437023&dopt=Abstract

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Screening for childhood obesity: international vs population-specific definitions. Which is more appropriate? Author(s): Fu WP, Lee HC, Ng CJ, Tay YK, Kau CY, Seow CJ, Siak JK, Hong CY. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 September; 27(9): 1121-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917720&dopt=Abstract

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Self-reported concern about food security associated with obesity--Washington, 19951999. Author(s): Centers for Disease Control and Prevention (CDC). Source: Mmwr. Morbidity and Mortality Weekly Report. 2003 September 5; 52(35): 8402. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966359&dopt=Abstract

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Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race. The CARDIA male hormone study. Author(s): Gapstur SM, Gann PH, Kopp P, Colangelo L, Longcope C, Liu K. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2002 October; 11(10 Pt 1): 1041-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12376505&dopt=Abstract

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Severe metabolic bone disease as a long-term complication of obesity surgery. Author(s): Goldner WS, O'Dorisio TM, Dillon JS, Mason EE. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 October; 12(5): 685-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12448393&dopt=Abstract

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Sex steroid hormones, upper body obesity, and insulin resistance. Author(s): Abate N, Haffner SM, Garg A, Peshock RM, Grundy SM. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 October; 87(10): 4522-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12364429&dopt=Abstract

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Should we recommend low-fat diets for obesity? Author(s): Pirozzo S, Summerbell C, Cameron C, Glasziou P. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 83-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760443&dopt=Abstract

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Sibutramine in the management of obesity. Author(s): Brunton S. Source: The Journal of Family Practice. 2003 August; 52(8): 635. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12899819&dopt=Abstract

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Simple index for screening overweight and obesity. Author(s): Pruenglampoo S, Pruenglampoo B, Kingkeow C, Mongkalabrug A. Source: Public Health Nutrition. 2003 April; 6(2): 225-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12675966&dopt=Abstract

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Sizes and obesity pattern of South Iranian adolescent females. Author(s): Ayatollahi SM. Source: Annals of Human Biology. 2003 March-April; 30(2): 191-202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637194&dopt=Abstract

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Skeletal muscle triglyceride: marker or mediator of obesity-induced insulin resistance in type 2 diabetes mellitus? Author(s): Goodpaster BH, Kelley DE. Source: Curr Diab Rep. 2002 June; 2(3): 216-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643176&dopt=Abstract

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Sleep apnea associated with antipsychotic-induced obesity. Author(s): Wirshing DA, Pierre JM, Wirshing WC. Source: The Journal of Clinical Psychiatry. 2002 April; 63(4): 369-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12000215&dopt=Abstract

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Social factors and obesity: an investigation of the role of health behaviours. Author(s): Ball K, Mishra GD, Crawford D. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 March; 27(3): 394-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629569&dopt=Abstract

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Societal change to prevent obesity. Author(s): Weisberg SP. Source: Jama : the Journal of the American Medical Association. 2002 November 6; 288(17): 2176. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413382&dopt=Abstract

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Socioeconomic aspects of spousal concordance for hypertension, obesity, and smoking in a community of Rio de Janeiro, Brazil. Author(s): Bloch KV, Klein CH, de Souza e Silva NA, Nogueira Ada R, Salis LH. Source: Arquivos Brasileiros De Cardiologia. 2003 February; 80(2): 179-86, 171-8. Epub 2003 February 25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640511&dopt=Abstract

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Some thoughts about childhood obesity. Author(s): Chambers S. Source: J Ark Med Soc. 2002 November; 99(5): 141. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12434622&dopt=Abstract

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Substrate oxidation, obesity and exercise training. Author(s): Blaak EE, Saris WH. Source: Best Practice & Research. Clinical Endocrinology & Metabolism. 2002 December; 16(4): 667-78. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12468414&dopt=Abstract

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Success of laparoscopic ovarian wedge resection is related to obesity, lipid profile, and insulin levels. Author(s): Duleba AJ, Banaszewska B, Spaczynski RZ, Pawelczyk L. Source: Fertility and Sterility. 2003 April; 79(4): 1008-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749446&dopt=Abstract

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Successes and challenges in treating obesity. Author(s): Elderkin AL, Bourbon A, Curtis LG, Dillard WC, Buskey RH, Nelson RL, Ulshafer C. Source: Jaapa. 2002 November; 15(11): 11-2, 15-6, 19 Passim. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12474429&dopt=Abstract

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Succinylcholine and morbid obesity. Author(s): Brodsky JB, Foster PE. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 138-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630630&dopt=Abstract

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Summary of the 2000 Surgeon General's listening session: toward a national action plan on overweight and obesity. Author(s): Jackson Y, Dietz WH, Sanders C, Kolbe LJ, Whyte JJ, Wechsler H, Schneider BS, McNally LA, Charles-Azure J, Vogel-Taylor M, Starke-Reed P, Hubbard VS, Johnson-Taylor WL, Troiano RP, Donato K, Yanovski S, Kuczmarski RJ, Haverkos L, McMurry K, Wykoff RF, Woo V, Noonan AS, Rowe J, McCarty K, Spain CB. Source: Obesity Research. 2002 December; 10(12): 1299-305. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490675&dopt=Abstract

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Suppression of fibrinolytic activity and obesity in young patients with myocardial infarction. Author(s): Saigo M, Abe S, Ogawa M, Maruyama I, Tei C. Source: Thrombosis and Haemostasis. 2002 November; 88(5): 878-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12428113&dopt=Abstract

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Surgery for morbid obesity. Author(s): Colquitt J, Clegg A, Sidhu M, Royle P. Source: Cochrane Database Syst Rev. 2003; (2): Cd003641. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804481&dopt=Abstract

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Surgery for obesity: demand soars amid scientific, ethical questions. Author(s): Mitka M. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1761-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684340&dopt=Abstract

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Surgical management of obesity. Author(s): Nehoda H. Source: Wiener Klinische Wochenschrift. 2002 September 30; 114(17-18): 744-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12416277&dopt=Abstract

154 Obesity

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Surgical treatment of severe obesity with a low-pressure adjustable gastric band: experimental data and clinical results in 625 patients. Author(s): Ceelen W, Walder J, Cardon A, Van Renterghem K, Hesse U, El Malt M, Pattyn P. Source: Annals of Surgery. 2003 January; 237(1): 10-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12496524&dopt=Abstract

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Survey of physician attitudes and practices related to pediatric obesity. Author(s): Jelalian E, Boergers J, Alday CS, Frank R. Source: Clinical Pediatrics. 2003 April; 42(3): 235-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739922&dopt=Abstract

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Sustaining dietary changes for preventing obesity and diabetes: lessons learned from the successes of other epidemic control programs. Author(s): Swinburn B. Source: Asia Pacific Journal of Clinical Nutrition. 2002; 11 Suppl 3: S598-606. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492653&dopt=Abstract

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Sympathetic neural activation in visceral obesity. Author(s): Alvarez GE, Beske SD, Ballard TP, Davy KP. Source: Circulation. 2002 November 12; 106(20): 2533-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12427647&dopt=Abstract

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Symptom status and functional status outcomes: humanistic outcomes in obesity disease management. Author(s): Ropka ME. Source: Obesity Research. 2002 November; 10 Suppl 1: 42S-49S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446858&dopt=Abstract

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Television viewing and risk of obesity. Author(s): Redelmeier DA, Stanbrook MB. Source: Jama : the Journal of the American Medical Association. 2003 July 16; 290(3): 332; Author Reply 332. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865370&dopt=Abstract

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Television watching and soft drink consumption: associations with obesity in 11- to 13-year-old schoolchildren. Author(s): Giammattei J, Blix G, Marshak HH, Wollitzer AO, Pettitt DJ. Source: Archives of Pediatrics & Adolescent Medicine. 2003 September; 157(9): 882-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963593&dopt=Abstract

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Testosterone supplementation in men with type 2 diabetes, visceral obesity and partial androgen deficiency. Author(s): Boyanov MA, Boneva Z, Christov VG. Source: The Aging Male : the Official Journal of the International Society for the Study of the Aging Male. 2003 March; 6(1): 1-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12809074&dopt=Abstract

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The "big picture" in obesity research. Author(s): Muhlhausler B. Source: Science. 2003 May 16; 300(5622): 1091-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750500&dopt=Abstract

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The association of dehydroepiandrosterone, obesity, waist-hip ratio and insulin resistance with fatty liver in postmenopausal women--a hyperinsulinemic euglycemic insulin clamp study. Author(s): Saruc M, Yuceyar H, Ayhan S, Turkel N, Tuzcuoglu I, Can M. Source: Hepatogastroenterology. 2003 May-June; 50(51): 771-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828082&dopt=Abstract

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The effect of the -308A allele of the TNF-alpha gene on insulin action is dependent on obesity. Author(s): Pihlajamaki J, Ylinen M, Karhapaa P, Vauhkonen I, Laakso M. Source: Obesity Research. 2003 July; 11(7): 912-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855762&dopt=Abstract

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The effects of weight loss on renal function in patients with severe obesity. Author(s): Chagnac A, Weinstein T, Herman M, Hirsh J, Gafter U, Ori Y. Source: Journal of the American Society of Nephrology : Jasn. 2003 June; 14(6): 1480-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761248&dopt=Abstract

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The epidemic of childhood overweight and obesity. Extent of the problem and prospects for change. Author(s): Molloy M, Kovach K, Bors P, Caldwell D, Lebeuf JS. Source: N C Med J. 2002 November-December; 63(6): 291-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970976&dopt=Abstract

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The etiology of obesity. Author(s): Gardner D. Source: Mo Med. 2003 May-June; 100(3): 242-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847865&dopt=Abstract

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The frequency of respiratory failure in patients with morbid obesity undergoing gastric bypass. Author(s): Blouw EL, Rudolph AD, Narr BJ, Sarr MG. Source: Aana Journal. 2003 February; 71(1): 45-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776650&dopt=Abstract

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The influence of obesity on the frequency and distribution of medication. Author(s): Dzien A, Pfeiffer KP, Dzien-Bischinger C, Hoppichler F, Lechleitner M. Source: Acta Medica Austriaca. 2003; 30(2): 51-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752089&dopt=Abstract

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The management of adult obesity. Author(s): Birmingham CL, Jones P, Hoffer LJ. Source: Eat Weight Disord. 2003 June; 8(2): 157-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12880194&dopt=Abstract

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The obesity charge. Author(s): Epperson S. Source: Time. 2003 September 8; 162(10): 100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14509905&dopt=Abstract

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The obesity epidemic: can we turn the tide? Author(s): Campbell I. Source: Heart (British Cardiac Society). 2003 May; 89 Suppl 2: Ii22-4; Discussion Ii35-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695431&dopt=Abstract

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The obesity epidemic--how states can trim the "fat". Author(s): Fierro MP. Source: N C Med J. 2002 November-December; 63(6): 304. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970979&dopt=Abstract

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The physiology of obesity. Author(s): Montague MC. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 56-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856442&dopt=Abstract

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The prevalence of obesity and undernutrition in Scottish children: growth monitoring within the Child Health Surveillance Programme. Author(s): Armstrong J, Reilly JJ. Source: Scott Med J. 2003 May; 48(2): 32-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774591&dopt=Abstract

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The public health burden of obesity in Missouri. Author(s): Kabeer NH, Simoes EJ. Source: Mo Med. 2003 May-June; 100(3): 236-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847864&dopt=Abstract

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The relationship between obesity and breast cancer. Author(s): Adderley-Kelly B, Williams-Stephens E. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 61-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856443&dopt=Abstract

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The relationship of obesity to the metabolic syndrome. Author(s): Lebovitz HE. Source: Int J Clin Pract Suppl. 2003 March; (134): 18-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793594&dopt=Abstract

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The role of the sympathetic nervous system in linking obesity with hypertension in white versus black Americans. Author(s): Eslami P, Tuck M. Source: Current Hypertension Reports. 2003 June; 5(3): 269-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724061&dopt=Abstract

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The significance of elevated levels of parathyroid hormone in patients with morbid obesity before and after bariatric surgery. Author(s): Hamoui N, Kim K, Anthone G, Crookes PF. Source: Archives of Surgery (Chicago, Ill. : 1960). 2003 August; 138(8): 891-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912749&dopt=Abstract

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The skinny on obesity and cancer. Obesity increases the risk of death from cancer, but being overweight isn't inescapable. Author(s): Blackburn GL. Source: Health News. 2003 June; 9(6): 3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793396&dopt=Abstract

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The TNF-alpha gene NcoI polymorphism at position -308 of the promoter influences insulin resistance, and increases serum triglycerides after postprandial lipaemia in familiar obesity. Author(s): Wybranska I, Malczewska-Malec M, Niedbal S, Naskalski JW, DembinskaKiec A. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2003 April; 41(4): 501-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747594&dopt=Abstract

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The treatment of obesity. Author(s): Mina WC, Burns RW, Terry BE. Source: Mo Med. 2003 May-June; 100(3): 248-55. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847866&dopt=Abstract

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Therapeutic role of peroxisome proliferator-activated receptors in obesity, diabetes and inflammation. Author(s): Ram VJ. Source: Prog Drug Res. 2003; 60: 93-132. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12790340&dopt=Abstract

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Treatment of obesity. Author(s): Sugerman HJ. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 476-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763401&dopt=Abstract

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Treatment of obesity: should we target the individual or society? Author(s): Tataranni PA. Source: Current Pharmaceutical Design. 2003; 9(15): 1151-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769743&dopt=Abstract

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Trends and predictors of overweight and obesity in East German children. Author(s): Frye C, Heinrich J. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 963-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861238&dopt=Abstract

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Tribunal clears obesity researcher of fraud. Author(s): Butler D. Source: Nature. 2003 July 3; 424(6944): 6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840722&dopt=Abstract

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Uncoupling protein genes and racial differences in obesity. Author(s): Polednak AP. Source: The American Journal of Clinical Nutrition. 2003 June; 77(6): 1527-8; Author Reply 1528. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791636&dopt=Abstract

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Uncoupling proteins, leptin, and obesity: an updated review. Author(s): Giacobino JP. Source: Annals of the New York Academy of Sciences. 2002 June; 967: 398-402. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079867&dopt=Abstract

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Uncoupling proteins: a molecular basis for racial differences in energy expenditure (and obesity?). Author(s): Schonfeld-Warden NA, Warden CH. Source: The American Journal of Clinical Nutrition. 2002 April; 75(4): 607-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11916746&dopt=Abstract

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Underdiagnosis of obesity at a community health center. Author(s): Lemay CA, Cashman S, Savageau J, Fletcher K, Kinney R, Long-Middleton E. Source: The Journal of the American Board of Family Practice / American Board of Family Practice. 2003 January-February; 16(1): 14-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12583646&dopt=Abstract

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Understanding obesity and program participation in the context of poverty and food insecurity. Author(s): Frongillo EA. Source: The Journal of Nutrition. 2003 July; 133(7): 2117-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840164&dopt=Abstract

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Understanding the complex journey to obesity in early adulthood. Author(s): Whitaker RC. Source: Annals of Internal Medicine. 2002 June 18; 136(12): 923-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12069566&dopt=Abstract

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Understanding the physiology of obesity: review of recent developments in obesity research. Author(s): Woods SC, Seeley RJ. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 December; 26 Suppl 4: S8-S10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12457292&dopt=Abstract

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Undertreatment of obesity. Author(s): Grizzard T. Source: Jama : the Journal of the American Medical Association. 2002 November 6; 288(17): 2177. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413383&dopt=Abstract

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Unemployment and obesity among young adults in a northern Finland 1966 birth cohort. Author(s): Laitinen J, Power C, Ek E, Sovio U, Jarvelin MR. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 October; 26(10): 1329-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12355341&dopt=Abstract

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Untreated hypertension among Australian adults: the 1999-2000 Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Author(s): Briganti EM, Shaw JE, Chadban SJ, Zimmet PZ, Welborn TA, McNeil JJ, Atkins RC; Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Source: The Medical Journal of Australia. 2003 August 4; 179(3): 135-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885281&dopt=Abstract

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Up to date. Gastroesophageal reflux disease (GERD) influence of obesity. Author(s): Chiocca JC. Source: Acta Gastroenterol Latinoam. 2002; 32(2): 95-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553162&dopt=Abstract

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Upper abdominal obesity, insulin resistance and breast cancer risk. Author(s): Stoll BA. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 June; 26(6): 747-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12037643&dopt=Abstract

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Urologic and plastic surgical collaboration for continent diversion when urine leakage is complicated by pressure ulcers or obesity. Author(s): Sterbis JR, Lewis VL, Bushman W. Source: J Spinal Cord Med. 2003 Summer; 26(2): 124-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828288&dopt=Abstract

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US paediatricians call for checks for childhood obesity. Author(s): Gottlieb S. Source: Bmj (Clinical Research Ed.). 2003 September 6; 327(7414): 518. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12958090&dopt=Abstract

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Use of beta-blockers in obesity hypertension: potential role of weight gain. Author(s): Pischon T, Sharma AM. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 November; 2(4): 275-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119998&dopt=Abstract

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Use of BMI as a measure of overweight and obesity in a field study on 5-7 year old children. Author(s): Mast M, Langnase K, Labitzke K, Bruse U, Preuss U, Muller MJ. Source: European Journal of Nutrition. 2002 April; 41(2): 61-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12083315&dopt=Abstract

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Use of somatostatin receptor ligands in obesity and diabetic complications. Author(s): Boehm BO, Lustig RH. Source: Best Practice & Research. Clinical Gastroenterology. 2002 June; 16(3): 493-509. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079271&dopt=Abstract

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Use of the health and activities limitation index as a measure of quality of life in obesity. Author(s): Livingston EH, Ko CY. Source: Obesity Research. 2002 August; 10(8): 824-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181392&dopt=Abstract

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Usefulness of anthropometrics and dual-energy x-ray absorptiometry for estimating abdominal obesity measured by magnetic resonance imaging in older men and women. Author(s): Stewart KJ, DeRegis JR, Turner KL, Bacher AC, Sung J, Hees PS, Shapiro EP, Tayback M, Ouyang P. Source: Journal of Cardiopulmonary Rehabilitation. 2003 March-April; 23(2): 109-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668933&dopt=Abstract

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Using mouse models to dissect the genetics of obesity. Author(s): Brockmann GA, Bevova MR. Source: Trends in Genetics : Tig. 2002 July; 18(7): 367-76. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12127777&dopt=Abstract

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Varicose veins of the lower limbs and venous capacitance in postmenopausal women: relationship with obesity. Author(s): Iannuzzi A, Panico S, Ciardullo AV, Bellati C, Cioffi V, Iannuzzo G, Celentano E, Berrino F, Rubba P. Source: Journal of Vascular Surgery : Official Publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter. 2002 November; 36(5): 965-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12422106&dopt=Abstract

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Venlafaxine treatment of binge-eating disorder associated with obesity: a series of 35 patients. Author(s): Malhotra S, King KH, Welge JA, Brusman-Lovins L, McElroy SL. Source: The Journal of Clinical Psychiatry. 2002 September; 63(9): 802-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12363121&dopt=Abstract

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Vertical gastric banding for morbid obesity: a long-term follow-up study. Author(s): Waaddegaard P, Clemmesen T, Jess P. Source: The European Journal of Surgery = Acta Chirurgica. 2002; 168(4): 220-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12440759&dopt=Abstract

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Very low energy diets in the treatment of obesity. Author(s): Mustajoki P, Pekkarinen T. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 February; 2(1): 61-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119638&dopt=Abstract

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Virtual gastroduodenoscopy: a new look at the bypassed stomach and duodenum after laparoscopic Roux-en-Y gastric bypass for morbid obesity. Author(s): Silecchia G, Catalano C, Gentileschi P, Elmore U, Restuccia A, Gagner M, Basso N. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 February; 12(1): 39-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11868296&dopt=Abstract

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Visceral fat and psychosocial stress in identical twins discordant for obesity. Author(s): Marniemi J, Kronholm E, Aunola S, Toikka T, Mattlar CE, Koskenvuo M, Ronnemaa T. Source: Journal of Internal Medicine. 2002 January; 251(1): 35-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11851863&dopt=Abstract

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Visceral obesity and hyperinsulinemia modulate the impact of the microsomal triglyceride transfer protein -493G/T polymorphism on plasma lipoprotein levels in men. Author(s): St-Pierre J, Lemieux I, Miller-Felix I, Prud'homme D, Bergeron J, Gaudet D, Nadeau A, Despres JP, Vohl MC. Source: Atherosclerosis. 2002 February; 160(2): 317-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11849654&dopt=Abstract

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Visceral obesity and metabolic syndrome. Author(s): Bosello O, Zamboni M. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2000 May; 1(1): 47-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119645&dopt=Abstract

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Visceral obesity attenuates the effect of the hepatic lipase -514C>T polymorphism on plasma HDL-cholesterol levels in French-Canadian men. Author(s): St-Pierre J, Miller-Felix I, Paradis ME, Bergeron J, Lamarche B, Despres JP, Gaudet D, Vohl MC. Source: Molecular Genetics and Metabolism. 2003 January; 78(1): 31-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559845&dopt=Abstract

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Visceral obesity is characterized by impaired nitric oxide-independent vasodilation. Author(s): Vigili de Kreutzenberg S, Kiwanuka E, Tiengo A, Avogaro A. Source: European Heart Journal. 2003 July; 24(13): 1210-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831815&dopt=Abstract

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Visceral obesity, hepatic lipase activity, and dyslipidemia in type 1 diabetes. Author(s): Sibley SD, Palmer JP, Hirsch IB, Brunzell JD. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 July; 88(7): 3379-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843191&dopt=Abstract

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Vitamin A deficiency in a newborn resulting from maternal hypovitaminosis A after biliopancreatic diversion for the treatment of morbid obesity. Author(s): Huerta S, Rogers LM, Li Z, Heber D, Liu C, Livingston EH. Source: The American Journal of Clinical Nutrition. 2002 August; 76(2): 426-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12145017&dopt=Abstract

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VLDL-triglyceride kinetics during hyperglycemia-hyperinsulinemia: effects of sex and obesity. Author(s): Mittendorfer B, Patterson BW, Klein S, Sidossis LS. Source: American Journal of Physiology. Endocrinology and Metabolism. 2003 April; 284(4): E708-15. Epub 2002 December 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475756&dopt=Abstract

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Waist circumference and obesity-associated risk factors among whites in the third National Health and Nutrition Examination Survey: clinical action thresholds. Author(s): Zhu S, Wang Z, Heshka S, Heo M, Faith MS, Heymsfield SB. Source: The American Journal of Clinical Nutrition. 2002 October; 76(4): 743-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12324286&dopt=Abstract

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Waist circumference, visceral obesity, and cardiovascular risk. Author(s): Poirier P, Despres JP. Source: Journal of Cardiopulmonary Rehabilitation. 2003 May-June; 23(3): 161-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12782898&dopt=Abstract

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Weighing in on obesity: America's growing health epidemic. Author(s): Grantmakers in Health, Washington, D.C., USA. Source: Issue Brief (Grantmakers Health). 2001 October 31; (11): 1-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14535290&dopt=Abstract

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Weight control and the management of obesity after menopause: the role of physical activity. Author(s): Dubnov G, Brzezinski A, Berry EM. Source: Maturitas. 2003 February 25; 44(2): 89-101. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12590004&dopt=Abstract

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Weight loss improves neurovascular and muscle metaboreflex control in obesity. Author(s): Trombetta IC, Batalha LT, Rondon MU, Laterza MC, Kuniyoshi FH, Gowdak MM, Barretto AC, Halpern A, Villares SM, Negrao CE. Source: American Journal of Physiology. Heart and Circulatory Physiology. 2003 September; 285(3): H974-82. Epub 2003 April 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714324&dopt=Abstract

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Weight loss increases circulating levels of ghrelin in human obesity. Author(s): Hansen TK, Dall R, Hosoda H, Kojima M, Kangawa K, Christiansen JS, Jorgensen JO. Source: Clinical Endocrinology. 2002 February; 56(2): 203-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11874411&dopt=Abstract

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Weight loss-induced plasticity of glucose transport and phosphorylation in the insulin resistance of obesity and type 2 diabetes. Author(s): Williams KV, Bertoldo A, Kinahan P, Cobelli C, Kelley DE. Source: Diabetes. 2003 July; 52(7): 1619-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829624&dopt=Abstract

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Weight maintenance and relapse in obesity: a qualitative study. Author(s): Byrne S, Cooper Z, Fairburn C. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 955-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861237&dopt=Abstract

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Weight reduction and long-term maintenance after 18 months treatment with orlistat for obesity. Author(s): Krempf M, Louvet JP, Allanic H, Miloradovich T, Joubert JM, Attali JR. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 May; 27(5): 591-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12704403&dopt=Abstract

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What are the most effective interventions to reduce childhood obesity? Author(s): Hill JC, Smith PC, Meadows SE. Source: The Journal of Family Practice. 2002 October; 51(10): 891. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401163&dopt=Abstract

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What can we do about the "epidemic" of obesity. Author(s): Hall JE, Jones DW. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2002 July; 15(7 Pt 1): 657-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12118917&dopt=Abstract

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What diets should we be recommending for obesity? Author(s): Hill JO, Astrup A. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 77-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760441&dopt=Abstract

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What do we do about the problem of overweight and obesity in the Americas? Author(s): Teelucksingh S. Source: Revista Panamericana De Salud Publica = Pan American Journal of Public Health. 2003 May; 13(5): 275-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846232&dopt=Abstract

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What will it take to stop obesity? Author(s): Potteiger CE, Still CD. Source: J Am Osteopath Assoc. 2003 April; 103(4): 168. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733545&dopt=Abstract

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Which aspects of socioeconomic status are related to obesity among men and women? Author(s): Ball K, Mishra G, Crawford D. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 April; 26(4): 559-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12075584&dopt=Abstract

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Which method should be used to determine the obesity, in patients with coronary artery disease? (body mass index, waist circumference or waist-hip ratio). Author(s): Sonmez K, Akcakoyun M, Akcay A, Demir D, Duran NE, Gencbay M, Degertekin M, Turan F. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 March; 27(3): 341-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629561&dopt=Abstract

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Why do we need an obesity review journal year 2000? Author(s): Astrup A. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2000 May; 1(1): 1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119639&dopt=Abstract

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Why should gastroenterologists be interested in nutrition and obesity? Author(s): Klein S. Source: Gastroenterology. 2002 October; 123(4): 967. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12360454&dopt=Abstract

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Work-related physical activity is not associated with body mass index and obesity. Author(s): Gutierrez-Fisac JL, Guallar-Castillon P, Diez-Ganan L, Lopez Garcia E, Banegas Banegas JR, Rodriguez Artalejo F. Source: Obesity Research. 2002 April; 10(4): 270-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11943836&dopt=Abstract

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World pandemic of obesity--any hope of its being controlled? Author(s): Walker AR. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 2003 August; 93(8): 598-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14531118&dopt=Abstract

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Years of life lost due to obesity. Author(s): Fontaine KR, Redden DT, Wang C, Westfall AO, Allison DB. Source: Jama : the Journal of the American Medical Association. 2003 January 8; 289(2): 187-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12517229&dopt=Abstract

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CHAPTER 2. NUTRITION AND OBESITY Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and obesity.

Finding Nutrition Studies on Obesity The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail: [email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “obesity” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.

7

Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.

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The following is a typical result when searching for recently indexed consumer information on obesity: •

Fatty acid composition of skeletal muscle membrane phospholipids, insulin resistance and obesity. Author(s): The Center for Genetics, Nutrition and Health, Washington, DC. Source: Simopoulos, A.P. Nutrition-today (USA). (February 1994). volume 29(1) page 1216. fats overweight insulin glucose metabolic disorders muscles membranes phospholipids fatty acids physiological functions genotypes diet polyunsaturated fatty acids lipid content risk disease control physical activity weight 0029-666X Summary: corps gras surpoids insuline glucose trouble du metabolisme muscle membrane phosphatide acide gras fonction physiologique genotype regime alimentaire acide gras polyinsature teneur en lipides risque controle de maladies activite physique poids

Additional consumer oriented references include: •

A 'cure' for obesity? Source: Tufts-University-diet-and-nutrition-letter (USA). (March 1995). volume 13(1) page 1-2. new york overweight pathogenesis genes medical sciences research 0747-4105

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Are there long term protective effects of breast feeding against later obesity? Author(s): Department of Pediatrics, Dr. von Haunersches Kinderspital, LudwigMaximilians-University of Munich, Germany. Source: Koletzko, B von Kries, R Nutr-Health. 2001; 15(3-4): 225-36 0260-1060

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Dehydroepiandrosterone (DHEA): useful or useless as an antiobesity agent? Source: Berdanier, C.D. Nutrition-today (USA). (December 1993). volume 28(6) page 3438. androgens overweight drug therapy appetite drugs metabolism 0029-666X

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Diabetes contributes to cholesterol metabolism regardless of obesity. Author(s): Department of Medicine, Division of Internal Medicine, University of Helsinki, Finland. [email protected] Source: Simonen, P P Gylling, H K Miettinen, T A Diabetes-Care. 2002 September; 25(9): 1511-5 0149-5992

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Dieting-induced obesity: a hidden hazard of weight cycling. Source: Environ-Nutr. New York : Environmental Nutrition, Inc. February 1987. volume 10 (2) page 1, 6. 0195-4024

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Do calories from alcohol contribute to obesity. Source: Kurtzweil, P. BNF-nutr-bull. London : The Foundation,. January 1996. volume 21 (77) page 45-53. 0141-9684

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EN speaks with obesity expert. Source: Milner, I. Environ-Nutr. New York, N.Y. : Environmental Nutrition, Inc. January 1990. volume 13 (1) page 1, 3. 0893-4452

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Factors associated with overweight and obesity among Kuwaiti college women. Author(s): Department of Community Medicine & Behavioural Sciences, Faculty of Medicine, University of Kuwait, Safat. Source: al Isa, A N Nutr-Health. 1998; 12(4): 227-33 0260-1060

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High red-meat intake, obesity linked to cancer. Source: Anonymous Health-News. 2002 February; 8(2): 9 1081-5880

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Leptin--the 'new' player in energy balance and obesity. Source: Porter, D.V. BNF-nutr-bull. London : The British Nutrition Foundation. Spring 1997. volume 22 (80) page 7-14. 0141-9684

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Natural hazards. Tonic or toxic? Americans are gobbling up nature's remedies for everything from obesity to depression. Source: Spake, A US-News-World-Repage 2001 February 12; 130(6): 42-9 0041-5537

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Obesity among Kuwaiti pre-school children aged 0-5 years: prevalence and comparison with the NCHS/CDC reference population. Author(s): Department of Community Medicine & Behavioural Sciences, Faculty of Medicine, University of Kuwait, Safat. Source: al Isa, A N Moussa, M A Nutr-Health. 1998; 12(4): 235-46 0260-1060

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Obesity, weight-reducing programmes and constipation. Source: Anderson, E. Davies, J. Nutr-food-sci. Bradford, West Yorkshire, England : MCB University Press. Nov/December 1999. (6) page 303-306. 0034-6659

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Overweight, obesity threaten U.S. health gains. Source: FDA-consum. Rockville, Md. : Food and Drug Administration, Department of Health & Human Services. Mar/April 2002. volume 36 (2) page 8. 0362-1332

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Professional singers with obesity or eating-related problems. Author(s): Frances Stern Nutrition Center. Source: Slover, A.N. Dwyer, J.T. Nutrition-today (USA). (June 1995). volume 30(3) page 123-127. overeating digestive disorders overweight occupational hazards music 0029666X

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Sugar gets a bad rap: not the villain in obesity or diabetes. Source: Ward, E.M. Environmental-nutrition (USA). (August 1993). volume 16(8) page 1, 6. sugar human nutrition 0893-4452

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Summary of the National Obesity and Weight Control Symposium. Source: VanItallie, T.B. Simopoulos, A.P. Nutrition-today (USA). (August 1993). volume 28(4) page 33-35. fats overweight weight diet weight gain aetiology 0029-666X

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Teen obesity: a heavy burden even in adulthood. Source: Tufts-University-diet-and-nutrition-letter (USA). (January 1993). volume 10(11) page 1-2. overweight youth diet physical activity disease control 0747-4105

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The effect of education and obesity on attitudes towards fads related to weight reduction among Arab women in Qatar. Source: Musaiger, A.O. Shahbeek, N.E. Nutr-food-sci. Bradford, West Yorkshire, England : MCB University Press. July/August 2001. volume 31 (4/5) page 201-204. 00346659

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The emerging epidemic of obesity in developing societies. Source: Schenker, S. BNF-nutr-bull. London : The British Nutrition Foundation. Spring 1999. volume 24 (86) page 8-13. 0141-9684

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The fruit bowl approach to the treatment of obesity. Source: Ashwell, M. BNF-nutr-bull. London : The Foundation,. Sept 1994. volume 19 (72) page 170-177. 0141-9684

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The news about overweight teens. Source: Weight-Watchers. New York, N.Y. : W/W Twentyfirst Corporation. March 1989. volume 22 (2) page 14, 16. 0043-2180

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The nutrient balance approach to obesity. Source: Bray, G.A. Nutrition-today (USA). (June 1993). volume 28(3) page 13-18. overweight nutrition physiology models nervous system nutrients hormones 0029-666X

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The other side of obesity: a bibliography of recent literature. Author(s): Illinois State University, Normal, IL. Source: Duran, N. Nutrition-today (USA). (April 1996). volume 31(2) page 80-81. overweight diet health hazards risk sociology 0029-666X

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Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome. Author(s): Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden. [email protected] Source: Riserus, U Arner, P BrisMarch, K Vessby, B Diabetes-Care. 2002 September; 25(9): 1516-21 0149-5992

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Understanding and treating human obesity: what's new. Source: Hill, J.O. Food-and-nutrition-news (USA). (Nov-December 1993). volume 65(5) page 29-31. overweight research energy balance men women 0015-6310

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Weight and overweight. Source: Youngs, Andrew. Nutr-Food-Sci. London, Eng. : Forbes Publications. May/June 1984. volume (88) page 16. 0034-6659

The following information is typical of that found when using the “Full IBIDS Database” to search for “obesity” (or a synonym): •

Acarbose improves indirectly both insulin resistance and secretion in obese type 2 diabetic patients. Author(s): Division of Therapeutic Education for Chronic Diseases, University Hospital Geneva, Switzerland. Source: Delgado, H Lehmann, T Bobbioni Harsch, E Ybarra, J Golay, A Diabetes-Metab. 2002 June; 28(3): 195-200 1262-3636

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Acute effects of valsartan on insulin sensitivity in obese, non-hypertensive subjects with and without type 2 diabetes. Author(s): Diabetes Research Unit, Llandough Hospital, Penlan Road, Penarth, S. Glam. CF64 2XX, Wales, UK. [email protected] Source: Luzio, S D Dunseath, G Owens, D R Horm-Metab-Res. 2002 May; 34(5): 271-4 0018-5043

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Characterisation of the mouse diabetes susceptibilty locus Nidd/SJL: islet cell destruction, interaction with the obesity QTL Nob1, and effect of dietary fat. Author(s): Institute of Pharmacology and Toxicology, Medical Faculty, Technical University of Aachen, Aachen, Germany. Source: Plum, L Giesen, K Kluge, R Junger, E Linnartz, K Schurmann, A Becker, W Joost, H G Diabetologia. 2002 Jun; 45(6): 823-30 0012-186X

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Defective amplification of the late phase insulin response to glucose by GIP in obese Type II diabetic patients. Author(s): Department of Internal Medicine F, Gentofte Hospital, University of Copenhagen, Niels Andersens Vej 65, 2900 Hellerup, Denmark. [email protected] Source: Vilsboll, T Krarup, T Madsbad, S Holst, J J Diabetologia. 2002 August; 45(8): 1111-9 0012-186X

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Diabetes mellitus and obesity. Author(s): Department of Family Practice, Mount Sinai School of Medicine, Jamaica Hospital Medical Center, 8900 Van Wyck Expressway, Jamaica, NY 11418, USA. [email protected] Source: Roth, A Prim-Care. 2002 June; 29(2): 279-95 0095-4543

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Differential effect of polyherbal, antiobesity preparation, OB-200G in male and female mice and monosodium glutamate-treated rats. Author(s): Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, 160 014, India. Source: Kaur, G Kulkarni, S K Indian-J-Exp-Biol. 2001 June; 39(6): 551-7 0019-5189

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Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. Author(s): Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan Medical School, 1150 West Medical Center Dr., Ann Arbor, MI 48109, USA. Source: Douyon, L Schteingart, D E Endocrinol-Metab-Clin-North-Am. 2002 March; 31(1): 173-89 0889-8529

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Effect of weight loss on QT dispersion in obesity. Author(s): Thoracic and Cardiovascular Institute and Sparrow Hospital Weight Management Center, Michigan State University, USA. [email protected] Source: Gupta, A K Xie, B Thakur, R K Maheshwari, A Lokhandwala, Y Carella, M J Indian-Heart-J. 2002 Jul-August; 54(4): 399-403 0019-4832

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Effects of the beta3 adrenergic receptor agonist on developmental obesity in oophorectomized rats. Author(s): Department of Obstetrics and Gynecology, Niigata University, Faculty of Medicine, Niigata, Japan. [email protected] Source: Tomita, M Kurabayashi, T Matsushita, H Honda, A Tanaka, K Horm-Metab-Res. 2002 July; 34(7): 389-93 0018-5043

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Evaluation and treatment of obesity. Author(s): Department of Internal Medicine, Division of Endocrinology, American University of Beirut Medical Center, Lebanon. [email protected] Source: Azar, S T Zantout, M S J-Med-Liban. 2000 Sep-October; 48(5): 310-4 0023-9852

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Free fatty acids-the link between obesity and insulin resistance. Author(s): Division of Endocrinology/Diabetes/Metabolism and the General Clinical Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA. Source: Boden, G Endocr-Pract. 2001 Jan-February; 7(1): 44-51 1530-891X

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Insulin signal transduction and glucose transport in human adipocytes: effects of obesity and low calorie diet. Author(s): Section of Integrative Physiology, Karolinska Institutet, Stockholm, Sweden. Source: Bjornholm, M Al Khalili, L Dicker, A Naslund, E Rossner, S Zierath, J R Arner, P Diabetologia. 2002 August; 45(8): 1128-35 0012-186X

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Is obesity associated with poor sleep quality in adolescents? Author(s): School of Public Health, University of Texas Health Science Center at Houston, Houston, Texas 77225, USA. Source: Gupta, N K Mueller, W H Chan, W Meininger, J C Am-J-Human-Biol. 2002 NovDecember; 14(6): 762-8 1042-0533

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Levels of hypothalamic neurotransmitters in lean and obese Zucker rats. Author(s): Obesity Research Program Department of Medicine, Louisiana State University Health Sciences Center, New Orleans 70112, USA. [email protected] Source: Svec, F Thompson, H Corll, C Porter, J Nutr-Neurosci. 2002 October; 5(5): 321-6 1028-415X

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Lifestyle factors are associated with osteoporosis in lean women but not in normal and overweight women: a population-based cohort study of 1222 women. Author(s): Department of Sports Medicine, Deaconess Institute of Oulu, Isokatu 43, 90100 Oulu, Finland. [email protected] Source: Korpelainen, R Korpelainen, J Heikkinen, J Vaananen, K Keinanen Kiukaanniemi, S Osteoporos-Int. 2003 January; 14(1): 34-43 0937-941X

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Metallothionein gene expression in human adipose tissue from lean and obese subjects. Author(s): School of Bioscience and Food Technology, Handong University, Pohang, Kyungbuk, Korea. Source: Do, M S Nam, S Y Hong, S E Kim, K W Duncan, J S Beattie, J H Trayhurn, P Horm-Metab-Res. 2002 June; 34(6): 348-51 0018-5043

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Neonatal nutrition: metabolic programming of pancreatic islets and obesity. Author(s): Department of Biochemistry, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, NY 14214, USA. Source: Srinivasan, M Laychock, S G Hill, D J Patel, M S Exp-Biol-Med-(Maywood). 2003 January; 228(1): 15-23 1535-3702

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Nutritional regulation of hypothalamic leptin receptor gene expression is defective in diet-induced obesity. Author(s): Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, PA 15261, USA. [email protected] Source: Sahu, A Nguyen, L O'Doherty, R M J-Neuroendocrinol. 2002 November; 14(11): 887-93 0953-8194

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Obese, older adults with knee osteoarthritis: weight loss, exercise, and quality of life. Author(s): Department of Health and Exercise Science, Wake Forest University, Winston-Salem, North Carolina 27109, USA. [email protected] Source: Rejeski, W J Focht, B C Messier, S P Morgan, T Pahor, M Penninx, B HealthPsychol. 2002 September; 21(5): 419-26 0278-6133

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Obesity and central adiposity in Japanese immigrants: role of the Western dietary pattern. Author(s): Preventive Medicine Department, the Federal University of Sao Paulo, SP, Brazil. Source: Ferreira, S R Lerario, D D Gimeno, S G Sanudo, A Franco, L J J-Epidemiol. 2002 November; 12(6): 431-8 0917-5040

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Obesity and medicinal plants. Author(s): Department of Pharmaceutical and Toxicological Chemistry, Study University of Naples Federico II, via D. Montesano 49, 80131, Naples, Italy. Source: Moro, C O Basile, G Fitoterapia. 2000 August; 71 Suppl 1: S73-82 0367-326X

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Obesity clinical trials in youth: concepts and challenges. Author(s): Department of Pediatrics, Medical College of Georgia, Augusta, Georgia 30912-3770, USA. [email protected] Source: Moore, D B Ethn-Dis. 2002 Fall; 12(4): S3-40-3 1049-510X

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Obesity correlates with increased blood pressures in urban Native American youth. Author(s): Department of Food Science and Nutrition, University of Minnesota, St Paul, Minnesota 55108, USA. [email protected] Source: Smith, C Rinderknecht, K Am-J-Human-Biol. 2003 Jan-February; 15(1): 78-90 1042-0533

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Obesity exacerbates chemically induced neurodegeneration. Author(s): HELD/TMBB, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Mailstop L-3014, 1095 Willowdale Road, Morgantown, WV 26505, USA. Source: Sriram, K Benkovic, S A Miller, D B O'Callaghan, J P Neuroscience. 2002; 115(4): 1335-46 0306-4522

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Obesity in Malaysia. Author(s): Department of Nutrition and Dietetics, University Kebangsaan Malaysia, Kuala, Lumpur. [email protected] Source: Ismail, M N Chee, S S Nawawi, H Yusoff, K Lim, T O James, W P ObesRevolume 2002 August; 3(3): 203-8 1467-7881

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Observation on the therapeutic effects of acupuncture for 60 cases of simple obesity. Author(s): Tianjin Municipal Hospital of TCM, Tianjin 300140. Source: Wang, H J-Tradit-Chin-Med. 2002 September; 22(3): 187-9 0254-6272

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Overweight is an independent risk factor for cardiovascular disease in Chinese populations. Author(s): Cardiovascular Institute, Fu Wai Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing. [email protected] Source: Zhou, B Wu, Y Yang, J Li, Y Zhang, H Zhao, L Obes-Revolume 2002 August; 3(3): 147-56 1467-7881

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Part III. Obesity. Author(s): Department of Surgery, University of Chicago Pritzker School of Medicine, Illinois, USA. Source: Boogerd, A Alverdy, J KuMarch, S Olson, D L Schwenk, W F Dis-Mon. 2002 November; 48(11): 725-42 0011-5029

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Pattern of dietary behaviour and obesity in Ahwaz, Islamic Republic of Iran. Author(s): Department of Community Medicine, School of Medicine, Ahwaz University of Medical Sciences, Ahwaz, Islamic Republic of Iran. Source: Soori, H East-Mediterr-Health-J. 2001 Jan-March; 7(1-2): 163-70 1020-3397

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Permanent prostate brachytherapy-induced morbidity in patients with grade II and III obesity. Author(s): Schiffler Cancer Center, Wheeling Hospital, Wheeling, West Virginia 260036300, USA. Source: Merrick, G S Butler, W M Wallner, K Galbreath, R W Anderson, R L Kurko, B S Lief, J H Urology. 2002 July; 60(1): 104-8 1527-9995

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Project Grow-2-Gether: a study of the genetic and environmental influences on child eating and obesity. Author(s): Weight and Eating Disorders Program, University of Pennsylvania School of Medicine, Philadelphia 19104, USA. [email protected] Source: Faith, M S Keller, K L Matz, P Johnson, S L Lewis, R Jorge, M A Ridley, C Han, H Must, S Heo, M Pietrobelli, A Heymsfield, S B Allison, D B Twin-Res. 2002 October; 5(5): 472-5 1369-0523

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Recent developments in the treatment of obesity-related hypertension. Author(s): Franz Volhard Clinic - HELIOS-Klinikum Berlin Buch, Charite, Medical Faculty of the Humboldt University Berlin, Max Delbruck Center for Molecular Medicine, Germany. Source: Pischon, T Sharma, A M Curr-Opin-Nephrol-Hypertens. 2002 September; 11(5): 497-502 1062-4821

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Resumption of fertility with diet in overweight women. Author(s): First Department of Obstetrics and Gynaecology, University of Milan, Via della Commenda 12, 20122 Milan, Italy. piergiorgio.crosignani.it Source: Crosignani, P G Vegetti, W Colombo, M Ragni, G Reprod-Biomed-Online. 2002 Jul-August; 5(1): 60-4 1472-6483

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School-based obesity prevention: a blueprint for taming the epidemic. Author(s): Children's Nutrition Research Center, Baylor College of Medicine, Houston, TX 77030-2600, USA. [email protected] Source: Baranowski, T Cullen, K W Nicklas, T Thompson, D Baranowski, J Am-J-HealthBehavolume 2002 Nov-December; 26(6): 486-93 1087-3244

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Synergic effect of overweight and cold on uncoupling proteins expression, a role of alpha(2)/beta(3) adrenergic receptor balance? Author(s): Departament de Biologia Fonamental i Ciencies de la Salut, Laboratori de Biologia Molecular, Nutricio i Biotecnologia, Universitat de les Illes Balears, Palma de Mallorca, 07071, Spain. Source: Rodriguez, A M Roca, P Palou, A Pflugers-Arch. 2002 July; 444(4): 484-90 00316768

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The effect of adrenalectomy on leptin levels and some metabolic parameters in rats with diet-induced obesity. Author(s): Department of Biochemistry, Faculty of Medicine, University of Ataturk, Erzurum, Turkey. Source: Yilmaz, A Suleyman, H Umudum, Z Sahin, Y N Biol-Pharm-Bull. 2002 May; 25(5): 580-3 0918-6158

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The effect of opioid antagonism on food intake behavior and body weight in a biobehavioral model of obese binge eating. Author(s): College of Nursing at Wayne State University, Detroit, Michigan 48202, USA. [email protected] Source: Jarosz, P A Metzger, B L Biol-Res-Nurs. 2002 April; 3(4): 198-209 1099-8004

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The effects of miglitol on glucagon-like peptide-1 secretion and appetite sensations in obese type 2 diabetics. Author(s): Department of Medicine, St Louis University Medical Center, and GRECC, St Louis VA Medical Center, St Louis, MO, USA. Source: Lee, A Patrick, P Wishart, J Horowitz, M Morley, J E Diabetes-Obes-Metab. 2002 September; 4(5): 329-35 1462-8902

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The effects of orlistat on body weight and glycaemic control in overweight patients with type 2 diabetes: a randomized, placebo-controlled trial. Author(s): Zentrum fur Klinische Studien, GWT-Technische Universitat Dresden, Dresden, Germany. [email protected] Source: Hanefeld, M Sachse, G Diabetes-Obes-Metab. 2002 November; 4(6): 415-23 14628902

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The elephant in the room: evolution, behavioralism, and counteradvertising in the coming war against obesity. Source: Anonymous Harv-Law-Revolume 2003 February; 116(4): 1161-84 0017-811X

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The epidemic of childhood obesity. Source: du Toit, G van der Merwe, M T S-Afr-Med-J. 2003 January; 93(1): 49-50 00382469

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The impact of a modified and supplemented diet on obesity syndrome in Kuwaiti citizens. Author(s): Dar Al-Shifa Hospital Kuwait Source: Rabie, M.M.A. Barlow, ,P.J. Taylor, K.D.A. Mansoura-University-Journal-ofAgricultural-Sciences (Egypt). (May 2001). volume 26 (5) page 2939-2957. Received 2002. foods food additives food hygiene overweight symptoms kuwait 1110-0346

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The lifecycle effects of nutrition and body size on adult adiposity, diabetes and cardiovascular disease. Author(s): Diabetes Unit, KEM Hospital Research Centre, Rasta Peth, Pune, India. [email protected] Source: Yajnik, C S Obes-Revolume 2002 August; 3(3): 217-24 1467-7881

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The obesity pandemic--implications for Pakistan. Author(s): Department of Community Health Sciences, Aga Khan University, Karachi. Source: Nanan, D J J-Pak-Med-Assoc. 2002 August; 52(8): 342-6 0030-9982

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Treatment of morbid obesity with intragastric balloon in association with diet. Author(s): Cattedra di Chirurgia Generale dell'Universita degli Studi di Milano, Unita Operativa di Chirurgia Generale, Istituto Clinico Sant'Ambrogio di Milano, Italy. [email protected] Source: Doldi, S B Micheletto, G Perrini, M N Librenti, M C Rella, S Obes-Surg. 2002 August; 12(4): 583-7 0960-8923

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Twenty-year changes in the prevalence of overweight in Japanese adults: the National Nutrition Survey 1976-95. Author(s): National Institute of Health and Nutrition, Tokyo, Japan. [email protected] Source: Yoshiike, N Seino, F Tajima, S Arai, Y Kawano, M Furuhata, T Inoue, S ObesRevolume 2002 August; 3(3): 183-90 1467-7881

Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •

healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0

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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov

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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov

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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/

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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/

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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/

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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/

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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/

Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats

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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html

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Google: http://directory.google.com/Top/Health/Nutrition/

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Healthnotes: http://www.healthnotes.com/

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Open Directory Project: http://dmoz.org/Health/Nutrition/

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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/

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WebMDHealth: http://my.webmd.com/nutrition

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,,00.html

The following is a specific Web list relating to obesity; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation (some Web sites are subscription based): •

Vitamins Vitamin D Alternative names: Calciferol, Calcitrol, Cholecalciferol, Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Vitamin E Source: Healthnotes, Inc. www.healthnotes.com

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Minerals Chromium Source: Integrative Medicine Communications; www.drkoop.com Chromium Source: Prima Communications, Inc.www.personalhealthzone.com

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Chromium Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10018,00.html Potassium Source: Prima Communications, Inc.www.personalhealthzone.com Vanadium Source: Prima Communications, Inc.www.personalhealthzone.com •

Food and Diet Atkins Diet Source: Healthnotes, Inc. www.healthnotes.com Beef Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,85,00.html Complex carbohydrates Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,993,00.html Fasting Diet Source: Healthnotes, Inc. www.healthnotes.com Guaraná Source: Healthnotes, Inc. www.healthnotes.com High-Fiber Diet Source: Healthnotes, Inc. www.healthnotes.com Hypertension Source: Healthnotes, Inc. www.healthnotes.com Low-Fat Diet Source: Healthnotes, Inc. www.healthnotes.com Low-Purine Diet Source: Healthnotes, Inc. www.healthnotes.com Low-Salt Diet Source: Healthnotes, Inc. www.healthnotes.com Omega-3 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com

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Vegetarian Diet Source: Healthnotes, Inc. www.healthnotes.com Weight Loss and Obesity Source: Healthnotes, Inc. www.healthnotes.com Weight Management Index Source: Healthnotes, Inc. www.healthnotes.com

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CHAPTER 3. ALTERNATIVE MEDICINE AND OBESITY Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to obesity. At the conclusion of this chapter, we will provide additional sources.

The Combined Health Information Database The Combined Health Information Database (CHID) is a bibliographic database produced by health-related agencies of the U.S. federal government (mostly from the National Institutes of Health) that can offer concise information for a targeted search. The CHID database is updated four times a year at the end of January, April, July, and October. Check the titles, summaries, and availability of CAM-related information by using the “Simple Search” option at the following Web site: http://chid.nih.gov/simple/simple.html. In the drop box at the top, select “Complementary and Alternative Medicine.” Then type “obesity” (or synonyms) in the second search box. We recommend that you select 100 “documents per page” and to check the “whole records” options. The following was extracted using this technique: •

Complementary Therapies and Health Promotion Source: British Journal of Community Nursing. 7(2): 102-7. February 2002. Summary: This journal article reviews evidence that supports the role of complementary therapies as adjunctive treatments to enable nurses to talk about their use with clients as part of their health options. It discusses the rational for complementary and alternative medicine (CAM) and the two definitions of CAM offered by the British Medical Association. Information on study results related to addictive behaviors, obesity, and stress (including anxiety and depression) is given, because these are three lifestyle behaviors that may respond to health promotion interventions in which CAM can play a part. Numerous references. 6 pages.

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Using the Body To Heal the Body: Exercise and Disease Intervention Source: Alternative and Complementary Therapies. 4(3): 169-172. June 1998.

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Summary: This journal article discusses the multiple health benefits of exercise, highlighting the work in this area by Dr. L. Goldberg and D. L. Elliot at the Human Performance Laboratory, Division of Health Promotion and Sports Medicine, Oregon Health Sciences University in Portland. Drs. Goldberg and Elliot have focused their work on the effects of exercise in hypertension, neuromuscular diseases, certain metabolic conditions, and obesity. Clinicians at the Human Performance Laboratory offer patients a choice of testing options, and develop individualized exercise plans specifying exercise mode, intensity, duration, frequency, and progression. They also help patients develop strategies to overcome potential barriers to plan compliance. Exercise, along with diet, stress reduction, and social support, also is an integral component of the Opening Your Heart Program developed by Dr. D. Ornish at the Preventive Medicine Research Center in Sausalito, California. Dr. Ornish emphasizes that exercise does not have to be vigorous to be beneficial, noting that consistency is more important than intensity. In addition to its benefits in heart disease, recent research suggests a role for exercise in reducing cancer risk and improving function in older age. The article includes a list of recommended readings and 14 references.

National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to obesity and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “obesity” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to obesity: •

A cost-analysis of adopting a healthful diet in a family-based obesity treatment program. Author(s): Raynor HA, Kilanowski CK, Esterlis I, Epstein LH. Source: Journal of the American Dietetic Association. 2002 May; 102(5): 645-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12008989&dopt=Abstract

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A cross-cultural analysis of 'motivation for eating' as a potential factor in the emergence of global obesity: Japan and the United States. Author(s): Hawks SR, Madanat HN, Merrill RM, Goudy MB, Miyagawa T. Source: Health Promotion International. 2003 June; 18(2): 153-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746387&dopt=Abstract

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A perspective on obesity. Author(s): Johnson RW, Broadnax PA. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 69-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856445&dopt=Abstract

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A randomized trial of a low-carbohydrate diet for obesity. Author(s): Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2082-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761365&dopt=Abstract

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A succulent cure to end obesity. Author(s): Habeck M. Source: Drug Discovery Today. 2002 March 1; 7(5): 280-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11854044&dopt=Abstract

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Acupuncture for the treatment of obesity: a review of the evidence. Author(s): Lacey JM, Tershakovec AM, Foster GD. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 419-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664074&dopt=Abstract

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Alternative therapies for obesity: benefit or rip-off. Author(s): Klein S. Source: Critical Reviews in Food Science and Nutrition. 2001 January; 41(1): 33-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11152043&dopt=Abstract

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Alternative therapies: Part I. Depression, diabetes, obesity. Author(s): Morelli V, Zoorob RJ. Source: American Family Physician. 2000 September 1; 62(5): 1051-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10997530&dopt=Abstract

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Beneficial effects of tea catechins on diet-induced obesity: stimulation of lipid catabolism in the liver. Author(s): Murase T, Nagasawa A, Suzuki J, Hase T, Tokimitsu I. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 November; 26(11): 1459-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439647&dopt=Abstract

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Beneficial role of dietary phytoestrogens in obesity and diabetes. Author(s): Bhathena SJ, Velasquez MT. Source: The American Journal of Clinical Nutrition. 2002 December; 76(6): 1191-201. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450882&dopt=Abstract

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Biocultural aspects of obesity in young Mexican schoolchildren. Author(s): Brewis A.

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Source: American Journal of Human Biology : the Official Journal of the Human Biology Council. 2003 May-June; 15(3): 446-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12704721&dopt=Abstract •

Biomarkers and functional foods for obesity and diabetes. Author(s): Hill JO, Peters JC. Source: The British Journal of Nutrition. 2002 November; 88 Suppl 2: S213-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495462&dopt=Abstract

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Body image disturbance in obese outpatients before and after weight loss in relation to race, gender, binge eating, and age of onset of obesity. Author(s): Sorbara M, Geliebter A. Source: The International Journal of Eating Disorders. 2002 May; 31(4): 416-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11948646&dopt=Abstract

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Breast cancer and obesity. Author(s): La Guardia M, Giammanco M. Source: Panminerva Medica. 2001 June; 43(2): 123-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11449184&dopt=Abstract

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Calorie use and obesity among diabetic and non-diabetic Mvskoke Indians. Author(s): Edwards KA, Pryor S, Campbell J, Jacobsen S, Booton-Hiser D. Source: J Cult Divers. 2000 Summer; 7(2): 36-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11249259&dopt=Abstract

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Chemical toxins: a hypothesis to explain the global obesity epidemic. Author(s): Baillie-Hamilton PF. Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 April; 8(2): 185-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006126&dopt=Abstract

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Childhood obesity in Europe: a growing concern. Author(s): Livingstone MB. Source: Public Health Nutrition. 2001 February; 4(1A): 109-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11255500&dopt=Abstract

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Childhood obesity reduction by school based programs. Author(s): Davis SP, Davis M, Northington L, Moll G, Kolar K. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2002 November-December; 13(6): 145-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592832&dopt=Abstract

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Childhood obesity: the genetic-environmental interface. Author(s): Maffeis C. Source: Bailliere's Best Practice & Research. Clinical Endocrinology & Metabolism. 1999 April; 13(1): 31-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10932675&dopt=Abstract

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Childhood obesity: the health issue. Author(s): Deckelbaum RJ, Williams CL. Source: Obesity Research. 2001 November; 9 Suppl 4: 239S-243S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11707548&dopt=Abstract

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Cholesterol absorption efficiency and sterol metabolism in obesity. Author(s): Miettinen TA, Gylling H. Source: Atherosclerosis. 2000 November; 153(1): 241-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11058720&dopt=Abstract

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Coagulation and fibrinolysis abnormalities in obesity. Author(s): De Pergola G, Pannacciulli N. Source: J Endocrinol Invest. 2002 November; 25(10): 899-904. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508953&dopt=Abstract

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Cultural considerations for treatment of childhood obesity. Author(s): Davis SP, Northington L, Kolar K. Source: J Cult Divers. 2000 Winter; 7(4): 128-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11855259&dopt=Abstract

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Current concepts in the management of obesity. An evidence based review. Author(s): Al-Quaiz AJ. Source: Saudi Med J. 2001 March; 22(3): 205-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11307103&dopt=Abstract

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Current status of medical and surgical therapy for obesity. Author(s): Mun EC, Blackburn GL, Matthews JB. Source: Gastroenterology. 2001 February; 120(3): 669-81. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179243&dopt=Abstract

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Developing health messages: qualitative studies with children, parents, and teachers help identify communications opportunities for healthful lifestyles and the prevention of obesity. Author(s): Borra ST, Kelly L, Shirreffs MB, Neville K, Geiger CJ.

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Source: Journal of the American Dietetic Association. 2003 June; 103(6): 721-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12778044&dopt=Abstract •

Diabetes mellitus and obesity. Author(s): Roth A. Source: Primary Care. 2002 June; 29(2): 279-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391712&dopt=Abstract

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Diet culture and obesity in northern Africa. Author(s): Mokhtar N, Elati J, Chabir R, Bour A, Elkari K, Schlossman NP, Caballero B, Aguenaou H. Source: The Journal of Nutrition. 2001 March; 131(3): 887S-892S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11238780&dopt=Abstract

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Dietary cyanidin 3-O-beta-D-glucoside-rich purple corn color prevents obesity and ameliorates hyperglycemia in mice. Author(s): Tsuda T, Horio F, Uchida K, Aoki H, Osawa T. Source: The Journal of Nutrition. 2003 July; 133(7): 2125-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840166&dopt=Abstract

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Dietary fat subtypes and obesity. Author(s): Storlien LH, Huang XF, Lin S, Xin X, Wang HQ, Else PL. Source: World Review of Nutrition and Dietetics. 2001; 88: 148-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11935947&dopt=Abstract

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Epidemiology of childhood obesity in Europe. Author(s): Livingstone B. Source: European Journal of Pediatrics. 2000 September; 159 Suppl 1: S14-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11011953&dopt=Abstract

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Ethnic issues in the epidemiology of childhood obesity. Author(s): Crawford PB, Story M, Wang MC, Ritchie LD, Sabry ZI. Source: Pediatric Clinics of North America. 2001 August; 48(4): 855-78. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11494640&dopt=Abstract

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Evidence based paediatrics: Evidence based management of childhood obesity. Author(s): Edmunds L, Waters E, Elliott EJ. Source: Bmj (Clinical Research Ed.). 2001 October 20; 323(7318): 916-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11668139&dopt=Abstract

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For the patient. Are vegetarians at less risk for obesity, diabetes, and hypertension? Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day

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Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 148. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723025&dopt=Abstract •

Gourmand savants and environmental determinants of obesity. Author(s): Myslobodsky M. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 121-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760447&dopt=Abstract

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Hepatothermic therapy of obesity: rationale and an inventory of resources. Author(s): McCarty MF. Source: Medical Hypotheses. 2001 September; 57(3): 324-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11516225&dopt=Abstract

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Herbal simulation of ephedrine and caffeine in treatment of obesity. Author(s): Dulloo AG. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 May; 26(5): 590-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12032740&dopt=Abstract

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Herbal therapy for management of obesity: observations from a clinical endocrinology practice. Author(s): Sindler BH. Source: Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2001 November-December; 7(6): 443-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11747280&dopt=Abstract

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Hunter-gatherers win profit-sharing deal for obesity drug. Author(s): Wise J. Source: Bulletin of the World Health Organization. 2003; 81(5): 382. Epub 2003 July 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856057&dopt=Abstract

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Integrating the prevention of eating disorders and obesity: feasible or futile? Author(s): Irving LM, Neumark-Sztainer D. Source: Preventive Medicine. 2002 March; 34(3): 299-309. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11902846&dopt=Abstract

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Integrative medicine approach to obesity and diabetes. Author(s): Shintani TT.

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Source: Hawaii Med J. 2001 October; 60(10): 262-3. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11732378&dopt=Abstract •

Laser acupuncture and low-calorie diet during visceral obesity therapy after menopause. Author(s): Wozniak P, Stachowiak G, Pieta-Dolinska A, Oszukowski P. Source: Acta Obstetricia Et Gynecologica Scandinavica. 2003 January; 82(1): 69-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580844&dopt=Abstract

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Managing obesity like any other chronic condition. Long-term therapy may reduce comorbidity as well. Author(s): Agrawal M, Worzniak M, Diamond L. Source: Postgraduate Medicine. 2000 July; 108(1): 75-6, 79-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10914120&dopt=Abstract

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Modulation of adipocyte lipoprotein lipase expression as a strategy for preventing or treating visceral obesity. Author(s): McCarty MF. Source: Medical Hypotheses. 2001 August; 57(2): 192-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11461172&dopt=Abstract

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Modulation of obesity by a green tea catechin. Author(s): Kao YH, Hiipakka RA, Liao S. Source: The American Journal of Clinical Nutrition. 2000 November; 72(5): 1232-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11063454&dopt=Abstract

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Morbidity of severe obesity. Author(s): Kral JG. Source: The Surgical Clinics of North America. 2001 October; 81(5): 1039-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11589244&dopt=Abstract

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Natural hazards. Tonic or toxic? Americans are gobbling up nature's remedies for everything from obesity to depression. Author(s): Spake A. Source: U.S. News & World Report. 2001 February 12; 130(6): 42-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11216231&dopt=Abstract

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Nutrition for health promotion: phytochemicals, functional foods, and alternative approaches to combat obesity. Author(s): Bloch AS.

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Source: Dent Clin North Am. 2003 April; 47(2): 411-23, Viii-Ix. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699239&dopt=Abstract •

Nutritional and other influences in childhood as predictors of adult obesity. Author(s): Power C, Parsons T. Source: The Proceedings of the Nutrition Society. 2000 May; 59(2): 267-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10946795&dopt=Abstract

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Obesity and associated modifiable environmental factors in Iranian adolescents: Isfahan Healthy Heart Program - Heart Health Promotion from Childhood. Author(s): Kelishadi R, Hashemi Pour M, Sarraf-Zadegan N, Sadry Gh G, Ansari R, Alikhassy H, Bashardoust N. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2003 August; 45(4): 435-442. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911481&dopt=Abstract

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Obesity and cortisol. Author(s): Bjorntorp P, Rosmond R. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2000 October; 16(10): 924-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11054598&dopt=Abstract

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Obesity and medicinal plants. Author(s): Moro CO, Basile G. Source: Fitoterapia. 2000 August; 71 Suppl 1: S73-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10930716&dopt=Abstract

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Obesity intervention among African-American children and adolescents. Author(s): Baskin ML, Ahluwalia HK, Resnicow K. Source: Pediatric Clinics of North America. 2001 August; 48(4): 1027-39. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11494636&dopt=Abstract

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Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 34-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723010&dopt=Abstract

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Obesity. Author(s): Yanovski SZ, Yanovski JA.

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Source: The New England Journal of Medicine. 2002 February 21; 346(8): 591-602. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11856799&dopt=Abstract •

Observation on the therapeutic effects of acupuncture for 60 cases of simple obesity. Author(s): Wang H. Source: J Tradit Chin Med. 2002 September; 22(3): 187-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400423&dopt=Abstract

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Overweight and obesity in women: health risks and consequences. Author(s): Hu FB. Source: Journal of Women's Health (2002). 2003 March; 12(2): 163-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737715&dopt=Abstract

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Platycodi radix affects lipid metabolism in mice with high fat diet-induced obesity. Author(s): Han LK, Xu BJ, Kimura Y, Zheng Y, Okuda H. Source: The Journal of Nutrition. 2000 November; 130(11): 2760-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11053518&dopt=Abstract

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Popular diets: correlation to health, nutrition, and obesity. Author(s): Kennedy ET, Bowman SA, Spence JT, Freedman M, King J. Source: Journal of the American Dietetic Association. 2001 April; 101(4): 411-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11320946&dopt=Abstract

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Possible lessons from the tobacco experience for obesity control. Author(s): Mercer SL, Green LW, Rosenthal AC, Husten CG, Khan LK, Dietz WH. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4 Suppl): 1073S1082S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663321&dopt=Abstract

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Prevention of childhood obesity: sociocultural and familial factors. Author(s): Bruss MB, Morris J, Dannison L. Source: Journal of the American Dietetic Association. 2003 August; 103(8): 1042-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12891156&dopt=Abstract

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Preventive strategies against weight gain and obesity. Author(s): Swinburn B, Egger G. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 November; 3(4): 289-301. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12458974&dopt=Abstract

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Principles and practices in the management of obesity. Author(s): Foster GD. Source: American Journal of Respiratory and Critical Care Medicine. 2003 August 1; 168(3): 274-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888610&dopt=Abstract

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Protective effects of a soy diet in preventing obesity-linked renal disease. Author(s): Maddox DA, Alavi FK, Silbernick EM, Zawada ET. Source: Kidney International. 2002 January; 61(1): 96-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11786089&dopt=Abstract

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Randomized controlled trial of the effect of n-3 fatty acid supplementation on the metabolism of apolipoprotein B-100 and chylomicron remnants in men with visceral obesity. Author(s): Chan DC, Watts GF, Mori TA, Barrett PH, Redgrave TG, Beilin LJ. Source: The American Journal of Clinical Nutrition. 2003 February; 77(2): 300-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540386&dopt=Abstract

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Recent findings of green tea extract AR25 (Exolise) and its activity for the treatment of obesity. Author(s): Chantre P, Lairon D. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2002 January; 9(1): 3-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11924761&dopt=Abstract

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Reduction of abdominal obesity in lipodystrophy associated with human immunodeficiency virus infection by means of diet and exercise: case report and proof of principle. Author(s): Roubenoff R, Schmitz H, Bairos L, Layne J, Potts E, Cloutier GJ, Denry F. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2002 February 1; 34(3): 390-3. Epub 2001 December 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11774087&dopt=Abstract

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Ripe for study: complementary and alternative treatments for obesity. Author(s): Evans M, Straus S. Source: Critical Reviews in Food Science and Nutrition. 2001 January; 41(1): 35-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11152044&dopt=Abstract

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Safety and efficacy of ephedra and ephedrine for enhancement of athletic performance, thermogenesis and the treatment of obesity. Author(s): Shekelle P, Hardy M.

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Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2002 January; 9(1): 78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11924769&dopt=Abstract •

Salacia reticulata and its polyphenolic constituents with lipase inhibitory and lipolytic activities have mild antiobesity effects in rats. Author(s): Yoshikawa M, Shimoda H, Nishida N, Takada M, Matsuda H. Source: The Journal of Nutrition. 2002 July; 132(7): 1819-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12097653&dopt=Abstract

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Self-help and long-term behavior therapy for obesity. Author(s): Latner JD, Wilson GT, Stunkard AJ, Jackson ML. Source: Behaviour Research and Therapy. 2002 July; 40(7): 805-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12074374&dopt=Abstract

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Self-help in the long-term treatment of obesity. Author(s): Latner JD. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 May; 2(2): 87-97. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119666&dopt=Abstract

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Single nucleotide polymorphism identification in candidate gene systems of obesity. Author(s): Irizarry K, Hu G, Wong ML, Licinio J, Lee CJ. Source: The Pharmacogenomics Journal. 2001; 1(3): 193-203. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11908756&dopt=Abstract

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Site-specific differences in the fatty acid composition of abdominal adipose tissue in an obese population from a Mediterranean area: relation with dietary fatty acids, plasma lipid profile, serum insulin, and central obesity. Author(s): Garaulet M, Perez-Llamas F, Perez-Ayala M, Martinez P, de Medina FS, Tebar FJ, Zamora S. Source: The American Journal of Clinical Nutrition. 2001 November; 74(5): 585-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11684525&dopt=Abstract

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The associations of a marine diet with plasma lipids, blood glucose, blood pressure and obesity among the inuit in Greenland. Author(s): Bjerregaard P, Pedersen HS, Mulvad G. Source: European Journal of Clinical Nutrition. 2000 September; 54(9): 732-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11002386&dopt=Abstract

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The cross cultural context of obesity: an INCLEN multicentre collaborative study. Author(s): Treloar C, Porteous J, Hassan F, Kasniyah N, Lakshmanudu M, Sama M, Sja'bani M, Heller RF.

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Source: Health & Place. 1999 December; 5(4): 279-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10984582&dopt=Abstract •

The Hawaii Diet: ad libitum high carbohydrate, low fat multi-cultural diet for the reduction of chronic disease risk factors: obesity, hypertension, hypercholesterolemia, and hyperglycemia. Author(s): Shintani TT, Beckham S, Brown AC, O'Connor HK. Source: Hawaii Med J. 2001 March; 60(3): 69-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11320614&dopt=Abstract

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The Influence of Obesity on the Self-Reported Health Status of Chamorros and other Residents of Guam. Author(s): Pinhey TK, Heathcote GM, Rarick J. Source: Asian Am Pac Isl J Health. 1994 Summer; 2(3): 195-211. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11567272&dopt=Abstract

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The pathogenesis of obesity. Author(s): Campfield LA, Smith FJ. Source: Bailliere's Best Practice & Research. Clinical Endocrinology & Metabolism. 1999 April; 13(1): 13-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10932674&dopt=Abstract

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The process of restructuring and the treatment of obesity in women. Author(s): Hayward LM, Nixon C, Jasper MP, Murphy KM, Harlan V, Swirda L, Hayward K. Source: Health Care for Women International. 2000 October-November; 21(7): 615-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11813769&dopt=Abstract

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The skinny on obesity and cancer. Obesity increases the risk of death from cancer, but being overweight isn't inescapable. Author(s): Blackburn GL. Source: Health News. 2003 June; 9(6): 3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793396&dopt=Abstract

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The treatment of obesity. Author(s): Mina WC, Burns RW, Terry BE. Source: Mo Med. 2003 May-June; 100(3): 248-55. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847866&dopt=Abstract

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Three-month tolerability of orlistat in adolescents with obesity-related comorbid conditions. Author(s): McDuffie JR, Calis KA, Uwaifo GI, Sebring NG, Fallon EM, Hubbard VS, Yanovski JA.

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Source: Obesity Research. 2002 July; 10(7): 642-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12105286&dopt=Abstract •

Treatment of child and adolescent obesity: reports from pediatricians, pediatric nurse practitioners, and registered dietitians. Author(s): Barlow SE, Trowbridge FL, Klish WJ, Dietz WH. Source: Pediatrics. 2002 July; 110(1 Pt 2): 229-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12094000&dopt=Abstract

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Triiodothyronine supplementation for hypothalamic obesity. Author(s): Fernandes JK, Klein MJ, Ater JL, Kuttesch JF, Vassilopoulou-Sellin R. Source: Metabolism: Clinical and Experimental. 2002 November; 51(11): 1381-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12404183&dopt=Abstract

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Use of quality control indices in moderately hypocaloric Mediterranean diet for treatment of obesity. Author(s): De Lorenzo A, Petroni ML, De Luca PP, Andreoli A, Morini P, Iacopino L, Innocente I, Perriello G. Source: Diabetes Nutr Metab. 2001 August; 14(4): 181-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11716286&dopt=Abstract

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What is an optimal diet? Relationship of macronutrient intake to obesity, glucose tolerance, lipoprotein cholesterol levels and the metabolic syndrome in the Whitehall II study. Author(s): Brunner EJ, Wunsch H, Marmot MG. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2001 January; 25(1): 45-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11244457&dopt=Abstract

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World pandemic of obesity: the situation in Southern African populations. Author(s): Walker AR, Adam F, Walker BF. Source: Public Health. 2001 November; 115(6): 368-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11781845&dopt=Abstract

Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •

Alternative Medicine Foundation, Inc.: http://www.herbmed.org/

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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats

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Chinese Medicine: http://www.newcenturynutrition.com/

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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html

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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm

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Google: http://directory.google.com/Top/Health/Alternative/

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Healthnotes: http://www.healthnotes.com/

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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine

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Open Directory Project: http://dmoz.org/Health/Alternative/

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HealthGate: http://www.tnp.com/

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WebMDHealth: http://my.webmd.com/drugs_and_herbs

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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,,00.html

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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/

The following is a specific Web list relating to obesity; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation (some Web sites are subscription based): •

General Overview Allergies and Sensitivities Source: Healthnotes, Inc. www.healthnotes.com Amenorrhea Source: Integrative Medicine Communications; www.drkoop.com Angina Source: Healthnotes, Inc. www.healthnotes.com Angina Source: Integrative Medicine Communications; www.drkoop.com Anorexia Nervosa Source: Integrative Medicine Communications; www.drkoop.com Asthma Source: Healthnotes, Inc. www.healthnotes.com Atherosclerosis Source: Healthnotes, Inc. www.healthnotes.com Birth Defects Prevention Source: Healthnotes, Inc. www.healthnotes.com Breast Cancer Source: Healthnotes, Inc. www.healthnotes.com

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Breast Cancer Source: Integrative Medicine Communications; www.drkoop.com Cancer, Breast Source: Integrative Medicine Communications; www.drkoop.com Cancer, Colorectal Source: Integrative Medicine Communications; www.drkoop.com Cancer, Skin Source: Integrative Medicine Communications; www.drkoop.com Candidiasis Source: Integrative Medicine Communications; www.drkoop.com Cardiovascular Disease Overview Source: Healthnotes, Inc. www.healthnotes.com Cataracts Source: Healthnotes, Inc. www.healthnotes.com Cholesterol, High Source: Integrative Medicine Communications; www.drkoop.com Cirrhosis Source: Integrative Medicine Communications; www.drkoop.com Colon Cancer Source: Healthnotes, Inc. www.healthnotes.com Colorectal Cancer Source: Integrative Medicine Communications; www.drkoop.com Depression Source: Integrative Medicine Communications; www.drkoop.com Diabetes Source: Healthnotes, Inc. www.healthnotes.com Diabetes Mellitus Source: Integrative Medicine Communications; www.drkoop.com Diverticular Disease Source: Healthnotes, Inc. www.healthnotes.com Diverticular Disease Source: Integrative Medicine Communications; www.drkoop.com Eating Disorders Source: Healthnotes, Inc. www.healthnotes.com

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Eating Disorders, Anorexia Source: Integrative Medicine Communications; www.drkoop.com Female Infertility Source: Healthnotes, Inc. www.healthnotes.com Gallstones Source: Healthnotes, Inc. www.healthnotes.com Gastroesophageal Reflux Disease Source: Healthnotes, Inc. www.healthnotes.com Gastroesophageal Reflux Disease Source: Integrative Medicine Communications; www.drkoop.com Gestational Hypertension Source: Healthnotes, Inc. www.healthnotes.com Gout Source: Healthnotes, Inc. www.healthnotes.com Hair Growth, Excessive Source: Integrative Medicine Communications; www.drkoop.com Heart Attack Source: Healthnotes, Inc. www.healthnotes.com Heartburn Source: Integrative Medicine Communications; www.drkoop.com Heat Exhaustion Source: Integrative Medicine Communications; www.drkoop.com High Blood Pressure Source: Integrative Medicine Communications; www.drkoop.com High Cholesterol Source: Healthnotes, Inc. www.healthnotes.com High Cholesterol Source: Integrative Medicine Communications; www.drkoop.com High Triglycerides Source: Healthnotes, Inc. www.healthnotes.com Hirsuitism Source: Integrative Medicine Communications; www.drkoop.com Hypercholesterolemia Source: Integrative Medicine Communications; www.drkoop.com

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Hypertension Source: Integrative Medicine Communications; www.drkoop.com Immune Function Source: Healthnotes, Inc. www.healthnotes.com Insulin Resistance Syndrome Source: Healthnotes, Inc. www.healthnotes.com Liver Disease Source: Integrative Medicine Communications; www.drkoop.com Low Back Pain Source: Healthnotes, Inc. www.healthnotes.com Ménière's Disease Source: Healthnotes, Inc. www.healthnotes.com Menstruation, Absence of Source: Integrative Medicine Communications; www.drkoop.com Obesity Source: Integrative Medicine Communications; www.drkoop.com Obesity Source: Integrative Medicine Communications; www.drkoop.com Osteoarthritis Source: Healthnotes, Inc. www.healthnotes.com Osteoarthritis Source: Integrative Medicine Communications; www.drkoop.com Pain Source: Healthnotes, Inc. www.healthnotes.com Preeclampsia Source: Healthnotes, Inc. www.healthnotes.com Pregnancy and Postpartum Support Source: Healthnotes, Inc. www.healthnotes.com Psoriasis Source: Integrative Medicine Communications; www.drkoop.com Pulmonary Edema Source: Integrative Medicine Communications; www.drkoop.com Pulmonary Hypertension Source: Integrative Medicine Communications; www.drkoop.com

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Skin Cancer Source: Integrative Medicine Communications; www.drkoop.com Sleep Apnea Source: Integrative Medicine Communications; www.drkoop.com Stroke Source: Healthnotes, Inc. www.healthnotes.com Vaginal Inflammation Source: Integrative Medicine Communications; www.drkoop.com Vaginitis Source: Integrative Medicine Communications; www.drkoop.com Varicose Veins Source: Healthnotes, Inc. www.healthnotes.com Varicose Veins Source: Integrative Medicine Communications; www.drkoop.com Varicose Veins Source: Prima Communications, Inc.www.personalhealthzone.com Wounds Source: Integrative Medicine Communications; www.drkoop.com Yeast Infection Source: Integrative Medicine Communications; www.drkoop.com •

Alternative Therapy Ayurveda Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,672,00.html Detoxification Therapy Source: Healthnotes, Inc. www.healthnotes.com Fasting Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,694,00.html Macrobiotics Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,714,00.html

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Nutrition Source: Integrative Medicine Communications; www.drkoop.com The Weigh Down Diet Alternative names: Weigh Down approach Weigh Down method Source: The Canoe version of A Dictionary of Alternative-Medicine Methods, by Priorities for Health editor Jack Raso, M.S., R.D. Hyperlink: http://www.canoe.ca/AltmedDictionary/w.html Traditional Chinese Medicine Source: Integrative Medicine Communications; www.drkoop.com •

Herbs and Supplements 5-HTP Source: Integrative Medicine Communications; www.drkoop.com 5-HTP (5-Hydroxytryptophan) Source: Prima Communications, Inc.www.personalhealthzone.com 5-Hydroxytryptophan Source: Healthnotes, Inc. www.healthnotes.com 5-Hydroxytryptophan (5-HTP) Source: Integrative Medicine Communications; www.drkoop.com 7-KETO Source: Healthnotes, Inc. www.healthnotes.com ALA Source: Integrative Medicine Communications; www.drkoop.com Alpha-Linolenic Acid (ALA) Source: Integrative Medicine Communications; www.drkoop.com Alpha-Lipoic Acid Source: Integrative Medicine Communications; www.drkoop.com Amino Acids Overview Source: Healthnotes, Inc. www.healthnotes.com Amlodipine Source: Healthnotes, Inc. www.healthnotes.com Antidepressants Source: Healthnotes, Inc. www.healthnotes.com Bladderwrack Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca

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Blue-Green Algae Source: Healthnotes, Inc. www.healthnotes.com Calciferol Source: Integrative Medicine Communications; www.drkoop.com Calcitrol Source: Integrative Medicine Communications; www.drkoop.com Cayenne Alternative names: Capsicum annuum, Capsicum frutescens Source: Healthnotes, Inc. www.healthnotes.com Chickweed Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Chitosan Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10016,00.html Cholecalciferol Source: Integrative Medicine Communications; www.drkoop.com Coenzyme Q10 Source: Healthnotes, Inc. www.healthnotes.com Coenzyme Q10 (CoQ10) Source: Prima Communications, Inc.www.personalhealthzone.com Coleus Alternative names: Coleus forskohlii Source: Healthnotes, Inc. www.healthnotes.com Conjugated linoleic acid Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10102,00.html Dehydroepiandrosterone (DHEA) Source: Healthnotes, Inc. www.healthnotes.com Dehydroepiandrosterone (DHEA) Source: Integrative Medicine Communications; www.drkoop.com DHA Source: Integrative Medicine Communications; www.drkoop.com DHEA Source: Integrative Medicine Communications; www.drkoop.com

200 Obesity

Diltiazem Source: Healthnotes, Inc. www.healthnotes.com Docosahexaenoic Acid (DHA) Source: Integrative Medicine Communications; www.drkoop.com Eicosapentaenoic Acid (EPA) Source: Integrative Medicine Communications; www.drkoop.com Enalapril Source: Healthnotes, Inc. www.healthnotes.com EPA Source: Integrative Medicine Communications; www.drkoop.com Ephedra Alternative names: Ephedra sinensis, Ma huang Source: Integrative Medicine Communications; www.drkoop.com Ephedra (Ma huang) Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,777,00.html Ephedra sinensis Source: Integrative Medicine Communications; www.drkoop.com Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Fiber Source: Integrative Medicine Communications; www.drkoop.com Garcinia cambogia Alternative names: Citrin, Gambooge Source: Alternative Medicine Foundation, Inc. www.amfoundation.org GLA (Gamma-Linolenic Acid) Source: Prima Communications, Inc.www.personalhealthzone.com Glucomannan Source: Healthnotes, Inc. www.healthnotes.com Green tea Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10032,00.html Guggul Alternative names: Commiphora mukul Source: Healthnotes, Inc. www.healthnotes.com

Alternative Medicine 201

Guggul Source: Prima Communications, Inc.www.personalhealthzone.com Gugulipid Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10033,00.html Hydroxycitric Acid Source: Healthnotes, Inc. www.healthnotes.com Hydroxycitric Acid Source: Prima Communications, Inc.www.personalhealthzone.com Indole-3-Carbinol Source: Healthnotes, Inc. www.healthnotes.com Insulin Alternative names: Humalog, Humulin, Iletin, Novolin, Velosulin Source: Prima Communications, Inc.www.personalhealthzone.com Ispaghula Source: Integrative Medicine Communications; www.drkoop.com Lipase Source: Integrative Medicine Communications; www.drkoop.com Lipase Source: Integrative Medicine Communications; www.drkoop.com Lipotropic combination Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,861,00.html Ma huang Source: Integrative Medicine Communications; www.drkoop.com Medium Chain Triglycerides Source: Healthnotes, Inc. www.healthnotes.com Metformin Source: Healthnotes, Inc. www.healthnotes.com Nadolol Source: Healthnotes, Inc. www.healthnotes.com Oral Hypoglycemics Source: Prima Communications, Inc.www.personalhealthzone.com

202 Obesity

Orlistat Source: Healthnotes, Inc. www.healthnotes.com Plantago isphagula Source: Integrative Medicine Communications; www.drkoop.com Plantago psyllium Alternative names: Psyllium, Ispaghula; Plantago psyllium/ovata Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Psyllium Alternative names: Plantago ovata, Plantago ispaghula Source: Healthnotes, Inc. www.healthnotes.com Psyllium Alternative names: Ispaghula,Plantago isphagula Source: Integrative Medicine Communications; www.drkoop.com Pyruvate Source: Healthnotes, Inc. www.healthnotes.com Pyruvate Source: Prima Communications, Inc.www.personalhealthzone.com Ribes Alternative names: Black Currant; Ribes nigrum L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Sibutramine Source: Healthnotes, Inc. www.healthnotes.com Thyroid Hormones Source: Healthnotes, Inc. www.healthnotes.com

General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.

203

CHAPTER 4. DISSERTATIONS ON OBESITY Overview In this chapter, we will give you a bibliography on recent dissertations relating to obesity. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “obesity” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on obesity, we have not necessarily excluded non-medical dissertations in this bibliography.

Dissertations on Obesity ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to obesity. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •

A Comparative Analysis of Absentee Rates and Health Care Costs for Obese and Nonobese Employees by Meesig Jondle, Mary Ann, Phd from The University of Toledo, 1989, 92 pages http://wwwlib.umi.com/dissertations/fullcit/8926339

•

A Comparison of Body Composition, Body Cathexis, and Attitude toward Obesity in Women with Different Levels of Physical Activity by Lai, Shu-mei Mary, Phd from Oregon State University, 1984, 145 pages http://wwwlib.umi.com/dissertations/fullcit/8407284

•

A Comparison of Different Exercise Prescriptions Combined with a Low-fat Ad Libitum Diet: Effects on Weight Loss, Health-related Variables and Psychological Well-being in Premenopausal Overweight Women by Brill, Janet Bond; Phd from University of Miami, 2001, 164 pages http://wwwlib.umi.com/dissertations/fullcit/3008195

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•

A Comparison of Hypnosis and Behavioral Treatments for Obesity with One Year Followup by Haynes, Judith A., Phd from The University of North Dakota, 1986, 137 pages http://wwwlib.umi.com/dissertations/fullcit/8702466

•

A Comparison of Intensity of Educational Intervention on Knowledge, Attitude, Weight and Metabolic Control in Obese Individuals with Type Ii Non-insulin Dependent Diabetes Mellitus by D'eramo, Gail Ann, Edd from Columbia University Teachers College, 1987, 157 pages http://wwwlib.umi.com/dissertations/fullcit/8804209

•

A Comparison of Physicians' Attitudes toward Obesity with Patients' Perceptions of Physicians' Attitudes toward Obesity by Siebring, Linda Lee, Phd from University of Arkansas, 1995, 97 pages http://wwwlib.umi.com/dissertations/fullcit/9536054

•

A Consideration of the Ventral Noradrenergic Bundle As a Discrete System Modulating Feeding Implications for Ventromedial Hypothalamic Obesity and Lateral Hypothalamic Hunger by Zacharko, Robert Michael; Phd from The University of Saskatchewan (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK49191

•

A Contextual Analysis of Obesity and Smoking among Women in Oklahoma City by Thompson, Virginia Marie, Phd from The University of Oklahoma, 1995, 128 pages http://wwwlib.umi.com/dissertations/fullcit/9538060

•

A Genetic Dissection of Obesity and Type 2 Diabetes Mellitus in the Mouse by Stoehr, Jonathan Paul; Phd from The University of Wisconsin - Madison, 2002, 235 pages http://wwwlib.umi.com/dissertations/fullcit/3060449

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A Naturalistic Exploration of Weight Tolerance and Primary Socialization Sources in Overweight African American Women by Gordon, Leslene Elaine; Phd from University of South Florida, 2003, 163 pages http://wwwlib.umi.com/dissertations/fullcit/3079983

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A Proposed Psychosocial Consequences Model of Childhood Obesity by Haydenwade, Helen Anne; Phd from University of California, San Diego, 2002, 93 pages http://wwwlib.umi.com/dissertations/fullcit/3044785

•

A Prospective Cohort Study of Maternal Factors in Childhood Asthma: Parity, Obesity, Fetal Growth, and Social Stressors by Held, Kathryn B. Phd from The University of Oklahoma, 2000, 312 pages http://wwwlib.umi.com/dissertations/fullcit/9985574

•

A Reanalysis of Schachter's Externality Theory the Relationship between Externality and Obesity by Buser, Mary M; Phd from The University of Manitoba (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK47190

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A Study of Self-concept and Obesity in Adult Females by Grzegorek Hagene, Lorraine Marie, Phd from Southern Illinois University at Carbondale, 1990, 126 pages http://wwwlib.umi.com/dissertations/fullcit/9129826

•

Adolescent Attitudes toward Obesity in Women: a Study of Sociodemographic Variables by Rubin, Marcia Ann, Phd from University of Illinois at Urbana-champaign, 1988, 235 pages http://wwwlib.umi.com/dissertations/fullcit/8908819

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•

An Empirical Validation of the Relationship between Contextual Correlates of Obesity and Enduring Self Variables by Haden, Tony Lynn, Phd from The University of Texas at Austin, 1987, 93 pages http://wwwlib.umi.com/dissertations/fullcit/8717425

•

An Ethnographic Analysis of the Family Dynamics of the Obese Adolescent by Mcvoy, Joseph Henry, Jr., Phd from Virginia Polytechnic Institute and State University, 1986, 91 pages http://wwwlib.umi.com/dissertations/fullcit/8624344

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An Exploratory Study of an Obesity Reduction Education Program by Turner, Freda Walker, Phd from Walden University, 1996, 122 pages http://wwwlib.umi.com/dissertations/fullcit/9804463

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An Investigation of the Relationship between Obesity and Demographic, Eating Habit, Nutrient Intake, and Health Status Factors among Adults by Boasi, Claire Bernadette, Edd from Temple University, 1986, 172 pages http://wwwlib.umi.com/dissertations/fullcit/8611814

•

Application of Exner's Rorschach System in the Study of Overweight, Restrained Eater and Normal Weight Comparison Subjects by Bunkis, Ruta Sternbergs, Edd from Boston University, 1987, 130 pages http://wwwlib.umi.com/dissertations/fullcit/8721314

•

Attributions towards Anorexic, Bulimic and Obese Others by Gousse, Alexandra; Ma from University of Guelph (canada), 2002, 72 pages http://wwwlib.umi.com/dissertations/fullcit/MQ65934

•

Beauty and the Beast: a Social Psychological Study of Weight Satisfaction and Dieting Behavior (gender, Obesity) by Huff-corzine, Linda Kathrine, Phd from Washington University, 1986, 142 pages http://wwwlib.umi.com/dissertations/fullcit/8708374

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Binge Eating Disorder and Its Relationship to Bulimia Nervosa and Obesity by Lacaille, Lara Schultz; Phd from Utah State University, 2002, 173 pages http://wwwlib.umi.com/dissertations/fullcit/3042740

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Biological and Cultural Effects of Obesity on Women during Menopause by Smith, Linda Kay, Phd from Wayne State University, 1987, 160 pages http://wwwlib.umi.com/dissertations/fullcit/8714563

•

Body Composition of Kuwaiti Youth: Prevalence of Obesity and Developmental Trends by Almarzouq, Hana Abdullah; Edd from University of Houston, 2001, 70 pages http://wwwlib.umi.com/dissertations/fullcit/3027881

•

Cardiovascular Consequences of Genetic and Diet-induced Obesity in Mice by Williams, Todd Dennis; Phd from The Florida State University, 2002, 90 pages http://wwwlib.umi.com/dissertations/fullcit/3055775

•

Central Obesity and Diet in Relation to Gallstone Disease by Tsai, Chung-jyi; Sd from Harvard University, 2002 http://wwwlib.umi.com/dissertations/fullcit/f241745

•

Central Obesity: Predisposing Factors and Consequences in Children Age 8 Through Young Adulthood by Appel, Susan J. Phd from The University of North Carolina at Chapel Hill, 2002, 132 pages http://wwwlib.umi.com/dissertations/fullcit/3046956

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Childhood Obesity: Determinants, Treatment, and Risk Factors for Chronic Disease by Ball, Geoffery Denis Charles; Phd from University of Alberta (canada), 2002, 210 pages http://wwwlib.umi.com/dissertations/fullcit/NQ68540

•

Comparison of Weight Control Treatment Programs (obesity) by Krieshok, Susan Mary, Phd from University of Kansas, 1990, 182 pages http://wwwlib.umi.com/dissertations/fullcit/9119090

•

Control of Brown Adipose Tissue Growth and Function in Rats and Hamsters Normalities in Genetic Models of Human Disease (obesity Muscular Dystrophy) by Triandafillou, Joan; Phd from University of Ottawa (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NK65634

•

Correlates of Obesity in Three Species of Captive Macaques by Klepper-kilgore, Nancy, Phd from Tulane University, 1986, 296 pages http://wwwlib.umi.com/dissertations/fullcit/8715185

•

Determining Rate of Subjective Time According to Subject Sex, Weight, and Locus of Control Orientation (obesity, Time Perception) by Faulkner, Kim Knox, Phd from The University of Southern Mississippi, 1985, 168 pages http://wwwlib.umi.com/dissertations/fullcit/8611219

•

Development and Evaluation of a Computer-based Resource Unit on Obesity and Weight Control for College Students by Hill, Charles Edward, Edd from State University of New York at Buffalo, 1972, 151 pages http://wwwlib.umi.com/dissertations/fullcit/7223526

•

Development and Evaluation of a Nutrition Curriculum to Prevent Obesity in Innercity Teens by Taitano, Rachael Tatiana, Phd from Colorado State University, 1998, 272 pages http://wwwlib.umi.com/dissertations/fullcit/9835036

•

Diet, Activity and Cardiovascular Disease Risk Factors in Western Samoan Men (cholesterol, Blood Pressure, Obesity) by Pelletier, David Louis, Phd from The Pennsylvania State University, 1984, 390 pages http://wwwlib.umi.com/dissertations/fullcit/8429123

•

Differences in Attitudes toward Obesity, Knowledge of Cvd, and Self-efficacy in Catch and Non-catch Physical Educators by Thompson, James Frederick; Ms from University of Houston, 2002, 66 pages http://wwwlib.umi.com/dissertations/fullcit/1409800

•

Differences in Physical Activity, Fitness Knowledge, and Obesity in Secondary Physical Education and Substitute Physical Education Students in Texas by Soukup, Gregory Jason, Sr. Edd from University of Houston, 2002, 75 pages http://wwwlib.umi.com/dissertations/fullcit/3056479

•

Differential Thermogenic Response in Juvenile-onset Type Obesity and Maturityonset Type Obesity (metabolism) by Oddou, William Eugene, Phd from Oregon State University, 1986, 233 pages http://wwwlib.umi.com/dissertations/fullcit/8527793

•

Discriminant Analysis of Variables Affecting Childhood Obesity by Rose, Frank Vincent, Phd from The University of Mississippi, 1988, 111 pages http://wwwlib.umi.com/dissertations/fullcit/8826327

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•

Early and On-time Puberty and the Relationship to Anorexia, Bulimia, and Obesity (menarche, Eating Disorders) by Davis, Emily Clifton, Edd from The University of Memphis, 1994, 172 pages http://wwwlib.umi.com/dissertations/fullcit/9506753

•

Eating Disordered Pathology in Obese Pre-adolescent Children by Tanofsky-kraff, Marian; Phd from The Catholic University of America, 2003, 107 pages http://wwwlib.umi.com/dissertations/fullcit/3067499

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Ecology of Obesity in West Philadelphia Adolescents by Gordon-larsen, Penny, Phd from University of Pennsylvania, 1997, 370 pages http://wwwlib.umi.com/dissertations/fullcit/9814876

•

Education and Self-efficacy As Predictors of Weight Loss among Older Obese Females (older Women) by Vaiani, Livia Lee, Edd from Rutgers the State University of New Jersey - New Brunswick, 1991, 174 pages http://wwwlib.umi.com/dissertations/fullcit/9130059

•

Effectiveness and Cost-effectiveness of Behavioral Self-help Manuals for the Treatment of Obesity a Study of Degree of Therapist Contact and Group Versus Individual Format by Pezzot-pearce, Terry Dianne; Phd from The University of Manitoba (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK47236

•

Effectiveness of a Self-administered Assertiveness Training Manual As a Component of a Counselor-directed Weight Loss Program (obesity, Bibliotherapy) by Mishou, Lucretia Virginia, Edd from University of Maine, 1985, 156 pages http://wwwlib.umi.com/dissertations/fullcit/8614146

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Effects of Obesity on the Clinical Judgments by Christian and Non-christian Mental Health Professionals by Duncan Hassel, Tricia Lynn; Psyd from Fuller Theological Seminary, School of Psychology, 2002, 65 pages http://wwwlib.umi.com/dissertations/fullcit/3046364

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Energy Balance, Obesity and Acculturation among Hualapai Indian Women of Arizona (indian Women) by Teufel, Nicolette Irene, Phd from University of Colorado at Boulder, 1989, 247 pages http://wwwlib.umi.com/dissertations/fullcit/8923537

•

Essential Hypertension in Urban Adolescents: the Epidemiology of Obesity and Physical Fitness by Wilson, Susan Louise, Phd from Southern Methodist University, 1982, 253 pages http://wwwlib.umi.com/dissertations/fullcit/8216732

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Evaluation of a Supervised Exercise Component in the Behavioral Control of Obesity by Blum, Miriam Deborah, Phd from The Pennsylvania State University, 1981, 233 pages http://wwwlib.umi.com/dissertations/fullcit/8205882

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Examination of a Self Concept Construct in Overweight and Non-overweight Elementary School-age Children (obesity) by Fisher, M. Lynette, Phd from Oklahoma State University, 1985, 100 pages http://wwwlib.umi.com/dissertations/fullcit/8611525

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Exercise Adherence in Obese Women: Evaluation of Two Intervention Strategies by Naylor, Patti-jean, Phd from University of Victoria (canada), 1992, 189 pages http://wwwlib.umi.com/dissertations/fullcit/NN79943

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Factors Related to Visceral Obesity in Black and White Women during Mid-life by Rexroad, Annette Reif; Phd from University of Pittsburgh, 2002, 270 pages http://wwwlib.umi.com/dissertations/fullcit/3054331

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Family of Origin and Support System Factors Affecting Body Weight Management in Gastroplasty Patients (obesity) by Brower, Penny Lynn, Phd from The University of Iowa, 1991, 171 pages http://wwwlib.umi.com/dissertations/fullcit/9212857

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Family Patterns of Obesity: the Use of Weight As a Predictor of Family Type by Barker, Brenda Crabtree, Phd from Texas Woman's University, 1989, 77 pages http://wwwlib.umi.com/dissertations/fullcit/9008481

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Food Behaviors and Obesity among Urban American Indian Women (health, Diet, Disease, Diabetes, New World Syndrome) by Kay, Nina W., Phd from Southern Methodist University, 1986, 235 pages http://wwwlib.umi.com/dissertations/fullcit/8616217

•

Household Characteristics Affecting Childhood Obesity by Colison, Charlene V. Ms from D'youville College, 2002, 84 pages http://wwwlib.umi.com/dissertations/fullcit/1410116

•

Human Leptin in Obesity and Diabetes: Anthropometric, Metabolic and Genetic Determinants by Wauters, Machteld; Phd from Universitaire Instelling Antwerpen (belgium), 2002, 268 pages http://wwwlib.umi.com/dissertations/fullcit/3042003

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Hypnotherapy and Client Suitability for the Treatment of Obesity by Cochrane, Gordon John, Edd from The University of British Columbia (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/f2118229

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Hypnotherapy and Client Suitability for the Treatment of Obesity by Cochrane, Gordon; Edd from The University of British Columbia (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NK66878

•

Independent Associations among Abdominal Obesity, Cardiorespiratory Fitness, Liver Fat and Lipid Variables in Men by Nguyen-duy, Thanh-binh; Msc from Queen's University at Kingston (canada), 2002, 64 pages http://wwwlib.umi.com/dissertations/fullcit/MQ73069

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Insulin and Cyclical Obesity in the Dormouse, Glis Glis by Melnyk, Roman Bohdan; Phd from University of Toronto (canada), 1981 http://wwwlib.umi.com/dissertations/fullcit/NK50313

•

Is There a Relationship between Bmi, Dietary Intake, and Parent's Report of Food Preferences of Obese Hispanic Toddlers? by Popejoy, April Pauline; Ms from Texas Woman's University, 2003, 90 pages http://wwwlib.umi.com/dissertations/fullcit/1413513

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Lipid Metabolism during Exercise in Beta-2 Adrenoceptor Gln27glu Polymorphism Homozygous Obese Women by Macho Azcarate, Tatiana; Dr from Universidad De Navarra (spain), 2002, 200 pages http://wwwlib.umi.com/dissertations/fullcit/f674689

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Logoanalysis As a Group Treatment for Existential Vacuum and Weight Loss in Obese Women by Horton, Robert Craig, Phd from University of Southern California, 1983 http://wwwlib.umi.com/dissertations/fullcit/f2688741

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•

Mapping Genes for Complex Traits: Obesity, Diabetes, Hypertension, and Dyslipidemia on the Pacific Island of Kosrae by Shmulewitz, Dvora; Phd from The Rockefeller University, 2002, 165 pages http://wwwlib.umi.com/dissertations/fullcit/3053194

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Measures of Therapeutics in the Treatment of Obesity by Kennedy, Christine Joy; Phd from University of Louisiana at Monroe, 2002, 124 pages http://wwwlib.umi.com/dissertations/fullcit/3062279

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Mitochondrial Proton Leak and Uncoupling Protein Expression in Transgenic Mice and Human Obesity by Monemdjou, Shadi; Phd from University of Ottawa (canada), 2002, 143 pages http://wwwlib.umi.com/dissertations/fullcit/NQ67976

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Mortality, Survivorship and Longevity in American Samoa, 1950 to 1981 (cardiovascular, Hypertension, Diabetes, Obesity, Cancer) by Crews, Douglas Earl, Phd from The Pennsylvania State University, 1985, 176 pages http://wwwlib.umi.com/dissertations/fullcit/8516013

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Motivational Characteristics Associated with Attrition in Worksite Obesity Treatment by Leshine, Paula L., Phd from University of Pennsylvania, 1986, 342 pages http://wwwlib.umi.com/dissertations/fullcit/8703234

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No Laughing Matter: Experiencing Obesity by Howard, Dorothy E., Phd from Boston University, 1987, 663 pages http://wwwlib.umi.com/dissertations/fullcit/8709640

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Obese-child-families: a Psychological Study by Fieman, Lawrence S., Edd from Boston University School of Education, 1983, 137 pages http://wwwlib.umi.com/dissertations/fullcit/8319890

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Obesity and Health Care Utilization by Zizza, Claire Ann; Phd from The University of North Carolina at Chapel Hill, 2002, 145 pages http://wwwlib.umi.com/dissertations/fullcit/3061745

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Obesity and Social Marketing: a Life Style Approach to Product Design and Market Segmentation. by Lewis, David Leroy, Phd from Georgia State University, 1978, 171 pages http://wwwlib.umi.com/dissertations/fullcit/7815559

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Obesity and Weight Loss in Weight Watchers: a Study of Deviance and Resocialization by Wernick, Sarah, Phd from Columbia University, 1973, 212 pages http://wwwlib.umi.com/dissertations/fullcit/7329875

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Obesity As a Factor in Self-concept and Attitude toward Physical Fitness and Exercise by Brown, Venie Edward, Edd from The University of Mississippi, 1971, 113 pages http://wwwlib.umi.com/dissertations/fullcit/7125680

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Obesity in Persons with Diabetes: a Sociological Analysis by Braitman, Leonard Edward, Phd from The University of Chicago, 1980 http://wwwlib.umi.com/dissertations/fullcit/T-27562

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Obesity in the United States: Stratifying Factors. by Benbrook, Sandra Leigh, Phd from University of Southern California, 1976 http://wwwlib.umi.com/dissertations/fullcit/f3611494

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Obesity: an Investigation of Personality Characteristics of Patients Participating in a Behaviorally-oriented Supplemented Fasting Program by Spiegelberg, Jane Slater, Phd from Kent State University, 1988, 176 pages http://wwwlib.umi.com/dissertations/fullcit/9332877

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On the Role of the Enteroinsular Axis in Obesity by Chan, Catherine Barbara; Phd from The University of British Columbia (canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL35053

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Organismic Characteristics and Psychosocial Functioning: Is Obesity a Risk Factor in Adolescents' Psychosocial Adjustment? by Sukariyah, Muhamad Bassam, Phd from Indiana University, 1992, 227 pages http://wwwlib.umi.com/dissertations/fullcit/9310361

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Patient Responsibility and Obesity in Determining Helping Behavior of Students in the Health Professions (patient Education, Nursing Students, Medical Students) by Kahan, Miriam Rhea, Phd from University of California, Los Angeles, 1992, 212 pages http://wwwlib.umi.com/dissertations/fullcit/9317422

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Patterns of Influence of Some Known Correlates of Obesity in Middle-class Black Women by Scott, Mildred Ware, Phd from University of Maryland College Park, 1980, 210 pages http://wwwlib.umi.com/dissertations/fullcit/8105137

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Perceptual/conceptual Disturbances in Anorexia Nervosa and Obesity by Garner, David M; Phd from York University (canada), 1975 http://wwwlib.umi.com/dissertations/fullcit/NK25712

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Personality Correlates and Psychosocial Dimensions of Obesity in Women: a Profile Analysis of Optifast Participants by Kayloe, Judith C., Phd from Kent State University, 1989, 186 pages http://wwwlib.umi.com/dissertations/fullcit/8919780

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Physical, Psychological, Behavioral and Family Factors Predicting Weight Loss and Weight Loss Maintenance in Morbidly Obese Children and Adolescents (obesity, Childhood Obesity) by Miller, Lisa Alison, Phd from Depaul University, 1991, 325 pages http://wwwlib.umi.com/dissertations/fullcit/9136823

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Physician Self-efficacy in the Treatment of Obesity by Stoffelmayr, Amy Stern, Phd from Michigan State University, 1994, 140 pages http://wwwlib.umi.com/dissertations/fullcit/9512148

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Predicting Attrition and Adherence in a Very Low Calorie Diet Behaviorally-based Treatment Program for Obesity by Kitto, Gary C., Phd from Kansas State University, 1992, 255 pages http://wwwlib.umi.com/dissertations/fullcit/9221988

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Primary Prevention of Atherosclerosis and Obesity in Young Adults Using Dietary and Educational Interventions by Matvienko, Oksana Alexandrovna; Phd from Iowa State University, 2002, 138 pages http://wwwlib.umi.com/dissertations/fullcit/3061845

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Psychological Methods of Obesity Reduction in Adolescent Girls by Carmichael, John Alexander; Phd from University of Victoria (canada), 1975 http://wwwlib.umi.com/dissertations/fullcit/NK25522

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Psychological Type and Obesity by Harris, Clifton Tumlin Bud, Jr., Phd from Georgia State University, 1985, 200 pages http://wwwlib.umi.com/dissertations/fullcit/8521695

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Racial Differences in Obesity between Black and White Women in the United States, 1986--1994 by Rucker, Toni Denise; Phd from University of Michigan, 2000, 202 pages http://wwwlib.umi.com/dissertations/fullcit/9977252

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Relationship between Habitual Physical Activity and Direct/indirect Costs among Overweight and Obese Adults by Wang, Feifei; Phd from University of Michigan, 2002, 104 pages http://wwwlib.umi.com/dissertations/fullcit/3068988

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Relationship between Weight Loss and Body Image in Obese Individuals Seeking Weight Loss Treatment by Reas, Deborah Lynn; Phd from Louisiana State University and Agricultural & Mechanical College, 2002, 85 pages http://wwwlib.umi.com/dissertations/fullcit/3069730

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Resistance Training and Therapist Contact in a Maintenance Program for Mild to Moderate Obesity by Binks, Martin; Phd from Fairleigh Dickinson University, 2002, 205 pages http://wwwlib.umi.com/dissertations/fullcit/3034808

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Resting Metabolic Rates in Child-onset and Adult-onset Obese Women by Summerfield, Liane M., Phd from University of Maryland College Park, 1989, 198 pages http://wwwlib.umi.com/dissertations/fullcit/8924238

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School-based Obesity Intervention by Wolf, Marlin Christian, Jr., Phd from Temple University, 1986, 274 pages http://wwwlib.umi.com/dissertations/fullcit/8627536

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Second-order Change Through Brief Therapy among Obese Clients of a Universitybased Weight Management Program by Munro, Janice Fay; Edd from University of Missouri - Saint Louis, 2002, 151 pages http://wwwlib.umi.com/dissertations/fullcit/3049604

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Sensitivity to Reward: a Factor in Overeating and Overweight by Strachan, Shaelyn Margaret; Ma from York University (canada), 2002, 101 pages http://wwwlib.umi.com/dissertations/fullcit/MQ71625

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Shedding the Obese Role: a Three-year Study of Twenty Obese Females, Ages 13-53, Who Had Surgery for Weight Loss (gastric Bypass, Intestinal Bypass) by Wrobel, Sylvia Burroughs, Phd from University of Kentucky, 1989, 221 pages http://wwwlib.umi.com/dissertations/fullcit/9014238

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Social Work Practitioners' Comparative Evaluations of Obese and Lean Clients by Lehmann, Barbara A. Phd from Case Western Reserve University, 2001, 133 pages http://wwwlib.umi.com/dissertations/fullcit/3036345

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Sociocultural Aspects of Body Image: Explorations of Body Size and Weight Problem Perceptions in a Southern Rural Community (obesity, Overweight) by Wright, Erma J., Phd from The University of North Carolina at Chapel Hill, 1986, 194 pages http://wwwlib.umi.com/dissertations/fullcit/8628275

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Socio-demographic Factors As Predictors of Obesity among Women by Hall, Claudia A., Phd from Mississippi State University, 1989, 113 pages http://wwwlib.umi.com/dissertations/fullcit/8917062

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Strength Training, Exercise and Diet in the Management of Obesity in Children by Yu, Chung Wah; Phd from Chinese University of Hong Kong (people's Republic of China), 2002, 351 pages http://wwwlib.umi.com/dissertations/fullcit/3066613

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Stress, Self-efficacy, Problem-solving Skills, and Levels of Obesity in Women: a Test of Group Differences by Kuntz, Carol B., Psyd from Central Michigan University, 1993, 95 pages http://wwwlib.umi.com/dissertations/fullcit/9334902

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Studies on Insulin Secretion and Glucose Tolerance in Experimental Obesity and Diabetes by Dalpé-scott, Marthe; Phd from University of Ottawa (canada), 1983 http://wwwlib.umi.com/dissertations/fullcit/NK65707

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The Addition of a Cognitive Intervention Based on Individualized Assessment to a Behavioral Intervention for Obesity by Delucia, Janice Lynn, Phd from The Pennsylvania State University, 1987, 243 pages http://wwwlib.umi.com/dissertations/fullcit/8727994

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The Association between Television Viewing and Related Video Activities, Physical Activity Level, and Weight in Obese and Nonobese Adolescents: a Multicultural Analysis by Albi, Kathleen Marie, Phd from University of Denver, 1997, 250 pages http://wwwlib.umi.com/dissertations/fullcit/9804090

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The Association between Television Viewing and Related Video Activities, Physical Activity Level, and Weight, in Obese and Nonobese Fourth-grade Children by Hammerberg, Diane Dehnert, Phd from University of Denver, 1992, 170 pages http://wwwlib.umi.com/dissertations/fullcit/9237590

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The Association of Obesity and Disability in Middle-aged Americans by Harrison, David Jeffrey; Phd from The University of North Carolina at Chapel Hill, 2002 http://wwwlib.umi.com/dissertations/fullcit/f653089

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The Association of Obesity and Physical Fitness with Inflammatory Markers in Children by Isasi, Carmen Rosa; Phd from Columbia University, 2002, 102 pages http://wwwlib.umi.com/dissertations/fullcit/3037721

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The Caloric Content, Macronutrient Composition, and Portion Size of Children's Meals in Restaurants: a Risk Factor for Childhood Obesity? by Hyder, Melissa L. Phd from University of Missouri - Kansas City, 2003, 69 pages http://wwwlib.umi.com/dissertations/fullcit/3085593

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The Child's Concept of Obesity by Wolfle, Jane Allen, Phd from Virginia Polytechnic Institute and State University, 1981, 174 pages http://wwwlib.umi.com/dissertations/fullcit/8121508

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The Cultural Beliefs and Values That Influence Perceptions of African American Mothers Regarding Obesity in Their Daughters by Senatore, Pamela Nichelle; Mph from California State University, Fresno, 2002, 97 pages http://wwwlib.umi.com/dissertations/fullcit/1412229

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The Development of an Instrument for the Assessment of Obesity-related Cognitions (obesity Cognition Inventory, Cognition Testing, Health Knowledge) by Christian, David Earl, Phd from Utah State University, 1992, 108 pages http://wwwlib.umi.com/dissertations/fullcit/9301633

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The Eating Disorder Inventory and Other Predictors of Successful Symptom Management in Bulimic and Obese Women Following an Inpatient Treatment

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Program Employing an Addictions Paradigm by Carroll, Mary Theodora, Phd from University of South Florida, 1993, 271 pages http://wwwlib.umi.com/dissertations/fullcit/9323672 •

The Effect of a Split Exercise Session on Excess Postexercise Oxygen Consumption in Young Obese Women (women) by Bronstein, Maridy Mcneff, Edd from The University of Alabama, 1992, 95 pages http://wwwlib.umi.com/dissertations/fullcit/9225803

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The Effect of a Token Reinforcement on Physical Activity, Body Weight, and Selfconcept of Overweight and Obese Adolescents with Serious Emotional Disturbances/behavioral Disorders (emotional Disturbances, Behavioral Disorders) by Hall, Darlene York, Phd from University of Idaho, 1992, 172 pages http://wwwlib.umi.com/dissertations/fullcit/9312472

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The Effect of Client Obesity on Counselor Clinical Judgments by Young, Laura Mim, Phd from The Catholic University of America, 1983, 121 pages http://wwwlib.umi.com/dissertations/fullcit/8313957

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The Effect of Pre-exercise Caffeine Ingestion on Free Fatty Acid Mobilization and Metabolism at Rest, During, and Following Prolonged Submaximal Exercise in Lean and Obese Volunteers by Kamimori, Gary H., Phd from Southern Illinois University at Carbondale, 1985, 203 pages http://wwwlib.umi.com/dissertations/fullcit/8610570

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The Effects of a Moderate Progressive Aerobic Exercise Program on the Severely and Morbidly Obese by Zelasko, Chester John, Phd from Michigan State University, 1987, 74 pages http://wwwlib.umi.com/dissertations/fullcit/8801890

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The Effects of Aerobic Exercise and Slow-speed Strength Training on Body Composition and Weight Loss in Obese Women by Silver, Francine J. Phd from Fairleigh Dickinson University, 2002, 176 pages http://wwwlib.umi.com/dissertations/fullcit/3036299

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The Effects of Assertion Training and Husband Involvement in the Behavioral Treatment of Obesity by Elterman, Michael Frank; Phd from Queen's University at Kingston (canada), 1981 http://wwwlib.umi.com/dissertations/fullcit/NK55934

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The Effects of Obesity on Skill Attainment in Twelve Year-old Children As Measured by Performance on Three Novel Manipulative Skills by Andrews, Stanley Cooper, Edd from The University of Mississippi, 1987, 99 pages http://wwwlib.umi.com/dissertations/fullcit/8724391

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The Effects of Some Sociological and Social Psychological Factors on the Outcome of Obesity Treatment Programs by Barker, Matilda Inez Nowell, Phd from University of California, Riverside, 1985, 216 pages http://wwwlib.umi.com/dissertations/fullcit/8520622

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The Efficacy of Geometric Versus Cluster Analysis on Assessing Psychosocial Adjustment Related to Obesity by Wong, Shu-yeng, Phd from Indiana University, 1980, 154 pages http://wwwlib.umi.com/dissertations/fullcit/8029264

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The Genetics of Obesity and Obesity-related Factors among Samoans by Choh, Audrey C. Phd from State University of New York at Albany, 2002, 167 pages http://wwwlib.umi.com/dissertations/fullcit/3072613

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The Impact of Kin, Friend and Neighbor Networks on Infantile Obesity. by Bryant, Carol Anne, Phd from University of Kentucky, 1978, 139 pages http://wwwlib.umi.com/dissertations/fullcit/7824381

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The Influence of Hyperandrogenism, Obesity and Infertility on the Psychosocial Health and Well-being of Women with Polycystic Ovary Syndrome by Mccook, Judy Griffin; Phd from University of Michigan, 2002, 150 pages http://wwwlib.umi.com/dissertations/fullcit/3042131

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The Management of Obesity in Everyday Life. by Hoover, Michael Coleman, Phd from The University of Tennessee, 1976, 319 pages http://wwwlib.umi.com/dissertations/fullcit/7710773

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The Medicalization Vs. the Politicization of Obesity in Women by Spencer, Barbara Duffy, Phd from St. John's University (new York), 1987, 567 pages http://wwwlib.umi.com/dissertations/fullcit/8914737

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The Ppar Pathway to Obesity and Type-2 Diabetes: a Multi-locus Approach to Understanding Complex Disease by Moffett, Susan Patricia; Phd from University of Pittsburgh, 2002, 176 pages http://wwwlib.umi.com/dissertations/fullcit/3068712

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The Prediction of Relapse from Obesity Treatment by Self-efficacy for Coping, Stress and Rationality of Beliefs by Macaulay, Mickle John, Edd from Northern Illinois University, 1998, 105 pages http://wwwlib.umi.com/dissertations/fullcit/9922468

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The Process of Overcoming Compulsive Overeating and Obesity by Spitalny, Gloria, Edd from Boston University School of Education, 1982, 142 pages http://wwwlib.umi.com/dissertations/fullcit/8300780

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The Relationship between Insulin Resistance Syndrome, Body Fat Distribution, Dietary Intake Variables and Subclinical Atherosclerosis in Obese Type 2 Diabetes by Hegazi, Refaat Mohamed; Phd from University of Pittsburgh, 2002, 179 pages http://wwwlib.umi.com/dissertations/fullcit/3054285

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The Relationship between Milk Consumption and Obesity among Low-income Hispanic Children Participating in the Special Supplemental Nutrition Wic Program by Grafton, Laura; Mph from Southern Connecticut State University, 2002, 57 pages http://wwwlib.umi.com/dissertations/fullcit/1410370

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The Relationship between the Age at Onset of Self-perceived Obesity and Personal Orientation by Creekmore, Carol Lynn, Edd from The University of Tulsa, 1984, 107 pages http://wwwlib.umi.com/dissertations/fullcit/8412635

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The Relationship of Obesity and Body Fat Distribution to Non-insulin Dependent Diabetes Mellitus in a Navajo Community by Hall, Teri-christine Ruan, Phd from The University of Wisconsin - Madison, 1990, 92 pages http://wwwlib.umi.com/dissertations/fullcit/9027499

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The Relationship of Obesity-related Metabolic Hormones and Prognosis in Young Women with Breast Cancer by Johnson, Lisa Godefroy; Phd from University of Washington, 2003, 89 pages http://wwwlib.umi.com/dissertations/fullcit/3079227

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The Relationship of Social Support Contracting to Worksite Weight Control (weight Loss, Obesity Treatment) by Wynne, Kathleen Louise, Edd from University of South Carolina, 1986, 188 pages http://wwwlib.umi.com/dissertations/fullcit/8704657

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The Relationship of Weight Loss in an Obesity Treatment Program to Expectancy of Success and to Selected Attribution Constructs by Niemeier, Dianne Frances, Phd from University of Southern California, 1982 http://wwwlib.umi.com/dissertations/fullcit/f91110

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The Relationships of Alexithymia, Body Image Distortion, and Body Image Dissatisfaction to Binge Eating in Obese Populations by Delaney, Letty Ward Lauffer; Phd from New York University, 2002, 221 pages http://wwwlib.umi.com/dissertations/fullcit/3045719

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The Relative Effects of Sociocultural Factors on Levels of Obesity among Africanamerican Women by Jordan, Audrey Denise; Phd from Virginia Commonwealth University, 1999, 192 pages http://wwwlib.umi.com/dissertations/fullcit/9938296

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The Role of Cognitive Thought Processes in the Maintenance of Weight Loss (obesity, Relapse) by Herb, Ellyn D., Phd from The Fielding Institute, 1985, 240 pages http://wwwlib.umi.com/dissertations/fullcit/8602957

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The Role of Obesity Screening and Health Risk in Canadians: Application of the National Cholesterol Education Program Adult Treatment Panel Iii Guidelines by Ardern, Christopher Ian; Msc from York University (canada), 2002, 108 pages http://wwwlib.umi.com/dissertations/fullcit/MQ77131

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The Social Stratification of Obesity: Bodily Assets and the Stylization of Health by Chang, Virginia Wei-wen; Phd from The University of Chicago, 2003, 280 pages http://wwwlib.umi.com/dissertations/fullcit/3077046

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The Symbolic World of Obesity: a Study of the Rhetorical Visions of Obese Women by Madden, Mary Jane, Phd from University of Minnesota, 1982, 174 pages http://wwwlib.umi.com/dissertations/fullcit/8301964

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The Validity of Convenient Obesity Indicators by Marshall, J. Dru; Phd from University of Alberta (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/NL55544

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The Validity of Convenient Obesity Indicators by Marshall, June Dru, Phd from University of Alberta (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/f3162852

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Treatment Acceptability for the Prevention of Obesity and Type 2 Diabetes Mellitus: the Effects of Ethnicity, Weight, and Genetic Predisposition by Thaw, Jean Marie; Phd from Louisiana State University and Agricultural & Mechanical College, 2002, 97 pages http://wwwlib.umi.com/dissertations/fullcit/3069735

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Use of Behavioral Stage-of-change and Preference for Weight Loss Interventions As a System for Client-matching Treatment of Obesity by Ostendorf, Wendy R., Edd from University of Sarasota, 1999, 187 pages http://wwwlib.umi.com/dissertations/fullcit/9929538

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Utilization of the Health Belief Model in Predicting Dieting and Exercising Behavior of Obese and Non-obese Adolescents by O'connell, Janelle Kay, Phd from The University of Toledo, 1984, 202 pages http://wwwlib.umi.com/dissertations/fullcit/8429739

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Variables Impacting Obesity among African American Women in Omaha (nebraska) by Blanchard, Shirley Ann; Phd from The University of Nebraska - Lincoln, 2002, 201 pages http://wwwlib.umi.com/dissertations/fullcit/3074068

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Weight Loss Maintenance in a Multicomponent Behavioral Treatment of Obesity by Barger, Sharon Ann, Phd from The University of Wisconsin - Madison, 1987, 383 pages http://wwwlib.umi.com/dissertations/fullcit/8712405

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Weight-based Stigmatization and Ideological Beliefs: Relation to Psychological Distress in an Obese, Treatment-seeking Population by Friedman, Kelli E. Phd from Duke University, 2002, 114 pages http://wwwlib.umi.com/dissertations/fullcit/3041578

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Why Lose? a Study of the Motivational Variables Operative in the Decision of Obese Individuals to Instigate Weight Reduction Activity (health Behavior, Decisionmaking) by Cregheur, Lucille Annette, Dsw from University of California, Berkeley, 1986, 184 pages http://wwwlib.umi.com/dissertations/fullcit/8624691

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Women, Weight, and Embodiment: an Intuitive Inquiry into Women's Psychospiritual Process of Healing Obesity by Coleman, Becky; Phd from Institute of Transpersonal Psychology, 2000, 470 pages http://wwwlib.umi.com/dissertations/fullcit/9969177

Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.

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CHAPTER 5. CLINICAL TRIALS AND OBESITY Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning obesity.

Recent Trials on Obesity The following is a list of recent trials dedicated to obesity.8 Further information on a trial is available at the Web site indicated. •

Diet and Physical Activity Interactions in Obesity Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The projects funded by this grant, primarily focus on environmental factors that promote weight-gain in the general human population, and how to modify these factors, to prevent further weight-gain in the future. In the coming years, the researchers at the University of Colorado-HSC hope to gain an understanding as to how small changes in diet and physical activity can be achieved and sustained to prevent weight-gain. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00067964

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Effects of Leptin Treatment on Weight Loss Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): Rockefeller University

8

These are listed at www.ClinicalTrials.gov.

218 Obesity

Purpose - Excerpt: This is a double blind placebo controlled clinical study designed to determine the effects of leptin on the changes that occur in the body during weight loss achieved by a very low calorie diet. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00050791 •

Effects of Oral Glucosamine on Insulin and Blood Vessel Activity in Normal and Obese People Condition(s): Obesity; Insulin Resistance Study Status: This study is currently recruiting patients. Sponsor(s): National Center for Complementary and Alternative Medicine (NCCAM) Purpose - Excerpt: This study will examine whether glucosamine affects the way the body responds to insulin. Insulin is a hormone that causes the body to use glucose (sugar). Insulin does not work as well in overweight people, causing a condition called insulin resistance. Insulin also increases the flow of blood into muscle by opening inactive blood vessels. This study will test whether glucosamine, a nutritional supplement that many people take to treat arthritis, can cause or worsen insulin resistance or change how blood vessels react to insulin in normal weight and overweight people. Healthy normal weight and overweight volunteers between 21 and 65 years of age may be eligible for this study. Candidates will be screened with a brief physical examination, medical history, and blood and urine tests. After screening, participants will have three additional outpatient clinic visits for the following procedures: Visit 1 - Glucose clamp test to measure the body's response to insulin: For this procedure, a needle is placed in a vein of each arm, one for drawing blood samples, and one for infusing glucose and a potassium solution. The glucose is infused continuously during this 4-hour test and blood is drawn frequently to monitor glucose and insulin levels. After the test, blood glucose levels are monitored for another 2 hours to make sure they remain at an adequate level to prevent hypoglycemia (low blood sugar). - Blood flow measurement: Blood flow in the brachial artery of the arm is measured to assess how many capillaries (very small blood vessels) are being used to supply nutrients and oxygen to the muscle in the forearm. This test is done at the same time as the glucose clamp test. Blood flow is measured using a technique called contrast ultrasound. A small amount of contrast agent consisting of gas-filled bubbles the size of red blood cells is infused over 10 minutes through one of the catheters placed in the vein for the glucose clamp test. The contrast agent is infused twice, once at the beginning of the glucose clamp test and once at the end of the test. The contrast material creates a signal in response to ultrasound that provides information about the distribution of capillaries in the forearm. - Assignment to medication group: Participants are randomly assigned to take either glucosamine or placebo three times a day by mouth for 6 weeks. At the end of the 6 weeks, no study drug is taken for 1 week, and then participants "cross-over" medications, those who took glucosamine for the first 6 weeks take placebo for the next 6 weeks and vice versa. Visits 2 and 3 For these visits, the glucose clamp test and blood flow measurements are repeated. Visit 2 is scheduled at the end of the first 6week treatment period, and Visit 3 is scheduled at the end of the second 6-week treatment period. Phase(s): Phase I

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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065377 •

Exercise Training in Obesity-prone Black and White Women Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Overweight premenopausal Black and White women are randomized to either diet-only, diet+aerobic or diet+resistance exercise training. Diet/behavior intervention, with or without the aerobic or resistance exercise training, will be provided throughout the 18 months of study. Major outcomes will include measures of perceived and physiologic difficulty of exercise (cardiac, ventilatory, electromyographic responses to standardized exercise tasks); aerobic fitness; strength fitness; and spontaneous freeliving energy expenditure (all derived from doubly labeled water). The results will provide insight into the effectiveness of, and the mechanisms by which, different types of exercise training can improve physical fitness, spontaneous engagement in physical activities of daily living and, in turn, weight-loss maintenance. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00067873

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FFA Metabolism in Different Types of Human Obesity Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: We will give intravenous fat molecules to help us understand how the fat that is released from peoples fat cells is used. This will be done when people are eating, not eating and walking. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00068900

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Genetics, Metabolism and Weight Loss in Older, Obese Veterans Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): Department of Veterans Affairs Medical Research Service Purpose - Excerpt: This study is designed to determine whether sequence variation in the lipoprotein lipase (LPQ) gene affects the amount of weight loss and metabolic responses during a hypocaloric diet treatment for overweight and obese (BMI=25-35 kg/m2), older (50-65 yrs), sedentary veterans. Study Type: Interventional Contact(s): see Web site below

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Web Site: http://clinicaltrials.gov/ct/show/NCT00018330 •

Girls Health Enrichment Multi-Site Studies (GEMS) Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To develop and test interventions to prevent obesity by decreasing weight gain during the high-risk transitional period from pre-puberty to puberty in African-American girls who are at high risk for developing obesity. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000615

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Heart Disease Risk Factors in African Americans Condition(s): Coronary Disease; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: It is unknown if obesity contributes to the development of heart disease in African American men and women. This study was created to determine whether there is a relationship between sex and body size and the incidence of heart disease in African American men and women. Researchers will attempt to associate obesity with the presence of heart disease risk factors. Risk factors that will be studied include; total body fat, body fat distribution, fat content of the blood (triglyceride concentration, low density lipoproteins [LDL], and high density lipoproteins [HDL]), how fast fat is removed from the blood, and how well insulin works in the body. Scientific studies have shown that obesity and increased levels of fat content in the blood are important risk factors for heart disease in Caucasian women. However, similar studies in African American women have failed to show the same correlation. In fact, it appears that African American women in all three body weight groupings, nonobese, overweight, and obese experience high death rates due to heart disease. In addition, prior research has shown that obese African American men tend to have elevated levels of fat in the blood while African American women have normal blood fat levels. Therefore, if high levels of triglycerides (fat found in the blood) are not seen in non-diabetic obese African American women, it cannot be considered a risk factor in this population. This suggests that studies conducted on Caucasian women may not provide insight into heart disease risk factors in African American women. The study will take 120 healthy nondiabetic African American men and women (ages 18-50) grouped by sex (60 men and 60 women) and body mass index 3 subgroups; nonobese, overweight and obese). Diabetes undeniably increases the risk of heart disease. Therefore patients suffering from diabetes will not be included in the study. Candidates for the study will undergo a series of tests and examinations over 5 outpatient visits. Subjects will have body fat analyses, resting energy expenditure measurements, an EKG (electrocardiogram), and specific blood tests. Researchers believe this study will provide significant insight into the causes of obesity and heart disease in African Americans. Study Type: Observational

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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001853 •

Impact of Non-Commercialism Policy in Seattle Schools Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This pilot study on the impact of a non-commercialism policy in Seattle schools will assess and evaluate obesity-related health outcomes of a real-life policy decision, recently voted on and adopted by the Seattle School Board. The policy reduces the exposure to advertising and other marketing pressures, including those from commercial food vendors. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00063700

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Inhibition of Intestinal Glucose Absorption by the Bioflavonoid Quercetin in the Obese and in Obese Type 2 Diabetes Condition(s): Diabetes Mellitus; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Postprandial hyperglycemia and the resultant hyperinsulinemia contribute to the cardiovascular complications seen in obesity and in type 2 diabetes. Epidemiological studies suggest that slow absorption of carbohydrates dampens glucose and insulin peaks, and reduces cardiovascular morbidity. The polyphenol quercetin is the most abundant flavanoid in plant-derived foods, and is sold as a dietary supplement. In vitro, quercetin is a potent and reversible inhibitor of glucose transport by the intestinal glucose transporter GLUT2. In vivo quercetin inhibits post absorptive glucose peaks in obese, diabetic rats. We hypothesize that quercetin blunts intestinal glucose absorption in humans, and attenuates postprandial hyperglycemia. We propose to test, in a double blind placebo controlled study, whether coadministration of 1 or 2 grams of quercetin with 50 grams of glucose will reduce plasma glucose concentrations during a 6 hour 50g oral glucose tolerance test in non-diabetic obese subjects and in obese type 2 diabetic subjects. Study subjects will be 19-65 years with a body mass index greater than or equal to 30, without complications of diabetes, or on any medication other than oral hypoglycemic agents and aspirin. We will study 16 obese non diabetic subjects and 16 obese type 2 diabetic. Each subject will have 3 oral glucose tolerance tests, and will serve as his or her own control. We will compare the peak plasma glucose concentrations achieved during oral glucose tolerance tests and the area under the curve of plasma glucose to determine whether quercetin inhibits glucose absorption in humans. Such inhibition may partially explain the protective effects of plant derived foods on cardiovascular disease, and enable us to use quercetin or related compounds to dampen intestinal glucose absorption. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below

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Web Site: http://clinicaltrials.gov/ct/show/NCT00065676 •

Metabolic Differences of Overweight Children and Children of Overweight Parents Condition(s): Cardiovascular Disease; Hypertension; Non Insulin Dependent Diabetes Mellitus; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: This study focuses on the way weight is gained. Individuals who gain weight primarily in their midsection (visceral weight) are at an increased risk for developing diabetes and high blood pressure. Research has shown that African Americans suffer more often from high blood pressure, diabetes (non-insulin dependent), and heart disease than Caucasian Americans. These conditions lead to significant numbers of deaths and diseases associated with and made worse by obesity. African American women in particular suffer from obesity and the associated conditions of obesity more than any other race or gender. However, it is unknown if the conditions seen in African American women are a result of the obesity or differences in their insulin sensitivity, glucose disposal, or fat metabolism. This study will compare body composition, total and resting energy expenditure, and glucose disposal of obese African American and Caucasian children and of non-obese children of obese African American and Caucasian parents, to characterize the timing and nature of factors that may contribute to the prevalence of obesity and its complications. Patients participating in this study will be followed for 15 years and be evaluated every 5 years during the study. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001522

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Metformin to Treat Obesity in Children with Insulin Resistance Condition(s): Hyperinsulinemia; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: This study will examine the safety and effectiveness of the medicine metformin to help overweight children control their food intake, weight, insulin, cholesterol, and triglyceride (blood fat) levels. Obesity and high insulin levels can lead to high blood pressure, diabetes, high cholesterol and triglyceride levels and heart disease. Metformin-approved by the Food and Drug Administration to treat adults with type 2 diabetes mellitus-helps lower insulin levels and may control weight gain in adults. Overweight children 6 to 11 years old who are in general good health may be eligible for this study. Children will be studied at the National Institutes of Health in Bethesda, Maryland, and at the Phoenix Indian Medical Center and the Gila River Reservation in the Phoenix, Arizona area. Candidates will have a medical history and physical examination and fasting blood test, and will provide a 7-day record of their food intake as part of the screening process. Those enrolled will be randomly assigned to receive either metformin or placebo (a look-alike tablet with no active medicine) twice a day for a six month period. After the 6 month study period, all children will be offered the opportunity to take metformin for another 6 months. Participants will be hospitalized for 2-3 days for the following procedures: history and physical

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examination; fasting blood test; several urine collections; X-ray studies to determine bone age and amount of body fat and muscle; magnetic resonance imaging (MRI) scan to measure body fat; "hyperglycemic clamp study" to evaluate insulin resistance; food intake testing; nutrition consultation; resting metabolic rate; and a "doubly labeled water" test. For the hyperglycemic clamp study, a catheter (thin flexible tube) is inserted into a vein in each arm. A sugar solution is given through one tube and blood samples are drawn every 5 minutes through the other to measure insulin. For the food intake testing, the child is asked about his or her hunger level, then given various foods he or she may choose to eat, then questioned again at various intervals both during and after finishing eating about his or her hunger level. The doubly labeled water study involves drinking "heavy water" (water which is enriched to have special kinds of hydrogen and oxygen). Urine specimens are collected 2, 3 and 4 hours after drinking the water. The child also drinks a special milk shake called a Scandishake and repeats the calorie intake and hunger study. (Two food intake studies are done on separate days.) One week after the heavy water test, additional urine samples are collected one week later. After completing the tests, the child will begin treatment with metformin or placebo, plus a daily vitamin tablet. Participants will be followed once a month with a brief history and physical examination, including a blood test. After 6 months, all of the tests described above will be repeated. All children who complete the second round of tests-both those who took metformin and those who took placebo-will be offered metformin for an additional 6 months and will be seen once a month for follow-up evaluations. Parents will not be told which children received metformin and which received placebo until all children in the study complete the first 6 months of the trial. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005669 •

Methods for Measuring Insulin Sensitivity Condition(s): Diabetes Mellitus; Healthy; Hypertension; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Patients with high blood pressure, diabetes, and who are overweight are known to have defects in the way their body responds to insulin. The purpose of this study is to develop better methods for measuring the way body tissue responds to insulin and sugar (glucose). Researchers are planning to study four groups of patients. 1. Normal volunteers 2. Patients who have mild to moderate high blood pressure 3. Patients who are overweight 4. Patients who have mild to moderate diabetes controlled with oral medication In this study patients and volunteers will undergo two separate tests designed to determine how well insulin is working in the body. The first test is called a glucose clamp test. Patients will have two needles placed in the veins of their arms. One needle will be used to take blood samples, the other needle will be used to inject doses of sugar (glucose) and insulin. The second test is called the frequently sample intravenous glucose tolerance test. In this test patients will have sugar (glucose) injected into their veins followed by a slow injected dose (infusion) of insulin. Researchers will periodically take blood samples during the test. Patients participating in the study will not directly benefit from it. However, the information gained from this

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study may be useful for improving the diagnosis and therapy of diseases such as diabetes, obesity, and high blood pressure (hypertension). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001625 •

Modifying the Home Television Watching Environment Condition(s): Obesity; Body Weight Changes Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The purpose of this study is to determine if limiting television and computer time will result in a stabilization or smaller increase in BMI, lower energy intake, and increased physical activity in 4-7 year old obese (>85th BMI percentile) children over two years. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065052

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Nutritional Restriction and Activity Thermogenesis Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: These studies will provide us with enormous insight regarding how obese patients adapt energetically during negative energy balance. We will gain fundamental information regarding the metabolic implications of combining food restriction with a walking program compatible to that advocated by statutory agencies. These studies will lead to improved understanding of the energetic adaptation that occurs during negative energy balance and how best to treat patients with obesity. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065338

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Obesity Prevention in African American School Children Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Obesity is the second leading preventable cause of disease and death in the United States. Low socioeconomic status (SES) and minorities are disproportionately affected. Obesity prevention among children and adolescents is a public health priority. Schools have been identified as key settings for obesity prevention; however, most health education interventions have had only a moderate effect on body weight. We propose a randomized intervention trial (pilot study) to test

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the feasibility and effectiveness of a school-based, environmental obesity prevention program in urban low-SES African American students. Schools, students and their families, and local communities will be involved to promote healthy eating and physical activity (HEPA) for prevention of childhood obesity. Six Chicago public schools will be randomly assigned as intervention (4 schools) and controls (2 schools). Focus group studies will assess needs and barriers for promotion of HEPA and guide the intervention. The intervention group will receive a School Environment Enrichment (SEE) program to modify the school physical and social environment, targeting food service, recess, physical education (PE) and school climate, and a Community Support & Environment Modification (CSEM) program, involving local corner and chain grocery stores to promote healthy eating among students and their families. Family involvement will be included for 5th and 6th graders, who will be followed for two years, to test ways to modify family environment. To assess the intervention effectiveness, multilevel data will be collected from schools (eg, food service, recess and PE), students (eg, body weight, eating and physical activity), parents (eg, family food purchasing practices) and communities (eg, available choices of snack foods in local stores). In addition, process evaluation data will be collected to assess the feasibility and acceptance (participation and satisfaction) of various intervention components by the target audience. The primary outcome variable is change in students' body weight status; secondary outcomes include changes in students' eating behavior and physical activity and changes in target environmental factors. In addition, cost-effectiveness of the intervention will be determined. If the intervention proves effective, a full-scale study will be developed. Findings from this study will provide insights into the prevention of obesity among low-SES and minority students. Study Type: Interventional Contact(s): Youfa Wang, PhD, MD 312 355 3382 [email protected]; Lisa Tussing, MS 312 996 0995 [email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00061165 •

Prevalence of carbohydrate intolerance in lean and obese children Condition(s): Obesity; Glucose Intolerance; Diabetes; Acanthosis Nigricans Study Status: This study is currently recruiting patients. Sponsor(s): National Center for Research Resources (NCRR) Purpose - Excerpt: The prevalence of obesity in children is reaching epidemic proportions. Excess adiposity is more than just a cosmetic problem, having substantial metabolic consequences. Insulin resistance, hyperinsulinemia, impaired glucose tolerance, and frank diabetes are often seen in obese children. In this study the prevalence of impaired glucose (carbohydrate) tolerance in lean children with a family history of diabetes and obese children with acanthosis nigricans with or without a family history of diabetes mellitus will be studied. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000112

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Safety and Efficacy of Xenical in Children and Adolescents with Obesity-Related Diseases Condition(s): Diabetes Mellitus; Hypertension; Metabolic Disease; Obesity; Sleep Apnea Syndrome Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: Obesity is a condition affecting one-third off the U.S. population and is a major risk actor for the development of Type 2 diabetes, hyperlipidemia (increased levels of fat in the blood), hypertension (high blood pressure), and other disorders of the heart and lungs. Individuals with the onset of obesity during childhood or adolescence are at an increased risk of obesity-related, diseases, both during adolescence and later in adult life. African American girls and women are at an increased risk for obesity, and have substantial rates of obesity-related diseases and causes of death. Further, many African American adult women fail to respond to many of the therapeutic approaches used to treat obesity. At present there are no medical therapies proven effective for the correction of severe obesity in children or adolescents. One medication that may have a favorable risk-benefit ratio in pediatric populations is Orlistat (Xenical, Hoffmann LaRoche). Orlistat works by preventing the action of enzymes in the digestive process, interfering with the absorption of approximately 1/3 of the fat eaten in the diet. Xenical appears to be effective for reducing weight and obesity-associated diseases in obese adults. Researchers propose to determine the safety, tolerability, and efficacy of Xenical in 12-17 year old severely obese African American and Caucasian children and adolescents who have one or more obesity-related disease (hypertension, hyperlipidemia, sleep apnea, hepatic steatosis, insulin resistance, impaired glucose tolerance, or Type 2 diabetes). Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001723

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Strength Training Following Gastric Bypass for Obesity Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: We will assess whether undesirable loss of lean tissue following gastric bypass surgery for obesity can be minimized by protein supplementation and exercise training. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065013

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Strength Training for Obesity Prevention Condition(s): Obesity Study Status: This study is currently recruiting patients.

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Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Recent obesity prevalence increases have made obesity prevention a clear and pressing public health issue. The average US. woman gains about 0.5 kg per year. Overweight women aged 25 to 44 have a higher prevalence of significant weight gains (BMI increases of > 5 kg/m2) than men or older or thinner women. The difficulty in successfully losing weight and maintaining weight loss has resulted in recommendations from several expert panels to advise overweight and mildly obese individuals free of co-morbidities to avoid weight gains rather than to lose weight. Physical activity is observed to decline with age while caloric intake remains stable or declines slightly. There is strong observational evidence that physical activity could prevent or attenuate age associated fat gains. This randomized, controlled behavioral intervention trial will test the hypothesis that regular participation in a twice weekly strength training program over 2 years, can prevent age associated body fat increases (total and abdominal fat) in 80 overweight to mildly obese premenopausal women between the ages of 25 and 44 years, compared to a 'standard care' group (n=80). The overall aim of the study is to prevent body fat gains and to reduce health risks associated with obesity. Treatment effects will be assessed for insulin sensitivity, blood pressure, blood lipids, muscle strength, and psychosocial predictors of strength training adherence. The innovation of this approach rests in its simplicity and the minimal time requirement for full participation (2 exercise sessions weekly). A preliminary study of this innovative approach resulted in 88% exercise session attendance over 12 months and maintenance of treatment effects on total body fat percentage to the end of pilot study measurements (9 months). This supports the feasibility and potential for long term efficacy of the proposed intervention approach. The long-term implication of success in this efficacy trial would be that this modest behavior change could prevent the fat gains and associated co-morbidities commonly observed in midlife women. Phase(s): Phase II Study Type: Interventional Contact(s): Robyn A Abear, MS 612-625-8056 [email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00030160 •

Supplemental Calcium in Overweight People Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: This study will examine the health effects of calcium supplements in overweight adults. overweight adults often eat a diet low in calcium. Some studies have found low calcium intake in people who have some of the medical problems often seen in overweight adults. This study will see if extra calcium improves the health of overweight adults. Volunteers in general good health 18 years of age or older who are overweight (body mass index equal to or greater than 25 kilograms per square meter of body surface) may be eligible for this study. Women who are pregnant or breastfeeding may not participate. The study includes four visits, described below. Visit 1 Volunteers will be screened for participation in the study with a medical history, physical examination, and blood and urine tests. At home, they will collect a 24-hour urine sample; fill out questionnaires to assess their average calcium intake; and record their food intake for 7 days. Those enrolled in the study will continue with the next 3 visits. Visit 2 Participants will complete a physical activity questionnaire, have their food diary

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reviewed, and meet with a dietitian for nutritional counseling. Triceps fold thickness and waist and hip circumferences will be measured three times. Body composition will be analyzed by a DEXA study. For this procedure, the subject lies on a flat table while a small dose of X-rays is passed through the body. Participants will be randomly assigned to take either calcium carbonate (1500 mg/day) or placebo capsules twice a day by mouth for 2 years. (The placebo looks like the calcium capsules but contains no calcium.) They will receive a 6-month supply of study capsules during visit 2 and return to NIH every 6 months for the next supply. They will also be sent questionnaires by mail every 3 months to complete information about health problems and how often the study capsules are being taken. Visits 3 and 4 Visit 3 is scheduled after participants have taken the study capsules for 1 year; visit 4 is scheduled after 2 years (the end of the study). At each of these visits, participants will have a DEXA scan, blood and urine tests, blood pressure measurements, and measurements of height, weight, waist and hip circumference. They will complete questionnaires about their medical history, side effects of the study medications, dietary calcium intake, and physical activity, and they will meet with one of the study investigators to talk about any concerns regarding the study. At the fourth visit, participants will answer some additional questions about their study participation and return the Diet History Questionnaire that was mailed to them before the visit. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00030238 •

Type 2 Diabetes Primary Prevention for At Risk Girls Condition(s): Obesity; Diabetes Mellitus; Prediabetic State Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Purpose: To evaluate two approaches to prevent obesity and type 2 diabetes in young girls. The Need: We are experiencing an epidemic of childhood obesity. Rates of obesity have doubled to tripled in the past two decades, with the highest rates among poor and ethnic minority girls. Type 2 diabetes (what used to be called adult-onset diabetes) is now showing up in overweight children, and more children are manifesting precursors of heart disease and stroke. Our Two Approaches: 1. A state-of-the-art nutrition education program with monthly newsletters mailed to girls and their parents and quarterly evening lectures/educational events at school sites, including cooking demonstrations and games to improve nutrition and increase physical activity. 2. After-school dance classes held five days per week all year long at school sites from the time school lets out until 6PM. Dance classes will include a 1-1.5 hour supervised homework study hall each day, and emphasize both traditional ethnic dances and popular dance. Participants: Second, third and fourth grade girls and their families will be eligible to participate. All activities are free of charge. To be able to perform a valid evaluation, to be able to accommodate all girls at their own school, and to be fair about which girls receive which program, families who wish to participate will be randomly selected to participate in either one program or the other (nutrition education or dance classes). Each family will participate for two years. Evaluation: Trained Stanford staff will perform all evaluation procedures with participating families

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in their own homes at the beginning and every six months. Families will be compensated for their participation. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00063674 •

APEX: Adiposity Prevention by Exercise in Black Girls Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine whether a one year afternoon exercise program will reduce adiposity in African American girls, ages 8 to 10. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006405

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Family Based Interventions: Preschool Children and Parent Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To assess the efficacy of a 2-year family-based weight prevention program in a cohort of overweight preschool children and overweight parent pairs. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00024843

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Genetic Determinants:Low HDL, High Triglycerides, Obesity Condition(s): Cardiovascular Diseases; Atherosclerosis; Hypertriglyceridemia; Obesity; Heart Diseases Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To conduct genetic studies of the metabolic syndrome which is characterized by very low levels of high density lipoprotein cholesterol (HDL-C), hypertriglyceridemia, and obesity. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049881

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Heavy Metals, Obesity and Cardiovascular Risk - Ancillary to Look AHEAD Condition(s): Diabetes Mellitus, non-insulin dependent; Cardiovascular Diseases; Obesity; Myocardial Infarction; Heart Diseases; Diabetes Mellitus Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To evaluate the relationship of baseline toenail chromium concentrations to weight loss, as well as the interaction between heavy metals and the beneficial effects of weight loss. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00031213

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Lifestyle, Adiposity and Cardiovascular Health in Youths Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the influences of diet and physical activity (PA) on total body fatness and regional fat distribution and the relationship of these to risk factors of cardiovascular disease during adolescence. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006402

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Obesity Prevention after Smoking Cessation in Menopause Condition(s): Obesity; Menopause Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute on Aging (NIA) Purpose - Excerpt: This study addresses the high risk of weight gain associated with smoking cessation in women. The obesity prevention pilot study is designed for the primary prevention of weight gain that can lead to overweight in normal-weight women, that can progress to obesity in women who are already overweight, and for the prevention of additional weight gain in obese women with BMI greater than or equal to 30.0. Fat and other macronutrient intake, specifically, sugar, complex carbohydrates, and protein, are analyzed as a target for individually tailored, weight control intervention following smoking cessation in Caucasian and African American women. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00064961

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Obesity Treatment in a Managed Care Setting Condition(s): Obesity; Weight Loss Study Status: This study is no longer recruiting patients.

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Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The aim of the present study is to evaluate the effectiveness of two different delivery formats for weight management in a managed care setting. Mailbased weight counseling and phone-based weight counseling will be compared to each other and a control condition. Primary outcomes are participation rates in programs, weight change, and cost. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00062985 •

Physical Activity and Childhood Obesity Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To measure associations between physical activity and obesity in a large, population-based cohort of children. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00063544

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The Assessment of a weight-gain agent for the Treatment of Olanzapine-Associated Anti-obesity Agent in Patients with Schizophrenia, Schizophreniform Disorder, Schizoaffective Disorder, and Bipolar I Disorder Condition(s): Schizophrenia; Psychotic Disorders; Bipolar Disorder Study Status: This study is no longer recruiting patients. Sponsor(s): Eli Lilly and Company Purpose - Excerpt: Olanzapine is currently marketed for the treatment of schizophrenia and acute manic episodes with bipolar 1 disorder. This Anti-obesity Agent is currently marketed for the management of obesity. In this study, the Anti-obesity Agent is being tested to see if it can treat weight gain that may be associated with taking olanzapine. The purposes of this study are to determine the safety of olanzapine when given in combination with the Anti-obesity Agent and any side effects that might be associated with it and whether weight-gain agent can help treat weight gain that may be associated with taking olanzapine. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00044187

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Theory-based Interventions for Smoking and Obesity (Challenge) Trial Condition(s): Smoking; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Neurological Disorders and Stroke (NINDS)

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Purpose - Excerpt: The purpose of this study is to examine a new theory for understanding the processes that govern behavior change by observing how people's beliefs and feelings about smoking cessation or weight loss change as they participate in smoking cessation or weight control programs. This study also seeks to improve the ability of treatment programs to help people maintain changes in their behavior. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00040287 •

Visceral Adiposity and CVD Risk in Women Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity; Diabetes Mellitus Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To investigate the influence of total body fat and visceral fat on risk factors of diabetes and cardiovascular disease (CVD) in black and white women. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00021879

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Adiposity and Fat Patterning in Black Americans Condition(s): Heart Diseases; Diabetes Mellitus; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine the relationships of obesity and fat patterning with morbidity and mortality in Black Americans. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005248

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Biobehavioral Determinants of Obesity in Black Women Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity; Telangiectasis Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine the biobehavioral determinants of obesity in Black as compared with white women. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005386

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Cardiovascular System in Obesity: Effect of Treatment Condition(s): Heart Diseases; Obesity; Vascular Diseases Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the long-term efficacy of the combination therapy of phentermine and fenfluramine in conjunction with diet, exercise, and behavior modification in the treatment of simple, moderate obesity. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000506

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Central Obesity and Disease Risk in Japanese Americans Condition(s): Cardiovascular Diseases; Heart Diseases; Atherosclerosis; Hypertension; Obesity; Diabetes Mellitus, non-insulin dependent; Hyperinsulinism; Insulin Resistance; Coronary Arteriosclerosis; Diabetes Mellitus Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To conduct a longitudinal study of central obesity and related risk factors found to be associated with hypertension and atherosclerotic cardiovascular disease (ASCVD) in a previously-examined cross-sectional cohort of second-generation Japanese Americans and in a newly-recruited cohort of third generation Japanese Americans. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005365

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Effectiveness of primary care physicians in delivering weight control counseling Condition(s): Obesity Study Status: This study is completed. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This randomized clinical trial will determine the efficacy of physicians providing weight control advice to their overweight and obese patients in primary care practice. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00017706

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Genetic Epidemiology of Blood Lipids and Obesity - Ancillary to NGHS Condition(s): Cardiovascular Diseases; Heart Diseases; Coronary Disease; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI)

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Purpose - Excerpt: To conduct a genetic epidemiologic study of the coronary heart disease (CHD) risk factors of blood lipids and obesity in Black and white girls who participated in the NHLBI-supported National Growth and Health Study (NGHS). The study was ancillary to NGHS. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005345 •

Genome Scan for Obesity in a Multi-Ethnic Sample Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To scan the genome for obesity in a multi-ethnic sample. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00037271

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Health Effects of Liposuction in Overweight Women with Elevated Insulin Levels, Impaired Glucose Tolerance and/or Type 2 Diabetes Condition(s): Glucose Intolerance; Hyperinsulinemia; Non Insulin Dependent Diabetes Mellitus; Obesity Study Status: This study is completed. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: This study is for women who have already decided to undergo liposuction at Georgetown University Medical Center in Washington, D.C. To take part in this study, a woman must first meet with the plastic surgeons there, and be accepted by them to have liposuction. This study will investigate whether large volume liposuction improves risk factors for heart disease in overweight women with type 2 (adult onset) diabetes, impaired glucose tolerance, or elevated blood insulin levels. Large volume liposuction is the surgical removal of at least 10 pounds (4.5 kg) of body fat, usually from the abdomen, hips or chest. Risk factors for heart disease include high blood pressure and elevated levels of blood lipids (cholesterol and triglycerides), blood glucose (sugar), and blood insulin. Subjects who participate in all parts of this study will receive a total of $930.00. overweight women 18 years or older with high blood insulin levels, impaired glucose tolerance, or type 2 diabetes, who are planning to have large volume liposuction performed at Georgetown University Medical Center in Washington, D.C., may be eligible for this study. For a subject to be accepted into this study, she must first meet with the plastic surgeons at Georgetown University Medical Center, and they have to agree to perform large volume liposuction. The decision that someone is suitable for liposuction is not under the control of the NIH or of any NIH investigator. Those enrolled will undergo the following procedures at four separate times - before undergoing liposuction, 4 weeks after surgery, 4 months after surgery and 1 year after surgery: - Body measurements - taken with calipers to measure several skinfold thicknesses (the width of a fat fold) and with a tape measure to measure the circumference of parts of the body. - Urine sample and 6-hour urine collection - to test for pregnancy and to evaluate kidney function. - Glucose tolerance test - measures

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insulin sensitivity and how the body uses sugar, how well insulin works, and insulin sensitivity. The procedure involves placement of two catheters (thin, flexible tubes) through a needle into a vein in each arm. Sugar water is infused into one catheter and 20 minutes into the test a small amount of insulin is injected. Blood samples are drawn from the other catheter at frequent intervals for a total of 5 hours. - Electrocardiogram (ECG) and echocardiography - measure the heart's electrical activity and function. Abdominal computerized tomography (CT) scan - produces images for measuring body fat in the abdomen. (not done at the 4-week visit). Takes about half an hour to complete. - DXA X-ray - measures body fat, muscle and bone mineral content. Takes about half an hour to complete. - Bod Pod - capsule-like device used to determine the proportion of body weight composed of fat and non-fat tissue. Takes less than 10 minutes - Bioelectric impedance analysis device - measures the proportions of body fat based on electrical conduction of a small electric current. Takes 2-3 minutes. - 24-hour blood pressure monitoring - a device attached to a blood pressure cuff strapped to the arm measures blood pressure every 15 to 30 minutes continuously for 24 hours. - Vascular reactivity tests - a blood pressure cuff is inflated for about 4 minutes before deflating, providing information on the function of the small blood vessels in the skin, as well as an idea of the function level of small blood vessels elsewhere in the body. Takes half an hour. Blood samples - collected to evaluate kidney and liver function and to measure body lipids, such as cholesterol, minerals, and other substances. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005760 •

NEW DAY: Nutrition, Exercise, Weight loss, Diabetes And You Condition(s): Diabetes Mellitus, Type 2; Obesity Study Status: This study is completed. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This clinical trial examines whether the addition of individual sessions of a motivational intervention to a state-of-the art behavioral group weight loss intervention for overweight women with Type 2 diabetes improves the weight losses and glycemic control outcomes. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00007800

•

Obese Patients with or without Comorbidities Condition(s): Obesity; Weight Loss Study Status: This study is completed. Sponsor(s): Sanofi-Synthelabo Purpose - Excerpt: To assess the effects of weight loss and weight maintenance over a period of two years when prescribed with a hypocaloric diet in obese patients with or without comorbidities Phase(s): Phase III

236 Obesity

Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029861 •

Obese Patients with Type 2 Diabetes Condition(s): Obesity; Diabetes Mellitus, Non-Insulin-Dependent; Obesity in Diabetes Study Status: This study is completed. Sponsor(s): Sanofi-Synthelabo Purpose - Excerpt: To assess the effect on weight loss and weight maintenance over a period of one year when prescribed with a hypocaloric diet in obese patients with Type 2 Diabetes Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029848

•

Obese Patients with Untreated Dyslipidemias Condition(s): Obesity; Dyslipidemia Study Status: This study is completed. Sponsor(s): Sanofi-Synthelabo Purpose - Excerpt: To assess the effect on weight loss and weight maintenance over a period of one year when prescribed with a hypocaloric diet in obese patients with untreated dyslipidemia Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029835

•

Overweight Adults--Ethnic, SES and Behavioral Influences Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine the effects of ethnicity, socioeconomic status (SES) and behavior in overweight adults. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005752

•

Randomized Trial of Dietary Intervention Therapy in Obese Hypertensives (DITOH) Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Obesity Study Status: This study is completed.

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Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the effects on blood pressure of dietary intervention, restricting caloric intake to 600 calories per day for 16 weeks compared to a control diet of 1200 calories per day in obese hypertensives. Secondary aims included a study of psychological characteristics at baseline and during the weight loss and maintenance phases of the study. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000515 •

School and Family-Based Obesity Prevention for Children Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To conduct an integrated, multiple-component, school- and community-based intervention targeting both primary and secondary prevention of obesity among third-fourth-and fifth-graders ("School- and Family-Based Obesity Prevention for Children"). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005750

•

Sex Steroids, Obesity and Lipids in Adolescent Females Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity; Hypercholesterolemia Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To prospectively explore the relationships of endogenous sex steroid hormones and obesity and their interactions with lipoprotein cholesterol and apolipoprotein levels in nine and ten year old Black and white adolescent girls for five years during puberty. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005210

•

Strong Heart Study Analyses Obesity and Lipoproteins Condition(s): Cardiovascular Diseases; Heart Diseases; Atherosclerosis; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine the relationship of obesity and body fat distribution to lipoprotein concentrations in members of the Strong Heart Study. Study Type: Observational

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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005510

Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “obesity” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •

For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/

•

For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html

•

For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/

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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm

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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm

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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm

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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp

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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm

•

For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/

•

For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm

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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm

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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm

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•

For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm

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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm

•

For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials

241

CHAPTER 6. PATENTS ON OBESITY Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “obesity” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on obesity, we have not necessarily excluded non-medical patents in this bibliography.

Patents on Obesity By performing a patent search focusing on obesity, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We

9Adapted

from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.

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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on obesity: •

.alpha.-Blocking agents in the treatment of obesity Inventor(s): Milavec; Maria (St. Louis, FR), Wagner; Heribert (Pfeffingen, CH) Assignee(s): Sandoz Ltd. (Basel, CH) Patent Number: 4,239,763 Date filed: June 22, 1979 Abstract: Alpha-blocking agents, especially 9,10-dihydroergot-peptide alkaloids, are anti-obesity agents. Excerpt(s): By way of example the following compositions may be used in the method of the invention.... If desired tablets may be made with 0.25 mg or 15 mg of dihydroergotoxin mesylate in analogous manner.... The above-mentioned tablets are useful in the treatment of obesity when administered 3 to 5 times a day. Web site: http://www.delphion.com/details?pn=US04239763__

•

Acute and chronic electrical signal therapy for obesity Inventor(s): Flesler; Melina (Misgav, IL), Mika; Yuval (Zichron Yaakov, IL), Belsky; Ziv (Haifa, IL), Ben Arie; Yaakov (Haifa, IL), Darvish; Nissim (Tzrufa, IL), Ben-Haim; Shlomo (Cesarea, IL) Assignee(s): Impulse Dynamics N.V. (Curacao, NL) Patent Number: 6,600,953 Date filed: December 11, 2000 Abstract: Apparatus is provided for treating a condition such as obesity. The apparatus includes a set of one or more electrodes, which are adapted to be applied to one or more respective sites in a vicinity of a body of a stomach of a patient. A control unit is adapted to drive the electrode set to apply to the body of the stomach a signal, configured such that application thereof increases a level of contraction of muscle tissue of the body of the stomach, and decreases a cross-sectional area of a portion of the body of the stomach for a substantially continuous period greater than about 3 seconds. Excerpt(s): The present invention relates generally to treatment of obesity, and specifically to invasive techniques and apparatus for treating obesity.... Invasive treatments for obesity are often recommended for patients with a body mass index (mass/height.sup.2 [kg/m.sup.2 ]) which is greater than 35 or 40. For such patients, their weight is commonly associated with increased risk of heart disease, diabetes, and arthritis. Preferably, the invasive treatments are accompanied by changes in lifestyle, such as improved eating habits and an appropriate exercise regimen.... U.S. Pat. No. 6,067,991 to Forsell, U.S. Pat. No. 5,601,604 to Vincent, and U.S. Pat. No. 5,234,454 to Bangs, and U.S. Pat. Nos. 5,449,368, 5,226,429 and 5,074,868 to Kuzmak, which are incorporated herein by reference, describe mechanical instruments for implantation in or around the stomach of an obese patient. Web site: http://www.delphion.com/details?pn=US06600953__

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•

Alkylated etiocholanolones erythropoietic agent

and

use

as

an

anti-diabetic,

anti-obesity

and

Inventor(s): Krsek; George (Culver, IN) Assignee(s): Progenics, Inc. (New York, NY) Patent Number: 4,602,008 Date filed: December 14, 1984 Abstract: 16-Alkylated and 16-alkylated-7-hydroxy 5.beta.-androstan-3-ol-17-one, and the esters and ethers thereof, are used as an anti-diabetic, anti-obesity and erythropoietic agent in mammals. Excerpt(s): The major function of the adrenal gland is to regulate metabolism in the body so that an intermittent intake of food can be regulated to maintain a constant metabolite supply to the cells. This is accomplished by producing steroid hormones which can control the conversion of incoming nutrients, such as aminoacids, glucose and fats into storage depots from which they can thereafter be released or interchanged, allowing a continuous flow of optimum energy and growth factors to the cells.... The steroid hormones are divided mainly into three classes. The first is glucocorticoids (cortisol), also known as gluconeogenic or diabetogenic steroids, which can convert aminoacids into glucose for direct use or store the glucose as glycogen for later use. Cortisol can therefore have an anti-anabolic effect through the depletion of aminoacids needed for protein synthesis and a diabetogenic effect through the direct release of glucose from the glycogen store.... A glucocorticoid excess, resulting from an excess of the pituitary hormone, adrenal cortico-trophic hormone (ACTH), which controls cortisol production, causes Cushing's Syndrome, an uncommon disease. Intake of an excess amount of cortisol from pharmacological use of steroids can also cause Cushing's Syndrome or Cushingoid-like disorders (hypercorticosteroidism, or more briefly hypercorticoidism) which are progeric in that they resemble the symptoms of the diseases of aging, e.g. obesity, hypertension, diabetes, renal stones, osteoporosis, mental disorder, menstrual disturbance, susceptibility to infection and poor wound healing. Web site: http://www.delphion.com/details?pn=US04602008__ •

Amino acid derivatives, pharmaceutical compositions containing these compounds and their use in the treatment of obesity Inventor(s): Rudolf; Klaus (Biberach, DE), Eberlein; Wolfgang (Biberach, DE), Engel; Wolfhard (Biberach, DE), Mihm; Gerhard (Biberach, DE), Doods; Henri (Warthausen, DE), Wieland; Heike A. (Biberach, DE), Willim; Klaus-Dieter (Schweinhausen/Hochdorf, DE), Krause; Jurgen (Ummendorf, DE), Dollinger; Horst (Ingelheim, DE), Esser; Franz (Ingelheim, DE), Schnorrenberg; Gerd (Gau-Algesheim, DE), Entzeroth; Michael (Warthausen, DE), Wienen; Wolfgang (Apfingen, DE) Assignee(s): Karl Thomae GmbH (Biberach an der Riss, DE) Patent Number: 5,616,620 Date filed: June 1, 1995 Abstract: Amino acid derivatives, suitable for the treatment of obesity. The following compound is exemplary of the class: (R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl) methyl]-argininamide-acetate.

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Excerpt(s): the tautomers, diastereomers and enantiomers thereof, mixtures thereof and salts thereof, more particularly the physiologically acceptable salts thereof with inorganic or organic acids or bases, and processes for preparing them.... T.sup.1 to T.sup.3, which may be identical or different, denote phenyl groups or 6-membered heteroaryl groups bound via carbon atoms and which each contain one or two nitrogen atoms.... and unless otherwise specified the above-mentioned alkyl and alkoxy moieties may each contain 1 to 3 carbon atoms. Web site: http://www.delphion.com/details?pn=US05616620__ •

Anti-obesity agents Inventor(s): Suzuki; Kunio (Saitama, JP), Nakata; Tadashi (Saitama, JP), Shimizu; Takeshi (Saitama, JP), Enomoto; Kotaro (Saitama, JP) Assignee(s): Institute of Physical and Chemical Research (Saitama, JP) Patent Number: 5,710,143 Date filed: March 27, 1996 Abstract: Disclosed are anti-obesity agents comprising 3-ketosteroidal compounds as defined in the specification. The present invention also discloses pharmaceutical compositions and use of these compounds in the prevention and treatment of obesity. Excerpt(s): This application is a 371 of PCT/JP94/01631 filed Sep. 30, 1994.... The present invention relates to anti-obesity agents, more specifically to anti-obesity agents which comprise as an active ingredient 3-ketosteroid compounds having ketone groups at the C.sub.3 position of the cholestane skeletons.... Obesity is a condition under which the proliferation of tissues of body-composing lipids is increased abnormally. This abnormal condition is produced when energy intake is continuously greater than energy consumption, with the resulting excess energy being converted into neutral lipid which is accumulated in lipid tissues. Web site: http://www.delphion.com/details?pn=US05710143__

•

Anti-obesity agents Inventor(s): Suzuki; Kunio (Saitama, JP), Nakata; Tadashi (Saitama, JP), Shimizu; Takeshi (Saitama, JP), Enomoto; Kotaro (Saitama, JP) Assignee(s): The Institute of Physical and Chemical Research (Saitama, JP) Patent Number: 5,846,962 Date filed: July 21, 1997 Abstract: Anti-obesity agents which comprise 3-ketosteroid compounds as an active ingredient are provided. The anti-obesity agents of the present invention have a high anti-obesity effect with little or no side effects and toxicity. Food products which contain anti-obesity agents comprising 3-ketosteroid compounds as an active ingredient, pharmaceutical compositions which comprise 3-ketosteroid compounds as an active ingredient and pharmaceutically acceptable carriers, and methods for preventing and treating obesity which comprise administering an effective amount of a 3-ketosteroid compound to a human are also provided.

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Excerpt(s): The present invention relates to anti-obesity agents, more specifically to antiobesity agents which comprise as an active ingredient 3-ketosteroid compounds having ketone groups at the C.sub.3 position of the cholestane skeletons.... Obesity is a condition under which the proliferation of tissues of body-composing lipids is increased abnormally. This abnormal condition is produced when energy intake is continuously greater than energy consumption, with the resulting excess energy being converted into neutral lipid which is accumulated in lipid tissues.... Obesity is important as a risk factor of the onset of diseases represented by geriatric diseases from hygienic and cosmetic viewpoints. Harmful influences of obesity have been recognized for a long time in advanced nations. Agents for preventing and/or treating obesity which have been developed until now have side effects or produce unsatisfactory effects. Web site: http://www.delphion.com/details?pn=US05846962__ •

Anti-obesity balloon placement system Inventor(s): Kullas; Karen E. (Taunton, MA), Giusto; Joseph (Warren, RI) Assignee(s): C. R. Bard, Inc. (Murray Hill, NJ) Patent Number: 4,723,547 Date filed: May 7, 1985 Abstract: An anti-obesity balloon and a placement system for the balloon includes a balloon with a needle-pierceable, self-sealing plug and an insertion catheter having a needle at its distal end. The needle is movable between an extended position in which it protrudes distally of the insertion catheter and a retracted position in which it is withdrawn interiorly of the insertion catheter. A handle arrangement is provided at the proximal end of the insertion catheter to control the position of the needle. Means are provided for aspirating and inflating the balloon. The balloon structure and insertion catheter structure protect and enclosed the sharp tip of the needle at all times during insertion and withdrawal of the insertion catheter. The insertion catheter is detachable from the balloon, after the balloon has been inflated in the patient's stomach, in a manner which imposes no force or load on the balloon. Excerpt(s): This invention relates to techniques for treating obesity by placement of a balloon in the patient's stomach to reduce the patient's appetite and control the patient's food intake.... Various techniques and devices have been proposed and used to treat obese patients so as to reduce their weight and to maintain their weight at a reduced, more acceptable level. The techniques have included surgical as well as non-surgical approaches. By way of example, one such surgical procedure involves an abdominal surgical procedure in which the stomach is surgically exposed and then is stapled in a manner to reduce the available volume of the stomach. In another surgical technique the stomach is wrapped in a non-expandable fabric or mesh so that it cannot expand beyond the volume defined by the wrap. Other surgical procedures for the treatment of obesity include shortening or placing shunts in the intestinal tract so as to reduce the time during which food is exposed to the patient's digestive process.... Also among the techniques which have been proposed has been to place a balloon within a patient's stomach so as to occupy a substantial volume of the stomach thereby to limit the available unfilled volume within the stomach and to provide the patient with an early sensation of satiety. The balloon systems which have been proposed have suffered from various difficulties and none is believed to have achieved any practical lasting use. Among the difficulties have been in the valving arrangement for inflating the balloon and for maintaining the balloon in an inflated condition over an extended period of

246 Obesity

time. Additionally, the balloon structures and placement techniques which have been proposed generally have been cumbersome and awkward. It is among the general objects of the present invention to provide an improved anti-obesity balloon and placement system which avoids the difficulties presented by the prior proposed devices. Web site: http://www.delphion.com/details?pn=US04723547__ •

Anti-obesity drugs Inventor(s): Shinitzky; Meir (Kfar Shmaryahu, IL), Shenfeld; Avner (Rehovot, IL) Assignee(s): Senyorina Ltd. (Kfar Shmaryahu, IL) Patent Number: 5,602,164 Date filed: March 18, 1996 Abstract: Obesity is treated by the administration to a subject of a compound having the general formula (I): R.sub.4 --(CH.sub.2).sub.n --CO--N(R.sub.1)--CH(R.sub.2)--CO(-R.sub.3), wherein R.sub.1 represents H or CH.sub.3; R.sub.2 represents a side chain of a naturally occurring amino acid; R.sub.3 represents OH, OCH.sub.2 CH.sub.3 and NH.sub.2; n is 6-18; and R.sub.4 represents CH.sub.3 or a group having the general formula (II): R.sub.3 --CO--CH(R.sub.2)--N(R.sub.1)--CO--, wherein R.sub.1, R.sub.2 and R.sub.3 have the above meanings. The compounds of formula (I) wherein R.sub.4 is a group of formula (II), are novel compounds. Excerpt(s): The present invention is in the field of treatment and prevention of obesity. The present invention provides compositions and methods for the treatment or prevention of such disorders utilizing, as active ingredient, lypophilic derivatives of natural amine acids. Furthermore, the present invention provides certain such novel compounds.... 1. Bar-Tana et al., J. Biol. Chem., 1985, 260, 8404-8410.... 2. Rose-Kakn et al., J. Biol. Chem., 1985, 260, 8411-8415. Web site: http://www.delphion.com/details?pn=US05602164__

•

Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,532,336 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to

Patents 247

recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05532336__ •

Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,552,522 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55:495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are

248 Obesity

largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05552522__ •

Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Heath, Jr. William F. (Fishers, IN), Schoner; Brigitte E. (Monrovia, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,552,523 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout. the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J, of Clin. Nut. 5: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due no the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05552523__

Patents 249

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Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Heath, Jr. William F. (Fishers, IN), Schoner; Brigitte E. (Monrovia, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,552,524 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 52: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05552524__

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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,525,705 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to

250 Obesity

overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer, J. Of Clin, Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Huch of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05525705__ •

Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Heath, Jr. William F. (Fishers, IN), Schoner; Brigitte E. (Monrovia, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,554,727 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fan tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for

Patents 251

cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits. are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05554727__ •

Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Heath, Jr. William F. (Fishers, IN), Schoner; Brigitte E. (Monrovia, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,559,208 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition.

252 Obesity

Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05559208__ •

Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,563,243 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05563243__

Patents 253

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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,563,244 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer, J., of Clin. Nut. 55: 495-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05563244__

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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,563,245 Date filed: January 31, 1995

254 Obesity

Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55:495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05563245__ •

Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,567,678 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the

Patents 255

Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05567678__ •

Anti-obesity proteins Inventor(s): Basinski; Margret (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,567,803 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are

256 Obesity

largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05567803__ •

Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffman; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,569,743 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05569743__

Patents 257

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Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,569,744 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55:495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05569744__

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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,574,133 Date filed: January 31, 1995

258 Obesity

Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Moist specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity inducted pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05574133__ •

Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,580,954 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the

Patents 259

Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05580954__ •

Anti-obesity proteins Inventor(s): Becker; Gerald W. (Fishers, IN), Hale; John E. (Fishers, IN), MacKellar; Warren C. (Plainfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,594,101 Date filed: March 3, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically, the invention relates to anti-obesity proteins that, when administered to a patient, regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med,. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute

260 Obesity

to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05594101__ •

Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,594,104 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55:495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05594104__

Patents 261

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Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,605,886 Date filed: May 17, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05605886__

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Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,691,309 Date filed: February 6, 1995

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Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05691309__ •

Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Hermeling; Ronald N. (Indianapolis, IN), Hoffmann; James A. (Greenwood, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,719,266 Date filed: March 17, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are overweight. Kuczmarski, Amer. J. of Clin. Nutr. 55: 495S-502S

Patents 263

(1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately, these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05719266__ •

Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,851,995 Date filed: August 4, 1997 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can, Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact

264 Obesity

that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05851995__ •

Apparatus and method for neuromodulation therapy for obesity and compulsive eating disorders using an implantable lead-receiver and an external stimulator Inventor(s): Boveja; Birinder R. (P.O. Box 210095, Milwaukee, WI 53221) Assignee(s): none reported Patent Number: 6,611,715 Date filed: April 19, 2001 Abstract: A system and method of neuromodulation adjunct (add-on) therapy for obesity and compulsive eating disorders, comprises an implantable lead-receiver and an external stimulator. Neuromodulation is performed using pulsed electrical stimulation. The external stimulator contains a power source, controlling circuitry, a primary coil, and predetermined programs which control the different levels of therapy. The primary coil of the external stimulator inductively transfers electrical signals to the lead-receiver, which is also in electrical contact with the left vagus nerve. The external stimulator emits electrical pulses to stimulate the vagus nerve according to a predetermined program. In a second mode of operation, an operator may manually override the predetermined sequence of stimulation. The predetermined programs have different levels of control, which is password protected. The external stimulator may also be equipped with a telecommunications module to control the predetermined programs remotely. Excerpt(s): This invention relates generally to medical device used for adjunct (add-on) treatment for obesity, more specifically a medical device used for adjunct (add-on) therapy for obesity and compulsive eating disorders with electrical stimulation neuromodulation using an implanted lead-receiver and an external stimulator.... Obesity results from excessive accumulation of fat in the body. It is caused by ingestion of greater amounts of food than can be used by the body for energy. The excess food, whether fats, carbohydrates, or proteins, is then stored almost entirely as fat in the adipose tissue, to be used later for energy. There can be various causes of obesity including, psychogenic, neurogenic, genetic, and other metabolic related factors. Treatment of obesity depends on decreasing energy input below energy expenditure. Treatment has included among other things various drugs, starvation and even stapling or surgical resection of a portion of the stomach.... Observations on the profound effect of electrical stimulation of the vagus nerve on central nervous system (CNS) activity extends back to the 1930's. In 1988 it was reported in the American Journal of Physiology, that the afferent vagal fibers from the stomach wall increased their firing rate when the stomach was filled. Accordingly, extra-physiologic electrical stimulation of the vagus nerve, from just above the stomach level, should produce appetite supression by causing the patient to experience satiety. Web site: http://www.delphion.com/details?pn=US06611715__

Patents 265

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Aryl-substituted cyclobutylalkylamines for treating obesity Inventor(s): Martin; Keith Frank (Nottingham, GB), Heal; David John (Nottingham, GB) Assignee(s): Knoll Aktiengesesllschaft (Ludwigshafen, DE) Patent Number: 6,127,424 Date filed: April 27, 1998 Abstract: Use of aryl-substituted cyclobutylalkylamines and their pharmaceutically suitable salts for treating obesity and its accompanying disorders are disclosed. Excerpt(s): The invention relates to use of aryl-substituited cyclobutylalkylamines for treating obesity. DE 32 12 682 C2 discloses aryl-substituted cyclobutylalkylamines. The compounds disclosed therein are employed as antidepressants.... and their pharmaceutically suitable salts, for treating obesity and its accompanying disorders.... The compounds used according to the invention have the advantage of very good bioavailability and show a more favorable spectrum of side effects. Web site: http://www.delphion.com/details?pn=US06127424__

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Azaftig, a proteoglycan for monitoring cachexia and for control of obesity Inventor(s): Prasad; Chandan (New Orleans, LA), Figueroa, II; Julio E. (New Orleans, LA), Vijayagopal; Parakat (Kenner, LA) Assignee(s): Board of Supervisors of Louisiana State University and Agricultural and (Baton Rouge, LA) Patent Number: 6,274,550 Date filed: June 28, 1999 Abstract: A proteoglycan ("azaftig") with a molecular weight of approximately 24,000 Dalton has been isolated and partially characterized from the urine of cachectic cancer and non-cancer patients. Azaftig has been shown to bind to receptors on fat cell membranes, and to cause lipolysis. Azaftig does not bind to muscle cell membranes, or cause proteolysis in muscle tissue. Azaftig detection in urine or other body fluids will allow early identification of patients in which weight loss may become a problem. Azaftig may also aid fat loss in humans in which obesity is a threat to health. Excerpt(s): This invention pertains to the detection of a propensity for cachexia and to the control of obesity.... Cachexia is defined as significant weight loss. It occurs commonly in cancer patients and HIV-infected individuals, but can also be caused by hypercatabolism due to cardiac failure (especially, right-sided or biventricular failure), hepatic failure, renal failure, burns, inflammation (including sepsis), infection or tuberculosis. See R. B. Verdery, "Reversible and irreversible weight loss (cachexia) in the elderly," in Textbook of Internal Medicine, 2d Edition (V. T. DeVita et at. eds.), Ch. 523, pp. 2424-2425 (1992); K. I. Marton, "Approach to patient with unintentional weight loss," in Textbook of Internal Medicine, 2d Edition (V. T. DeVita et al. eds.), Ch. 444, pp. 21132115 (1992); R. M. Jordan et al., "Weight loss," in Internal Medicine, 4th Edition (J. H. Stein ed.), Ch. 152, pp. 1260-1262 (1994); C. P. Artz et al., "Burns: Including cold, chemical, and electrical injuries," in Textbook of Surgery, 11th Edition (D. C. Sabiston, Jr. ed.), Ch. 15, pp. 295-322 (1977); E. Braunwald, "Heart Failure," in Harrison's Principles of Internal Medicine, 13th Edition (K. J. Isselbacher ed.), Ch. 195, pp. 998-1009 (1994); and D. W. Foster, "Gain and loss in weight," in Harrison's Principles of Internal Medicine, 13th Edition (K. J. Isselbacher ed.), Ch. 40, pp. 221-223 (1994). Over 50% of cancer and

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HIV-infected patients experience an unintended weight loss of greater than 10% of their baseline weight. Moreover, this weight loss is associated with an increase in morbidity and mortality. Many cachectic patients manifest multiple physiological problems involving the immune system, muscular system, and hepatic function that can be directly related to loss of body weight or wasting. Therefore, understanding the mechanisms of cachexia in patients can lead to better treatment and consequently can have a substantial impact on the quality of life and survival of many cancer and HIV/AIDS patients. See G. O. Coodley et al., "The HIV Wasting Syndrome: a Review," Journal of Acquired Immune Deficiency Syndromes, vol. 7, pp. 681-694 (1994); L. M. Hecker et al., "Malnutrition in patients with AIDS," Nutrition Reviews, vol. 48, pp. 393401 (1990); N. M. Graham et al., "Clinical factors associated with weight loss related to infection with Human Immunodeficiency Virus Type 1 in the multicenter AIDS cohort study," American Journal of Epidemiology, vol. 137, pp. 439-46 (1993); and K. A. Nelson et al., "The cancer anorexia-cachexia syndrome," Journal of Clinical Oncology, vol. 12, pp. 213-25 (1994).... Despite the prevalence of weight loss in cancer patients, the mechanisms underlying the weight loss are unknown. Current explanations for cancer or AIDS-associated weight loss are divided into two general categories--(1) mechanisms that decrease food intake (anorexia); and (2) mechanisms that increase energy expenditure through altered or increased metabolism. Hecker et al., 1990. Any mismatch between energy intake and expenditure will result in a change in weight. Web site: http://www.delphion.com/details?pn=US06274550__ •

Combination anorexiant drug therapy for obesity using phentermine and an SSRI drug Inventor(s): Anchors; J. Michael (16220 Frederick Rd. Suite 210, Gaithersburg, MD 20877) Assignee(s): none reported Patent Number: 5,795,895 Date filed: June 13, 1997 Abstract: This is a new therapy and method used to treat moderate and severe exogenous obesity by combining generic phentermine with an SSRI (selective serotonin reuptake inhibitor) drug in specific doses for a brief or even a long duration, 12 months or more. The preferred drugs for the combination are fluoxetine hydrochloride(Prozac), sertraline (Zoloft), fluvoxamine maleate (Luvox) and trazodone hydrochloride (Desyrel). Excerpt(s): Abenhaim L, Moride Y, Brenot F, et al. Appetite-suppressant drugs and the risk of primary pulmonary hypertension. N Engl J Med. 1996;335:609-616.... Anchors M. Fluoxetine Is a Safer Alternative to Fenfluramine in the Medical Treatment of Obesity. Arch Int Med. 1997;157:1270.... Anchors M. Better Than Phen-Fen PRIMA Publishing, Sacramento Calif. 1997, 250 pages. Web site: http://www.delphion.com/details?pn=US05795895__

Patents 267

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Combination therapy for the treatment of diabetes and obesity Inventor(s): Smith; Roy G. (Westfield, NJ), Cascieri; Margaret A. (East Windsor, NJ), MacIntyre; Euan (Scotch Plains, NJ), MacNeil; Douglas J. (Westfield, NJ), Menke; John G. (Morganville, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 5,908,830 Date filed: October 30, 1997 Abstract: The combination of a metabolic rate modifying agent (e.g., a.beta..sub.3 adrenergic receptor agonist) and a feeding behavior modifying agent (e.g., a NPY5 antagonist) is useful in the treatment of obesity and diabetes, either as compounds, pharmaceutically acceptable salts, pharmaceutical composition ingredients. Methods of treating obesity and diabetes are also described. Excerpt(s): The present invention provides a combination useful in the treatment of obesity and diabetes, either as compounds, pharmaceutically acceptable salts or pharmaceutical composition ingredients. Methods of treating obesity and diabetes are also disclosed. More particularly, the combination of the present invention comprises a metabolic rate modifying agent and a feeding behavior modifying agent; and the pharmaceutically acceptable salts and esters thereof.... Obesity, which can be defined as a body weight more than 20% above the ideal body weight, is a major health concern in Western societies, since it is accompanied by numerous complications such as hypertension, non-insulin dependent diabetes mellitus and arteriosclerosis, which in turn cause heart disease, stroke and premature death. Obesity is the result of a positive energy balance, as a consequence of increased ratio of caloric intake to energy expenditure. The molecular factors regulating food intake and body weight balance are incompletely understood. ›B. Staels et al., J. Biol. Chem. 270(27), 15958 (1995); F. Lonnquist et al., Nature Medicine 1(9), 950 (1995)!. Although the genetic and/or environmental factors leading to obesity are poorly understood, several genetic factors have recently been identified.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines. Web site: http://www.delphion.com/details?pn=US05908830__

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Compositions and methods, for the treatment of body weight disorders, including obesity Inventor(s): Tartaglia; Louis Anthony (Waterstown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 5,741,666 Date filed: August 23, 1994 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight

268 Obesity

regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... Body weight disorders, including eating disorders, represent major health problems in all industrialized countries. Obesity, the most prevalent of eating disorders, for example, is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to other diseases. For example, this disorder is responsible for increased incidences of diseases such as coronary artery disease, stroke, and diabetes. Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity. The nature, however, of the genetic factors which control body composition are unknown, and attempts to identify molecules involved in such control have generally been empiric and the parameters of body composition and/or substrate flux are monitored have not yet been identified (Friedman, J. M. et al., 1991, Mammalian Gene 1:130-144). Web site: http://www.delphion.com/details?pn=US05741666__ •

Compositions containing compounds with adrenergic activity and vegetable extracts of Crataegus and gingko biloba for the treatment of overweight and obesity Inventor(s): Stankov; Bojidar M. (Milan, IT) Assignee(s): Ambros Pharma S.R.L. (Milan, IT) Patent Number: 6,447,818 Date filed: October 10, 2000

Patents 269

Abstract: Compositions containing compounds with adrenergic activity and an extract of Crataegus standardized in flavonoids, combined with an extract of Gingko biloba standardized in flavonglucosides in appropriate weight ratios are suitable for pharmaceutical administration or as food supplements for the treatment of weight loss and obesity in humans. The formulations are appropriate for the administration of the active ingredients in a form that increases patient compliance and the efficacy of the therapeutic or dietary intervention, but reduces the untoward effects of the compounds with adrenergic activity. Excerpt(s): This invention relates to compositions for the treatment of overweight and obesity.... The management of body weight is a complex phenomenon that generally varies according to nutritive equilibrium. The amount of energy introduced with the intake of food and that used by the organism for the maintenance of vital functions (metabolism, respiration, thermoregulation, movement etc.) determines the energetic balance, which, if positive for long-term periods, inevitably leads to increased body weight and obesity.... a) The loss of weight, obtained by a low-calorie diet, gives rise, as a defense mechanism, to an exacerbated attraction for food, especially carbohydrates which are transformed into fat by the organism. Subsequently, the temporary weight loss is replaced by a fast and often uncontrolled weight increase. Web site: http://www.delphion.com/details?pn=US06447818__ •

Compositions for the treatment of body weight disorders including obesity Inventor(s): Tartaglia; Louis Anthony (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,057,109 Date filed: December 14, 1998 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body

270 Obesity

weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight-related processes, including body weight disorders such as obesity and cachexia. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, 1985, Essays in Biochem. 20:110-165; Himms-Hagen J., 1989, Prog. Lipid Res. 28:67-115). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, 1984, Physiol. Rev. 64:1-64). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg M., 1990, Trends Biochem. Sci. 15:108-112; Klaus S. et al., 1991, Int. J. Biochem. 23:791-801). UCP-mediated uncoupling is not only capable of increasing body temperature in coldacclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, 1986, In Brown Adipose Tissue. Trayhurn P., Nicholls D. G., Eds., London, Arnold, p. 269-298; Spiegelman & Flier, 1996, Cell 87:377-389; Hamann & Flier, 1996, Endocrinology 137:2129). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, 1996, Endocrinology 137:2129; Lowell B. B. et al., 1993, Nature 366:740-742; Kopecky J. et al., 1995, J. Clin. Invest. 96:2914-2923; Cummings D. E. et al., 1996, Nature 382:622-626).... In humans, body weight homeostasis is poorly understood, but is also thought to involve regulated thermogenesis (Rothwell & Stock, 1981, Annu. Rev. Nutr. 1:235-56; Segal K. R. et al., 1992, J. Clin. Invest. 89:824-833; Jensen M. D. et al., 1995, Am. J. Physiol. 268:E433-438). However, the importance of the UCP in adult humans is questionable due to the low levels of BAT and consequently the low levels of UCP expression (Huttunen P. et al., 1981, Eur. J. Appl. Physiol. 46:339-345; Cunningham S. et al., 1985, Clin. Sci. 69:343-348; Schulz L., 1987, J. Am. Diet Assoc. 87:761-764; Santos G. C. et al., 1992, Arch. Pathol. Lab Med. 116:1152-1154). Web site: http://www.delphion.com/details?pn=US06057109__ •

Compositions for the treatment of body weight disorders, including obesity Inventor(s): Tartaglia; Louis Anthony (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,121,017 Date filed: October 8, 1997 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments

Patents 271

of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight-related processes, including body weight disorders such as obesity and cachexia. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, 1985, Essays in Biochem. 20:110-165; Himms-Hagen J., 1989, Prog. Lipid Res. 28:67-115). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, 1984, Physiol. Rev. 64:1-64). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg M., 1990, Trends Biochem. Sci. 15:108-112; Klaus S. et al., 1991, Int. J. Biochem. 23:791-801). UCP-mediated uncoupling is not only capable of increasing body temperature in coldacclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, 1986, In Brown Adipose Tissue. Trayhurn P., Nicholls D. G., Eds., London, Arnold, p. 269-298; Spiegelman & Flier, 1996, Cell 87:377-389; Hamann & Flier, 1996, Endocrinology 137:2129). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, 1996, Endocrinology 137:2129; Lowell B. B. et al., 1993, Nature 366:740-742; Kopecky J. et al., 1995, J. Clin. Invest. 96:2914-2923; Cummings D. E. et al., 1996, Nature 382:622-626).... In humans, body weight homeostasis is poorly understood, but is also thought to involve regulated thermogenesis (Rothwell & Stock, 1981, Annu. Rev. Nutr. 1:235-56; Segal K. R. et al., 1992, J. Clin. Invest. 89:824-83.3; Jensen M. D. et al., 1995, Am. J. Physiol. 268:E433-438). However, the importance of the UCP in adult humans is questionable due to the low levels of BAT and consequently the low levels of UCP expression (Huttunen P. et al., 1981, Eur. J. Appl. Physiol. 46:339-345; Cunningham S. et al., 1985, Clin. Sci. 69:343-348; Schulz L., 1987, J. Am. Diet Assoc. 87:761-764; Santos G. C. et al., 1992, Arch. Pathol. Lab Med. 116:1152-1154). Web site: http://www.delphion.com/details?pn=US06121017__

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Compounds for the treatment of obesity Inventor(s): Elliott; Richard L. (East Lyme, CT), Hank; Richard F. (No. Stonington, CT), Hammond; Marlys (Salem, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,514,966 Date filed: January 4, 2001 Abstract: NPY antagonists, methods of using such NPY antagonists and pharmaceutical compositions containing such NPY antagonists. The NPY antagonists are useful for the treatment of NPY mediated disease/conditions including obesity. Excerpt(s): This invention relates to NPY antagonists, particularly NPY-5 antagonists, and pharmaceutical compositions containing such antagonists and the use of such antagonists to treat, for example, obesity, feeding disorders, as well as other NPY mediated diseases/conditions in mammals, including humans, dogs, cats and horses.... Neuropeptide Y (NPY), a 36 amino acid peptide neurotransmitter, is a member of the pancreatic polypeptide class of neurotransmitters/neurohormones which has been shown to be present in both the periphery and central nervous system. NPY is one of the most potent orexogenic agents known and has been shown to play a major role in the regulation of food intake in animals. At least 6 NPY receptor subclasses have been identified and cloned to date, with two of these subclasses, NPY-1 and NPY-5, thought to be the most important receptor subtypes modulating food intake and energy expenditure.... Various animal studies have shown that activation of neuropeptide Y receptors is related to stimulation of consummatory behavior, Food and Morley Peptides, 10:963-966 (1989), Leibowitz and Alexander, Peptides, 12:1251-1260 (1991), and Stanley et al. Peptides, 13:581-587 (1992), and to vasoconstriction, Wahlestedt et al. Regul. Peptides, 13:307-318 (1986), McCauley and Westfall J. Pharmacol. Exp. Ther. 261:863-868 (1992), and Grundemar et al. Br. J. Pharmacol. 105:45-50 (1992). Web site: http://www.delphion.com/details?pn=US06514966__

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Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz; Martin C. (1150 - 88th Ave. West, Duluth, MN 55808) Assignee(s): none reported Patent Number: 6,403,657 Date filed: October 5, 1999 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): Safer than Phen-Fen (copyright 1997), Written by Michael Anchors, MD Ph.D. Pulmonary Vascular Disease, Medical Clinics of North America Nov. 6, 1997,

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Written by Donald Heath, MD Ph.D.... The "Phen-pro" Diet Drug Combination Is Not Associated with Valvular Heart Disease. Jan. 12, 1998 Archives of Internal Medicine. Written by: Len Griffen, MD and Michael Anchors, MD Ph.D.... Fluoxetine (Prozac) and Other Drugs for Treatment of Obesity, Nov. 25, 1994 The Medical Letter. Web site: http://www.delphion.com/details?pn=US06403657__ •

Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz; Martin C. (1150 - 88th Ave. W., Duluth, MN 55808) Assignee(s): none reported Patent Number: 6,548,551 Date filed: August 30, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): The medications stop working during therapy where at least 40% to 50% of patients quit losing weight (plateau) on an average of 3.3 months into therapy; and 5% to 8% of patients who receive drug therapy for weight problems experience the complication where the medications fail to assist in appetite suppression where the patient therefore does not lose significant weight.... In the past long term treatment, defined as treatment longer than 3 months to many years, with drugs has been a problem due to long term safety issues including, medication intolerability by the patient, medication side effects and most important ineffectiveness of the drugs or the cessation of benefit of the drugs which in turn causes the patient to fall out of appetite suppression and terminate weight loss.... A weight loss procedure using SSRI medication is disclosed in U.S. Pat. No. 5,795,895. The potential for patients to obtain goal weight loss under the process of U.S. Pat. No. 5,795,895 is low, and the failure of the drugs to provide a desired level of performance is at the heart of the problem. Web site: http://www.delphion.com/details?pn=US06548551__

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Creatine analogues for treatment of obesity Inventor(s): Kaddurah-Daouk; Rima (Belmont, MA) Assignee(s): Avicena Group, Inc. (Cambridge, MA) Patent Number: 5,998,457 Date filed: October 25, 1996 Abstract: The present invention relates to the use of creatine compounds for treating or preventing a metabolic disorder related to body weight control such as obesity, and it's associated diseases in a patient experiencing said disorder. The creatine compounds

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which can be used in the present method include (1) analogues of creatine which can act as substrates or substrate analogues for the enzyme creatine kinase; (2) compounds which can act as inhibitors of creatine kinase; (3) compounds which can modulate the creatine transporter (4) N-phosphocreatine analogues bearing transferable or nontransferable moieties which mimic the N-phosphoryl group. (5) compounds which modify the association of creatine kinase with other cellular components. Excerpt(s): The present invention provides for new use for creatine compounds (creatine analogues and compounds which modulate one or more of the structural or functional components of the creatine kinase/creatine phosphate system) as therapeutic agents. More particularly, the present invention provides a method of treating or preventing certain metabolic disorders of human and animal metabolism relating to aberrant body weight regulation as manifested in obesity and it's related disorders.... There are several metabolic diseases of human and animal metabolism, eg., obesity and severe weight loss that relate to energy imbalance--where caloric intake versus energy expenditure--is imbalanced. Obesity, which can be defined as a body weight more than 20% in excess of the ideal body weight, is a major health problem in Western affluent societies. It is associated with an increased risk for cardiovascular disease, hypertension, diabetes, hyperlipidaemia and an increased mortality rate. Obesity is the result of a positive energy balance, as a consequence of an increased ratio of caloric intake to energy expenditure. The molecular factors regulating food intake and body weight balance are incompletely understood. Five single-gene mutations resulting in obesity have been described in mice, implicating genetic factors in the etiology of obesity. (Friedman, J. M., and Leibel, R. L. Cell 69: 217-220 (1990)). In the ob mouse a single gene mutation, obese, results in profound obesity, which is accompanied by diabetes (Friedman, J. M., et. al. Genomics 11: 1054-1062 (1991)). Cross-circulation experiments have suggested that the ob mice are deficient of a blood-borne factor regulating nutrient intake and energy metabolism (Coleman, D. L. Diabetologia 14: 141-148 (1978)). Using positional cloning technologies, the mouse ob gene, and subsequently its human homologue, have been recently cloned (Zhang, Y., et. al., Nature 372: 425-432 (1994)). Daily intraperitoneal injections of either mouse or human recombinant OB protein reduced the body weight of obese mice ob/ob by 30% after 2 weeks of injection. The protein reduced food intake and increased energy expenditure in the ob/ob mice (Halaas et. al., Science 269: 543-546 (1995)).... Cachexia on the other hand is characterized by severe weight loss and imbalanced energy expenditure, examples being patients with cancer or HIV infections. Web site: http://www.delphion.com/details?pn=US05998457__ •

Detection of dinucleotide repeat polymorphism in exon 18 of LDL receptor gene for determining predisposition to obesity Inventor(s): Griffiths; Lynette Robyn (Burleigh Heads, AU) Assignee(s): Griffith University (Queensland, AU) Patent Number: 5,688,647 Date filed: December 8, 1995 Abstract: A method detects whether an individual is predisposed to obesity. The method includes the steps of (i) obtaining a sample containing human genomic DNA from the individual; (ii) detecting whether the genomic DNA in the sample has a 7 AT tandem repeat in exon 18 of the low density lipoprotein receptor gene on one or both chromosomes; and (iii) correlating the absence of the 7 AT tandem repeat on the chromosome or chromosomes with a predisposition to obesity in the individual.

Patents 275

Excerpt(s): This invention relates to a method for detecting individuals who are predisposed to obesity. This invention further relates to genetic techniques for detecting a low density lipoprotein receptor gene (LDLR) microsatellite polymorphism.... Obesity is a common nutritional disorder that affects approximately 30% of adults in the Western world. Obesity is a multifactorial condition in which both environmental and genetic factors are important determinants in susceptibility to body fat accumulation (Despres et al., 1992, Molecular and Cellular Biochemistry, 113, 151-169). Adoption studies have implicated genetic control, rather than childhood environment, as the main influence on the development of adult obesity (Sorensen, T. I. & Stunkard, A. J., 1993, Acta Psychiatrica Scandinavica, 370, 67-72). Obesity, essential hypertension, impaired glucose tolerance, non-insulin-dependent diabetes mellitus and dyslipidaemia tend to cluster in families. Collectively, these abnormalities constitute the multiple metabolic syndrome or Syndrome X, which is associated with cardiovascular disease (Kesaniemi et. al., 1992, Annals of Medicine (Helsinki), 24, 461-464).... Lipida and cholesterol ingested in an individuals' diet are essential for body maintenance. These molecules are transported through the body in lipoproteins. There are four types of lipoproteins each responsible for transporting varying amounts of lipid and cholesterol. It has been shown that lipoprotein concentration in the blood is proportional to abdominal fat disposition in obese individuals (Nishina et al., 1992, Proceeding of the National Academy of Science U.S.A., 89, 708-712). The low density lipoprotein (LDL) receptor is responsible for regulating LDL levels and hence cholesterol and plasma lipids in the blood. The gene encoding the LDL receptor (LDLR) is located at chromosome 19 position p13.2. Web site: http://www.delphion.com/details?pn=US05688647__ •

Dietary system high in oil intake for the treatment of obesity and for the lowering of saturated fats Inventor(s): McLean; Linsey (4267 S. State Rd., Davison, MI 48423) Assignee(s): none reported Patent Number: 5,484,623 Date filed: January 10, 1994 Abstract: A dietary system for the treatment of obesity and for the lowering of saturated fats in the blood. The system includes a diet that restricts the patient to the intake of certain foods in certain amounts and combines this intake with specific supplements. The prescribed foods comprise those low in saturated fats and carbohydrates, those having moderate amounts of proteins, and oils high in monounsaturates and certain fatty acids such as olive oil and canola oil. The supplements include prescribed amounts of vitamins and minerals. By providing the patient with a diet high in essential fatty acids, the glucagon-driven pathway of the patient is stimulated and less fat is stored by the body. In addition, more body fat is catalyzed for the production of energy for use by the body. Excerpt(s): The present invention relates to diets for humans. More particularly, the present invention relates to a dietary system for the treatment of obesity and for the lowering of saturated fats in the blood. The system includes a diet that restricts the patient to the intake of certain foods in certain amounts and combines this intake with specific supplements. The prescribed foods comprise those that are low in saturated fats and carbohydrates, those having moderate amounts of proteins, and oils high in monounsaturates and certain fatty acids. The supplements include selected vitamins and minerals.... The patient presenting with obesity is known to require a modified diet

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to effect weight reduction. This same patient also typically presents with a high concentration of saturated fat in the blood.... Whatever the underlying psychological or physiological basis the common belief is that for most cases of obesity overeating or eating the "wrong" foods are the main avenues to weight gain. Accordingly, conventional approaches to resolving obesity include both behavior modification and diet modification. The former approach requires significant psychological adjustment with varying results and the latter is much more common and includes a broad array of diets with many plans producing instantaneous results but being unworkable and even counterproductive over time. Web site: http://www.delphion.com/details?pn=US05484623__ •

Endoscopic stomach insert for treating obesity and method for use Inventor(s): Ellias; Yakub A. (2272 Renshaw Ave., Dayton, OH 45439) Assignee(s): none reported Patent Number: 5,868,141 Date filed: May 14, 1997 Abstract: An endoscopic stomach insert for treating obesity in humans by reducing the desire for eating, comprising a base-sized for passing through a human mouth and esophagus; a plurality of flexible blades coupled at one end thereof to the base and circumferentially arranged about the base central axis, where the blades are biased to extend substantially radially outward and downward from the base; and a retainer for releasably coupling the distal portions of the blades within close proximity to each other about the central axis of the base. The insert is thus adapted to be passed through the mouth and esophagus and into a human stomach, and upon releasing the retainer within the stomach, the blades are biased to flare outwardly into the form of a domeshaped cage, applying pressure to the stomach, and thus causing a sensation of fullness within the stomach and reducing the desire for eating. Excerpt(s): The present invention is an apparatus and method for treating obesity in humans, and particularly, a device for endoscopic insertion into the stomach of a human to cause a reduced desire for eating.... Obesity is arguably one of the most serious health problems in the United States, afflicting over 60 million people of all ages. Apart from physical and psychological effects, especially on the younger population, obesity predisposes to serious diseases such as coronary artery disease, hyperlipidemia, hypertension, and diabetes mellitus. The costs to the health system is a staggering $39 billion per year.... Weight reduction can be achieved either by increasing caloric expenditure through exercise and/or by reducing caloric intake. Reduced caloric intake can be achieved in a number of ways; surgical procedures to reduce the stomach capacity or increase the food transit time in the gastrointestinal tract, appetite suppressants like amphetamines or noradrenargic compounds, or other methods such as introducing balloons into the stomach. Surgical procedures to reduce the stomach capacity or increase food transit time in the gastrointestinal tract carry with them the risk of surgery as well as post-operative complications. The appetite suppressants act on the central nervous system and are associated with considerable morbidity and side effects. Balloon inserts have several disadvantages, which include failure due to bursting or dislodging, intestinal obstruction (blockage of the intestinal lumen), and the requirement of complicated devices and/or procedures to secure the balloons within the stomach.

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Web site: http://www.delphion.com/details?pn=US05868141__ •

Fatty analogues for the treatment of obesity, hypertension and fatty liver Inventor(s): Berge; Rolf (B.o slashed.nes, NO) Assignee(s): Thia Medica AS (Bergen, NO) Patent Number: 6,441,036 Date filed: January 27, 2001 Abstract: The present invention relates to novel fatty acid analogous of the general forumla I: CH.sub.3 --[CH.sub.2 ].sub.m --[x.sub.i --CH.sub.2 ].sub.n --COOR, as defined in the specification, which can be used for the treatment and/or prevention of obesity, fatty liver and hypertension. Further, the invention relates to a nutritional composition comprising such fatty acid analogues, and a method for reducing the total weight, or the amount of adipose tissue in an animal. The invention also relates to a method for improving the quality of product such as meat, milk and eggs. Excerpt(s): The present invention relates to novel fatty acid analogous which can be used for the treatment and/or prevention of obesity, fatty liver and hypertension. Further, the invention relates to a nutritional composition comprising such fatty acid analogues, and a method for reducing the total weight, or the amount of adipose tissue in an animal. The invention also relates to a method for improving the quality of product such as meat, milk and eggs.... Hyperlipidemia and obesity afflict an increasing proportion of the population in Western societies and are associated with the development of serious conditions such as atherosclerosis, hypertension, fatty liver and insulin resistance. These conditions may eventually lead to the clinical manifestations of coronary heart diseases (CD) and non-insulin dependent diabetes mellitus (NIDDM).... Treatment with modified fatty acids represent a new way to treat these diseases. Web site: http://www.delphion.com/details?pn=US06441036__

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Fatty-acid monoesters of estrogens for the treatment of obesity and/or overweight Inventor(s): Alemany; Maria (Barcelona, ES) Assignee(s): Laboratorios S.A.L.V.A.T., S.A. (Esplugues de Llobregat, ES) Patent Number: 5,798,348 Date filed: October 30, 1996 Abstract: The pharmaceutical and/or cosmetic compositions for treatment of obesity and/or overweight contain an effective amount of a fatty-acid monoester of an estrogen and a fatty acid wherein the estrogen is estrone, diethylstilbestrol, estriol, estradiol or ethinyl estradiol and the fatty acid is oleic, linoleic, linolenic, stearic, palmitic, palmitoleic or arachidonic acids. The fatty-acid monoesters mimic the function of estrone monooleate, as a signal that informs the brain of the size of fat tissue mass. In preferred pharmaceutical and/or cosmetic compositions for intravenous injection the monoester is incorporated in a lipidic suspension, prepared from lipoproteins or from liposome components, such as soy oil and egg phospholipids. When administered to rats with a 15% of total adipose tissue, they produce weight reduction of about 10%, by a new and unexpected mechanism. They are useful for the treatment of obesity and/or overweight in mammals, with the advantages of high efficacy and low toxicity. New

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substantially pure fatty-acid monoesters including diethylstilbestrol monooleate are also described.

estrone

monooleate

and

Excerpt(s): This invention refers to products, compositions and uses thereof, for therapeutic and/or cosmetic treatment of obesity and/or overweight in mammals.... Treatment of obesity and/or overweight is a therapeutic or cosmetic problem of major importance that does not have a satisfactory solution yet. Attempts to solve the problem by reducing food intake or by doing physical exercise, are well known. But also known are the difficulties, limitations and general lack of success of all these approaches. Apparently the sheer complexity of mechanisms involved in the control of body mass allow little room for external manipulation, thus limiting the possible damage to body reserves by increased thermogenic stimulation or diminished energy intake.... In the therapeutic fight against obesity and/or overweight considerable research has been focused on trying to find some signal that informs the brain of the size of fat tissue mass. It is believed that such information is required by the brain to promote either the accumulation of fat reserves or their burning by the thermogenic system, via the natural homeostatic mechanisms set to maintain the body mass stable. According to a recent discovery based on a mutation of a gene, one such signal could be a protein named leptin (cf. Y. Zhang et al., Nature 1994, vol. 372, pp. 425-32). From this discovery the invention of using leptin for the preparation of a medicament for treating obesity by injection could be derived. But, even if this approach proves to be useful in the future, it would be very expensive because leptin must be prepared by genetic engineering. Web site: http://www.delphion.com/details?pn=US05798348__ •

Indoline derivatives and method of treating obesity Inventor(s): Bentley; Jonathan Mark (Oakdene Court, 613 Reading Court, Winnersh, Wokingham RG41 5UA, GB), Davidson; James Edward Paul (Oakdene Court, 613 Reading Court, Winnersh, Wokingham RG41 5UA, GB), Mansell; Howard Langham (Oakdene Court, 613 Reading Court, Winnersh, Wokingham RG41 5UA, GB), Monck; Nathaniel Julius Thomas (Oakdene Court, 613 Reading Court, Winnersh, Wokingham RG41 5UA, GB) Assignee(s): none reported Patent Number: 6,479,534 Date filed: October 15, 2001 Abstract: The present invention relates to indoline derivatives. These compounds are especially useful for the prevention and treatment of disorders of the central nervous system; damage to the central nervous system; cardiovascular disorders; gastrointestinal disorders; diabetes, sleep apnea, and especially for the treatment and prevention of obesity. Excerpt(s): The present invention relates to indoline derivatives, to processes and intermediates for their preparation, to pharmaceutical compositions comprising them and to their medicinal use. The active compounds of the present invention are useful in treating obesity, diabetes and other disorders.... It has been recognised that obesity is a disease process influenced by environmental factors in which the traditional weight loss methods of dieting and exercise need to be supplemented by therapeutic products (S. Parker, "Obesity: Trends and Treatments", Scrip Reports, PJB Publications Ltd, 1996).... Whether someone is classified as overweight or obese is generally determined on the basis of their body mass index (BMI) which is calculated by dividing body weight (kg)

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by height squared (m.sup.2). Thus, the units of BMI are kg/m.sup.2 and it is possible to calculate the BMI range associated with minimum mortality in each decade of life. Overweight is defined as a BMI in the range 25-30 kg/m.sup.2, and obesity as a BMI greater than 30 kg/m.sup.2. There are problems with this definition in that it does not take into account the proportion of body mass that is muscle in relation to fat (adipose tissue). To account for this, obesity can also be defined on the basis of body fat content: greater than 25% and 30% in males and females, respectively. Web site: http://www.delphion.com/details?pn=US06479534__ •

Inflatable gastric device for treating obesity Inventor(s): Berson; Daniel (199 Kings Highway, Congers, NY 10920) Assignee(s): none reported Patent Number: 4,246,893 Date filed: July 5, 1978 Abstract: Apparatus for treating extreme obesity comprising means for compressing the stomach and reducing its capacity and procedures employing said apparatus. Excerpt(s): This invention relates to procedures and apparatus for treating obesity in human patients.... In the past, rather drastic surgical procedures have been employed to treat morbidly or mortally obese patients, i.e., patients whose body weight is at least twice their appropriate weight. One set of surgical procedures induces a pathophysiologic abnormality of the gastrointestinal tract by gastric or jejunoileal bypass operations in which as much as 95% of the tract is surgically bypassed. These procedures result in a patient who is a metabolic cripple having surgically induced malabsorption, and are associated with long term complications often requiring additional surgical procedures. The jejunoileal bypass, for example, has been used extensively in this country and around the world. This procedure bypasses about 95% of the small bowel, leaving about 40 cm. of functioning jejunum and ileum. The physiologic effect of this is massive diarrhea and malabsorption of nutrients, leading to weight loss secondary to poor absorption of nutrients, as well as aversion to eating. The procedure is performed an estimated five thousand to twenty thousand times per year in the United States, but has been abandoned by many institutions, including the Cleveland Clinic, because of unacceptable operative mortality averaging 6% nationwide, as well as severe complications including wound infection and breakdown, progressive liver failure, hypocalcemia, calcium oxalate urinary calculi and bypass enteropathy. Mechanical problems such as intestinal obstruction and hernia formation are frequent.... Approximately 32% of the patients having jejunoileal bypass operations are rehospitalized within one year. These operations have also been associated with liver dysfunctions most likely caused by the preferential absorption of carbohydrates in the remaining small bowel, with resulting relative protein starvation. Web site: http://www.delphion.com/details?pn=US04246893__

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Inhibition of adipose tissue development and obesity Inventor(s): Serrero; Ginette (Lake Placid, NY) Assignee(s): W. Alton Jones Cell Science Center, Inc. (Lake Placid, NY) Patent Number: 5,723,115 Date filed: December 2, 1993 Abstract: Epidermal growth factor (EGF), which can act as a potent inhibitor of adipocyte differentiation in vitro, affects adipose tissue differentiation in vivo and can suppress obesity. Methods are provided for inhibiting the differentiation of adipocyte precursor cells, and for treating or preventing obesity, which comprise administering an effective amount of a composition capable of binding to and activating the EGF receptor, preferably epidermal EGF or a functional derivative thereof, TGF.alpha., an antibody specific for the EGF receptor or an anti-idiotypic antibody specific for an idiotope on an antibody specific for EGF. Also provided is a method for determining the susceptibility of a subject to obesity or determining the presence of obesity associated with an abnormality in EGF or EGF receptor, which comprises measuring EGF in a body fluid or the amount or activity of EGF receptor protein or mRNA in adipocyte precursors. Excerpt(s): The invention in the field of cell biology, physiology and medicine relates to methods for treating obesity and methods for determine susceptibility to obesity.... Obesity has been declared a public health hazard by the National Institutes of Health. To combat this health problem, both prophylactic and therapeutic approaches are necessary. For prophylactic purposes, it would be useful to be able to predict and measure a person's propensity or susceptibility to obesity For therapeutic purposes, a means for interfering with the development or differentiation of adipocytes (fat cells) would be of great benefit. Furthermore, as a broader preventative approach to obesity, the ability to limit the fat content of food mammals would be of great importance. None of these desired objectives has been achieved. Early-onset obesity cannot be efficiently controlled by a weight reduction program once the obesity is apparent. Therefore, a means for early detection of early-onset obesity is imperative for its prevention.... The identification of the hormones controlling adipocyte proliferation and differentiation is very important for understanding normal adipose tissue development and for designing approaches for controlling abnormal states of adipose tissue development such as obesity. Several adipogenic cell lines able to undergo differentiation in vitro into fully mature adipocytes have served as model systems for investigating differentiation at the cellular and molecular levels (1-3). Using these cell lines, several hormones and growth factors have been shown to have adipogenic (3-5) or anti-adipogenic activities (6-9). Web site: http://www.delphion.com/details?pn=US05723115__

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Lipolytic composition and method of treating obesity Inventor(s): Traunecker; Werner (Munster-Sarmsheim, DE), Frolke; Wilhelm (Ingelheim am Rhein, DE), Kreuzer; Heinrich (Gau-Algesheim, DE), Kollmer; Hans P. (Wackernheim, DE) Assignee(s): Boehringer Ingelheim KG (Ingelheim am Rhein, DE) Patent Number: 4,499,106 Date filed: May 20, 1983

Patents 281

Abstract: Lipolytic pharmaceutical composition containing 1-(4-hydroxy-3dimethylamino-sulfonamidophenyl)-1-hydroxy-2-(1-phenoxy-iso propylamino)ethane or a pharmaceutically acceptable acid addition salt thereof as the active ingredient, and a method of combatting obesity therewith. Excerpt(s): This invention relates to pharmaceutical compositions which contain as the active ingredient the compound 1-(4-hydroxy-3-dimethylamino-sulfonamidophenyl)-1hydroxy-2-(1-phenoxy-iso propylamino)ethane (Me 693), and to a method of treating both generalized and also localized obesity in warm-blooded animals therewith.... It is known from West German Pat. No. 2,115,926 that a group of sulfonamides, which includes 1-(4-hydroxy-3-dimethylamino-sulfonamidophenyl)-1-hydroxy-2-(1-phenoxyiso propylamino)ethane (Me 693), having a dilating effect upon the peripheral blood vessels, influence blood pressure, increase the capacity of the heart, and have broncholytic properties.... Compounds which exhibit activities of this kind are known as.beta.-adrenergics. Known.beta.-adrenergics have, in addition to the properties mentioned above, a marked glycogenolytic effect on the skeletal muscle, which is accompanied by lactacidemia. Web site: http://www.delphion.com/details?pn=US04499106__ •

Medicament for treating obesity and improving lipid metabolism Inventor(s): Suzuki; Kunio (1238-8, Gomigaya, Tsurugashima-shi, Saitama 350-2202, JP), Shimizu; Takeshi (Saitama, JP), Nakata; Tadashi (Saitama, JP) Assignee(s): Riken (Saitama, JP), Suzuki; Kunio (Saitama, JP) Patent Number: 6,531,462 Date filed: January 7, 2002 Abstract: A medicament for preventive and therapeutic treatment of obesity and a disease with abnormal lipid metabolism which comprises a 24-alkylcholest-5-en-3-one as an active ingredient. Excerpt(s): The present invention relates to medicaments useful for preventive and/or therapeutic treatment of obesity, and to medicaments of improving lipid metabolism.... Obesity is caused by insufficient exercise of habitual hyperphagia, or by metabolic disturbance due to genetic causes or endocrine diseases and other. Obesity may be a risk factor that causes various adult diseases such as myocardial infarct or arterial sclerosis, and it may also be a cause for deteriorating these diseases. Therefore, early therapeutic and preventive treatment of obesity is very important. Diet therapies or exercise therapies have been applied heretofore as the treatment of mild obesity, and drug therapies are sometimes used for serious obesity in combination with these therapies.... Hormone drugs, metabolic accelerators and other have been used heretofore for drug therapies of obesity and lipid metabolic disorder. For example, androgens such as dehydroepiandrosterone and 3-keto-.DELTA..sup.9 -19-norsteroid are known to have anti-obesity action (Japanese Patent Unexamined Publication No. (Hei)2-275895/1990). These androgens are considered to activate intramuscular anabolism to induce the consumption of depot lipid. It is also known that 3-ketosteroids such as 4-cholesten-3one (Japanese Patent Unexamined Publication No. (Hei)5-170651/1993) and 5-cholesten3-one (Japanese Patent Unexamined Publication No. (Hei)7-165587/1995) have reducing activity on serum lipid and anti-obesity action. However, the aformentioned cholestenones, which have the enone structure derived from cholesterol, may possibly

282 Obesity

be absorbed and accumulated in the body, and therefore, they are not satisfactory medicaments from a viewpoint of safety. Web site: http://www.delphion.com/details?pn=US06531462__ •

Method and apparatus for reducing obesity Inventor(s): Berman; Edward J. (3426 N. Meridian, Indianapolis, IN 46208), Rowe; George A. (3426 N. Meridian, Indianapolis, IN 46208) Assignee(s): none reported Patent Number: 4,133,315 Date filed: December 27, 1976 Abstract: An apparatus for reducing obesity in human beings having an inflatable bag to which a flexible tube is attached. The bag is positioned in the stomach, usually by swallowing, and the tube extends up through the esophagus and out of a nasal cavity or out from the abdomen when a gastrostomy is performed. The bag is inflated by attachment of a supply of fluid to the end of the tube, and then the tube is closed so that the bag will maintain its inflated conditon. With a portion of the open cavity of the patient's stomach occupied by the inflated bag, the patient will sense a feeling of being "filled-up" with only a small amount of food intake. Excerpt(s): This invention relates in general to dietary devices for medical treatment of obesity.... Those who have a problem with obesity have few options available to them with respect to a solution. The typical approach is to rely on the person's willpower to stick to a particular diet or to use diet pills to try and reduce the desire for food. These may be effective measures, depending upon the individual, but if the person is either physically or mentally unable to control his weight gain, he may be subject to more drastic measures, such as surgical reduction of the size of the stomach or bypassing much of the small intestines. Unfortunately, such measures have resulted in death to the patient in a substantial number of cases. Even if death is not the result, the operation is often permanent and the patient is still subjected to the after-effects once the problem with obesity is corrected. One approach to correcting obesity involves reducing the desire for food. This can be accomplished by partially filling the stomach so as to produce the sensation of being "filled-up." One way of accomplishing this is to place an inflatable, elastomeric bag in the stomach and inflate the bag with fluid.... Inflatable bag and tube combination devices are known in the field of medicine and have experienced use by the medical profession in the treatment of gastric disorders such as stomach ulcers and hemorrhages in the upper gastrointestinal tract. Cook, U.S. Pat. No. 3,227,154 discloses a device in which the bag must be fully inflated so that its impressionablesettable outer surface can make impressions in the walls of cavities which have restricted outlets. Another use of inflatable bag and tube combination devices as disclosed by Gawura, U.S. Pat. No. 3,768,484 and Seaman, U.S. Pat. No. 3,174,481, is to transfer and retain a cooling solution at a particular internal location. The bag acts merely as a container for this solution and the characteristic of being inflatable allows a single bag to be used with a wide range of cavity sizes. These prior art references all disclose tubes with a plurality of passageways and a liquid to inflate the bag. Web site: http://www.delphion.com/details?pn=US04133315__

Patents 283

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Method and apparatus for treating obesity Inventor(s): Garren; Lloyd R. (P.O. Box 3738, Wilmington, DE 19807), Garren; Mary L. (P.O. Box 3738, Wilmington, DE 19807) Assignee(s): none reported Patent Number: 4,416,267 Date filed: December 10, 1981 Abstract: A stomach insert for treating obesity in humans by reducing the stomach volume comprises a flexible torus-shaped inflatable balloon having a central opening extending therethrough. At least a portion of the balloon has a self-sealing substance to facilitate puncture thereof with a needle for inflating the balloon and sealing of the puncture upon removal of the needle. The method herein comprises positioning the balloon inside the stomach of the person being treated for obesity so as to reduce the stomach volume. Excerpt(s): The present invention relates to the medical treatment of obesity in humans, and more particularly to apparatus and methods for curbing the appetite of persons being treated for obesity.... Extreme obesity is a major illness in the United States and other countries. Its complications include hypertension, diabetes, coronary artery disease, stroke, congestive heart failure, venous disease, multiple orthopedic problems and pulmonary insufficiency with markedly decreased life expectancy. Medical management including dietary, psychotherapy, medications and behavioral modification techniques have yielded extremely poor results in multiple trials. Several surgical techniques have been tried which have bypassed the absorptive surface of the small intestine or have been aimed at reducing the stomach size by either partition or bypass. These procedures have been proven both hazardous to perform in morbidly obese patients and have been fraught with numerous life-threatening postoperative complications. Moreover such operative procedures are often difficult to reverse.... Nonsurgical approaches for the treatment of obesity include voluntary dieting which is often unsuccessful since most persons do not possess sufficient willpower to limit the intake of food. Other approaches include the use of stomach fillers such as methyl cellulose, often taken in the form of tablets. The methyl cellulose expands in the stomach leaving the person with a filled-up feeling. Also, inflatable bag and tube combinations have been proposed wherein the bag is swallowed into the stomach and the tube attached thereto is used to periodically inflate the bag, particulary just prior to mealtime or during the meal. Once the person has eaten, the bag can be deflated all at once, or it can be deflated gradually over a period of a few hours so as to simulate the condition of digestion occurring and the gradual reduction of stomach contents. Web site: http://www.delphion.com/details?pn=US04416267__

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Method and appartus for treating obesity Inventor(s): Garren; Lloyd R. (P.O. Box 3738, Wilmington, DE 19807), Garren; Mary L. (P.O. Box 3738, Wilmington, DE 19807) Assignee(s): none reported Patent Number: 4,899,747 Date filed: September 6, 1983

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Abstract: A stomach insert for treating obesity in humans by reducing the stomach volume comprises a flexible, free floating and unattached, inflatable balloon, the balloon being inflatable to a volume effective to reduce the stomach volume of a person being treated. At least a portion of the balloon has a self-sealing substance to facilitate puncture thereof with insufflation means through which the balloon is inflated and to facilitate sealing of the puncture upon removal of the insufflation means. The method herein comprises positioning the balloon inside the stomach of the person being treated for obesity so as to reduce the stomach volume. Excerpt(s): The present invention relates to a medical treatment of obesity in humans, and more particularly to both apparatus and method for curbing the appetite of persons being treated for obesity.... Extreme obesity is a major illness in the United States and other countries. Its complications include hypertension, diabetes, coronary artery disease, stroke, congestive heart failure, venous disease, multiple orthopedic problems and pulmonary insufficiency with markedly decreased life expectancy. Medical management including dietary, psychotherapy, medications and behavioral modification techniques have yielded extremely poor results in multiple trials. Several surgical techniques have been tried which have bypassed the absorptive surface of the small intestine or have been aimed at reducing the stomach size by either partition or bypass. These procedures have been proven both hazardous to perform in morbidly obese patients and have been fraught with numerous life-threatening postoperative complications. Moreover such operative procedures are often difficult to reverse.... Nonsurgical approaches for the treatment of obesity include voluntary dieting which is often unsuccessful since most persons do not possess sufficient willpower to limit the intake of food. Other approaches include the use of stomach fillers such as methyl cellulose, often taken in the form of tablets. The methyl cellulose expands in the stomach leaving the person with a filled-up feeling. Also, inflatable bag and tube combinations have been proposed wherein the bag is swallowed into the stomach and the tube attached thereto is used to periodically inflate the bag, particularly just prior to mealtime or during the meal. Once the person has eaten, the bag can be deflated all at once, or it can be deflated gradually over a period of a few hours so as to simulate the condition of digestion occurring and the gradual reduction of stomach contents. Web site: http://www.delphion.com/details?pn=US04899747__ •

Method and composition for treating obesity and related disorders in animals comprising dehydroepiandrosterone (DHEA), or a derivative thereof, and an anorectic agent Inventor(s): Svec; Frank (Metairie, LA), Porter; Johnny (Metairie, LA) Assignee(s): Louisiana State University Medical Center Foundation (New Orleans, LA) Patent Number: 5,795,880 Date filed: December 30, 1996 Abstract: The invention describes a method and composition for treating obesity or related disorders in animals using an anorectic agent and dehydroepiandrosterone (DHEA). The composition effectively diminishes caloric intake, may alter metabolism, weight gain, or a combination thereof. Excerpt(s): A method and composition for treating obesity and related disorders in animals comprising dehydroepiandrosterone (DHEA), or a derivative thereof, and an anorectic agent.... This invention describes an effective method and composition for

Patents 285

treating obesity and related disorders in humans and animals, such as dogs, cats, or any other suitable animal, using DHEA or a derivative thereof and an anorectic agent. The method and composition are useful in veterinary as well as human applications.... Obesity may be the major health problem of the Western world. Nearly 20% of the United States' adult population is overweight and its prevalence is rising. The medical and economic importance of obesity go far beyond effects on self-image. Obesity is the dominant risk factor for the expression of adult-onset diabetes mellitus, and thus leads to complications of cardiovascular, renal, and peripheral vascular disease. Obesity is also a leading factor in the development of complications after surgical procedures. Web site: http://www.delphion.com/details?pn=US05795880__ •

Method and composition for treating obesity comprising dehydroepiandrosterone (DHEA), or a derivative thereof, and an anorectic agent Inventor(s): Svec; Frank (Metairie, LA), Porter; Johnny (Metairie, LA) Assignee(s): Louisiana State Univ. Medical Center Foundation (New Orleans, LA) Patent Number: 5,527,788 Date filed: January 18, 1994 Abstract: The invention describes a method and composition for treating obesity or related disorders in animals using an anorectic agent and dehydroepiandrosterone (DHEA). The composition effectively diminishes caloric intake, may alter metabolism, weight gain, or a combination thereof. Excerpt(s): A method and composition for treating obesity and related disorders in animals comprising dehydroepiandrosterone (DHEA), or a derivative thereof, and an anorectic agent.... This invention describes an effective method and composition for treating obesity and related disorders in humans and animals, such as dogs, cats, or any other suitable animal, using DHEA or a derivative thereof and an anorectic agent. The method and composition are useful in veterinary as well as human applications.... Obesity may be the major health problem of the Western world. Nearly 20% of the United States' adult population is overweight and its prevalence is rising. The medical and economic importance of obesity go far beyond effects on self-image. Obesity is the dominant risk factor for the expression of adult-onset diabetes mellitus, and thus leads to complications of cardiovascular, renal, and peripheral vascular disease. Obesity is also a leading factor in the development of complications after surgical procedures. Web site: http://www.delphion.com/details?pn=US05527788__

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Method and composition for treating obesity, drug abuse, and narcolepsy Inventor(s): Hohenwarter; Mark (Mobile, AL) Assignee(s): Serotonin Industries of Charleston (Charleston, SC) Patent Number: 4,843,071 Date filed: December 5, 1986 Abstract: Compositions and methods are disclosed for the treatment of obesity, depression, drug abuse, and narcolepsy. The compositions comprise a norepinephrine precursor such as L-tyrosine or L-phenylalanine in combination with a norepinephrine re-uptake inhibitor such as desipramine. In another embodiment of the invention, the

286 Obesity

compositions further norepinephrine.

comprise

enzymatic

cofactors

for

the

biosynthesis

of

Excerpt(s): This invention relates to compositions comprising a norepinephrine precursor, such as L-tyrosine or L-phenylalanine in combination with a norepinephrine re-uptake inhibitor such as desipramine. The compositions are useful in controlling obesity, depression, drug abuse, and narcolepsy in animals. The invention also relates to said compositions further comprising one or more enzymatic cofactors for the biosynthesis of norepinephrine. This invention further relates to a method of controlling obesity, depression, drug abuse, or narcolepsy in an animal comprising administering an effective amount of the compositions of this invention to said animal.... The use of appetite supressants such as diethylproprion and phenylpropanolamine operate by directly and/or indirectly stimulating noradrenergic receptors in the brain. However, long-term use of these drugs is met with increasing tolerance in most patients, requiring increased dosage and more frequent administration to achieve continued appetite suppression. Tolerance to these products occurs as the result of a depletion of norepinephrine from storage sites in the neuron with the use of indirect-acting agents.... Catecholamines are stored in subcellular granules and released by exocytosis in the adrenal medulla and sympathetic nerve endings. The biosynthesis of catecholamines proceeds from the amino acid phenylalanine which is sequentially hydroxylated to form tyrosine, then 3,4-dihydroxyphenylalanine (DOPA). DOPA is decarboxylated to form dopamine. Hydroxylation on the beta position of the side chain forms norepinephrine. Web site: http://www.delphion.com/details?pn=US04843071__ •

Method for combating obesity Inventor(s): Munter; Klaus (Mannheim, DE), Kirchengast; Michael (Mannheim, DE) Assignee(s): Knoll Aktiengesellschaft (Ludwigshafen, DE) Patent Number: 6,197,780 Date filed: April 27, 2000 Abstract: Diseases caused by obesity are treated with endothelin receptor antagonists. Diseases treated include those frequently associated with obesity such as hypertension, type 2 diabetes, hyperlipidemia, chronic kidney failure, arteriosclerosis and gout. Excerpt(s): The present invention relates to a method for controlling obesity and diseases caused by obesity.... The peptide hormone endothelin is known for its strong vasoconstrictor properties. Endothelin receptor antagonists are therefore mainly being tested in cardiovascular pathologies.... The invention relates to the use of endothelin receptor antagonists for producing drugs for controlling obesity and diseases caused by obesity. Web site: http://www.delphion.com/details?pn=US06197780__

Patents 287

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Method for control of obesity, overweight and eating disorders Inventor(s): Clegg; Charles T. (1418 Thayer Ave., Los Angeles, CA 90024), Wallace; Garn A. (1647 Manning Ave., Los Angeles, CA 90024) Assignee(s): none reported Patent Number: 4,823,808 Date filed: July 6, 1987 Abstract: Methods for the treatment of obesity, overweight, compulsive overeating, emotional overeating, binge eating, bulimia and anorexia comprises the steps of monitoring physiological parameters in the esophageal and/or gastrointestinal tract which are associated with gastric relaxation, gastric filling, gastric contractions, gastric secretions, and gastric emptying. The measurement are transmitted either directly to a receiver or via radiotelemetry to a receiver. The receiver has a data processor associated therewith, and the data processor produces audio and/or visual feedback for the person under treatment to hear and/or see. This feedback is used for purposes of teaching behavior modification and other psychotherapeutic purposes. In the most simple form of the invention, a warning sound is generated by the data processor indicating when sufficient food has been ingested. This warning can be generated by the monitoring apparatus much sooner than the biological signal of fullness transmitted by the stomach to the brain of the person. The person can thereby discontinue eating before otherwise becoming unconsciously too full. Excerpt(s): The present invention relates generally to methods for the control of obesity, overweight, and eating disorders, including anorexia, bulimia, and compulsive overeating. In particular, the invention relates to methods for sensing the quantity of food consumed and/or the monitoring of various physiological changes during food ingestion and digestion, with the monitored data being presented visually or through auditory means or other sensations to a person who is participating in a program of treatment involving voluntary limitation of dietary intake and/or behavior modification.... Obesity has been treated in many ways, with the overall goal being to reduce ingestion below energy expenditure so as to result in a weight loss. Energy expenditure is increased by physical activity increases, and the physical activity further results in an increase in metabolic rate lasting beyond the period of exercise. Energy intake is reduced through dietary restriction or other means. Numerous theories exist regarding various topics which are believed to influence body weight, such as genetics, fat cell number behavior, and developmental psychology. Finally systems theory has also been used to partially account for difficulties with overweight, obesity, and eating disorders.... Currently used treatments for obesity and overeating include psychological interventions, dietetics, exercise, gastric balloons, stomach staping, jaw wiring, surgery, drugs and behavior modifications. An important of the psychological interventions may also include assessment and treatment of body image. Behavior modification, including assessment and treatment of body image, is a most effective treatment when combined with diet and exercise. Web site: http://www.delphion.com/details?pn=US04823808__

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Method for imparting ability of preventing obesity and impaired glucose tolerance to foods and foods and sugar preparations exhibiting such preventive effects Inventor(s): Wakabayashi; Shigeru (Takarazuka, JP), Hoshii; Yasuhiro (Fujiidera, JP) Assignee(s): Matsutani Chemical Industries Co., Ltd. (Hyogo, JP) Patent Number: 5,505,981 Date filed: August 3, 1993 Abstract: Preventing obesity and impaired glucose tolerance by incorporating indigestible dextrin containing at least 30% by weight of indigestible components into a food in an amount ranging from 1 g to 30 g per meal of the food. Excerpt(s): The present invention relates to a method for imparting an ability of preventing obesity and impaired glucose tolerance to foods, and a food and a sugar preparation exhibiting such preventive effects.... Recently, eating habits have been improved, but the population of patients suffering from geriatric diseases represented by obesity and diabetes increases steadily because of hypernutrition and unbalanced diet as well as lack of exercise. Under such social background, there have been developed various agents for inhibiting an increase in the blood-sugar level and excess insulin-secretion for preventing healthy person from suffering from obesity and/or diabetes or for treating patients requiring the control of the blood-sugar level such as those suffering from diabetes. As such agents, there have been known, for instance, Acarbose (available from Bayer Yakuhin, Ltd.) and A0-128 (available from Takeda Chemical Industries, Ltd.) which are substances having an effect of inhibiting the gastrointestinal absorption of sugar and starch and inhibitors for enzymes involved in digestion, but both of them are medicines and the ingestion or intake thereof for the preventive purpose becomes a cause of various problems. For instance, they suffer from a problem of safety, since they would be dangerous because of possible side-effects. Moreover, polymers of glucose moieties bonded through.alpha.-1,6-bonds such as isomaltotriose, dextran and pullulan have been known to have an effect of inhibiting an increase in the blood-sugar level in response to ingestion of sugar. Isomaltotriose and dextran as such are digested and absorbed and, in particular, dextran suffers from a problem of safety since it has been proved that dextran exhibits side-effects such as an effect of elongating the blood-coagulation time. On the other hand, pullulan can inhibit any increase in the blood-sugar level after the ingestion of sugar, but is substantially ineffective for the control of the blood-sugar level after the ingestion of glucose and maltose. Moreover, the effect thereof for controlling the insulin-secretion has not yet been proved. Furthermore, pullulan has been known to control an increase in the body weight when it is administered to a young rat and to inhibit the growth thereof.... On the other hand, the effect of insulin is very important for controlling the sugar-metabolism in patients suffering from diabetes, persons whose probability of suffering from diabetes is high or patients suffering from obesity and, therefore, it is needed for these persons or patients to protect, hold and/or enhance the effect of insulin. There have been used, for instance, solutions for transfusion and foods containing monosaccharides or sugar alcohols such as fructose, sorbitol and xylitol; disaccharides and their alcohols such as maltitol, maltose and leucrose; and glucose polymers (U.S. Pat. No. 3,928,135), capable of being digested in and absorbed by living bodies independent of the effect of insulin, for the prevention of temporal hyperglycemia after the ingestion of these sugars, for saving the insulin-secretion, for the supplementation of energy or for controlling the osmotic pressure of transfusion solutions. However, these mono- and poly-saccharides and their alcohols have high degrees of sweetness, but the quality of sweetness thereof is inferior to that of sugar. In addition, sugar alcohols often becomes a cause of diarrhea.

Patents 289

Moreover, it has been known that the glucose polymers do not stimulate any insulinsecretion when it is used in the form of a transfusion solution, but the transfusion is a medical act and cannot be commonly adopted. Web site: http://www.delphion.com/details?pn=US05505981__ •

Method for screening potential anti-obesity agents Inventor(s): Hamilton; Bradford S. (D7 - 245 Howland Avenue, Toronto, Ontario, CA), Roncari, deceased; Daniel A. K. (late of North York, CA), Roncari, executor; by Lubov (144 Esther Crescent, Thornhill, Ontario, CA) Assignee(s): none reported Patent Number: 5,783,408 Date filed: June 7, 1995 Abstract: A method for screening a compound as a potential anti-obesity agent by determining whether the compound stimulates micro motion of cells in vitro is described Excerpt(s): The present invention relates to a method for screening compounds having potential as anti-obesity agents.... Obesity is a significant health problem in many countries and has been extensively reviewed in the literature..sup.1,2,3,4,5,6 Obesity is frequently associated with such cardiovascular risk factors as dyslipidemias (particularly, elevated levels of very-low-density lipoprotein-triglycerides and depressed levels of high-density lipoproteins), hypertension, hyperinsulinemia, and non-insulin dependent diabetes mellitus..sup.1,2,3,4,5,6 Massive corpulence (body weight greater than 170% of reference or body mass index greater than 37 kg/m.sup.2) is also characterized by high morbidity and mortality..sup.1,2,6 Massive obesity, which features diffuse distribution of adiposity, is particularly associated with the mixed (central and obstructive) sleep-apnea syndrome, and at times the full hypoventilation syndrome, gallbladder disease, non-insulin dependent diabetes, trauma and psychosocial problems.... It has been estimated that approximately 34 million American adults were obese in 1980..sup.7 The economic costs in 1986 of obesity were estimated conservatively to be $39.3 billion. Web site: http://www.delphion.com/details?pn=US05783408__

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Method for the treatment of obesity Inventor(s): Hornkvist; Per-Erik (Goteborg, SE) Assignee(s): Imperial Chemical Industries plc (London, GB2) Patent Number: 4,933,340 Date filed: November 26, 1986 Abstract: The invention concerns the use of N-(2-[RS-2-hydroxy-3-(4hydroxyphenoxy)propylamino]ethyl)-morpholinoformam ide or a salt thereof in the production of a medicament for the treatment of obesity and/or related conditions in warm-blooded animals including man. Excerpt(s): This invention concerns a therapeutic agent for use in the treatment of obesity and/or related conditions such as obesity of maturity onset diabetes, affecting

290 Obesity

warm-blooded animals, especially humans or domestic animals. More particularly, the invention concerns the novel use of the known pharmaceutical agent xamoterol, its Senantiomer or a salt in the treatment of obesity and/or related conditions in humans or domestic animals, and in the manufacture of a new medicament for such use.... According to the invention there is provided a method for the treatment of obesity and/or related conditions in warm-blooded animals, such as humans or domestic animals which comprises the administration of a therapeutically effective amount of a therapeutic agent selected from N-(2-[RS-2-hydroxy-3-(4hydroxyphenoxy)propylamino]ethyl)morpholinoformami de of formula I (also known as xamoterol) and the S-laevorotatory enantiomer thereof, or of a pharmaceutically acceptable acid-addition salt of said agent, to humans or domestic animals requiring such treatment.... Particularly suitable pharmaceutically acceptable acid-addition salts include, for example, salts derived from a suitable inorganic acid, such as hydrochloric, hydrobromic, phosphoric and sulphuric acids, and salts derived from a suitable organic acid, such as oxalic, fumaric, lactic, acetic, salicylic, citric, benzoic, 2-naphthoic and adipic acid, 1,1-methylene-bis(2-hydroxy-3-naphthoic acid), and from an acidic synthetic resin, such as a sulphonated polystyrene resin. Web site: http://www.delphion.com/details?pn=US04933340__ •

Method for treating morbid obesity Inventor(s): Silverman; David E. (Palo Alto, CA), Stein; Alan (Moss Beach, CA) Assignee(s): SciMed Life Systems, Inc. (Maple Grove, MN) Patent Number: 6,540,789 Date filed: November 10, 2000 Abstract: A method for treating morbid obesity in a body of a mammal having a gastrointestinal tract extending through a stomach and a pyloric sphincter and a wall forming the stomach and pyloric sphincter. At least one implant is formed in the wall in the vicinity of the pyloric sphincter to inhibit emptying of the stomach. Excerpt(s): This invention pertains to the treatment of morbid obesity.... Numerous modalities are purported to treat morbid obesity. These include patient-specific dietary restrictions and nutritional supplementation, abdominoplasty or panniculectomy, gastric banding and/or stapling and the more invasive and surgically aggressive gastric bypass. There is a need for a method which is less invasive and more clinically efficacious in treating morbid obesity.... In general, it is an object of the present invention to provide a method for creating implants in natural body cavities accessible by natural body openings and more preferably in gastrointestinal tract passageways in order to treat morbid obesity. Web site: http://www.delphion.com/details?pn=US06540789__

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Method for treating obesity Inventor(s): Lassen; Joergen B. (Glostrup, DK) Assignee(s): A/S Ferrosan (Soberg, DK) Patent Number: 4,745,122 Date filed: December 4, 1985

Patents 291

Abstract: A method for treating obesity in humans or non-human animals, which method comprises administering an effective, non-toxic amount of paroxetine or a pharmaceutically acceptable salt thereof, to obese humans or animals and compositions for use in such treatment. Excerpt(s): The present invention relates to a method for the treatment of obesity and to a compound for use in such method.... U.S. Pat. No. 4,007,196 discloses the compound, ()-trans-4-(4'-fluorophenyl)-3-(3',4'-methylenedioxyphenoxymethyl)piperid ine, and, in Example 2, a process by which it can be prepared. The compound, which is referred to herein by its common name, paroxetine, is described in the patent as an inhibitor of 5hydroxytryptamine and, therefore, is of use in the treatment of depression. The patent also mentions that paroxetine is useful in the treatment of Parkinson's disease.... It has now been discovered that paroxetine also has activity against obesity. Web site: http://www.delphion.com/details?pn=US04745122__ •

Method for treatment of morbid obesity Inventor(s): Angelchik; Jean P. (1728 W. Glendale Ave., Phoenix, AZ 85021) Assignee(s): none reported Patent Number: 4,607,618 Date filed: January 11, 1985 Abstract: Morbid obesity is treated by implacement in the fundus of a hollow shaped appliance. The appliance is formed of semi-rigid skeleton members and is collapsible to a dimension and shape which can be inserted into the stomach through the esophagus and cardiac opening. Upon release of the collapsed device in the stomach, it autogenously re-assumes its normal uncollapsed shape. Excerpt(s): This invention pertains to medical treatment methods and apparatus useful therein.... In a more particular respect, the invention concerns a method for treating morbid obesity.... In another particular respect, the invention concerns an appliance useful in such treatment. Web site: http://www.delphion.com/details?pn=US04607618__

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Method for treatment of obesity Inventor(s): Viner; Norman (Ottawa, CA) Assignee(s): Synapse Pharmaceuticals International, Inc. (Ottawa, CA) Patent Number: 5,900,418 Date filed: February 10, 1997 Abstract: A method is provided for the control of obesity comprising administering to a mammal including humans suffering from obesity an acetylcholine esterase reactivator or prodrug derivative thereof optionally in association with an acetylcholine receptor antagonist. Excerpt(s): The present invention is directed to a method for the control and/or treatment of obesity.... It is well understood that obesity is a widespread problem. Obesity is linked to a variety of medical conditions including hypertension, diabetes, cardiovascular disease, etc. obesity is also linked to a variety of psychological

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maladjustments. By contemporary medical standards an obese person is judged to be overweight by at least 10 percent. At present, only a limited number of treatments are available to treat obesity. Exemplary treatments are disclosed in U.S. Pat. Nos. 3,867,539 (administration of histidine); 4,446,138 (administration of L-Dopa); 4,588,724 (administration of beta adrenergic stimulant or alpha-2 adrenergic inhibitor); 4,745,122 (administration of paroxetine); 5,019,594 (sympathomimetic drug and tyrosine); 5,300,298 (administration of 8-phenylxanthines); 5,403,851 (tryptamine); 5,567,714 (administration of neuropeptide Y); 5,573,774 (nicotinic metabolites); and 5,578,613 (administration of 2-phenyl-3-aroylbenzothiophenes). Amphetamine has also been used as an appetite suppressant.... Unfortunately, none of the above methods of treatment have been very successful. While such treatments may bring short-term relief to the person, long-term success has not been easily achieved. The cessation of tobacco use has frequently contributed to weight gain. Also, comorbid addictions, stress, psychiatric disorders and environmental factors may exacerbate the difficulty encountered by a particular person in alleviating obesity. It is believed, for example, that xenobiotic toxic agents such as pesticides, insecticides, fungicides, oxidants, solvents and other environmental toxins encountered by the person by various means (e.g., via drinking water and/or food impurities, etc.) may contribute to the inability of the person to control obesity. Web site: http://www.delphion.com/details?pn=US05900418__ •

Method for treatment of obesity using prolactin modulators and diet Inventor(s): Cincotta; Anthony H. (Andover, MA), Meier; Albert H. (Andover, MA) Assignee(s): The Board of Supervisors of Louisiana State University and Agriculture (Baton Rouge, LA), Ergo Research Corporation (Wakefield, RI) Patent Number: 5,760,047 Date filed: May 10, 1995 Abstract: The present invention is directed to an improvement in a method of weight and/or body-fat reduction comprising a (preferably moderate) reduction in the caloric intake of a subject in need of such treatment in combination with administration to said subject of a prolactin inhibitor. Additionally, the present invention is directed to an improvement in a method for altering and/or resetting prolactin profiles (and thereby controlling one or more metabolic disorders such as obesity, excessive body fat, hyperlipidemia, hyperlipoproteinemia, hyperglycemia, hypercholesterolemia, hyperinsulinemia, insulin resistance, glucose intolerance, and Type II diabetes) comprising administration to a subject in need of such treatment of a prolactin inhibitor at a predetermined time or times during a 24-hour period in combination with a (preferably moderate) reduction of the caloric intake of said subject. Excerpt(s): This invention relates to an improved method for the reduction in a subject, vertebrate animal or human, of weight and/or body fat stores. This method involves a reduction in caloric intake, in combination with the administration of a prolactin inhibitor.... In another aspect, this invention relates to an improved method for altering and/or resetting prolactin profiles of a vertebrate subject (including a human), by administering to such subjects a prolactin inhibitor in combination with restricting the caloric intake of the subject, thereby effecting an amelioration in abnormal metabolic indices of said subject.... The reduction of body weight and/or fat stores in man is of significant benefit, both cosmetically and physiologically. Whereas controlled diet and exercise can produce modest results in the reduction of weight and body fat deposits,

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these results are often unsatisfactory due to the substantial reduction in metabolic rate which accompanies a reduced calorie diet. Further, although a loss in body weight is seen with reduced caloric intake, this loss is often temporary and/or due to a reduction in lean body weight (as opposed to loss of fat). Various studies have shown that most calorie restriction diets result in weight loss approximately 40% of which is body fat lost and the remainder is lean body mass loss. Web site: http://www.delphion.com/details?pn=US05760047__ •

Method for treatment or prevention of obesity Inventor(s): Clark; Ross G. (Pacifica, CA) Assignee(s): Genentech, Inc. (South San Francisco, CA) Patent Number: 5,597,797 Date filed: November 19, 1993 Abstract: A method is disclosed for treating obese mammals or preventing obesity from occurring in mammals. This method involves administering to the mammal an effective amount of growth hormone in combination with an effective amount of IGF-I. Preferably, the growth hormone is given so as to have a maintained, continual therapeutically effective presence in the blood, such as by continuous infusion or frequent injections, or by use of a long-acting formulation. Excerpt(s): This invention relates to a method of restoring ideal population-based body composition in obese mammals or preventing obesity especially in humans.... Obesity is a chronic disease that is highly prevalent in modern society and is associated not only with a social stigma, but also with decreased life span and numerous medical problems, including adverse psychological development, reproductive disorders such as polycystic ovarian disease, dermatological disorders such as infections, varicose veins, Acanthosis nigricans, and eczema, exercise intolerance, diabetes mellitus, insulin resistance, hypertension, hypercholesterolemia, cholelithiasis, osteoarthritis, orthopedic injury, thromboembolic disease, cancer, and coronary heart disease. Rissanen et al., British Medical Journal, 301: 835-837 (1990).... Obese subjects tend to have low basal levels of growth hormone (GH) and fail to secrete significant amounts of GH in response to a variety of stimuli, including growth hormone releasing hormone (GHRH). Williams, New Engl. J. Med., 311: 1403 (1984) Kopelman, Clin. Endocrinol., 23: 87 (1985); Kopelman, Clin. Endocrinol., 24: 157 (1986) Loche, Clin. Endocrinol., 27: 145 (19871) Ghigo et al., Metabolism, 41: 560-563 (1992). The GH responsiveness to GHRH in obese rats shows sexual dimorphism. Cocchi et al., Pharmacol. Res., 25: Suppl. 2, 336-337 (1992). This failure to secrete GH has been postulated to be the result of a hypothalamic disorder (Kopelman, 1986, supra), leading to a chronic state of somatostatin hypersecretion. Cordido, J. Clin. Endocrinol. Metab., 68: 290 (1989). This defect in GH secretion appears to be a result rather than a cause of obesity, since it is, at least in part, reversible with weight reduction. Web site: http://www.delphion.com/details?pn=US05597797__

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Method of controlling obesity with purified active principle of fruit of Synsepalum dulcificum Inventor(s): Henkin; Robert I. (Bethesda, MD), Giroux; Eugene L. (Strasbourg, FR) Assignee(s): The United States of America as represented by the Department of Health, (Washington, DC) Patent Number: 3,995,031 Date filed: July 23, 1974 Abstract: A process for the purification of the active principle of the fruit of the plant Synsepalum dulcificum is disclosed. The process includes contacting the fruit with a suspension of polyvinyl pyrrolidone, followed by adsorption of the active principle by means of chromatography procedures. By following the process in accordance with the present invention, proteases and tannins are substantially completely eliminated from the final product. The active principle of this fruit, when prepared in accordance with the present invention, has been found to be particularly useful in controlling obesity in human beings. Excerpt(s): The present invention relates to a process for purification of the active principle of the fruit of the plant Synsepalum dulcificum. Also disclosed is a method for the use of this active principle in the control of obesity.... The botanical plant species of Synsepalum dulcificum is indigenous to tropical West Africa, where it is often referred to as "miracle fruit." The plant, which grows in the form of a shrub, yields ripe red berries from December to June, the berries being ellipsoidal in shape and about 0.75 inch long, and composed of a thin layer of pulp surrounding a single large seed. These berries have the unique property of modifying the taste of sour foods to make such foods taste sweet after the fruit pulp has been chewed.... Previous methods for the purification of the active principle of plants such as Synsepalum dulcificum have been characterized by a complex series of steps involving bulky equipment and long periods of time for the separation of an active principle which in many cases has been of a low degree of purity, often containing contaminants such as proteases and tannins in relatively large amounts. Such prior art methods include those described by Inglett et al., J. Agri. Food Chem., 13:284 (1965), Brouwer et al., Nature 220:373 (1968) and Beidler et al., Science 161:1241 (1968). The method of Inglett et al. involves purification of the active principle of miracle fruit in phases A and B, with phase A involving successive treatment of the plant parts with petroleum ether, chloroform, ethyl acetate, acetone, absolute ethanol and water, and phase B including successive treatment with water, aqueous alcohol, absolute alcohol, acetone, chloroform and n-hexane, followed by hydrolysis of fractions A and B. By removal of inactive matter, a five-fold concentration of the active material was achieved. Web site: http://www.delphion.com/details?pn=US03995031__

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Method of preventing or alleviating mammalian obesity Inventor(s): Mikami; Toshiyuki (Ibaraki, JP), Spiegelman; Bruce (Waban, MA), Wright; Harold (Watertown, MA) Assignee(s): Sumitomo Chemical Company, Limited (Osaka, JP), Dana-Farber Cancer Institute, Inc. (Boston, MA) Patent Number: 6,033,656 Date filed: May 4, 1999

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Abstract: The present invention provides methods of suppressing the activation of Peroxisome Proliferator-Activated Receptor gamma in a mammalian body by administering an effective amount of bisphenol A diglycidyl ether to a mammal, methods of suppressing the accumulation of fat in the mammalian fat cell or adipose tissue by administering an effective amount of bisphenol A diglycidyl ether to a mammal, methods of preventing or alleviating mammalian obesity by administering an effective amount of bisphenol A diglycidyl ether to a mammal, bisphenol A diglycidyl ether for use as an active pharmaceutical substance or composition for the treatment of obesity, and uses of bisphenol A diglycidyl either for the preparation of a pharmaceutical composition for the treatment of obesity. Excerpt(s): The present invention relates to a method of preventing or alleviating mammalian obesity.... Fat cells have the ability to store fat in their cells and are typically present in the adipose tisses of the subcutaneous abdominal region, the femoral region, the gluteal region, the pectoral region and the like, and the adipose tissues which are in the abdominal cavity and in the vicinity of the mesenterium, kidney, epididymis, and the like, which are in the body of a mammal, such as a human. For example, promoting the storage of fat in fat cells generally results in an obese mammal, which is generally accompanied by an increase in body fat content and an increase in the mass of adipose tissue which is typically in the abdominal cavity of the mammal. It is knovwn that such obesity thereby induces disorders such as the impairment in glucose tolerance [Journal of Clinical Investigation, vol.72, pp. 1150 (1983)], diabetes [National Diabetes Data Group: Diabetes in America. Bethesda, Md., U.S. Dept. of Health and Human Services, (1985), Diabetes Care, vol.19, pp.613 (1996), Diabetes & Metabolisme, vol.20, pp.375 (1994), Obesity: Advances in Understanding and Treatment, Published by IBC Biomedical Library, Chapter 3.1, (1996)], hyperglycemia, hyperlipemia, hypertension [Journal of Clinical Investigation, vol.72, pp. 1150 (1983)], coronary arterial diseases [Diabetes & Metabolisme, vol.20, pp.375 (1994)], obstructive arterial sclerosis and the like [WHO Expert Committee on Diabetes Mellitus. Second report, WHO Tech Rep 646 Geneva: World Health Organization (1980)].... The fat cells are generally produced by differentiating progenitor fat cells. To differentiate progenitor fat cells into fat cells, it is essential to activate a function of a protein called Peroxisome Proliferator-Activated Receptor gamma (hereinafter refereed to as "PPAR.gamma.")[Peter Tontonoz, et al., Cell, vol.79, 1147-1156, 1994]. For example, the accumulation of fat in a fat cell can occur from having a thiazolidinedione derivative bind to PPAR.gamma. in the progenitor fat cell so that PPAR.gamma. can be activated, which induces the differentiation of the progenitor fat cell to a fat cell, and which then further expresses genes associated with fat accumulation [Jurgen of M. Lehman, et al., Journal of Biological Chemistry, vol. 270, No. 22, 12953-12956, 1995]. PPAR.gamma. is a nuclear receptor type transcription regulating factor [Issenman and Green, Nature 347-645-650 (1990)]. Web site: http://www.delphion.com/details?pn=US06033656__ •

Method of reducing bodyweight and treating obesity Inventor(s): Remmereit; Jan (Volda, NO) Assignee(s): Natural Nutrition Ltd. AS (NO) Patent Number: 6,034,132 Date filed: March 19, 1998 Abstract: The present invention discloses method for reducing body weight and treating obesity. The method comprises administering a nutritionally effective amount of

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conjugated linoleic acid to a human. The conjugated linoleic acid may be provided in the form of a free fatty acid in a pill, or as a component of a prepared food product. Excerpt(s): This invention relates to the administration of a dietary supplement, conjugated linoleic acid, to induce bodyweight reduction, thereby providing a treatment for obesity.... Obesity is the most common disorder of the developed world. The ready availability of food in most areas, a shift to relatively sedentary lifestyles, and changing food sources have contributed to this problem.... Researchers have hypothesized that recent changes in food sources have led to an imbalance in the optimal ratio of fatty acid intake. These imbalances may influence obesity. Specifically, modern diets have increased amounts of omega-6 fatty acids as compared to omega-3 fatty acids, as noted in Simopoulos, "Evolutionary Aspects of Diet: Fatty Acids, Insulin Resistance and Obesity", in Obesity: New Directions in Assessment and Management, VanItallie and Simonpoulos ed., The Charles Press, Philadelphia, 241-61 (1995). Omega-6 fatty acids are represented by linoleic acid and omega-3 fatty acids are represented by alpha-linolenic acid. A balance between omega-6 and omega-3 fatty acids existed for most of human history and has now been changed to a ratio of about 20 to 25:1 in the favor of omega-6 fatty acids. This increase in omega-6 fatty acids is due the increased intake of vegetable oils and increased amounts saturated and monounsaturated fatty acids (depot fat) in domestic meat as compared to meat from wild game. The replacement of saturated fats with unsaturated fats has been widely recommended, resulting in increased intake of omega-6 fatty acids from vegetable oils and trans fatty acids from margarine. This means that humans have been exposed to pharmacological doses of omega-6 fatty acids from the first time in their evolutionary history. Web site: http://www.delphion.com/details?pn=US06034132__ •

Method of treating obesity Inventor(s): Klein; Ira (5 Windermere, Houston, TX 77063) Assignee(s): none reported Patent Number: 5,498,424 Date filed: November 30, 1994 Abstract: The present invention provides a simple, pharmacological method for treating obesity without risk of undesirable side effects. It has been discovered that intake of a megadose of a macrolide antibiotic creates an anorexigenic reaction in the human sufficient to result in weight loss. This method can also be used advantageously to assist non-obese persons in losing weight. The present invention relates to a method of treating obesity, comprising the steps of identifying a patient needing to lose weight and administering an appetite suppressing dose of a macrolide antibiotic compound to the patient. The dose of the macrolide antibiotic preferably ranges between a dose greater than a normal clinical dose used to treat bacterial infections and a maximum dose capable of being safely received by the patient without toxicity. In another preferred embodiment, the method includes the additional step of readministering the dose at an interval as required to maintain a desired level of appetite suppression throughout the treatment. In a preferred embodiment of the present invention, the macrolide antibiotic compound is clarithromycin. Excerpt(s): The present invention relates to methods of inducing weight loss in mammals, and in particular to methods of treating obesity.... Excess adiposity, in its extreme form obesity, is generally regarded as a disorder of energy regulation. This

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disorder is increasingly prevalent in industrialized nations because of the abundance of food and the reduced activity levels that accompany the movement of populations from rural to urban settings. Obesity is loosely defined as an excess of body fat over that needed to maintain health.... Obesity is associated with increased morbidity and mortality. Detrimental effects of obesity on health, include an increased risk of cardiovascular disease and the associated conditions of hypertension, diabetes, and hyperlipidemia. Millions of people are clinically obese (i.e., a Body Mass Index value above the 851 h percentile), and, in view of the deleterious effects of obesity on health, would benefit from treatment. Additionally, many people, although not clinically obese, can improve their health and well-being by losing weight. Web site: http://www.delphion.com/details?pn=US05498424__ •

Method of treating obesity by the oral administration of a predigested protein composition Inventor(s): Gans; Arnold M. (Closter, NJ), Goren; Alvin J. (North Bergen, NJ), Gorenberg; Eli M. (Fair Lawn, NJ) Assignee(s): Control Drug, Inc. (Port Reading, NJ) Patent Number: 4,042,687 Date filed: June 22, 1976 Abstract: A method of preventing obesity which comprises ingestion of a pre-digested protein composition formed from hydrolyzed gelatin to which has been added an effective amount of tryptophane, said composition containing all of the essential amino acids and having a palatable taste and odor. Excerpt(s): This invention relates to a method and composition for providing a highly efficient source of nutrition without undesirable side effects, and it especially relates to the provision of a source of protein in concentrated but highly palatable form.... One of the most significant aspects of the present invention is its utilization in the prevention of nutritional deficiency, and particularly that form of nutritional deficiency which is caused by disease or which is an undesirable condition in the treatment of a disease or surgical procedure.... The crucial effect in the body's response to nutritional deficiency or starvation is the preservation of the size and character of the body cell mass. The term "body cell mass" denotes the total mass of living, functioning, energy-exchanging, and mitotically active cells of the body comprising two large groups of tissues, namely skeletal muscle and visceral parenchyma. Web site: http://www.delphion.com/details?pn=US04042687__

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Method of treatment of obesity Inventor(s): Holloway; Brian R. (Congleton, GB2), Howe; Ralph (Macclesfield, GB2), Rao; Balbir S. (Holmes Chapel, GB2), Stribling; Donald (Prestbury, GB2) Assignee(s): Imperial Chemical Industries PLC (London, GB2) Patent Number: 4,937,267 Date filed: March 10, 1987 Abstract: A method of treatment of obesity or diabetes mellitus in a warm-blooded animal requiring such treatment which comprises administering to said animal an

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effective amount of the compound N-(2-[2-hydroxy-3-phenoxypropyl]aminoethyl)isobutyramide in racemic (R,S) or levorotatory optically active (S) form, or of a pharmaceutically acceptable acid-addition salt thereof. Excerpt(s): The invention concerns novel therapeutic agents having thermogenic properties for use in the treatment of obesity and/or related conditions such as diabetes mellitus especially of maturity onset, in warm-blooded animals such as man. More particularly, the invention provides a new method of treatment of obesity and/or related conditions involving administration of a known pharmaceutical agent and the use of said agent in the manufacture of a novel medicament.... According to the invention there is provided a method of treatment of obesity and/or a related condition affecting a warm-blooded animal which comprises administering to said animal an effective amount of the compound N-(2-[2-hydroxy-3phenoxypropyl]aminoethyl)isobutyramide of formula I (set out hereinafter) in racemic (R,S) or laevorotatory optically active (S) form, or a pharmaceutically acceptable acidaddition salt thereof.... The invention also provides the use of the compound of formula I in racemic (R,S) or laevorotatory optically active (S) form, or of a pharmaceutically acceptable salt thereof, in the manufacture of a novel medicament for the treatment of obesity and/or related conditions in warm-blooded animals, including man. Web site: http://www.delphion.com/details?pn=US04937267__ •

Methods and compositions for the diagnosis and treatment of body weight disorders, including obesity Inventor(s): Moore; Karen (Maynard, MA), Nagle; Deborah Lynn (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,274,339 Date filed: February 5, 1999 Abstract: The present invention relates to mammalian mahogany genes, including the human mahogany gene, which are novel genes involved in the control of mammalian body weight. The invention encompasses nucleotide sequences of the mahogany gene, host cell expression systems of the mahogany gene, and hosts which have been transformed by these expression systems, including transgenic animals. The invention also encompasses novel mahogany gene products, including mahogany proteins, polypeptides and peptides containing amino acid sequences mahogany proteins, fusion proteins of mahogany proteins polypeptides and peptides, and antibodies directed against such mahogany gene products. The present invention also relates to methods and compositions for the diagnosis and treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia, and for the identification of subjects susceptible to such disorders. Further, the invention relates to methods of using the mahogany gene and gene products of the invention for the identification of compounds which modulate the expression of the mahogany gene and/or the activity of the mahogany gene product. Such compounds can be useful as therapeutic agents in the treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia. Excerpt(s): The present invention relates to mammalian mahogany genes, including the human mahogany gene, which are novel genes involved in the control of mammalian body weight. The invention encompasses nucleotide sequences of the mahogany gene, host cell expression systems of the mahogany gene, and hosts which have been

Patents 299

transformed by these expression systems, including transgenic animals. The invention also encompasses novel mahogany gene products, including mahogany proteins, polypeptides and peptides containing amino acid sequences mahogany proteins, fusion proteins of mahogany proteins polypeptides and peptides, and antibodies directed against such mahogany gene products.... The present invention also relates to methods and compositions for the diagnosis and treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia, and for the identification of subjects susceptible to such disorders. Further, the invention relates to methods of using the mahogany gene and gene products of the invention for the identification of compounds which modulate the expression of the mahogany gene and/or the activity of the mahogany gene product. Such compounds can be useful as therapeutic agents in the treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia.... Obesity represents the most prevalent of body weight disorders, and it is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa, which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS. Web site: http://www.delphion.com/details?pn=US06274339__ •

Methods and reagents for regulating obesity Inventor(s): Bernfield; Merton (Boston, MA), Reizes; Ofer (Newton, MA) Assignee(s): Children's Medical Center Corporation (Boston, MA) Patent Number: 6,284,729 Date filed: May 6, 1998 Abstract: It has now been demonstrated that syndecan binds to and interacts with MC4R, and thereby modulates neuropeptide regulation of body weight, via the agouti/MC4R signaling pathway. Transgenic animals were made initially using a construct including a cytomegalovirus promoter and the 3' untranslated region, including the polyadenylation site, of the bovine growth hormone gene, as well as cDNA encoding syndecan-1. The mice express the syndecan-1 transgene in many tissues, with expression in the brain occurring preferentially in their hypothalamus. These mice are characterized by elevated levels of circulating syndecan-1 ectodomain and exhibit enormous weight gain after reaching sexual maturity, but have a relatively normal distribution of fat, are completely healthy and heterozygotes reproduce, and show other indicators associated with obesity in humans. Agouti mice which are transgenic for syndecan-1 ectodomain demonstrate that syndecan-1 and agouti interact, potentiating obesity. The double heterozygote shows both an earlier onset, and greater extent, of obesity than either normal agouti or the original transgenic syndecan-1 mice.Based on these studies and animal models, one can design and test compounds regulating obesity. These mice are also useful in understanding the factors involved in weight regulation and in designing and screening for drugs which are involved in weight regulation and that can either enhance or reduce appetite and activity. Excerpt(s): Obesity is a well established risk factor for a number of potentially lifethreatening diseases such as atherosclerosis, hypertension, diabetes, stroke, pulmonary embolism, and cancer. Furthermore, it complicates numerous chronic conditions such as respiratory diseases, osteoarthritis, osteoporosis, gall bladder disease, and

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dyslipidemias. The enormity of this problem is best reflected in the fact that death rates escalate with increasing body weight. More than 50% of all-cause mortality is attributable to obesity-related conditions once the body mass index (BMI) exceeds 30 kg/m.sup.2, as seen in 35 million Americans. (Lee1992. JAMA. 268:2045-2049). By contributing to greater than 300,000 deaths per year, obesity ranks second only to tobacco smoking as the most common cause of potentially preventable death. (McGinnis 1993 MA.270:2207-2212). Accompanying the devastating medical consequences of this problem is the severe financial burden placed on the health care system in the United States. The estimated economic impact of obesity and its associated illnesses from medical expenses and loss of income are reported to be in excess of $68 billion/year. (Colditz G. 1992. Am J Clin Nutr. 55:503S-507S). This does not include the greater than $30 billion per year spent on weight loss foods, products, and programs. (Wolf 1994. Pharmacoeconomics. 5:34-37).... A major reason for the long-term failure of established approaches is their basis on misconceptions and a poor understanding of the mechanisms of obesity. Conventional wisdom maintained that obesity is a self-inflicted disease of gluttony. Comprehensive treatment programs, therefore, focused on behavior modifications to reduce caloric intake and increase physical activity using a myriad of systems. These methods have limited efficacy and are associated with recidivism rates exceeding 95%. (NIH Technology Assessment Conference Panel. 1993. Ann Intern Med. 119:764-770). Failure of short-term approaches, together with the recent progress made in elucidating the pathophysiology of obesity, have lead to a reappraisal of pharmacotherapy as a potential long-term, adjuvant treatment. (National Task Force on Obesity. 1996. JAMA. 276:1907-1915). The premise is that body weight is a physiologically controlled parameter similar to blood pressure and obesity is a chronic disease similar to hypertension. The goal of long-term (perhaps life long) medical therapy would be to facilitate both weight loss and subsequent weight maintenance in conjunction with a healthy diet and exercise. To assess this approach, the long-term efficacy of currently available drugs must be judged against that of nonpharmacological interventions alone. Currently, no single drug regimen emerges as superior in either promoting or sustaining weight loss. Although promising, the success of this approach is limited by the efficacy of currently available anorexiant drugs. Surgical interventions, such as gastric partitioning procedures, jejunoileal bypass, and vagotomy, have also been developed to treat severe obesity. (Greenway 1996. Endo Metab Clin N Amer. 25:1005-1027). Although these procedures induce similar rates of early weight loss as nonsurgical interventions, they have been shown to maintain a weight loss of up to 33% for more than 10 years. (Long 1994. Diabetes Care. 17:372-375). While still far from optimal, this is a substantial improvement over that achieved with behavioral and medical management alone. The superior long-term outcome with surgical procedures in attributed to the inherent permanence of the intervention which addresses the chronic nature of the disease. Although advantageous in the long run, the acute risk benefit ratio has reserved these invasive procedures for morbidly obese patients according to the NIH consensus conference on obesity surgery (BMI>40 kg/m.sup.2). (NIH Conference. 1991. Ann Intern Med. 115:956-961). Therefore, this is not an alternative for the majority of overweight patients unless and until they become profoundly obese and are suffering the attendant complications.... No one knows all of the mechanisms involved in regulation of weight gain, although it is believed that many genetic as well as environmental factors, including diet and exercise, play major, interrelated roles. A number of publications have reported the discovery of genes that have been "knocked out" or overexpressed in transgenic mice, resulting in affected animals becoming incredibly obese, or vice versa. See, for example, Ezzell, "Fat Times for Obesity Research: Tons of New Information, but How Does It All Fit Together" J. NIH Res. 7, 39-43 (October 1995). Researchers have reported the cloning of at least two

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distinct genes, Ob which encodes a protein "leptin" believed to cause weight reduction in obese animals, and Db, which is believed to cause weight gain in animals. Other genes which have been reported include the fat, tub, agouti, and melanocortin 4 receptor genes. Recent reviews relating to the insights regarding the mechanisms involved in obesity help to understand these complex pathways. See, for example, Trish Gura, Science 275, 752-753 (Feb. 7, 1997) and Jeffrey S. Flier, Proc. Natl. Acad. Sci. USA 94, 4242-4245 (April 1997). Leptin, discovered in 1994 by Jeffrey Friedman's team at Rockefeller University, NY, is a 16 kD protein produced by the obesity (ob) gene of mice. Homozygotes with defective ob genes are unable to reproduce, stay warm, or grow normally, and become grossly overweight. The receptor for leptin has now been identified and cloned. Defects in the receptor also result in grossly obese animals. The receptor is expressed in the brain primarily in four regions, including the arcuate nucleus. In humans, however, the linkage between obesity and overexpression of leptin does not seem to be closely correlated, and no individuals have been identified that have a mutated Ob receptor or gene. Another molecule which appears to be important in weight control is the appetite-stimulating neurotransmitter referred to as neuropeptide Y or "NPY". NPY levels are elevated in animals with decreased levels of leptin. Genetic studies with knockout NPY and ob/ob animals indicate that NPY plays a role in, but is not a controlling factor, in obesity. Another line of research has implicated a role in obesity for the melanocortin receptor ("MCR"). Two MCRs, MCR3 and MCR4, are produced in the arcuate nucleus of the hypothalamus, a prime target of leptin action as well as of NPY production. Synthetic peptides mimicking melanocortins which bind to MCR-4 suppress feeding. Animals in which the gene encoding MCR-4 has been knocked out show the opposite behavior, exhibiting high weight gain and high NPY expression. Web site: http://www.delphion.com/details?pn=US06284729__ •

Methods for identifying compositions for the treatment of body weight disorders, including obesity Inventor(s): Tartaglia; Louis Anthony (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 5,853,975 Date filed: February 26, 1997 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis. Specifically, the present invention identifies and describes genes which

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are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight-related processes, including body weight disorders such as obesity and cachexia. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, 1985, Essays in Biochem. 20:110-165; Himms-Hagen J., 1989, Prog. Lipid Res. 28:67-115). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, 1984, Physiol. Rev. 64:1-64). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg M., 1990, Trends Biochem. Sci. 15:108-112; Klaus S. et al., 1991, Int. J. Biochem. 23:791-801). UCP-mediated uncoupling is not only capable of increasing body temperature in coldacclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, 1986, In Brown Adipose Tissue. Trayhurn P., Nicholls D.G., Eds., London, Arnold, p. 269-298; Spiegelman & Flier, 1996, Cell 87:377-389; Hamann & Flier, 1996, Endocrinology 137:2129). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, 1996, Endocrinology 137:2129; Lowell B. B. et al., 1993, Nature 366:740-742; Kopecky J. et al., 1995, J. Clin. Invest. 96:2914-2923; Cummings D. E. et al., 1996, Nature 382:622-626).... In humans, body weight homeostasis is poorly understood, but is also thought to involve regulated thermogenesis (Rothwell & Stock, 1981, Annu. Rev. Nutr. 1:235-56; Segal K. R. et al., 1992, J. Clin. Invest. 89:824-833; Jensen M. D. et al., 1995, Am. J. Physiol. 268:E433-438). However, the importance of the UCP in adult humans is questionable due to the low levels of BAT and consequently the low levels of UCP expression (Huttunen P. et al., 1981, Eur. J. Appl. Physiol. 46:339-345; Cunningham S. et al., 1985, Clin. Sci. 69:343-348; Schulz L., 1987, J. Am. Diet Assoc. 87:761-764; Santos G. C. et al., 1992, Arch. Pathol. Lab Med. 116:1152-1154). Web site: http://www.delphion.com/details?pn=US05853975__ •

Methods for the diagnosis of body weight disorders including obesity Inventor(s): Tartaglia; Louis Anthony (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 5,702,902 Date filed: August 23, 1995 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body

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weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... Body weight disorders, including eating disorders, represent major health problems in all industrialized countries. Obesity, the most prevalent of eating disorders, for example, is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to other diseases. For example, this disorder is responsible for increased incidences of diseases such as coronary artery disease, stroke, and diabetes. Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity. The nature, however, of the genetic factors which control body composition are unknown, and attempts to identify molecules involved in such control have generally been empiric and the parameters of body composition and/or substrate flux are monitored have not yet been identified (Friedman, J. M. et al., 1991, Mammalian Gene 1:130-144). Web site: http://www.delphion.com/details?pn=US05702902__

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Methods for treating obesity and weight gain using optically pure (-)-bupropion Inventor(s): Young; James W. (Palo Alto, CA) Assignee(s): Sepracor (Marlborough, MA) Patent Number: 6,110,973 Date filed: January 28, 1999 Abstract: Methods are disclosed utilizing the optically pure (-)-isomer of bupropion, which is a potent drug for treating obesity and weight gain. Excerpt(s): This invention relates to methods of treatment and pharmaceutical compositions employing the compound (-)-bupropion.... Many organic compounds exist in optically active forms, i.e., they have the ability to rotate the plane of plane-polarized light. In describing an optically active compound, the prefixes D and L or R and S are used to denote the absolute configuration of the molecule about its chiral center(s). The prefixes (+) and (-) or d and l are employed to designate the sign of rotation of planepolarized light by the compound, with (-) or l meaning that the compound is levorotatory. A compound prefixed with (+) or d is dextrorotatory. For a given chemical structure, these compounds, called stereoisomers, are identical except that they are mirror images of one another. A specific stereoisomer may also be referred to as an enantiomer, and a mixture of such isomers is often called an enantiomeric or racemic mixture.... Stereochemical purity is of importance in the field of pharmaceuticals, where 16 of the 20 most prescribed drugs exhibit chirality. A case in point is provided by the Lform of the.beta.-adrenergic blocking agent, propranolol, which is known to be 100 times more potent than the D-enantiomer. Web site: http://www.delphion.com/details?pn=US06110973__

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Methods of producing weight loss and treatment of obesity Inventor(s): Kozachuk; Walter E. (Kensington, MD) Assignee(s): none reported Patent Number: 6,191,117 Date filed: July 10, 2000 Abstract: Methods are disclosed for the acute and chronic treatment of obesity using drugs whose mechanism includes the interaction and antagonism of the kainate/AMPA receptor. Methods are disclosed for employing the drug topiramate (topomax) as monotherapy or in combination therapy with lamotrigene, valproic acid, valproic acid and carbamezepine combination, or felbamate (felbatol). Excerpt(s): The present invention relates to pharmaceutical compositions, whose mechanisms of action(s) are at the kainate/AMPA receptor that can be used to treat the medical condition of obesity.... Obesity is one of the most common medical disorders, which affects 30-40% of the population of which 10% may be severe and morbid. Complications of obesity include insulin resistance, diabetes mellitus, hypertension, cardiovascular disease, pseudotumor cerebri, hyperlipidemia, sleep apnea, cancer, pulmonary hypertension, cholecystitis, and osteoarthritis. The mortality from obesity is estimated at 300,000 to 400,000 per annum in the United States. Obesity in humans is commonly measured by the BMI (body mass index) which is the weight in kilograms divided by the height in meters squared. The degree of obesity is determined by comparisons against standard deviations above the means for males and females. The

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exact etiology of obesity is unknown but occurs when energy intake exceeds energy expenditure. The amount and distribution of body fat may have some genetic predisposition and be under some hormonal control. Hypothalamic structures, which have complex interconnections with the limbic system and other brain structures, control appetite. Some neurochemicals known to be involved in appetite control include: leptin, a substance released from adipose tissue, GLP-1 (glucagon-like peptidel) which promotes satiety, and neuropeptide-Y, a potent stimulator of appetite.... The present invention proposes a theory of obesity in which dysfunction of the AMPA/kainate and/or NMDA is a contributing etiology. Administration of drugs whose mechanism or action is antagonism of the AMPA/kainate receptor, with or without the combination of glycine-site antagonists, is proposed as a treatment for obesity. Web site: http://www.delphion.com/details?pn=US06191117__ •

Methods of screening for modulators of uncoupling protein-2 (UCP-2) as potential treatments for obesity Inventor(s): Lind; Peter (Uppsala, SE), Walum; Erik (.ANG.kersberga, SE) Assignee(s): Pharmacia & Upjohn AB (Stockholm, SE) Patent Number: 6,001,578 Date filed: June 26, 1998 Abstract: The invention relates to a method for treatment of obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus by administering a drug capable of modulating the regulation of UCP-2, the use of a drug capable of modulating the regulation of UCP-2 for the production of drug for treatment of obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus and pharmaceutical composition comprising a pharmaceutically effective amount of such a drug. The invention is also related to methods for screening for potential drugs against obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus and the use of cDNA probe for determination of upregulation of UCP-2 for potential drugs against obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus. Excerpt(s): The present invention relates to method for treatment of obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus by administering a drug capable of modulating the regulation of UCP-2. The present invention also relates to the use of a drug capable of modulating the regulation of UCP-2 for the production of a drug for treatment of obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus. The present invention also relates to method for screening for potential drugs against obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus comprising the measurement of UCP-2 activity by biochemical, chemical or physical methods.... Obesity is a disease with strongly increasing prevalence, and has reached epidemic proportions in the industrialized world. This disease is essentially characterized by an unbalance between energy intake and expenditure, which, without interference, leads to an endless increase in adipose tissue mass and body weight.... Appetite and energy intake are influenced by several hormonal effectors and neurotransmitters acting in the peripheral as well as the central nervous system. Examples of neurotransmitters acting to increase appetite and, concomitantly, body weight, are neuropeptide Y, melanin concentrating hormone, galanin, as well as glucocorticoid hormones. Examples of hormones or neurotransmitters that counteract feeding and stimulate reduction in adipose mass are

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melanocortin, corticotropin releasing factor, as well as the recently described peptide hormone leptin. Web site: http://www.delphion.com/details?pn=US06001578__ •

Methods of treating obesity with purine related compounds Inventor(s): LaNoue; Kathryn F. (Hershey, PA) Assignee(s): The Pennsylvania Research Corporation (University Park, PA) Patent Number: 5,300,298 Date filed: May 6, 1992 Abstract: There is disclosed a method of treating obesity in warm-blooded animals, including humans, as well as a method of increasing the muscle mass to fat ratio in farm animals. The methods entail administering to an animal in need thereof, an effective amount of certain 8-phenylxanthines substituted in the 3- or 4-position of the phenyl group by an alkenylene, alkenyleneoxy, alkynylene or alkynyleneoxy bearing a terminal acetic grouping. Excerpt(s): The present invention pertains to a method of treating obesity in warmblooded animals, including humans, and to methods of increasing the ratio of muscle mass to fat in farm animals.... U.S. Pat. No. 4,879,296, issued Nov. 7, 1989 and U.S. Pat. No. 4,981,857, issued Jan. 1, 1991, disclose purine derivatives of Formula I described below, which are useful in the present invention. Methods of preparing the compounds are disclosed in both U.S. Pat. Nos. 4,879,296 and 4,981,857. The patents also disclose that the compounds provided therein are useful in human and veterinary therapy, particularly for conditions associated with the cell surface effects of adenosine. Even so, there is no disclosure in either U.S. patent that the compounds provided therein are useful as anti-obesity agents, or as agents capable of increasing the ratio to muscle mass to fat in farm animals. Instead, both patents are concerned with using the compounds disclosed therein in the treatment or prophylaxis of AIDS and other retroviral infections and for pathophysiological disorders arising from the cell surface effects of adenosine. Such pathophysiological disorders caused by adenosine/cell surface interaction are disclosed in both U.S. patents as including those arising within the cardiovascular, gastrointestinal or neuroendocrine systems, including heart block, asthma, and irritable bowel syndrome. U.S. Pat. No. 4,879,269 and 4,981,857 are each incorporated herein by reference, in their entirety.... The present invention provides a method of treating obesity in warm-blooded animals. In particular, the present invention provides a method of treating obesity (e.g., adult onset obesity, lifelong obesity and morbid obesity.sup.7) in humans. The method entails administering to a patient in need thereof, an effective amount of one of the anti-obesity agents encompassed by Formula I, as shown below. Such compounds are advantageously administered to a patient in need thereof in the form of a pharmaceutical composition, in combination with a pharmaceutically acceptable carrier. Web site: http://www.delphion.com/details?pn=US05300298__

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Methods of treating or preventing weight gain, obesity, and related disorders Inventor(s): Jerussi; Thomas P. (19 Garvey Rd., Framingham, MA 01701), Senanayake; Chrisantha H. (11 Old Farm Cir., Shrewsbury, MA 01545), Fang; Qun K. (35 Atwood St., Wellesley, MA 02181) Assignee(s): none reported Patent Number: 6,538,034 Date filed: December 4, 2001 Abstract: Methods are disclosed for the treatment and prevention of obesity, weight gain, and eating disorders. The methods comprise the administration of racemic or optically pure sibutramine metabolites and pharmaceutically acceptable salts, solvates, and clathrates thereof. Excerpt(s): The invention relates to methods of using, and compositions comprising, dopamine reuptake inhibitors and, in particular, racemic and optically pure metabolites of sibutramine.... Sibutramine, chemically named [N-1-[1-(4-chlorophenyl)cyclobutyl]-3methylbutyl]-N,N-dimethylamine, is a neuronal monoamine reuptake inhibitor which was originally disclosed in U.S. Pat. Nos. 4,746,680 and 4,806,570. Sibutramine inhibits the reuptake of norepinephrine and, to a lesser extent, serotonin and dopamine. See, e.g., Buckett et al., Prog. Neuro-psychopharm. & Biol. Psychiat., 12:575-584, 1988; King et al., J. Clin. Pharm., 26:607-611 (1989).... Racemic sibutramine is sold as a hydrochloride monohydrate under the tradename MERIDIA.RTM., and is indicated for the treatment of obesity. Physician's Desk Reference.RTM. 1494-1498 (53.sup.rd ed., 1999). The treatment of obesity using racemic sibutramine is disclosed, for example, in U.S. Pat. No. 5,436,272. Web site: http://www.delphion.com/details?pn=US06538034__

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Novel anti-obesity compounds and method of use Inventor(s): Ruhe; Rodney C. (1000 Willmar Ave., SW., Willmar, MN 56201) Assignee(s): none reported Patent Number: 4,897,390 Date filed: July 21, 1987 Abstract: The present invention provides novel compounds for controlling mammalian obesity by simultaneous action upon caloric intake and caloric expenditure. This is accomplished by the administration of pharmaceutically acceptable and therapeutically active analogs of.alpha.-HET and.beta.-HET, having a methyl group at the 3.beta. position to avoid metabolically induced conjugation of the molecule to an inactive species while retaining the structural integrity of the molecule. Excerpt(s): This invention relates generally to the use of steroid compounds in the reduction of mammalian obesity. In particular, this invention relates to the synthesis and use of etiocholanone derivatives as anti-obesity agents.... Weight reduction is accomplished when the body takes in fewer calories than it expends. Thus, all weight control measures involve strategies for either reducing caloric intake, or, increasing energy expenditure. For example, diets achieve weight reduction by directing an individual to consume food sufficient to maintain nutritional balance but insufficient to maintain body weight. U.S. Pat. No. 4,137,327 to Marshall claims an analogous process whereby a mixture of albumin and oxethazine is swallowed prior to eating. The mixture

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purportedly clings to the walls of the stomach and anesthetizes the nerve endings which activate digestive fluids. The process thereby permits eating without caloric intake. On the other hand, exercise or activity programs achieve weight reduction by increasing the body's rate of caloric expenditure. Such programs are effective when they specify normal levels of food consumption and greater than normal levels of exercise.... It follows that the most efficient weight reduction strategy would simultaneously decrease caloric intake while increasing caloric expenditure. To this end, dehydroepiandrosterone ("DHEA") is a promising antiobesity agent. The exact mechanism by which DHEA effects weight loss is not known. However, experimental evidence suggests that DHEA inhibits particular metabolic enzymes (and thus caloric intake) while simultaneously increasing the overall metabolic rate (and therefor caloric expenditure). Web site: http://www.delphion.com/details?pn=US04897390__ •

Ob receptor and methods for the diagnosis and treatment of body weight disorders, including obesity and cachexia Inventor(s): Tartaglia; Louis A. (Watertown, MA), Tepper; Robert I. (Weston, MA), Culpepper; Janice A. (Brookline, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,548,269 Date filed: April 26, 1996 Abstract: The present invention relates to the discovery, identification and characterization of nucleotides that encode Ob receptor (ObR), a receptor protein that participates in mammalian body weight regulation. The invention encompasses obR nucleotides, host cell expression systems, ObR proteins, fusion proteins, polypeptides and peptides, antibodies to the receptor, transgenic animals that express an obR transgene, or recombinant knock-out animals that do not express the ObR, antagonists and agonists of the receptor, and other compounds that modulate obR gene expression or ObR activity that can be used for diagnosis, drug screening, clinical trial monitoring, and/or the treatment of body weight disorders, including but not limited to obesity, cachexia and anorexia. Excerpt(s): The present invention relates to the discovery, identification and characterization of nucleotides that encode Ob receptor (ObR), a receptor protein that participates in mammalian body weight regulation. The invention encompasses obR nucleotides, host cell expression systems, ObR proteins, fusion proteins, polypeptides and peptides, antibodies to the receptor, transgenic animals that express an obR transgene, or recombinant knock-out animals that do not express the ObR, antagonists and agonists of the receptor, and other compounds that modulate obR gene expression or ObR activity that can be used for diagnosis, drug screening, clinical trial monitoring, and/or the treatment of body weight disorders, including but not limited to obesity, cachexia and anorexia.... Obesity represents the most prevalent of body weight disorders, and it is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to other diseases. For example, this disorder is responsible for increased incidences of

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diseases such as coronary artery disease, stroke, and diabetes. (See, e.g., Nishina, P. M. et al., 1994, Metab. 43:554-558.) Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity (Friedman, J. M. et al., 1991, Mammalian Gene 1:130-144). The epidemiology of obesity strongly shows that the disorder exhibits inherited characteristics (Stunkard, 1990, N. Eng. J. Med. 322:1483). Moll et al. have reported that, in many populations, obesity seems to be controlled by a few genetic loci (Moll et al. 1991, Am. J. Hum. Gen. 49:1243). In addition, human twin studies strongly suggest a substantial genetic basis in the control of body weight, with estimates of heritability of 80-90% (Simopoulos, A. P. & Childs B., eds., 1989, in "Genetic Variation and Nutrition in Obesity", World Review of Nutrition and Diabetes 63, S. Karger, Basel, Switzerland; Borjeson, M., 1976, Acta. Paediatr. Scand. 65:279-287). Web site: http://www.delphion.com/details?pn=US06548269__ •

Obesity associated genes Inventor(s): North; Michael (La Jolla, CA), Nishina; Patsy (Bar Harbor, ME), NobenTrauth; Konrad (Bar Harbor, ME), Naggert; Juergen (Bar Harbor, ME) Assignee(s): Sequana Therapeutics, Inc. (La Jolla, CA), The Jackson Laboratory (Bar Harbor, ME) Patent Number: 5,776,762 Date filed: September 17, 1996 Abstract: The gene responsible for the autosomal recessive mouse obesity mutation tub was identified by positional cloning. The homologous human gene is also provided. The genes are used to produce tubby protein; in screening for compositions that modulate the expression or function of the tubby protein; and in studying associated physiological pathways. The DNA is further used as a diagnostic for genetic predisposition to obesity, retinal degeneration or cochlear degeneration. The mutation responsible for the tub phenotype is a G to T transversion that abolishes a donor splice site in the 3' coding region and results in a larger transcript containing the unspliced intron. A second, prematurely truncated transcript arises from the introduction of a premature polyadenylation site in the unspliced intron. Excerpt(s): The field of this invention is genes associated with obesity in mammals.... Human obesity is a widespread and serious disorder, affecting a high percentage of the adult population in developed countries. In spite of an association with heart disease, type II diabetes, cancer, and other conditions, few persons are able to permanently achieve significant weight loss. Failure to treat obesity may be at least partially attributed to the complexity of the disease. Genetic, psychological and environmental factors all play a role in individual patterns of weight gain or loss, making it exceedingly difficult to define the contribution of any single element.... An understanding of the genetic factors that underlie obesity may aid in treatment. However, defining the exact genetic loci involved in a human polygenic trait requires extensive family studies. Because there are so many genes that can affect the single trait of obesity, in humans it may be virtually impossible to statistically determine the contribution of one locus. An attempt at such mapping studies can be further complicated by the interaction and linkage of genes. Also, environmental effects cannot be assumed to be the same for all

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genotypes. As an alternative to the complexities of human genetic mapping, animal models may be useful. Web site: http://www.delphion.com/details?pn=US05776762__ •

Obesity protein analog compounds and formulations thereof Inventor(s): Hoffmann; James Arthur (Greenwood, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,831,017 Date filed: January 24, 1997 Abstract: The present invention provides novel compounds, which comprise an obesity protein analog complexed with a divalent metal cation, pharmaceutical formulations thereof, and methods of using such compounds for treating obesity, and disorders associated with obesity such as diabetes, cardiovascular disease and cancer. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/011,055, filed Jan. 25, 1996.... The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. More specifically, the present invention relates to compounds and formulations of an obesity protein analog.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are overweight. Kuczmarski, Amer. J. of Clin. Nutr. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society. Web site: http://www.delphion.com/details?pn=US05831017__

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Obesity treatment tools and methods Inventor(s): Deem; Mark E. (Mountain View, CA), Sutton; Douglas S. (Pacifica, CA), Gifford, III; Hanson S. (Woodside, CA), Andreas; Bernard H. (Redwood City, CA), French; Ronald G. (Santa Clara, CA) Assignee(s): Satiety, Inc. (Redwood City, CA) Patent Number: 6,558,400 Date filed: May 30, 2001 Abstract: Various obesity treatment tools and methods are described herein, as well as treatments for other gastric-related diseases, e.g., GERD. Treatment includes reducing the size of the stomach pouch to limit the caloric intake as well as to provide an earlier feeling of satiety. This may be done by creating a smaller gastric pouch within the stomach directly from the interior of the stomach itself. The smaller pouches may be made through the use of individual anchoring devices, rotating probes, or volume reduction devices. A pyloroplasty procedure may also be performed to render the pyloric sphincter incompetent. A gastric bypass procedure may additionally be

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performed using atraumatic magnetic anastomoses devices so that sugars and fats are passed directly to the bowel while bypassing the stomach. Many of these procedures may be done in a variety of combinations. Treatment may create enforced behavioral modifications by discouraging the ingestion of high-caloric foods. Excerpt(s): The present invention relates generally to tools and methods for the treatment of obesity. More particularly, the present invention relates to tools and methods for performing less traumatic gastroplasty procedures.... Obesity is considered a major health problem with annual associated costs reaching $100 billion in the U.S. alone. Morbid obesity is a condition of obesity with the presence of a secondary debilitating progressive disease and is generally associated with a body mass index (BMI).gtoreq.40 kg/m.sup.2. While the basic mechanism of obesity is simply an imbalance between caloric intake and burn rate, the underlying factors are varied and complex and conservative attempts at sustained weight loss with this population are almost always unsuccessful. Often, there are genetic and other biological influences that may override environmental causes. Consequently, obesity is a disease that eludes a simple treatment, with a recurrence rate above 90% for those who attempt to lose weight. Moreover, long-term results using conservative treatments for morbid obesity are generally unsuccessful and are typically associated with further loss of self-esteem with the regaining of weight. Hypertension, cardiovascular disease, diabetes, along with a host of other comorbidities all make morbid obesity second only to smoking as a preventable cause of death.... Surgical procedures for obesity date back to 1889 (Billroth) with the earliest peer reviewed procedure being the jejuno-ileal bypass in 1954 (Kreman). A successful procedure is commonly defined as one that results in at least 50% excess weight loss at 2 years. Today, the most commonly done operation is the Roux-en-Y gastric bypass (RYGB), with around 35,000 performed annually in the U.S. Other forms of bariatric surgery include Fobi pouch, bilio-pancreatic diversion, and gastroplasty or "stomach stapling". The single existing procedure that involves an implanted device is the Lap-Band, which is a laparoscopically installed inflatable cuff that is placed around the top of the stomach just below the lower esophageal sphincter (LES). This device affects satiety only (no reduced caloric absorption). Because there is more to obesity than simple overeating, it is unlikely that Lap-Band by itself will ever be as effective as a surgery that includes other physiologic feedback mechanisms. Web site: http://www.delphion.com/details?pn=US06558400__ •

Oxadiazole benzenesulfonamides as selective.beta..sub.3 Agonist for the treatment of Diabetes and Obesity Inventor(s): Biftu; Tesfaye (Westfield, NJ), Fisher; Michael H. (Ringoes, NJ), Feng; Danqing Dennis (Branchburg, NJ), Kuo; Chan-Hwa (South Plainfield, NJ), Liang; GuiBai (Scotch Plains, NJ), Naylor; Elizabeth M. (Scotch Plains, NJ), Weber; Ann E. (Scotch Plains, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 6,034,106 Date filed: June 4, 1997 Abstract: Oxadiazole substituted benzenesulfonamides are selective.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride

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levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for increasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptormediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus. Web site: http://www.delphion.com/details?pn=US06034106__ •

Percutaneous intragastric balloon catheter for the treatment of obesity Inventor(s): De Hoyos Garza; Andres (Mexico City, MX) Assignee(s): none reported Patent Number: 6,454,785 Date filed: February 23, 2001 Abstract: The present invention relates to a percutaneous intragastric balloon catheter for the treatment of obesity. The invention occupies a portion of the gastric cavity causing a feeling of satiety and decreasing the consumption of food by an obese patient. This invention consists in a percutaneous intragastric balloon that is placed in a nonsurgically form. The percutaneous intragastric balloon catheter is collocated by percutaneous endoscopic gastrotomy (PEG). The invention comprises an affixed valve for regulating the amount of fluid introduced or evacuated from the percutaneous intragastric balloon. Excerpt(s): This invention relates to gastrostomy devices for use in the treatment of obesity. More particularly, the invention relates to percutaneous balloon catheters positioned in the stomach for medical treatment of morbid obesity in humans.... Morbid obesity is a chronic medical illness defined as overweight of 50 to 100 percent above the ideal body weight. Obesity is a major medical problem affecting millions of people worldwide. In addition to the phychosocial stigmas associated with the condition or disease, many serious health ramifications may develop. Hypertension, hyperlipidemia, exacerbation of diabetes mellitus, heart disease, degenerative arthritis, and Pickwickian syndrome. Certain types of cancer, gallstones, varicose veins, thromboembolism and

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hernias are more common among overweight individuals. In addition, morbid obesity can lead to psychosocial difficulties such as depression, loss of self-esteem and decreased employability.... To date, numerous attempts have been made to cause weight loss in morbidly obese patients. None of them have been entirely successful. The weight loss methods can be broadly divided into behavioral modification, vigorous exercise, use of pharmaceuticals, medical diets, surgical procedures and devices. Web site: http://www.delphion.com/details?pn=US06454785__ •

Peroral apparatus for morbid obesity treatment Inventor(s): Angelchik; Jean P. (1728 W. Glendale Ave., Phoenix, AZ 85021) Assignee(s): none reported Patent Number: 4,648,383 Date filed: July 22, 1985 Abstract: Apparatus for peroral treatment of morbid obesity includes a collapsible intragastric appliance which can be temporarily deformed to pass through the esophagus and cardiac opening of the stomach and to autogenously assume a normal shape after it is received in the stomach to stimulate neuro-receptors in the sub-mucosa of the gastric fundus. Means are provided for detachably connecting the appliance to the lower end of an elongate, semi-rigid inserter rod which is passed through an aperture formed in the appliance to effect the detachable connection. Downward pressure on the inserter rod forces the collapsed appliance through the esophagus and cardiac opening into the stomach and slight upward force of the inserter rod is thereafter applied to detach the rod from the appliance. Excerpt(s): This invention relates to apparatus for peroral treatment of morbid obesity without surgery.... In still another aspect, the invention concerns such improved apparatus in which a collapsible intra-gastric appliance is emplaced in the gastric fundus with improved convenience and reduced discomfort for the patient.... In still another aspect the invention relates to peroral emplaceable applicances for treatment of morbid obesity which may have biodegradable parts which dissolve under normal stomach conditions after a preselected time to permit the remains of the appliance to be passed from the body through the intestines, such that removal of the appliance by surgery is unnecessary. Web site: http://www.delphion.com/details?pn=US04648383__

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Pharmaceutical composition for treatment of obesity Inventor(s): Langer; Salomon (Paris, FR) Assignee(s): Synthelabo (Paris, FR) Patent Number: 4,791,119 Date filed: September 9, 1987 Abstract: A method of treatment of obesity which comprises administering to a subject liable thereto or suffering therefrom an effective dose of 4-(2naphthylmethoxy)piperidine.

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Excerpt(s): The present invention relates to pharmaceutical compositions.... 4-(2naphthylmethoxy)piperidine is described in French Patent of Addition No. 81/19,025 (2,514,353) dated Oct. 9, 1981, to Pat. No. 80/09,513, as having antidepressant properties.... We have suprisingly found, according to the present invention, that 4-(2naphthylmethoxy)piperidine possesses anorexigenic properties and that it may therefore be employed in the treatment of obesity. Web site: http://www.delphion.com/details?pn=US04791119__ •

Polypeptide for obesity and type II diabetes mellitus Inventor(s): Shuldiner; Alan R. (Columbia, MD), Walston; Jeremy (Baltimore, MD), Silver; Kristi (Baltimore, MD), Roth; Jesse (Baltimore, MD) Assignee(s): The Johns Hopkins University School of Medicine (Baltimore, MD) Patent Number: 5,877,283 Date filed: June 15, 1998 Abstract: The present invention provides a novel polypeptide characterized by a nonconservative missense mutation, Trp64Arg, in the.beta.3-adrenergic receptor (.beta.3AR) that increases susceptibility to obesity and non-insulin dependent diabetes mellitus (NIDDM; type II diabetes). Also provided are methods of diagnosis and methods of treatment of subjects having or at risk of having type II diabetes/obesity. Excerpt(s): This invention relates generally to non-insulin dependent diabetes mellitus (NIDDM) (type II) and obesity, and specifically to a novel Trp64Arg mutation in the.beta.3-adrenergic receptor that increases susceptibility to obesity and type II diabetes.... Non-insulin dependent diabetes mellitus (NIDDM) is one of the most common inherited diseases in man with an estimated prevalence in Caucasian populations of 8-10% (Harris, et al., Diabetes, 36:523-534, 1987). Although most forms of NIDDM do not exhibit simple Mendelian inheritance, the contribution of heredity is well recognized (Rotter, et al., Diabetes Mellitus: Theory and Practice, 378-413, 1990). The genetic basis of a few rare monogenic syndromes of NIDDM have been elucidated, but together, these syndromes account for a very small minority of cases (Taylor, et al., Endocrine Rev., 13:566-595, 1992; Froguel, et al., N. Engl. J. Med., 328:697-702, 1993; Steiner, et al., Diabetes Care, 13:600-609, 1990; and Kadowaki, et al., N. Engl. J. Med., 330:962-968, 1994). It is likely that the common forms of NIDDM are complex and heterogenous, and result when a pool of mutant genes, each of which contributes modestly and in a subtle way, interact with each other and with environmental, aging and behavioral influences to lead to the expression of the disease. This pool of genes may vary between populations and among individuals within a population, despite the illusion of a clinically homogenous phenotype.... Obesity is a known risk factor for the development of NIDDM (Barrett-Conner, E., Epidemiol. Rev., 11:172-181, 1989; and Knowler, et al., Am. J. Clin. Nutr., 53:1543-1551, 1991), and although less well studied than NIDDM, also has clear genetic determinants (Bouchard, C., World Rev. Nutr. Diet, 72:68-77, 1993; and Stunkard, et al., N. Engl. J. Med., 314:193-197,1986). Potential candidate genes for obesity (and therefore also NIDDM) include those that influence energy expenditure. In adult Pima Indians, resting metabolic rate (RMR) is familial (Bogardus, et al., N. Engl. J Med, 315:96-100, 1986 ), and in prospective studies, a low RMR is a risk factor for weight gain and obesity (Ravussin, et al., N. Engl. J Med, 318:467-472, 1988). Studies in other populations (Bouchard, et al., Metabolism, 38:364370, 1989; and Griffith, et al., Lancet, 336:76-78, 1990), as well as in animal models (Coleman, D. L., Diabetes, 31:1-6, 1992), support the relationship between heredity, low

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RMR and obesity. In rodents, RMR is regulated by the sympathetic nervous system and acts through modulation of thermogenesis in brown adipose tissue (Lowell, et al., Nature, 366:740-749, 1993). Although humans do not have anatomically distinct deposits of brown adipose tissue, the identification of human uncoupling protein, a molecular marker widely regarded as being specific for brown adipose tissue, suggests that modulation of thermogenesis in adipose tissue may also be important in humans (Cassard, et al., J. Cell Biochem., 43:255-264, 1990). Web site: http://www.delphion.com/details?pn=US05877283__ •

Polypeptides involved in body weight disorders, including obesity Inventor(s): Tartaglia; Louis Anthony (Waterstown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 5,861,485 Date filed: June 6, 1995 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... Body weight disorders, including eating disorders, represent major health problems in all industrialized countries. Obesity, the most prevalent of eating disorders, for example, is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to

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other diseases. For example, this disorder is responsible for increased incidences of diseases such as coronary artery disease, stroke, and diabetes. Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity. The nature, however, of the genetic factors which control body composition are unknown, and attempts to identify molecules involved in such control have generally been empiric and the parameters of body composition and/or substrate flux are monitored have not yet been identified (Friedman, J. M. et al., 1991, Mammalian Gene 1:130-144). Web site: http://www.delphion.com/details?pn=US05861485__ •

Process and device for treating obesity and syndromes related to motor disorders of the stomach of a patient Inventor(s): Cigaina; Valerio (Via 4 Novembre 3a, 31050 Villorba (Treviso) Assignee(s): none reported Patent Number: 5,423,872 Date filed: May 26, 1993 Abstract: The process for treating obesity and syndromes related to motor disorders of the stomach of a patient consists in artificially altering, by means of sequential electrical pulses and for preset periods of time, the natural gastric motility of the patient to prevent emptying or to slow down gastric transit. Excerpt(s): The present invention relates to a process and to a device for treating obesity and syndromes related to motor disorders of the stomach of a patient. As is known, the treatment of obesity related to hyperalimentation, i.e. to a subject who introduces food in excess of his actual caloric requirements (energy expenditure related to motor activity, work, environmental activity, etc.) is based on psychotherapeutic, pharmacological or dietary provisions or, in selected cases (pathogenic obesity), on surgical provisions.... The modern surgical orientation (surgery is the only therapy that ensures real results in patients who have exceeded obesity values close to, or in excess of, 40 BMI, i.e. the ratio of weight to the square of the height) entails the reduction of gastric compliance, with the aim of limiting the subject's ability to ingest food, or of reducing the food absorption surface by shortening or bypassing part of the digestive canal; both aims are sought in some surgical procedures.... All of the surgical procedures currently in use have some immediate and/or delayed risks and surgery must thus be considered as an extreme solution. Web site: http://www.delphion.com/details?pn=US05423872__

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Process for electrostimulation treatment of morbid obesity Inventor(s): Cigaina; Valerio (Treviso, IT) Assignee(s): Transneuronix, Inc. (Mt. Arlington, NJ) Patent Number: 6,615,084 Date filed: November 15, 2000

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Abstract: An improved process using electrostimulation for treating obesity, especially morbid obesity, and other syndromes related to motor disorders of the stomach is provided. The improved method of this invention provides electrostimulation on the lesser curvature of the stomach, preferably on the lower or distal end of the lesser curvature, which provides improved control of obesity and other syndromes related to motor disorders of the stomach. In one embodiment, the process employs stimulation of the lesser curvature at a rate of about 2 to about 14 pulses/minute with each pulse lasting about 0.5 to about 4 seconds such that there is a pause of about 3 to about 30 between the pulses. Preferably, the pulse rate is about 12 pulses/minute with each pulse lasting about 2 seconds with a pause of about 3 seconds between pulses. Preferably, the pulse amplitude is about 0.5 to about 15 milliamps. More preferable, each pulse consists of a train of micro-bursts with a frequency of about 5 to about 100 sec.sup.-1. Excerpt(s): The present invention relates to an improved process using electrostimulation for treating obesity, especially morbid obesity, and other syndromes related to motor disorders of the stomach. The improved method of this invention provides electrostimulation on the lesser curvature of the stomach which provides improved control of obesity and other syndromes related to motor disorders of the stomach.... The modern surgical orientation with regard to obesity generally entails the reduction of gastric compliance, with the aim of limiting the subject's ability to ingest food, or of reducing the food absorption surface by shortening or bypassing part of the digestive canal; both aims are sought in some surgical procedures. Until recently, surgery was the only therapy that ensures real results in patients who have exceeded obesity values close to or greater than about 40 BMI (ratio of weight to the square of the height).... All of the major surgical procedures (e.g., removal or blocking off of a portion of the stomach) currently in use have some immediate and/or delayed risks. Thus, surgery is usually considered as an extreme solution when all less invasive procedures fail. Furthermore, even surgical treatment fails in some cases, thereby requiring the surgeon to restore the original anatomical situation. Web site: http://www.delphion.com/details?pn=US06615084__ •

Process for preparing anti-obesity protein Inventor(s): MacKellar; Warren C. (Plainfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,614,379 Date filed: April 26, 1995 Abstract: The present invention is directed to a novel process of preparing an antiobesity protein using dipeptidyl-aminopeptidase isolated from the cellular slime mold, Dictyostelium discodeum. The process produces an anti-obesity protein in high yield. Excerpt(s): This invention is in the field of biotechnology. More specifically, this invention concerns a process for preparing an anti-obesity protein of SEQ ID NO: 1 using dipeptidyl-aminopeptidase isolated from the slime mold, Dictyostelium discoideum.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for

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cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately, these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05614379__ •

Process for preparing obesity protein analogs Inventor(s): Atkinson; Paul Robert (Indianapolis, IN), Foster; Lisa Kay (Greenwood, IN), Furman; Thomas Charles (Indianapolis, IN), MacKellar; Warren Cameron (Plainfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,840,517 Date filed: March 24, 1997 Abstract: The present invention is directed to an improved process for preparing in high yield an obesity protein analog using a dipeptidylaminopeptidase isolated from the slime mold, Dictyostelium discoideum. Excerpt(s): 1. Field of the Invention.... This invention is in the field of enzyme technology. More specifically, this invention concerns a process for preparing an obesity protein analog using dipeptidylaminopeptidase isolated from the slime mold, Dictyostelium discoideum.... 2. Background Information. Web site: http://www.delphion.com/details?pn=US05840517__

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Prolonged acting appetite suppressant and anti-obesity compositions containing amphetamine adipate, dextroamphetamine adipate, amphetamine sulfate and dextroamphetamine sulfate as the active agents Inventor(s): Cohen; Louis (Yonkers, NY) Assignee(s): Delco Chemical Company, Inc. (Mount Vernon, NY) Patent Number: 4,049,791 Date filed: January 26, 1976 Abstract: A prolonged acting appetite suppressant and anti-obesity composition in oral administration form which comprises an effective amount of a synergistic combination of amphetamine adipate, dextroamphetamine adipate, amphetamine sulfate and dextroamphetamine sulfate in equal or substantially equal amounts as the active agents

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in combination with a pharmaceutically acceptable carrier and is useful in suppressing one's appetite and in treating obesity. Excerpt(s): The present invention is concerned with prolonged-acting appetite suppressant and anit-obesity compositions. More particularly, the present invention is concerned with compositions in oral administration form which comprise an effective amount of a combination of at least two active agents selected from the group consisting of amphetamine adipate, dextroamphetamine adipate, amphetamine sulfate and dextroamphetamine sulfate in combination with a pharmaceutically-acceptable solid vehicle or carrier.... The compositions are preferably in the form of tablets or capsules.... The compositions of the present invention are effective for diminishing the rate of excretion by prolonging blood levels above the minimum effective concentration while avoiding peak concentrations and those side effects which may be encountered with respect to prior known amphetamine preparations. The use of a combination of the active agents set forth above have a stabilizing effect on the enzyme d-amino oxidase thereby prolonging appetite-suppressant effect of amphetamine and dextroamphetamine in the treatment of exogenous obesity while reducing undesired or adverse side effects encountered with amphetamine and dextroamphetamine. Web site: http://www.delphion.com/details?pn=US04049791__ •

Stereotactic hypothalamic obesity probe Inventor(s): Howard, III; Matthew A. (Iowa City, IA) Assignee(s): The University of Iowa Research Foundation (Iowa City, IA) Patent Number: 6,129,685 Date filed: June 27, 1997 Abstract: Apparatus and methods for regulating the appetite of an individual suffering from morbid obesity, the apparatus including a plurality of stimulation electrodes arranged longitudinally on at least one electrode support shaft for insertion within the hypothalamus for outputting electrical discharges to specific sites within the hypothalamus. Each of the plurality of stimulation electrodes may be independently controlled. Electrical discharge of various frequencies transmitted from one or more of the plurality of stimulation electrodes, and delivered to a region of the hypothalamus that is involved with either stimulating or inhibiting appetite, may be used to regulate appetite in the individual. Alternatively, an individual's appetite may be regulated by the microinfusion from at least one microinfusion catheter of an appropriate quantity of a suitable drug to a distinct site or region within the hypothalamus. Excerpt(s): This invention relates generally to an apparatus and method for delivering and detecting electrical signals to/from the patient's brain. In one embodiment, this invention also relates to an apparatus and method for performing ablative surgery on a patient. In particular the invention is concerned with an apparatus and method for performing brain surgery; and more particularly the invention is concerned with an apparatus and method for performing brain surgery by monitoring and selectively inactivating specific regions within the brain. The invention is also concerned with an apparatus and method for delivering therapeutic drugs, and more particularly is concerned with an apparatus and method for delivering therapeutic drug to a specific region within a patient's brain tissues, by monitoring and selectively delivering a drug to the target tissue. In one embodiment, this invention also relates to an apparatus and method for selective electrical stimulation of a patient's hypothalamus for the purpose of

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appetite regulation. In yet another embodiment, this invention relates to an apparatus and method for localized drug treatment for the purpose of appetite regulation by drug microinfusion into certain regions of the hypothalamus.... Prior to the nineteenth century, physicians and scientists believed the brain was an organ with functional properties distributed equally through its mass. Localization of specific functions within subregions of the brain was first demonstrated in the 1800's, and provided the fundamental conceptual framework for all of modern neuroscience and neurosurgery.... As it became clear that brain subregions served specific functions such as movement of the extremities, and touch sensation, it was also noted that direct electrical stimulation of the surface of these brain regions could cause partial reproduction of these functions. Morgan, J. P., "The first reported case of electrical stimulation of the human brain," J. History of Medicine, January 1982:51-63, 1982; Walker, A. E., "The development of the concept of cerebral localization in the nineteenth century," Bull. Hist. Med., 31:99-121, 1957. Web site: http://www.delphion.com/details?pn=US06129685__ •

Substituted benzylidene hydrazines for treating hyperglycemia, obesity and inflammation Inventor(s): Houlihan; William J. (Mountain Lakes, NJ), Manning; Robert E. (Mountain Lakes, NJ) Assignee(s): Sandoz, Inc. (E. Hanover, NJ) Patent Number: 3,982,020 Date filed: September 5, 1972 Abstract: Substituted benzylidene hydrazines e.g. N-(4-phenylbenzylidene)-N'-amidino hydrazine and their use as hypoglycemic-antihyperglycemic agents, anti-obesity agents and anti-inflammatory agents. Excerpt(s): This invention relates to substituted benzylidene hydrazines. More particularly, it relates to novel N-(4-substituted benzylidene)-N' amidino hydrazines and acid addition salts thereof. The invention also relates to the use of these and other substituted benzylidene hydrazines as hypoglycemic-antihyperglycemic agents, antiobesity agents and anti-inflammatory agents to pharmaceutical compositions containing the compounds as an active ingredient thereof, and the method of using such compositions for the treatment of hyperglycemia, obesity and inflammation.... 4. both R.sup.1 and R.sup.5 are methyl only, when R.sub.2, R.sub.3 and R.sub.4 are other than hydrogen.... Where R.sup.1, R.sup.2, R.sup.3, R.sup.4 and R.sup.5 are as defined above. Web site: http://www.delphion.com/details?pn=US03982020__

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Substituted or unsubstituted 2-phenylbenzimidazoles as anti-obesity agents Inventor(s): Houlihan; William J. (Mt. Lakes, NJ) Assignee(s): Sandoz, Inc. (E. Hanover, NJ) Patent Number: 4,212,876 Date filed: June 21, 1978 Abstract: Certain substituted or unsubstituted 2-phenylbenzimidazoles, e.g., 1-methyl-2phenylbenzimidazole, are useful as anti-obesity agents.

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Excerpt(s): This invention relates to the pharmaceutical activity of substituted or unsubstituted 2-phenylbenzimidazoles. More particularly, this invention concerns the use of substituted or unsubstituted 2-phenylbenzimidazoles in the treatment of obesity. The invention also relates to pharmaceutical compositions containing these compounds as an active ingredient thereof.... R.sub.2 represents hydrogen, fluoro or chloro.... The compounds of formula (I) above are known and may be prepared according to methods disclosed in the literature from known materials. The present invention contemplates only the novel use of such compounds as anti-obesity agents. Web site: http://www.delphion.com/details?pn=US04212876__ •

Substituted phenyl sulfonamides as selective.beta. 3 agonists for the treatment of diabetes and obesity Inventor(s): Fisher; Michael H. (Ringoes, NJ), Mathvink; Robert J. (Jersey City, NJ), Ok; Hyun O. (Edison, NJ), Parmee; Emma R. (Hoboken, NJ), Weber; Ann E. (Scotch Plains, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 5,451,677 Date filed: December 15, 1993 Abstract: Substituted phenylsulfonamides are selective.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted alkyl epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for increasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptormediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxtion (.beta..sub.2)- These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus. Web site: http://www.delphion.com/details?pn=US05451677__

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Substituted sulfonamides as selective.beta..sub.3 agonists for the treatment of diabetes and obesity Inventor(s): Fisher; Michael H. (Ringoes, NJ), Naylor; Elizabeth M. (Scotch Plains, NJ), Ok; Dong (Edison, NJ), Weber; Ann E. (Scotch Plains, NJ), Shih; Thomas (Edison, NJ), Ok; Hyun (Edison, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 5,561,142 Date filed: May 22, 1995 Abstract: Substituted sulfonamides are selective.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for increasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptormediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus. Web site: http://www.delphion.com/details?pn=US05561142__

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Substituted sulfonamides as selective.beta.-3 agonists for the treatment of diabetes and obesity Inventor(s): Fisher; Michael H. (Ringoes, NJ), Naylor; Elizabeth M. (Scotch Plains, NJ), Parmee; Emma R. (Hoboken, NJ), Shih; Thomas (Edison, NJ), Ok; Hyun (Edison, NJ), Weber; Ann E. (Scotch Plains, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 5,705,515 Date filed: July 25, 1996

Patents 323

Abstract: Substituted sulfonamides are selective.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for increasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptormediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus. Web site: http://www.delphion.com/details?pn=US05705515__ •

Susceptibility gene for obesity and type II diabetes mellitus Inventor(s): Shuldiner; Alan R. (Columbia, MD), Walston; Jeremy (Baltimore, MD), Silver; Kristi (Baltimore, MD), Roth; Jesse (Baltimore, MD) Assignee(s): The Johns Hopkins University School of Medicine (Baltimore, MD) Patent Number: 5,766,851 Date filed: May 19, 1995 Abstract: The present invention provides a novel polypeptide characterized by a nonconservative missense mutation, Trp64Arg, in the.beta.3-adrenergic receptor (.beta.3AR) that increases susceptibility to obesity and non-insulin dependent diabetes mellitus (NIDDM; type II diabetes). Also provided are methods of diagnosis and methods of treatment of subjects having or at risk of having type II diabetes/obesity. Excerpt(s): This invention relates generally to non-insulin dependent diabetes mellitus (NIDDM) (type II) and obesity, and specifically to a novel Trp64Arg mutation in the.beta.3-adrenergic receptor that increases susceptibility to obesity and type II diabetes.... Non-insulin dependent diabetes mellitus (NIDDM) is one of the most common inherited diseases in man with an estimated prevalence in Caucasian populations of 8-10% (Harris, et al., Diabetes, 36:523-534, 1987). Although most forms of

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NIDDM do not exhibit simple Mendelian inheritance, the contribution of heredity is well recognized (Rotter, et al., Diabetes Mellitus: Theory and Practice, 378-413, 1990). The genetic basis of a few rare monogenic syndromes of NIDDM have been elucidated, but together, these syndromes account for a very small minority of cases (Taylor, et al., Endocrine Rev., 13:566-595, 1992; Froguel, et al., N. Engl. J. Med., 328:697-702, 1993; Steiner, et al., Diabetes Care, 13:600-609, 1990; and Kadowaki, et al., N. Engl. J. Med., 330:962-968, 1994). It is likely that the common forms of NIDDM are complex and heterogenous, and result when a pool of mutant genes, each of which contributes modestly and in a subtle way, interact with each other and with environmental, aging and behavioral influences to lead to the expression of the disease. This pool of genes may vary between populations and among individuals within a population, despite the illusion of a clinically homogenous phenotype.... Obesity is a known risk factor for the development of NIDDM (Barrett-Conner, E., Epidemiol. Rev., 11:172-181, 1989; and Knowler, et al., Am. J. Clin. Nutr., 53:1543-1551, 1991), and although less well studied than NIDDM, also has clear genetic determinants (Bouchard, C., World Rev. Nutr. Diet, 72:68-77, 1993; and Stunkard, et al., N. Engl. J. Med., 314:193-197, 1986). Potential candidate genes for obesity (and therefore also NIDDM) include those that influence energy expenditure. In adult Pima Indians, resting metabolic rate (RMR) is familial (Bogardus, et al., N. Engl. J. Med., 315:96-100, 1986), and in prospective studies, a low RMR is a risk factor for weight gain and obesity (Ravussin, et al., N. Engl. J. Med., 318:467-472, 1988). Studies in other populations (Bouchard, et al., Metabolism, 38:364370, 1989; and Griffith, et al., Lancet, 336:76-78, 1990), as well as in animal models (Coleman, D. L., Diabetes, 31:1-6, 1992), support the relationship between heredity, low RMR and obesity. In rodents, RMR is regulated by the sympathetic nervous system and acts through modulation of thermogenesis in brown adipose tissue (Lowell, et al., Nature, 366:740-749, 1993). Although humans do not have anatomically distinct deposits of brown adipose tissue, the identification of human uncoupling protein, a molecular marker widely regarded as being specific for brown adipose tissue, suggests that modulation of thermogenesis in adipose tissue may also be important in humans (Cassard, et al., J. Cell Biochem., 43:255-264, 1990). Web site: http://www.delphion.com/details?pn=US05766851__ •

System for preventing and curing osteoporosis and obesity Inventor(s): Hirano; Shinnosuke (Kanagawa, JP) Assignee(s): Kohgen Kizai Kabushiki Kaisha (Yokohama, JP) Patent Number: 5,836,997 Date filed: November 25, 1996 Abstract: A system for preventing and curing osteoporosis and obesity, which has a mat essentially consisting of a first sheet made from a semiconductive or insulating material and having a volume resistivity of less than 10.sup.4.OMEGA..cm and a second sheet made from a semiconductive or insulating material, laminated on the first sheet and having a volume resistivity of 10.sup.4.OMEGA..cm or more; an electric power source; an electrical circuit to apply DC voltage of 25-800 to the first sheet; and a control unit. A normal person or patient is made contact with the mat, so as to put his body in electrostatic field to be formed on the mat. In another embodiment, a third sheet of a material having a volume resistivity of more than 10.sup.12.OMEGA..cm is used such that the first sheet is sandwiched between the third and second sheets.

Patents 325

Excerpt(s): The present invention relates to a system for preventing and curing osteoporosis and obesity, by putting a human body in an electrostatic field.... In recent years, medical techniques have greatly advanced to prolong the average span of human life and as a result, so-called "adult and senior diseases" tend to increase. Therefore, it has been emphasized in the medical world that so-called "Health medical science" will be required, in which each individual controls his health by himself to prevent a disease or pays his possible effort to overcome the diseases.... Among the diseases, osteoporosis has often been found in senior persons and women in menopause and it has been said that number of the patients with this disease reaches 6 million or more, even in Japan only. Web site: http://www.delphion.com/details?pn=US05836997__ •

Thiazole benzenesulfonamides as.beta.3 agonists for treatment of diabetes and obesity Inventor(s): Mathvink; Robert J. (Red Bank, NJ), Parmee; Emma R. (Highland Park, NJ), Tolman; Samuel (Jersey City, NJ), Weber; Ann E. (Scotch Plains, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 6,011,048 Date filed: January 15, 1998 Abstract: Thiazole substituted benzenesulfonamides are.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for decreasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptor mediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus.

326 Obesity

Web site: http://www.delphion.com/details?pn=US06011048__ •

Treatment for obesity Inventor(s): Horrobin; David F. (Montreal, CA) Assignee(s): Efamol Limited (London, GB2) Patent Number: 4,393,049 Date filed: June 10, 1981 Abstract: Use of.gamma.-linolenic acid and related materials alone or with zinc or.beta.lactam antibiotics to treat obesity. Excerpt(s): This invention relates to the treatment of obesity primarily, but not exclusively, in the field of human medicine.... Considerable interest has been shown in recent years in the use of prostaglandin (PG) precursors in medicine.... Prior art within this general area includes the following patents and papers. Web site: http://www.delphion.com/details?pn=US04393049__

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Treatment of insulin resistance in obesity linked type II diabetes using antagonist to TNF-alpha function Inventor(s): Hotamisligil; Gokhan S. (Charlestown, MA), Spiegelman; Bruce M. (Waban, MA) Assignee(s): Dana-Farber Cancer Institute, Inc. (Boston, MA) Patent Number: 5,730,975 Date filed: June 8, 1994 Abstract: An induction of TNF-.alpha. mRNA expression has been observed in adipose tissue from four different insulin resistant rodent models of obesity and diabetes. TNF.alpha. protein was also elevated locally and systemically. Neutralization of TNF-.alpha. in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. A method of treating an animal suffering from insulin resistance in obesity linked Type II diabetes mellitus is disclosed. The method includes providing a therapeutic agent that includes an antagonist to TNF-.alpha. function in a pharmaceutically acceptable carrier substance and administering a pharmacologically effective amount of the therapeutic agent to the animal. Excerpt(s): Obesity and diabetes are among the most common human health problems in industrialized societies. Obesity, which is the result of an imbalance between caloric intake and energy expenditure, is highly correlated with insulin resistance and diabetes in experimental animals and humans. However, the molecular mechanisms that are involved in obesity-diabetes syndromes are not clear. Since adipose tissue is the major site for energy storage and mobilization, many investigators have focused on finding abnormalities in adipocyte physiology or metabolism (Plata-Salaman, Brain Behav. Immun. 3:193, 1989; Lardy et al., Annu. Rev. Biochem. 59:689, 1990).... It has been shown that several cytokines such as tumor necrosis factor (TNF)-.alpha. have direct effects on adipocyte metabolism as well as other important metabolic actions (Le et al., Lab. Invest. 56:234, 1987; Dinarello, Immunol. Lett. 16:227, 1987; Kunkel et al., Crit. Rev. Immunol. 9:93, 1989;Grunfeld et al., Biotherapy 3:143, 1991). TNF-.alpha. acts in vitro on murine adipocytes to suppress expression of most adipose specific genes including enzymes

Patents 327

involved in lipogenesis (Kawakami et al., Proc. Natl. Acad. Sci. USA 79:912, 1982; Price et al., Arch. Biochem. Biophys. 251:738, 1986). However, some of these effects are not observed in primary cultures of human or rat adipocytes (Grunfeld et al., Biotherapy 3:143, 1991; Kern, J. Lipid Res. 29:909, 1988).... In vivo, TNF-.alpha. expression has been associated with catabolic states leading to a "wasting syndrome," termed cachexia (Beutler et al., Nature 316:552, 1985; Beutler et al., Science 232:977, 1986; Beutler et al., Nature 320:584, 1986; Oliff et al., Cell 50:555, 1987; Beutler et al., Ann. Rev. Immunol. 7:625, 1989), but this effect of TNF-.alpha. has been challenged by several groups of investigators (Semb et al., J. Biol. Chem. 262:8390, 1987; Grunfeld et al., J. Lipid Res. 30:579, 1989; Feingold et al., J. Clin. Invest. 83:1116, 1989; Patton et al., J. Clin. Invest. 80:1587 (1987); Kettlehut et al., J. Clin. Invest. 81:1384, 1988; Tracey et al., J. Clin. Invest. 86:2014, 1990; Socher et al., J. Exp. Med. 167:1957, 1988; Mullen et al., Proc. Soc. Exp. Biol. Med. 193:318, 1990; Teng et al., Proc. Natl. Acad. Sci. USA 88:3535, 1991; for reviews see C. Grunfeld et al., Cancer Res. 49:2554, 1989; Fiers, FEBS 285:199, 1991). Web site: http://www.delphion.com/details?pn=US05730975__ •

Treatment of insulin resistance in obesity linked type II diabetes using antagonists to TNF-.alpha. function Inventor(s): Hotamisligil; Gokhan S. (Charlestown, MA), Spiegelman; Bruce M. (Waban, MA) Assignee(s): Dana-Farber Cancer Institute, Inc. (Boston, MA) Patent Number: 6,015,558 Date filed: March 10, 1998 Abstract: An induction of TNF-.alpha. mRNA expression has been observed in adipose tissue from four different insulin resistant rodent models of obesity and diabetes. TNF.alpha. protein was also elevated locally and systemically. Neutralization of TNF-.alpha. in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. A method of treating an animal suffering from insulin resistance in obesity linked Type II diabetes mellitus is disclosed. The method includes providing a therapeutic agent that includes an antagonist to TNF-.alpha. function in a pharmaceutically acceptable carrier substance and administering a pharmacologically effective amount of the therapeutic agent to the animal. Excerpt(s): Obesity and diabetes are among the most common human health problems in industrialized societies. Obesity, which is the result of an imbalance between caloric intake and energy expenditure, is highly correlated with insulin resistance and diabetes in experimental animals and humans. However, the molecular mechanisms that are involved in obesity-diabetes syndromes are not clear. Since adipose tissue is the major site for energy storage and mobilization, many investigators have focused on finding abnormalities in adipocyte physiology or metabolism (Plata-Salaman, Brain Behav. Immun. 3:193, 1989; Lardy et al., Annu. Rev. Biochem. 59:689, 1990).... It has been shown that several cytokines such as tumor necrosis factor (TNF)-.alpha. have direct effects on adipocyte metabolism as well as other important metabolic actions (Le et al., Lab. Invest. 56:234, 1987; Dinarello, Immunol. Lett. 16:227, 1987; Kunkel et al., Crit. Rev. Immunol. 9:93, 1989; Grunfeld et al., Biotherapy 3:143, 1991). TNF-.alpha. acts in vitro on murine adipocytes to suppress expression of most adipose specific genes including enzymes involved in lipogenesis (Kawakami et al., Proc. Natl. Acad. Sci. USA 79:912, 1982; Price et al., Arch. Biochem. Biophys. 251:738, 1986). However, some of these effects are not observed in primary cultures of human or rat adipocytes (Grunfeld et al., Biotherapy

328 Obesity

3:143, 1991; Kern, J. Lipid Res. 29:909, 1988).... In vivo, TNF-.alpha. expression has been associated with catabolic states leading to a "wasting syndrome," termed cachexia (Beutler et al., Nature 316:552, 1985; Beutler et al., Science 232:977, 1986; Beutler et al., Nature 320:584, 1986; Oliff et al., Cell 50:555, 1987; Beutler et al., Ann. Rev. Immunol. 7:625, 1989), but this effect of TNF-.alpha. has been challenged by several groups of investigators (Semb et al., J. Biol. Chem. 262:8390, 1987; Grunfeld et al., J. Lipid Res. 30:579, 1989; Feingold et al., J. Clin. Invest. 83:1116, 1989; Patton et al., J. Clin. Invest. 80:1587 (1987); Kettlehut et al., J. Clin. Invest. 81:1384, 1988; Tracey et al., J. Clin. Invest. 86:2014, 1990; Socher et al., J. Exp. Med. 167:1957, 1988; Mullen et al., Proc. Soc. Exp. Biol. Med. 193:318, 1990; Teng et al., Proc. Natl. Acad. Sci. USA 88:3535, 1991; for reviews see C. Grunfeld et al., Cancer Res. 49:2554, 1989; Fiers, FEBS 285:199, 1991). Web site: http://www.delphion.com/details?pn=US06015558__ •

Treatment of obesity Inventor(s): Ng; Frank Man-Woon (Kew, AU), Natera; Siria Helen-Anna (Mount Waverly, AU), Jiang; Woei-Jia (Clayton, AU) Assignee(s): Monash University (Clayton, AU) Patent Number: 5,869,452 Date filed: November 15, 1994 Abstract: A method for the treatment of obesity in an animal such as a human, comprises administering to the animal an effective amount of a peptide which comprises the carboxyl-terminal sequence of a growth hormone, particularly the carboxyl-terminal sequence of human growth hormone containing amine acid residues 177-191. A pharmaceutical composition for use in the treatment of obesity is also disclosed. Excerpt(s): This invention relates to the treatment of obesity in animals. In particular, the invention relates to the treatment of obesity in humans, although it is to be understood that the present invention also extends to the treatment of obesity in non-human mammals, for example, for the improvement of meat qualities in farm animals used in food production.... The critical role of human growth hormone (hGH) in postnatal growth in humans is well recognised. Less obvious is the impact of this hormone on the regulation of lipid and carbohydrate metabolism, due to lack of detailed molecular studies.... It is well documented that the predominant form of hGH is a globular protein with a molecular weight of 22,000 daltons (22-KD) and consists of 191 amino acid residues in a single-chain, folded by 2 disulphide bonds with a small loop at the carboxyl terminus between residues 182 and 189. Recent crystallographic studies also show that the hGH molecule contains four anti-parallel.alpha.-helices which are arranged in a left-twisted, tightly-packed helical bundle.sup.1. The concept that there are discrete functional domains within the hGH molecule responsible for specific metabolic actions of the hormone is generally accepted. The amino-terminus has been identified as the functional domain responsible for the insulin-like actions of the hGH molecule.sup.2,3. Web site: http://www.delphion.com/details?pn=US05869452__

Patents 329

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Treatment of obesity Inventor(s): Ng; Frank Man-Woon (Kew, AU), Natera; Siria Helen Anna (Mount Waverly, AU), Jiang; Woei-Jia (Clayton, AU) Assignee(s): Metabolic Pharmaceuticals, Inc. (Toorak, AU) Patent Number: 6,335,319 Date filed: February 8, 1999 Abstract: A method for the treatment of obesity in an animal such as a human, comprises administering to the animal an effective amount of a peptide which comprises the carboxyl-terminal sequence of a growth hormone, particularly the carboxyl-terminal sequence of human growth hormone containing amine acid residues 177-191. A pharmaceutical composition for use in the treatment of obesity is also disclosed. Excerpt(s): This invention relates to the treatment of obesity in animals. In particular, the invention relates to the treatment of obesity in humans, although it is to be understood that the present invention also extends to the treatment of obesity in non-human mammals, for example, for the improvement of meat qualities in farm animals used in food production.... The critical role of human growth hormone (hGH) in postnatal growth in humans is well recognised. Less obvious is the impact of this hormone on the regulation of lipid and carbohydrate metabolism, due to lack of detailed molecular studies.... It is well documented that the predominant form of hGH is a globular protein with a molecular weight of 22,000 daltons (22-KD) and consists of 191 amino acid residues in a single-chain, folded by 2 disulphide bonds with a small loop at the carboxyl terminus between residues 182 and 189. Recent crystallographic studies also show that the hGH molecule contains four anti-parallel.alpha.-helices which are arranged in a left-twisted, tightly-packed helical bundle.sup.1. The concept that there are discrete functional domains within the hGH molecule responsible for specific metabolic actions of the hormone is generally accepted. The amino-terminus has, been identified as the functional domain responsible for the insulin-like actions of the hGH molecule.sup.2,3. Web site: http://www.delphion.com/details?pn=US06335319__

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Treatment of obesity and diabetes using sapogenins Inventor(s): Applezweig; Norman (New York, NY) Assignee(s): Progenics, Inc. (New York, NY) Patent Number: 4,680,289 Date filed: June 5, 1985 Abstract: Obesity and diabetes obesity syndromes are treated with 5.beta.-sapogenin or.DELTA..sup.5 sapogenin. Excerpt(s): This invention is related to U.S. patent application Ser. No. 683,423, filed Dec. 19, 1984 for Treatment of Obesity, Diabetes and Other Symptoms of Hypercorticoidism Using Etiocholanolones, and to U.S. patent application Ser. No. 515,354, filed on July 19, 1983 for "Method for Treating Diabetes Using DHEA Components" and the contents of these applications are incorporated herein by reference.... The major function of the adrenal gland is to regulate metabolism in the body so that an intermittent intake of food can be regulated to maintain a constant metabolite supply to the cells. This is

330 Obesity

accomplished by producing steroid hormones which can control the conversion of incoming nutrients, such as aminoacids, glucose and fats into storage depots from which they can thereafter be released or interchanged, allowing a continuous flow of optimum energy and growth factors to the cells.... One category of steroids is known as the adrenal androgens. Dehydroepiandrosterone (DHEA) is the principal representative of this category. The adrenal androgens which have an anabolic action are produced with puberty, reach a peak in early adulthood and then, beyond the age of 50, decline to very low levels. Web site: http://www.delphion.com/details?pn=US04680289__ •

Treatment of obesity and essential hypertension and related disorders Inventor(s): Cooper; Garth J. S. (Solana Beach, CA), Leighton; Brendan (Eynsham, GB2) Assignee(s): Amylin Pharmaceuticals, Inc. (San Diego, CA) Patent Number: 5,364,841 Date filed: June 21, 1993 Abstract: The administration of antagonists and blockers of amylin or CGRP or both for the treatment of obesity and essential hypertension and associated lipid disorders and atherosclerosis. Excerpt(s): The field of the invention is medicine, and more particularly, the effect of amylin antagonists and amylin blockers on glucose metabolism in peripheral tissues as a treatment for obesity and essential hypertension and associated lipid disorders and atherosclerosis.... Publications and other materials including patent applications used to illuminate the specification are incorporated herein by reference.... A 37-amino acid peptide called amylin has been isolated, purified, sequenced and characterized. The present invention discloses the use of amylin antagonists and amylin receptor blockers to control glucose and lipid metabolism for the treatment of obesity and essential hypertension and associated lipid abnormalities and atherosclerosis. Web site: http://www.delphion.com/details?pn=US05364841__

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Treatment of obesity, diabetes and other symptoms of hypercorticoidism using etiocholanolones Inventor(s): Coleman; Douglas L. (Seal Harbor, ME), Applezweig; Norman (New York, NY) Assignee(s): Jackson Lab. (Bar Harbor, ME), Progenics, Inc. (New York, NY) Patent Number: 4,666,898 Date filed: December 19, 1984 Abstract: Obesity, diabetes obesity syndromes and associated hypercorticoidism are treated with.alpha. and/or.beta.-etiocholanolone. Excerpt(s): The major function of the adrenal gland is to regulate metabolism in the body so that an intermittent intake of food can be regulated to maintain a constant metabolite supply to the cells. This is accomplished by producing steroid hormones which can control the conversion of incoming nutrients, such as aminoacids, glucose and fats into storage depots from which they can thereafter be released or interchanged,

Patents 331

allowing a continuous flow of optimum energy and growth factors to the cells.... The steroid hormones are divided mainly into three classes. The first is glucocorticoids (cortisol), also known as gluconeogenic or diabetogenic steriods, which can convert aminoacids into glucose for direct use or store the glucose as glycogen for later use. Cortisol can therefore have an anti-anabolic effect through the depletion of aminoacids needed for protein synthesis and a diabetogenic effect through the direct release of glucose from the glycogen store.... A glucocorticoid excess, resulting from an excess of the pituitary hormone, adrenal cortico-trophic hormone (ACTH), which controls cortisol production, causes Cushing's Syndrome, an uncommon disease. Intake of an excess amount of cortisol from pharmacological use of steroids can also cause Cushing's Syndrome or Cushingoid-like disorders (hypercorticosteroidism, or more briefly hypercorticoidism) which are progeric in that they resemble the symptoms of the diseases of aging, e.g. obesity, hypertension, diabetes, renal stones, osteoporosis, mental disorder, menstrual disturbance, susceptibility to infection and poor wound healing. Web site: http://www.delphion.com/details?pn=US04666898__ •

Treatments for obesity and methods for identifying compounds useful for treating obesity Inventor(s): Hadcock; John R. (East Lyme, CT), Swick; Andrew G. (East Lyme, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,451,783 Date filed: January 16, 2001 Abstract: The present invention provides a method of treating obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the method comprising the step of administering to a patent having or at risk of having one of the above-mentioned diseases a therapeutically effective amount of a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not attenuate the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors. The present invention also provides a method of identifying a compound that is useful for the treatment or prevention of obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the method comprising the steps of: 1) determining if a compound affects the binding of agoutirelated protein to melanocortin receptors; 2) determining if a compound affects the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors; and 3) selecting a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not affect the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors. Excerpt(s): The present invention provides methods of treating obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the methods comprising the step of administering to a patient having or at risk of having one of the above-mentioned diseases or conditions a therapeutically effective amount of a compound that attenuates the binding of agouti-related protein to

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melanocortin receptors, but does not attenuate the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors.... The present invention also provides methods of identifying a compound that is useful for the treatment of obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the methods comprising the steps of: 1) determining if a compound affects the binding of agouti-related protein to melanocortin receptors; 2) determining if a compound affects the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors; and 3) selecting a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not attenuate the binding of cc-melanocyte stimulating hormone to melanocortin receptors.... Obesity is a devastating disease. In addition to harming physical health, obesity can wreak havoc on mental health because obesity affects self-esteem, which ultimately can affect a person's ability to interact socially with others. Unfortunately, obesity is not well understood, and societal stereotypes and presumptions regarding obesity only tend to exacerbate the psychological effects of the disease. Because of the impact of obesity on individuals and society, much effort has been expended to find ways to treat obesity, but little success has been achieved in the long-term treatment and/or prevention of obesity. Web site: http://www.delphion.com/details?pn=US06451783__ •

Use of agonists of the peroxisome proliferator activated receptor alpha for treating obesity Inventor(s): Willson; Timothy Mark (Durham, NC) Assignee(s): Glaxo Wellcome Inc. (Research Triangle Park, NC) Patent Number: 6,028,109 Date filed: September 28, 1998 Abstract: The use of agonists of the peroxisome proliferator activated receptor alpha (PPAR.alpha.) for the manufacture of a medicament for the treatment of obesity and methods of treating obesity comprising the administration of a therapeutic amount of a PPAR.alpha. agonist. Excerpt(s): The present invention is concerned with medicaments, and more particularly medicaments for use in the treatment of obesity.... Obesity can be described as a state of excessive accumulation of body fat, and is widely considered to be a major public health problem, being associated with substantially increased morbidity and mortality, as well as psychological problems, reduced economic achievement, and discrimination. Examples of health and social problems thought to be caused or exacerbated by obesity include coronary heart disease, stroke, obstructive sleep apnoea, diabetes mellitus, gout, hyperlipidemia, osteoarthritis, reduced fertility, impaired psychosocial function, reduced physical agility and increased risk of accidents, impaired obstetrical performance, reduced economic performance and discrimination and prejudice.... Causes of obesity remain unclear, however whether obesity is of genetic origin or is promoted by a genotype-environment interaction, or both, it remains true that energy intake must have exceeded metabolic and physical (work) energy expenditure for there to have been surplus energy available for fat deposition. There remains considerable uncertainty, however, over the relative importance of different mechanisms in achieving this positive energy balance.

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Web site: http://www.delphion.com/details?pn=US06028109__ •

Use of an NK-1 receptor antagonist and an SSRI for treating obesity Inventor(s): Hefti; Franz Fridolin (Much Hadham, GB) Assignee(s): Merck Sharp & Dohme Limited (Hoddesdon, GB) Patent Number: 6,162,805 Date filed: October 22, 1999 Abstract: The present invention relates to the use of an NK-1 receptor antagonist and a selective serotonin reuptake inhibitor for the treatment or prevention of obesity. Excerpt(s): This invention relates to the treatment or prevention of obesity by the administration of a combination of a NK-1 receptor antagonist and a selective serotonin reuptake inhibitor.... Obesity is a chronic disease that is highly prevalent in modern society and is associated not only with a social stigma, but also with decreased life span and numerous medical problems, including adverse psychological development, reproductive disorders such as polycystic ovarian disease, dermatological disorders such as infections, varicose veins, Acanthosis nigricaits, and eczema, exercise intolerance, diabetes mellitus, insulin resistance, hypertension, hypercholesterolemia, cholelithiasis, osteoarthritis, orthopedic injury, thromboembolic disease, cancer, and coronary heart disease. Rissanen et al, British Medical Journal, 301:835-837 (1990).... Treatment regimens for obesity typically include the use of selective serotonin reuptake inhibitors (SSRIs). SSRIs alter the synaptic availability of serotonin through their inhibition of presynaptic reaccumulation of neuronally released serotonin. The SSRI, fluoxetine, has found to be of use in the treatment of obesity. Web site: http://www.delphion.com/details?pn=US06162805__

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Use of CNTF (ciliary neurotrophic factor) receptor activators for the treatment of obesity Inventor(s): Ciliberto; Gennaro (Rome, IT), Costa; Patrizia (Rome, IT), Paonessa; Giacomo (Rome, IT), Lazzaro; Domenico (Rome, IT), Gloaguen; Isabelle (Scoppito L'Aquila, IT), Di Marco; Annalise (Rieti, IT), De Martis; Anna (Rome, IT), Laufer; Ralph (Rome, IT), Cortese; Riccardo (Rome, IT) Assignee(s): Istituto di Ricerche di Biologia Molecolare P. Angeletti S.p.A. (Pomezia, IT) Patent Number: 6,565,869 Date filed: July 19, 1999 Abstract: The present invention refers to the use of hCNTF (human ciliary neurotrophic factor), mutants thereof or other molecules that activate the CNTF receptor, for the preparation of drugs for the treatment of obesity and associated disease, for example hyperglycemia. FIG. 1 shows the anti-obesity effect of hCNTF and leptin on body weight (left panels) and on food intake (right panels) in genetically obese mice and in mice with diet-induced obesity (DIO). Excerpt(s): The present application is the national stage under 35 U.S.C. 371 of PCT/IT97/00283, filed Nov. 18, 1997.... The subject of the present invention is the use of molecules that activate the CNTF (ciliary neurotrophic factor) receptor--such as hCNTF (human CNTF) or mutants of hCNTF--as active principles in the formulation of

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pharmaceutical compositions suitable for the treatment of obesity and of related diseases. The term hCNTF mutant is intended to mean an amino acid sequence that can in theory be derived from hCNTF by substitution of one or more amino acids.... Obesity, which affects >30% of the adult population in the industrial world, is a major public health problem, since it is associated with type II diabetes, hypertension, hyperlipidemia and increased mortality rate. Obesity is the result of a positive energy balance, as a consequence of an increased ratio of caloric intake to energy expenditure. Treatment is generally unsuccessful due to the operation of mechanisms that restore adipose mass after both intentional or unintentional changes (1). The lipostasis theory postulates that the size of the body fat depot is regulated by a feedback loop, constituted by adipocytederived circulating molecules that act on the hypothalamus to decrease appetite and increase energy expenditure (2). Web site: http://www.delphion.com/details?pn=US06565869__ •

Use of droloxifene for the treatment of protastic disease, endometriosis and obesity Inventor(s): Thompson; David D. (Gales Ferry, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 5,852,059 Date filed: January 6, 1997 Abstract: This invention provides a method for treating a condition or disease selected from endometriosis, obesity, benign prostatic hypertrophy and prostatic carcinoma in mammals which comprises administering to said mammal an amount of droloxifene or a pharmaceutically acceptable salt thereof which is effective in treating said condition or disease. Excerpt(s): Droloxifene is a known compound disclosed in U.S. Pat. No. 5,047,431 in which it is disclosed as an anti-tumor agent, particularly for treatment and prevention of cancer of the breast. Droloxifene is also useful for the relief of bone diseases caused by the deficiency of estrogen or the like, which are often observed in women after menopause or those with the ovaries removed. U.S. Pat. No. 5,254,594.... Gill-Sharma, et al., J. Reproduction and Fertility (1993) 99, 395, disclose that tamoxifen at 200 and 400 mg/kg/day reduces the weights of the testes and secondary sex organs in male rats.... Neubauer, et al., The Prostate 23: 245 (1993) teach that raloxifene treatment of male rats produced regression of the ventral prostate. Web site: http://www.delphion.com/details?pn=US05852059__

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Viral obesity methods and compositions Inventor(s): Atkinson; Richard L. (Fitchburg, WI), Dhurandhar; Nikhil V. (Madison, WI) Assignee(s): Obetech, LLC (Fitchburg, WI) Patent Number: 6,127,113 Date filed: April 6, 1998 Abstract: A source of viral induced obesity has been discovered. A virus known as AD36P has been found to be associated with obesity in both animals and humans. Diagnostic DNA sequences are presented so that DNA based tests for the presence of the obesity associated virus can be conducted.

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Excerpt(s): This invention concerns obesity in humans caused by viruses and methods and compositions for diagnosing, treating and preventing this disease.... The invention also concerns methods and compositions for reducing levels of triglycerides and cholesterol in humans.... More particularly, the invention concerns methods and compositions for diagnosing whether obesity in a human is caused by a virus or whether a person is susceptible to becoming obese because of having been infected with and obesity-causing virus, methods for testing or screening body fluids (e.g., donated human blood) for the presence of obesity-causing viruses, methods for treating and preventing viral obesity in humans, methods for preparing vaccine compositions for treating and preventing viral obesity in humans, such vaccine compositions themselves, and viruses which cause viral obesity in humans. Web site: http://www.delphion.com/details?pn=US06127113__

Patent Applications on Obesity As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to obesity: •

2-amino-benzoxazinone derivatives for the treatment of obesity Inventor(s): Palmer, Richard Michael John; (Beckenham, GB), Dunk, Christopher Robert; (Ely, GB), Mitchell, Timothy John; (Cambridge, GB), Downham, Robert; (Cambridge, GB), Hodson, Harold Francis; (Beckenham, GB), Carr, Beverley Jane; (Royston, GB) Correspondence: Choate, Hall & Stewart; Exchange Place; 53 State Street; Boston; MA; 02109; US Patent Application Number: 20030013707 Date filed: July 6, 2001 Abstract: The use of a compound comprising formula (I): 1(I)or a salt, ester, amide or prodrug therof in the inhibition of an enzyme whose preferred mode of action is to catalyse the hydrolysis of an ester functionality, e.g. in the control and inhibition of unwanted enzymes in products and processes. The compounds are also useful in medicine e.g. in the treatment of obesity and related conditions. The invention also relates to novel compounds within formula (I), to processes for preparing them and pharmaceutical compositions containing them.In formula (I) A is a 6-membered aromatic or heteroaromatic ring; andR.sup.1 is a branched or unbranched alkyl (optionally interrupted by one or more oxygen atoms), alkenyl, alkynyl, cycloalkyl, cycloalkenyl, aryl, arylalkyl, reduced arylalkyl, arylalkenyl, heteroaryl, heteroarylalkyl, heteroarylalkenyl, reduced aryl, reduced heteroaryl, reduced heteroarylalkyl or a substituted derivative of any of the foregoing groups. Excerpt(s): This application is a continuation of international application number PCT/GB00/00031, filed on Jan. 6, 2000, entitled "2-Amino-Benzoxazinone Derivatives for the Treatment of Obesity", which PCT application claims priority to GB 9900416.0, filed on Jan. 8, 1999, and the entire contents of each of these is hereby incorporated by reference.... The present invention provides known and novel compounds, their use in

10

This has been a common practice outside the United States prior to December 2000.

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the inhibition of an enzyme whose preferred mode of action is to catalyse the hydrolysis of an ester functionality (in vivo, as the enzyme naturally occurs), their use in medicine, and particularly in the prevention and/or treatment of obesity or an obesity-related disorder. Also provided are methods for the prevention and/or treatment of obesity or an obesity-related disorder and for promoting/aiding non-medical weight loss and the use of the compounds in the manufacture of a medicament for the aforementioned indications. In respect of novel compounds the invention also provides processes for their manufacture, compositions containing them, and methods for manufacturing such compositions.... In the last 20 years, there has been an increasing trend in obesity in the populations of the developed world. The increased incidence of obesity is due in part to the ready availability of food in numerous retail outlets and westernised diets that have high saturated fat and lower fibre contents such that the food is energy dense. The lifestyle of the populations of the developed world has also become more sedentary with the increased mechanisation of society and the steady reduction of manual labour intensive industries. There now exists an energy imbalance between the energy intake from calorie dense foods and the reduced energy expenditure required for a sedentary lifestyle. Some of the excess energy intake is stored as fat in the adipose tissue, the accumulation of which over a period of time results in obesity and can be a significant contributory factor to other diseases and disorders. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

2-Oxy-benzoxazinone derivatives for the treatment of obesity Inventor(s): Palmer, Richard Michael John; (Kent, GB), Downham, Robert; (Cambridge, GB), Mitchell, Timothy John; (Cambridge, GB), Hodson, Harold Francis; (Beckenham, GB), Carr, Beverley Jane; (Royston, GB), Dunk, Christopher Robert; (Ely, GB) Correspondence: Choate, Hall & Stewart; Exchange Place; 53 State Street; Boston; MA; 02109; US Patent Application Number: 20030027821 Date filed: July 6, 2001 Abstract: The use of a compound comprising formula (I): 1(I)or a salt, ester, amide or prodrug therof in the inhibition of an enzyme whose preferred mode of action is to catalyse the hydrolysis of an ester functionality, e.g. in the control and inhibition of unwanted enzymes in products and processes. The compounds are also useful in medicine e.g. in the treatment of obesity and related conditions. The invention also relates to novel compounds within formula (I), to processes for preparing them and pharmaceutical compositions containing them.In formula (I) A is a 6-membered aromatic or heteroaromatic ring; and R.sup.1 is a branched or unbranched alkyl (optionally interrupted by one or more oxygen atoms), alkenyl, alkynyl, cycloalkyl, cycloalkenyl, aryl, arylalkyl, reduced arylalkyl, arylalkenyl, heteroaryl, heteroarylalkyl, heteroarylalkenyl, reduced aryl, reduced heteroaryl, reduced heteroarylalkyl or a substituted derivative of any of the foregoing groups. Excerpt(s): This application is a continuation of international application number PCT/GB00/00032, filed on Jan. 6, 2000, entitled "2-Oxy-Benzoxazinone Derivatives for the Treatment of Obesity", which PCT application claims priority to GB 9900413.7, filed on Jan. 8, 1999, and GB 9917294.2, filed on Jul. 22, 1999, and the entire contents of each of these is hereby incorporated by reference.... The present invention provides known and novel compounds, their use in the inhibition of an enzyme whose preferred mode of action is to catalyse the hydrolysis of an ester functionality (in vivo, as the enzyme

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naturally occurs) their use in medicine, and particularly in the prevention and/or treatment of obesity or an obesity-related disorder. Also provided are methods for the prevention and/or treatment of obesity or an obesity-related disorder and for promoting/aiding non-medical weight loss and the use of the compounds in the manufacture of a medicament for the aforementioned indications. In respect of novel compounds the invention also provides processes for their manufacture, compositions containing them and methods for manufacturing such compositions.... In the last 20 years, there has been an increasing trend in obesity in the populations of the developed world. The increased incidence of obesity is due in part to the ready availability of food in numerous retail outlets and westernised diets that have high saturated fat and lower fibre contents such that the food is energy dense. The lifestyle of the populations of the developed world has also become more sedentary with the increased mechanisation of society and the steady reduction of manual labour intensive industries. There now exists an energy imbalance between the energy intake from calorie dense foods and the reduced energy expenditure required for a sedentary lifestyle. Some of the excess energy intake is stored as fat in the adipose tissue, the accumulation of which over a period of time results in obesity and can be a significant contributory factor to other disease and disorders. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Acute and chronic electrical signal therapy for obesity Inventor(s): Darvish, Nissim; (Tzrufa, IL), Ben-Haim, Shlomo; (Cesarea, IL), Ben Arie, Yaakov; (Haifa, IL), Belsky, Ziv; (Haifa, IL), Mika, Yuval; (Zichron Yaakov, IL), Flesler, Melina; (Misgav, IL) Correspondence: William H. Dippert; Cowan, Liebowitz & Latman, P. C. 1133 Avenue of the Americas; New York; NY; 10036-6799; US Patent Application Number: 20020161414 Date filed: December 11, 2000 Abstract: Apparatus is provided for treating a condition such as obesity. The apparatus includes a set of one or more electrodes, which are adapted to be applied to one or more respective sites in a vicinity of a body of a stomach of a patient. A control unit is adapted to drive the electrode set to apply to the body of the stomach a signal, configured such that application thereof increases a level of contraction of muscle tissue of the body of the stomach, and decreases a cross-sectional area of a portion of the body of the stomach for a substantially continuous period greater than about 3 seconds. Excerpt(s): The present invention relates generally to treatment of obesity, and specifically to invasive techniques and apparatus for treating obesity.... Invasive treatments for obesity are often recommended for patients with a body mass index (mass/height.sup.2 [kg/m.sup.2]) which is greater than 35 or 40. For such patients, their weight is commonly associated with increased risk of heart disease, diabetes, and arthritis. Preferably, the invasive treatments are accompanied by changes in lifestyle, such as improved eating habits and an appropriate exercise regimen.... U.S. Pat. No. 6,067,991 to Forsell, U.S. Pat. No. 5,601,604 to Vincent, and U.S. Pat. No. 5,234,454 to Bangs, and U.S. Pat. Nos. 5,449,368, 5,226,429 and 5,074,868 to Kuzmak, which are incorporated herein by reference, describe mechanical instruments for implantation in or around the stomach of an obese patient. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Administration of estradiol metabolites for the treatment or prevention of obesity, metabolic syndrome, diabetes, and vascular and renal disorders Inventor(s): Tofovic, Stevan P. (Pittsburgh, PA), Jackson, Edwin K. (Pittsburgh, PA), Dubey, Raghvendra K. (Glenshaw, PA) Correspondence: Mary-Elizabeth Buckles; REED SMITH, LLP; Suite 1100 - East Tower; 1301 K Street, N.W. Washington; DC; 20005; US Patent Application Number: 20030050294 Date filed: August 19, 2002 Abstract: Methods are provided for preventing or treating risk factors for cardiovascular disease in an individual, comprising administering a therapeutically effective amount of a composition comprising an estradiol metabolite to said individual. Such risk factors include obesity, the metabolic syndrome, diabetes mellitus, vascular disorders, and renal disorders. Preferred estradiol metabolites include 2-methoxyestradiol, 4methoxyestradiol, 2-hydroxyestradiol, and 4-hydroxyestradiol or prodrugs thereof. The compositions may also be in the form of a controlled release formulation. Methods are also provided for use of estradiol metabolites to treat or prevent insulin resistance, vascular endothelial dysfunction, hyperlipidemia, hypertension, diabetic nephropathy, proteinuria and reducing leptin levels. In addition, the methods provide a method of stabilizing glucose levels. These treatments may be used in either gender because of their lack of a feminizing estrogenic effect. Excerpt(s): This application claims priority from U.S. Provisional Application No. 60/312,741 filed Aug. 17, 2001.... The present invention relates generally to methods and compositions for use in the prevention or treatment of risk factors for cardiovascular diseases such as obesity, metabolic syndrome, diabetes, and vascular and renal disorders. More particularly, the present invention relates to the use of estradiol metabolites with little estrogenic activity such as 2-hydroxyestradiol, 4hydroxyestradiol, 2-methoxyestradiol and 4-methoxyestradiol, all of which may be delivered in a controlled release formulation for the prevention or treatment of such disorders.... Obesity is pandemic and worsening in developed countries (see e.g., Mokdad, A. H., et al., J. Am. Medical Assoc. 284:1650 (2000), the disclosure of which is incorporated herein by reference). Obesity contributes importantly to the metabolic syndrome (see e.g., Grundy, S. M., Endocrine 13:155 (2000) (hereinafter, "Grundy, 2000"); Bergman, R. N., et al., Journal of Investigative Medicine 49:119 (2001) (hereinafter, "Bergman, 2001"), the disclosures of which are incorporated herein by reference), a disorder characterized by hypertension, insulin resistance and hyperlipidemia (Grundy, 2000; Bergman, 2001). The metabolic syndrome in turn contributes to heart and vascular disease (see e.g., Colditz, G. A., Medicine & Science in Sports & Exercise 31:S663 (1999), the disclosure of which is incorporated herein by reference), and to the accelerating epidemic of end stage renal failure (see e.g., Hall, W. D, et al., American Journal of the Medical Sciences 313:195 (1997); Hall, J. E. et al., Annals of the New York Academy of Sciences 892:91 (1999), the disclosures of which are incorporated herein by reference). Unfortunately, pharmacological management of obesity has caused, rather than attenuated, cardiovascular disease. For example, a popular phentermine/fenfluramine combination produces valvular heart disease (see e.g., Lepor, N. E., et al., American Journal of Cardiology 86:107 (2000), the disclosure of which is incorporated herein by reference), while another popular treatment option, phenylpropanolamine, causes stroke (see e.g., Kernan, W. N., et al., New England J. Med. 343:1826 (2000), the disclosure of which is incorporated herein by reference). Thus, drugs that prevent or

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treat obesity and its metabolic, vascular and renal sequelae, without adversely affecting the heart, are badly needed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Agents for preventing or ameliorating insulin resistance and/or obesity Inventor(s): Hashimoto, Hiroyuki; (Nagoya-shi, JP), Jomori, Takahito; (Nagoya-shi, JP), Yamashita, Tokuyuki; (Nagoya-shi, JP), Tubamoto, Yoshiharu; (Naguya-shi, JP), Seino, Yutaka; (Amagasaki-shi, JP), Ban, Nobuhiro; (Kyoto-shi, JP), Yamada, Yuichiro; (Hirakata-shi, JP), Miyawaki, Kazumasa; (Kyoto-shi, JP), Takeda, Motohiro; (Hagoyashi, JP) Correspondence: FISH & RICHARDSON, PC; 4350 LA JOLLA VILLAGE DRIVE; SUITE 500; SAN DIEGO; CA; 92122; US Patent Application Number: 20030157107 Date filed: April 9, 2003 Abstract: An object of the present invention is to provide a prophylactic or ameliorative agent for insulin resistance and/or obesity based on a new concept, and a screening method therefor.The present inventors found that GIP causes insulin resistance and obesity by a new mechanism, and obtained a new concept that a GIP function inhibitory compound exhibits the ameliorative effect of insulin resistance and anti-obesity effect, thereby completing the present invention. That is, the present invention is a prophylactic or ameliorative agent for insulin resistance and/or obesity, having a GIP function inhibitory compound as an active ingredient, and a screening method for a prophylactic or ameliorative agent for insulin resistance and/or obesity, characterized by selecting a GIP function inhibitory compound. Excerpt(s): The present invention relates to a prophylactic or ameliorative agent for insulin resistance and/or obesity, and more specifically to a prophylactic or ameliorative agent for insulin resistance and/or obesity, on the basis of a technological concept that a compound inhibiting a function of GIP (gastric inhibitory polypeptide or glucosedependent insulinotropic peptide) serves as a prophylactic or ameliorative agent for insulin resistance and/or obesity, and a screening method therefor.... GIP is one of gastrointestinal hormones belonging to Glucagon-secretin family. GIP, along with glucagon-like peptide 1 (GLP-1), is called incretin, is secreted on feeding from the K cells existing in the small intestine, and regulates the kinetics of nutrients after eating in the body by stimulating an insulin secretion on.beta.-cells of the pancreas in response to glucose. In addition, GIP has been said to inhibit the gastric motor activity and stimulates the secretion of intestinal juice. However, a doubt exists at present as to its inhibitory effect on gastric acid secretion proposed just after its discovery. The GIPreceptor genes are expressed widely in addition to the.beta.-cells in the pancreas and the adipocytes, so it is assumed that GIP has some effects in other tissues though they have not been clear in details. Naturally, its relationship with insulin resistance is unknown.... Examples of GIP-receptor antagonists include GIP (6-30)-NH.sub.2 (Regulatory Peptide, 69: 151-154, 1997) and GIP (7-30)-NH.sub.2 (Am J Physiol, 276: E1049-1054, 1999). However, they have not been studied as insulin resistance ameliorative agents or antiobesity agents. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Anti-obesity 1,2,3,4,10,10-a-hexahydropy razino [1,2-a] indoles Inventor(s): Roever, Stephan; (Inzlingen, DE), Muller, Marc; (Saint-Louis, FR), Hebeisen, Paul; (Basle, CH), Bentley, Jonathan M. (Reading, GB), Richter, Hans; (GrenzachWyhlen, DE) Correspondence: HOFFMANN-LA ROCHE INC. PATENT LAW DEPARTMENT; 340 KINGSLAND STREET; NUTLEY; NJ; 07110 Patent Application Number: 20020035110 Date filed: July 25, 2001 Abstract: The present invention is directed to 1,2,3,4,10,10a,-hexahydropyrazino[1,2- -a] indole derivatives as well as pharmaceutically acceptable salts, solvates and esters thereof, wherein R.sup.1 to R.sup.8 have the significance given in claim 1 be used in the form of pharmaceutical preparations for the treatment or prevention of disorders of the central nervous system, damage to the central nervous system, cardiovascular disorders, gastrointestinal disorders, diabetes insipidus, obesity and sleep apnea. Excerpt(s): It has been recognised that obesity is a disease process influenced by environmental factors in which the traditional weight loss methods of dieting and exercise need to be supplemented by therapeutic products (S. Parker, "Obesity: Trends and Treatments", Scrip Reports, P J B Publications Ltd, 1996).... Whether someone is classified as overweight or obese is generally determined on the basis of their body mass index (BMI) which is calculated by dividing body weight (kg) by height squared (m.sup.2). Thus, the units of BMI are kg/m.sup.2 and it is possible to calculate the BMI range associated with minimum mortality in each decade of life. Overweight is defined as a BMI in the range 25-30 kg/m.sup.2, and obesity as a BMI greater than 30 kg/m.sup.2. There are problems with this definition in that it does not take into account the proportion of body mass that is muscle in relation to fat (adipose tissue). To account for this, obesity can also be defined on the basis of body fat content: greater than 25% and 30% in males and females, respectively.... As the BMI increases there is an increased risk of death from a variety of causes that is independent of other risk factors. The most common diseases with obesity are cardiovascular disease (particularly hypertension), diabetes, including Type I and Type II diabetes, (obesity aggravates the development of diabetes), gall bladder disease (particularly cancer) and diseases of reproduction. Research has shown that even a modest reduction in body weight can correspond to a significant reduction in the risk of developing coronary heart disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Aryl boronate functionalized polymers for treating obesity Inventor(s): Polomoscanik, Steven Craig; (Bedford, MA), Huval, Chad Cori; (Somerville, MA), Dhal, Pradeep K. (Westford, MA), Mandeville, W. Harry III; (Lynnfield, MA), Holmes-Farley, Stephen Randall; (Arlington, MA), Li, Xinhua; (Newton, MA) Correspondence: HAMILTON, BROOK, SMITH & REYNOLDS, P.C. 530 VIRGINIA ROAD; P.O. BOX 9133; CONCORD; MA; 01742-9133; US Patent Application Number: 20030059399 Date filed: June 27, 2002 Abstract: Disclosed are polymers comprising one or more phenyl boronate ester, boronamide or boronate thioester groups. The phenyl boronate ester, boronamide and

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boronate thioester groups are represented by one of the following structural formulas: 1Ar in Structural Formulas (I) and (II) is substituted or unsubstituted; and each Z is --O-, --NH-- or --S-- and is independently selected. Pharmaceutically acceptable salts of the polymer are also included. The aryl boronate ester, boronamide or boronate thioester can be cleaved to release the corresponding aryl boronic acid.Also disclosed are pharmaceutical compositions comprising the polymers of the present invention and a pharmaceutically acceptable carrier or diluent; and methods of treating a subject for obesity with the polymers of the present invention. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/302,221, filed Jun. 29, 2001, and U.S. Provisional Application No. 60/359,473, filed Feb. 22, 2002, the entire teachings of which are incorporated herein by reference.... Human obesity is a recognized health problem with approximately ninety-seven million people considered clinically overweight in the United States. Various chemical approaches have been used for treating obesity. In one such approach, a medicament which inhibits lipases is administered to the obese patient. Lipases are key enzymes in the digestive system which break down diglycerides and triglycerides into monoglycerides and fatty acids. Diglycerides and triglycerides have a high caloric content but are not absorbed by the small intestine until broken down by the lipases. Therefore, inhibition of lipases within the digestive system results in a reduction in the absorption of fat and consequently a decrease in caloric uptake. XENICAL is an example of a commercially available lipase inhibitor that is used for treating obesity.... Administration of lipase inhibitors results in stools with a high fat or oil content from the undigested diglycerides and triglycerides. Leakage of oil from the stool is an unpleasant side effect that often occurs when stools have a high fat or oil content. This condition is referred to as "oily stool" or "leaky stool". It has been reported in U.S. application Ser. No. 09/166,453 that fat-binding polymers, when co-administered with lipase inhibitors, can bind with or "stabilize" the oil and thereby reduce or eliminate the leakage of oil from the stool. However, the need to administer two drugs can reduce patient compliance because it is burdensome and inconvenient. The development of new drugs which both inhibit lipases and bind the lipids which cause "leaky stools" would be an advance with respect to managing and treating obesity in patients. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Aryl boronic acids for treating obesity Inventor(s): Dhal, Pradeep K. (Westford, MA), Huval, Chad Cori; (Somerville, MA), Mandeville, W. Harry III; (Lynnfield, MA), Holmes-Farley, Stephen Randall; (Arlington, MA), Li, Xinhua; (Newton, MA) Correspondence: HAMILTON, BROOK, SMITH & REYNOLDS, P.C. 530 VIRGINIA ROAD; P.O. BOX 9133; CONCORD; MA; 01742-9133; US Patent Application Number: 20030064963 Date filed: June 27, 2002 Abstract: Disclosed is a phenyl boronic acid compound represented by Structural Formula (I): 1Ar is a substituted or unsubstituted aryl group.Z and Z' are independently --O--. --NH-- or --S--.X is an electron withdrawing group.R is a substituted or unsubstituted straight chained hydrocarbyl group optionally comprising one or more amine, ammonium, ether, thioether or phenylene linking groups and Y is --H, an amine, --[NH--(CH.sub.2).sub.q]-.sub.r--NH.sub.2, halogen, --CF.sub.3, thiol ammonium, alcohol, --COOH, --SO.sub.3H, --OSO.sub.3H or phosphonium group covalently bonded

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to the terminal position of R. Each --NH-- in --[NH--(CH.sub.2).sub.q].sub.r--NH-.sub.2 is optionally N-alkylated or N,N-dialkylated and --NH.sub.2 in --[NH-(CH.sub.2).sub.q].sub.r--NH.sub.2 is optionally N-alkylated, N,N-dialkylated or N,N,Ntrialkylated.q is an integer from 2 to about 10 and r is an integer from 1 to about 5.R.sub.1 and R.sub.1' are independently --H, an aliphatic group, a substituted aliphatic group, an aryl group or a substituted aryl group, or, taken together, are a C2-C5 substituted or unsubstituted alkylene group optionally comprising an amine linking group [--N.sup.+(R.sup.1a)--]. Each R.sub.1 is Structural Formula (I) is preferably -H.R.sup.1a is --H, alkyl, substituted alkyl, phenyl or substituted phenyl.Also disclosed is a method of treating obesity in a subject by administering an effective amount of a compound represented by Structural Formula (I) and a pharmaceutical composition comprising the compound and a pharmaceutically acceptable carrier or diluent. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/302,081, filed Jun. 29, 2001 and U.S. Provisional Application No. 60/359,467, filed Feb. 22, 2002. The entire teachings of the above application(s) are incorporated herein by reference.... Human obesity is a recognized health problem with approximately ninetyseven million people considered clinically overweight in the United States. Various chemical approaches have been used for treating obesity. In one such approach, a medicament which inhibits lipases is administered to the obese patient. Lipases are key enzymes in the digestive system which break down diglycerides and triglycerides into monoglycerides and fatty acids. Diglycerides and triglycerides have a high caloric content but are not absorbed by the small intestine until broken down by the lipases. Therefore, inhibition of lipases within the digestive system results in a reduction in the absorption of fat and consequently a decrease in caloric uptake. XENICAL is an example of a commercially available lipase inhibitor that is used for treating obesity.... There is still a need, however, for improved lipase inhibitors. For example, administration of lipase inhibitors results in stools with a high fat or oil content from the undigested diglycerides and triglycerides. Leakage of oil from the stool is an unpleasant side effect that often occurs when stools have a high fat or oil content. This condition is referred to as "oily stool" or "leaky stool". It has been reported in U.S. application Ser. No. 09/166,453 that fat-binding polymers, when co-administered with lipase inhibitors, can bind with or "stabilize" the oil and thereby reduce or eliminate the leakage of oil from the stool. It would be desirable to develop a single compound which is both a lipase inhibitor and a fat-binder. In addition, a lipase inhibitor should be minimally absorbed by the intestines to prevent systemic side-effects. Other desirable features include ease and economy of manufacture. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Aza- indolyl derivatives for treating obesity Inventor(s): Taylor, Sven; (Riedisheim, FR), Hebeisen, Paul; (Basle, CH), Bentley, Jonathan Mark; (Reading, GB) Correspondence: HOFFMANN-LA ROCHE INC. PATENT LAW DEPARTMENT; 340 KINGSLAND STREET; NUTLEY; NJ; 07110 Patent Application Number: 20010025039 Date filed: February 27, 2001 Abstract: Novel compounds of formula (I): 1wherein X.sup.1, X.sup.2, X.sup.3 and X.sup.4, n, R.sup.1, R.sup.2 and R.sup.3 are defined in the specification, and pharmaceutically acceptable salts and prodrugs of the compounds of formula (I) have

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therapeutic uses. These compounds are useful for the treatment of disorders of the central nervous system; damage to the central nervous system; cardiovascular disorders; gastrointestinal disorders; diabetes insipidus, and sleep apnea. They are particularly useful for the treatment of obesity. Excerpt(s): The present invention relates to new aza-indolyl derivatives, to processes and intermediates for their preparation, to pharmaceutical compositions containing them and to their medicinal use. The active compounds of the present invention are useful in treating obesity and other disorders.... It has been recognized that obesity is a disease process influenced by environmental factors in which the traditional weight loss methods of dieting and exercise need to be supplemented by therapeutic products (S. Parker, "Obesity: Trends and Treatments", Scrip Reports, PJB Publications Ltd, 1996).... Whether someone is classified as overweight or obese is generally determined on the basis of their body mass index (BMI) which is calculated by dividing body weight (kg) by height squared (m.sup.2). Thus, the units of BMI are kg/m.sup.2 and it is possible to calculate the BMI range associated with minimum mortality in each decade of life. Overweight is defined as a BMI in the range 25-30 kg/m.sup.2, and obesity as a BMI greater than 30 kg/m.sup.2. There are problems with this definition in that it does not take into account the proportion of body mass that is muscle in relation to fat (adipose tissue). To account for this, obesity can also be defined on the basis of body fat content: greater than 25% and 30% in males and females, respectively. Using BMI and/or other conventional diagnosis tools, prescribing doctors are well able to determine which of their patients are in need of treatment for obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Beta-adrenoceptor genetic polymorphisms and obesity Inventor(s): Johnson, Julie A. (Melrose, FL) Correspondence: SALIWANCHIK LLOYD & SALIWANCHIK; A PROFESSIONAL ASSOCIATION; 2421 N.W. 41ST STREET; SUITE A-1; GAINESVILLE; FL; 326066669 Patent Application Number: 20020187491 Date filed: February 12, 2002 Abstract: The present invention provides a method for identifying a subject having a risk of developing obesity, coronary microvascular dysfunction, or hypertension, comprising detection of the presence of a single nucleotide polymorphism (SNP) in a nucleic acid encoding an element of at least one.beta.-adrenergic receptor from the subject. The presence of the SNP is correlated with obesity, coronary microvascular dysfunction, or hypertension, and thereby identifies the subject as having a risk of developing obesity, coronary microvascular dysfunction, or hypertension. The subject invention also provides methods of identifying patients likely to benefit from the prescription of beta blocker hypertension medications. In various embodiments, the nucleic acids detected include those genes encoding ADRB1 (.beta..sub.1AR), ADRB2 (.beta..sub.2AR), ADRB3 (.beta..sub.3AR), GNB3 (G protein.beta.3 subunit), or GNAS1 (G.sub.S protein alpha subunit). Methods of treating identified individuals are also provided. Excerpt(s): The prevalence of obesity has increased dramatically in Westernized societies. It represents a major health problem, because it markedly increases the risk of cardiovascular disease, diabetes, lipid disorders, and some cancers. Obesity clearly has a heritable basis, with estimates that 40% to 70% of the variability in body weight is

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genetically mediated. Thus, understanding the genetic basis of variability in BMI or obesity is important. The range of treatments for obesity reflects the complexity of the processes involved in weight regulation and the current lack of understanding of these processes. Recent reports have even implicated viruses as a possible causative factor in obesity (U.S. News and World Report, Aug. 7, 2000). In addition, human twin studies strongly suggest a substantial genetic basis in the control of body weight, with estimates of heritability of 80% to 90% (Simopoulos, A. P. and Childs, B., eds. [1989] "Genetic Variation and Nutrition in Obesity", World Review of Nutrition and Diabetes, 63, S. Karger, Basel, Switzerland; Boijeson, M. [1976] Acta. Paediatr. Scand. 65:279-287).... The regulation of body weight, and particularly body fat, in animals is a complex process having enormous implications for the health and well being of humans and other animals. Excess body weight and/or an excess of body fat relative to lean body mass has been associated with a wide range of health problems. Obesity is a major health problem in the United States, with estimates that 50% to 60% of Americans over age 30 are overweight and 25% to 30% are clinically obese (Wickelgren, L. [1998] "Obesity: How Big a Problem?"[news], Science 280(5368):1364-7). Obesity is of concern because numerous studies link obesity with increased risk of cardiovascular disease, metabolic disorders (such as Type II diabetes mellitus and lipid abnormalities) and some forms of cancer.... Individuals 20% over ideal weight guidelines are considered obese. Obesity is classified as mild (20-40% overweight), moderate (41-100% overweight), and severe (>100%). Severe obesity is relatively rare, affecting less than 0.5% of all obese individuals and about 0.1% of the total population. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Botanical composition and methods for the treatment or prevention of obesity Inventor(s): Tseng, Albert Peng Sheng; (New South Wales, AU), Lim, Yoland Sim Huat; (VICTORIA, AU), Sun, Hai Ping; (New South Wales, AU) Correspondence: Mark D. Moore; Williams, Morgan & Amerson, P.C. Suite 250; 7676 Hillmont; Houston; TX; 77040; US Patent Application Number: 20020197338 Date filed: June 6, 2001 Abstract: Disclosed are botanical compositions, and more particularly to compositions having particularly beneficial therapeutic or prophylactic properties in a mammal. In particular, the compositions of the present inventions are useful inter alia in the treatment and/or prophylaxis of obesity, overeating, and other eating disorders, as well as an oral supplement in place of, or commensurate with, the consumption of food. The compositions of the present invention may be conveniently formulated for suitable administration, such as, for example, as a dried composition. In particularly preferred embodiments, the compositions of the present invention encompass formulations that comprise, consist essentially of, or consist of, a plurality of at least three herbal plants, horticultural and/or botanical equivalents, and/or extracts thereof, having similar or equivalent medicinal or therapeutic properties. Excerpt(s): The present application claims priority from U.S. Provisional Application Serial No. 60/209,544, filed Jun. 6, 2000, the entire contents of which is specifically incorporated herein by reference in its entirety.... The present invention relates generally to a composition and more particularly to a composition having therapeutic properties. The composition of the present invention is useful inter alia in the treatment and/or prophylaxis of obesity as well as an oral supplement in place of or commensurate with

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the consumption of food. The composition of the present invention is conveniently packaged for consumption as a dried formulation. In a particularly preferred embodiment, the composition of the present invention is a formulation derived from three or more herbal plants or horticultural and/or botanical equivalents thereof having similar or equivalent medicinal or therapeutic properties and/or extracts therefrom.... Obesity is one of the more significant problems frequently associated with affluent societies. Obesity is not confined to middle age and is now an increasing problem with younger children and adolescents. Although medical conditions leading to obesity exist, modem obesity frequently appears as a consequence of less exercise and an increase in the availability of fatty foods and high calorie foods at affordable prices. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Cobalt-porphyrin complexes and use thereof as an anti-obesity agent Inventor(s): Ghosh, Soumitra S. (San Diego, CA), Szabo, Tomas R. (San Diego, CA), Davis, Robert E. (San Diego, CA) Correspondence: SEED INTELLECTUAL PROPERTY LAW GROUP PLLC; 701 FIFTH AVE; SUITE 6300; SEATTLE; WA; 98104-7092; US Patent Application Number: 20020165216 Date filed: December 14, 2001 Abstract: Cobalt-porphyrin (Co-P) complexes for use as anti-obesity agents, and compositions and methods related thereto. The Co-P complexes exhibit reduced redox activity compared to cobalt mesoporphyrin (Co-MP) and cobalt protoporphyrin (CoPP), which alleviates the deleterious effects associated with administration of Co-P associated with oxidative stress, particularly in the context of injection site toxicity. Excerpt(s): The present invention relates generally to cobalt-porphyrin complexes which are useful as anti-obesity agents, as well as to compounds, compositions and methods related to the same.... Cobalt protoporphyrin ("Co-PP") has been reported to regulate food intake and body weight in rats (Galbraith and Kappas, Proc. Natl. Acad Sci. U.S.A. 86:7653-7657, 1989), as well as in other animals such as rats, dogs and monkeys. A single subcutaneous injection of Co-PP produces a prompt dose-dependent decrease in food intake in Sprague Dawley rats. This result is accompanied by a sustained decrease in body weight, that is characterized by decreases in carcass fat content without changes in protein content. Smaller doses of Co-PP delivered by intracerebroventricular administration has also been found to elicit the same effect.... The regulatory effect of Co-PP has also been extended to animals that are genetically destined to become markedly obese. Thus, subcutaneous administration of Co-PP to Zucker rats whose obesity is conferred by homozygosity of the fa gene (fa/fa) produces long-sustained reduction in body weight (Galbraith and Kappas, Pharmacology 41:292-298, 1990). The effect of Co-PP is profound and believed to be caused by the phenotype of gene expression in the fa/fa animal to revert to a phenotype similar to that of the heterozygous lean animal. Whereas cobalt mesoporphyrin ("Co-MP") has a comparable biological profile, the same effect is not found upon administration of inorganic cobalt, or a number of other metal chelates of porphyrins. The mechanism of action of Co-PP for regulation of body weight is unknown, and it has been shown that the weight loss in rats is not mediated by the neuropeptide Y system (Choi et al, Brain Research 729:223227, 1996; Turner et al, Physiology and Behavior 56:10009-1014, 1994). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Combination of a CB1 receptor antagonist and of sibutramine, the pharmaceutical compositions comprising them and their use in the treatment of obesity Inventor(s): Petitet, Francois; (Creteil, FR), Picaut, Philippe; (Fontenay Aux Roses, FR), Piot-Grosjean, Odile; (Choisy Le Roi, FR) Correspondence: Finnegan, Henderson, Farabow,; Garrett & Dunner, L.L.P. 1300 I Street, N.W. Washington; DC; 20005-3315; US Patent Application Number: 20020091114 Date filed: October 3, 2001 Abstract: The present invention relates to the combination of a CB1 receptor antagonist and of sibutramine, to the pharmaceutical compositions comprising them and to their use in the treatment of obesity. Excerpt(s): The present invention relates to the combination of a CB1 receptor antagonist and of sibutramine, to the pharmaceutical compositions comprising them and to their use in the treatment of obesity.... CB1 receptor antagonists are known for their effect on food intake and their use as anorexigenic (G. Colombo et al., Life Sciences, 63 (8), 113117 (1998); J. Siamand et al., Behavioural Pharmacol., 9, 179-181 (1998)).... Sibutramine (BTS 54524; N-{1-[1-(4-chlorophenyl)cyclobutyl]-3-methy- lbutyl}-N,N-dimethylamine; Meridia.sup.R, Reductil.sup.R), its hydrate and its pharmaceutically acceptable salts and in particular its hydrochloride reduces food intake and is of use in the treatment of obesity (WO 90/061110; D. H. Ryan et al., Obesity Research, 3 (4), 553 (1995); H. C. Jackson et al., British Journal of Pharmacology, 121, 1758 (1997); G. Fanghanel et al., Inter. J. Obes., 24 (2), 144 (2000); G. A. Bray et al., Obes. Res., 7 (2), 189 (1999)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Composition for treating obesity and esthetic treatment process Inventor(s): Rombi, Max; (Bordighera, IT) Correspondence: BURNS, DOANE, SWECKER & MATHIS, L.L.P. P.O. Box 1404; Alexandria; VA; 22313-1404; US Patent Application Number: 20030104081 Date filed: October 22, 2002 Abstract: The invention relates to a composition for the curative and prophylactic treatment of obesity, comprising a catechol-rich extract of green tea, in particular containing from 20% to 50% by mass of catechols expressed as epigallocatechol gallate (EGCG). Excerpt(s): The therapeutic objective as regards obesity is well defined: it is a matter either of allowing the individual to lose a significant amount of weight, or of helping the individual to maintain a weight level which is as low as desired.... Several types of approach have been envisaged to date.... Nutritional approaches are directed toward reducing the supply of energy in the form of foods. This can be achieved either by drastically reducing the energy supplies or by replacing high-energy nutrients with others which are lower in energy: such as indigestible substitute fats, structured triglycerides which are difficult to assimilate or dietary fibers which cannot be assimilated. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Compositions and methods for the diagnosis and treatment of body weight disorders, including obesity Inventor(s): Nagle, Deborah Lynn; (Watertown, MA), Moore, Karen; (Maynard, MA) Correspondence: PENNIE AND EDMONDS; 1155 AVENUE OF THE AMERICAS; NEW YORK; NY; 100362711 Patent Application Number: 20020150973 Date filed: June 27, 2001 Abstract: The present invention relates to mammalian mahogany genes, including the human mahogany gene, which are novel genes involved in the control of mammalian body weight. The invention encompasses nucleotide sequences of the mahogany gene, host cell expression systems of the mahogany gene, and hosts which have been transformed by these expression systems, including transgenic animals. The invention also encompasses novel mahogany gene products, including mahogany proteins, polypeptides and peptides containing amino acid sequences mahogany proteins, fusion proteins of mahogany proteins polypeptides and peptides, and antibodies directed against such mahogany gene products. The present invention also relates to methods and compositions for the diagnosis and treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia, and for the identification of subjects susceptible to such disorders. Further, the invention relates to methods of using the mahogany gene and gene products of the invention for the identification of compounds which modulate the expression of the mahogany gene and/or the activity of the mahogany gene product. Such compounds can be useful as therapeutic agents in the treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia. Excerpt(s): Obesity represents the most prevalent of body weight disorders, and it is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa, which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to other diseases. For example, this disorder is responsible for increased incidence of diseases such as coronary artery disease, hypertension, stroke, diabetes, hyperlipidemia, and some cancers (See, e.g., Nishina, P. M. et al., 1994, Metab. 43: 554-558; Grundy, S. M. & Barnett, J. P., 1990, Dis. Mon. 36: 641-731). Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity (Friedman, J. M. et al., 1991, Mammalian Gene 1: 130-144).... The epidemiology of obesity strongly shows that the disorder exhibits inherited characteristics (Stunkard, 1990, N. Eng. J. Med. 322: 1438). Moll et al. have reported that, in many populations, obesity seems to be controlled by a few genetic loci (Moll et al., 1991, Am. J. Hum. Gen. 49: 1243). In addition, human twin studies strongly suggest a substantial genetic basis in the control of body weight, with estimates of heritability of 80-90% (Simopoulos, A. P. & Childs, B., eds., 1989, in "Genetic Variation and Nutrition in Obesity", World Review of Nutrition and Diabetes 63, S. Karger, Basel, Switzerland; Borjeson, M., 1976, Acta. Paediatr. Scand. 65: 279-287).

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Compounds for the treatment of obesity Inventor(s): Hank, Richard F. (No. Stonington, CT), Elliott, Richard L. (East Lyme, CT), Hammond, Marlys; (Salem, CT) Correspondence: Gregg C. Benson; Pfizer Inc. Patent Department, MS 4159; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20010039277 Date filed: January 4, 2001 Abstract: NPY antagonists, methods of using such NPY antagonists and pharmaceutical compositions containing such NPY antagonists. The NPY antagonists are useful for the treatment of NPY mediated disease/conditions including obesity. Excerpt(s): This application claims priority from provisional application U.S. Ser. No. 60/132,029 filed Apr. 30, 1999, the benefit of which is hereby claimed under 37 C.F.R..sctn.1.78(a)(3).... This invention relates to NPY antagonists, particularly NPY-5 antagonists, and pharmaceutical compositions containing such antagonists and the use of such antagonists to treat, for example, obesity, feeding disorders, as well as other NPY mediated diseases/conditions in mammals, including humans, dogs, cats and horses.... Neuropeptide Y (NPY), a 36 amino acid peptide neurotransmitter, is a member of the pancreatic polypeptide class of neurotransmitters/neuroho- rmones which has been shown to be present in both the periphery and central nervous system. NPY is one of the most potent orexogenic agents known and has been shown to play a major role in the regulation of food intake in animals. At least 6 NPY receptor subclasses have been identified and cloned to date, with two of these subclasses, NPY-1 and NPY-5, thought to be the most important receptor subtypes modulating food intake and energy expenditure. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz, Martin C. (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20020040054 Date filed: August 29, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program.

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Excerpt(s): Safer than Phen-Fen (copyright 1997), Written by Michael Anchors, MD Ph.D. Pulmonary Vascular Disease, Medical Clinics of North America Nov. 6, 1997, Written by Donald Heath, MD Ph.D.... The "Phen-pro" Diet Drug Combination Is Not Associated with Valvular Heart Disease. Jan. 12, 1998 Archives of Internal Medicine. Written by: Len Griffen, MD and Michael Anchors, MD Ph.D.... Fluoxetine (Prozac) and Other Drugs for Treatment of Obesity, Nov. 25, 1994 The Medical Letter. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz, Martin C. (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20020065311 Date filed: August 30, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): Safer than Phen-Fen (copyright 1997), Written by Michael Anchors, MD Ph.D. Pulmonary Vascular Disease, Medical Clinics of North America November 6, 1997, Written by Donald Heath, MD Ph.D.... The "Phen-pro" Diet Drug Combination Is Not Associated with Valvular Heart Disease. Jan. 12, 1998 Archives of Internal Medicine. Written by: Len Griffen, MD and Michael Anchors, MD Ph.D.... Fluoxetine (Prozac) and Other Drugs for Treatment of Obesity, Nov. 25, 1994 The Medical Letter. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz, Martin C. (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20020072537 Date filed: August 29, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and

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Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): The medications stop working during therapy where at least 40% to 50% of patients quit losing weight (plateau) on an average of 3.3 months into therapy; and 5% to 8 % of patients who receive drug therapy for weight problems experience the complication where the medications fail to assist in appetite suppression where the patient therefore does not lose significant weight.... In the past long term treatment, defined as treatment longer than 3 months to many years, with drugs has been a problem due to long term safety issues including, medication intolerability by the patient, medication side effects and most important ineffectiveness of the drugs or the cessation of benefit of the drugs which in turn causes the patient to fall out of appetite suppression and terminate weight loss.... A weight loss procedure using SSRI medication is disclosed in U.S. Pat. No. 5,795,895. The potential for patients to obtain goal weight loss under the process of U.S. Pat. No. 5,795,895 is low, and the failure of the drugs to provide a desired level of performance is at the heart of the problem. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Comprehensive pharmacologic therapy for treatment of obesity including cysteine Inventor(s): Hinz, Martin C. (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20020094969 Date filed: September 6, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity including Cysteine is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, Cysteine, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): This application is a continuation-in-part application from Ser. No. 09/412,701 filed Oct. 5, 1999, the entire contents of which are hereby incorporated by reference.... The medications stop working during therapy where at least 40% to 50% of patients quit losing weight (plateau) on an average of 3.3 months into therapy; and 5% to 8% of patients who receive drug therapy for weight problems experience the complication where the medications fail to assist in appetite suppression where the patient therefore does not lose significant weight.... In the past long term treatment, defined as treatment longer than 3 months to many years, with medications, has raised safety issues including, medication intolerability by the patient, medication side effects and most important ineffectiveness of the drugs or the cessation of benefit of the drugs which in turn causes the patient to fall out of appetite suppression and terminate weight loss.

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Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Derivatives of C2-substituted indan-1 ol systems for the prophylaxis or treatment of obesity Inventor(s): Bickel, Martin; (Bad Homburg, DE), Krone, Volker; (Hofheim, DE), Jaehne, Gerhard; (Frankfurt, DE), Gossel, Matthias; (Hofheim, DE) Correspondence: HELLER EHRMAN WHITE & MCAULIFFE LLP; 1666 K STREET,NW; SUITE 300; WASHINGTON; DC; 20006; US Patent Application Number: 20030134881 Date filed: August 29, 2002 Abstract: Derivatives of C2-substituted indan-1-ol compounds of the formula I: 1its physiologically acceptable salts, and its physiologically functional derivatives for the prophylaxis or treatment of obesity are disclosed herein. Compositions comprising the same, methods for preparing the instant compounds, and methods for reducing weight in mammals and for the prophylaxis or treatment of obesity are also described. Excerpt(s): The instant application takes priority from DE 10142660.7 filed Aug. 31, 2001 which is incorporated herein by reference in its entirety.... The invention relates to C2substituted indan-1-ol systems and their physiologically acceptable salts and physiologically functional derivatives for the prophylaxis or treatment of obesity.... EP 0009554 discloses indan-1-one and -1-ol derivatives as herbicides and analgesics. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Diet food formula for overweight people and diabetics Inventor(s): Li, Rui; (Arcadia, CA), Liu, Tian Xiao; (Arcadia, CA), Liu, Xue Wu; (Arcadia, CA), Liu, Xuewen; (Arcadia, CA) Correspondence: Joe Nieh; Suite 411; 17800 Castleton Street; City of Industry; CA; 91748; US Patent Application Number: 20020068110 Date filed: December 4, 2000 Abstract: A diet food formula for overweight people and diabetics, comprising of agar, carrageenans, alginate, chlorella, spirulina, and water. The diet food formula comprises of all natural materials. The diet food formula cannot be metabolized by the human body after ingestion and will supply the human body with proper nutrients that it requires. Excerpt(s): The present invention relates to a diet food formula for overweight people and diabetics.... People with overweight problems and/or diabetes have extremely limited choices of food that both satisfies their desire to eat and satisfies the body's nutrient requirements.... People with overweight problems are often instructed by their physicians to limit their intake of food while attempting to also maintain a healthy diet by including food with nutrients that the body needs or by taking dietary supplements such as vitamins. However, limiting the intake of food is extremely difficult to do since the body craves for food to fulfill the hunger sensation. Furthermore, the more one tries to limit the intake of food, the more the body craves for them. Therefore attempting to limit food intake to the body often becomes a self-defeating process.

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Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Fibroblast growth factor-19 (FGF-19) nucleic acids and polypeptides and methods of use for the treatment of obesity and related disorders Inventor(s): Yu, Xing Xian; (Carlsbad, CA), Stewart, Timothy A. (San Francisco, CA), Gurney, Austin L. (Belmont, CA), Goddard, Audrey; (San Francisco, CA), Adams, Sean; (Randolph Township, NJ), Tomlinson, Elizabeth; (Griswold, CT) Correspondence: GENENTECH, INC. 1 DNA WAY; SOUTH SAN FRANCISCO; CA; 94080; US Patent Application Number: 20020155543 Date filed: August 7, 2001 Abstract: The present invention is directed to novel polypeptides belonging to the fibroblast growth factor family and to nucleic acid molecules encoding those polypeptides. Also provided herein are vectors and host cells comprising those nucleic acid sequences, chimeric polypeptide molecules comprising the polypeptides of the present invention fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides of the present invention and to methods for producing the polypeptides of the present invention. Furthermore, methods of treating obesity are provided. Excerpt(s): The present invention relates generally to the identification and isolation of novel DNA and to the recombinant production of novel polypeptides designated herein as fibroblast growth factor-19 (FGF-19) polypeptides, and to methods, compositions and assays utilizing such polypeptides for the therapeutic treatment of obesity and related disorders and for producing pharmaceutically active materials having therapeutic and pharmacologic properties including those associated with the treatment of obesity and related disorders.... Obesity is a chronic disease that is highly prevalent in modem society and is associated not only with a social stigma, but also with decreased life span and numerous medical problems, including adverse psychological development, reproductive disorders such as polycystic ovarian disease, dermatological disorders such as infections, varicose veins, Acanthosis nigricans, and eczema, exercise intolerance, diabetes mellitus, insulin resistance, hypertension, hypercholesterolemia, cholelithiasis, osteoarthritis, orthopedic injury, thromboembolic disease, cancer, and coronary heart disease. Rissanen et al., British Medical Journal, 301: 835-837 (1990).... Existing therapies for obesity include standard diets and exercise, very low calorie diets, behavioral therapy, pharmacotherapy involving appetite suppressants, thermogenic drugs, food absorption inhibitors, mechanical devices such as jaw wiring, waist cords and balloons, and surgery. Jung and Chong, Clinical Endocrinology, 35: 11-20 (1991); Bray, Am. J. Clin. Nutr., 55: 538S-544S (1992). Protein-sparing modified fasting has been reported to be effective in weight reduction in adolescents. Lee et al., Clin. Pediatr., 31: 234-236 (April 1992). Caloric restriction as a treatment for obesity causes catabolism of body protein stores and produces negative nitrogen balance. Protein-supplemented diets, therefore, have gained popularity as a means of lessening nitrogen loss during caloric restriction. Because such diets produce only modest nitrogen sparing, a more effective way to preserve lean body mass and protein stores is needed. In addition, treatment of obesity would be improved if such a regimen also resulted in accelerated loss of body fat. Various approaches to such treatment include those discussed by Weintraub and Bray, Med. Clinics N. Amer., 73: 237 (1989); Bray, Nutrition Reviews, 49: 33 (1991).

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Ginseng berry extracts and pharmaceutical compositions from ginseng berry for the treatment of type 2 diabetes and obesity Inventor(s): Yuan, Chun-Su; (Chicago, IL) Correspondence: MARK B WILSON; FULBRIGHT & JAWORSKI LLP; 600 CONGRESS AVENUE; SUITE 2400; AUSTIN; TX; 78701; US Patent Application Number: 20020136785 Date filed: October 9, 2001 Abstract: The present invention relates to methods and compositions for the use in treating type 2 diabetes and obesity. More specifically, the invention relates to the methods of screening for the active compound from berries from plants of the Panax genus that decreases blood glucose and decreases body weight. It is contemplated that the active compound may comprise a ginsenoside or a combination thereof. Excerpt(s): This application claims priority to U.S. Provisional Application No. 60/246,628, filed Nov. 7, 2000.... The present invention relates generally to the fields of physiology and medicine. More particularly, it relates to pharmaceutical compositions and the methods of screening for constituents that are anti-hyperglycemic or antiobesity agents. Such constituents can be extracted from ginseng berry.... Diabetes mellitus is a major health problem, affecting approximately 5% of the total population in the U.S., and 3% of the population world-wide. Diabetes mellitus is a chronic metabolic disease that can cause blindness, kidney failure, or nerve damage. In addition, diabetes mellitus confers an increased risk of ischemic heart disease, stroke and peripheral vascular disease. Over 90% of diabetics are classified as type 2, or non-insulindependent diabetes mellitus (NIDDM); the rest fall into the category of type 1, or insulin-dependent diabetes mellitus (IDDM). Although the two types of diabetes have distinct pathogeneses, hyperglycemia and various life-threatening complications resulting from long-term hyperglycemia are the most common features. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Health food and preparation having an anti-obesity effect Inventor(s): Ueda, Ryohei; (Yokohama, JP), Hirayama, Shin; (Yokohama, JP) Correspondence: OBLON SPIVAK MCCLELLAND MAIER & NEUSTADT PC; FOURTH FLOOR; 1755 JEFFERSON DAVIS HIGHWAY; ARLINGTON; VA; 22202; US Patent Application Number: 20030026811 Date filed: July 2, 2002 Abstract: The present invention discloses an anti-obesity agent comprising:D-cysteinolic acid represented by Formula I, as an active ingredient: 1 Excerpt(s): This application is based upon and claims the benefit of priority from prior Japanese Patent Applications No. 2001-226298 filed Jul. 26, 2001; and No. 2001-353609 filed Nov. 19, 2001, the entire contents of both of which are incorporated herein by reference.... The present invention relates to an anti-obesity agent, food and pharmaceutical product containing a component suppressing adipogenesis, which is used as a raw material for pharmaceutical products, and pharmaceutical compositions

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as well as an additive for health foods and health beverages.... D-cysteinolic acid (C.sub.3H.sub.9NO4S: molecular weight: 155) was first isolated from red algae and identified by B. Wickberg in 1957 (Acta Chem Scand 11, 506 (1957)). In 1963, Itoh (University of Hiroshima) found that D-cysteinolic acid is also present in green algae and brown algae of seaweed (Bull. Jpn. Scient. Fish., 29, 771 (1963)). Recently, it was found that sardine contain D-cysteinolic acid. Since D-cysteinolic acid has an anticlotting effect, its use as a raw material for pharmaceutical products has been expected. Indeed, an invention directed to thrombosis treatment and a preventive drug for thrombosis using D-cysteinolic acid from sardine has already been filed under Japanese Patent Application Publication No. 61-47880. Also, an invention directed to a cholesterol-reducing drug using D-cysteinolic acid or a cysteinolic acid/bile acid conjugate has been filed under Japanese Patent Application Publication No. 3-49113. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

HMGI PROTEINS IN CANCER AND OBESITY Inventor(s): ZHOU, XIANJIN; (PISCATAWAY, NJ), TKACHENKO, ALEX; (NEW BRUNSWICK, NJ), ASHAR, HENA; (EDISON, NJ), CHADA, KIRAN K. (NORTH BRUNSWICK, NJ) Correspondence: LYON & LYON LLP; 633 WEST FIFTH STREET; SUITE 4700; LOS ANGELES; CA; 90071; US Patent Application Number: 20030051260 Date filed: January 6, 1999 Abstract: The present invention pertains to a method for treating obesity in a mammal which comprises reducing the biological activity of HMGI genes in the mammal. In another embodiment, the invention pertains to a method for treating a tumor in a patient by reducing the biological activity of normal HMGI genes which comprises administering to the patient a therapeutically effective amount of an inhibitor compound active against normal HMGI-C or HMGI(Y) genes. In another embodiment, the invention pertains to a method of producing a transgenic non-human mammal, the germ cells and somatic cells of which contain an inactivated HMGI gene sequence introduced into the mammal at an embryonic stage. In another embodiment, the invention pertains to a method for screening candidate compounds capable of inhibiting the biological activity of normal HMGI proteins. In another embodiment, the invention pertains to a method for screening candidate compounds capable of inhibiting the biological activity of normal HMGI genes. In another embodiment, the invention pertains to a method for detecting normal HMGI proteins as a diagnostic marker for a tumor using a probe. that recognizes normal HMGI proteins, which comprises the steps of (a) contacting normal HMGI proteins from a sample from a patient with a probe which binds to HMGI proteins; and (b) analyzing for normal HMGI proteins by detecting levels of the probe bound to the normal HMGI proteins, wherein the presence of normal HMGI proteins in the sample is positive for a tumor. In another embodiment, the invention pertains to a method for detecting antibodies to normal HMGI proteins using a probe that recognizes antibodies to HMGI normal proteins, which comprises the steps of (a) treating a sample from a patient with a probe which binds to antibodies to normal HMGI proteins; and (b) analyzing for antibodies to HMGI proteins by detecting levels of the probe bound to the antibodies to HMGI proteins, wherein the presence of antibodies to normal HMGI proteins in the sample is positive for a tumor. In another

Patents 355

embodiment, the invention pertains to HMGI genes and proteins for use as a starting point to isolate downstream target genes regulated by the HMGI genes and proteins. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 08/852,666, filed May 7, 1997, which application is a continuation-in-part of U.S. patent application Ser. No. 08/679,529, filed Jul. 12, 1996.... The present invention pertains to a method for treating obesity in a mammal which comprises reducing the biological activity of HMGI genes in the mammal. In another embodiment, the invention pertains to a method for treating a tumor in a patient by reducing the biological activity of normal HMGI genes which comprises administering to the patient a therapeutically effective amount of an inhibitor compound active against normal HMGI-C or HMGI(Y) genes. In another embodiment, the invention pertains to a method of producing a transgenic non-human mammal, the germ cells and somatic cells of which contain an inactivated HMGI gene sequence introduced into the mammal, or an ancestor of the mammal, at an embryonic stage. In another embodiment, the invention pertains to a method for screening candidate compounds capable of inhibiting the biological activity of normal HMGI proteins, or a fragment thereof, which comprises the steps of (a) incubating a HMGI protein, or a fragment thereof, with a candidate compound under conditions which promote optimal interaction; and (b) measuring the binding affinity of the candidate compound to the HMGI protein, or a fragment thereof; and (c) determining from the binding affinity which candidate compounds inhibit the biological activity of HMGI proteins, or a fragment thereof. In another embodiment, the invention pertains to a method for screening candidate compounds capable of inhibiting the biological activity of normal HMGI genes which comprises the steps of (a) transfecting into a cell a DNA construct which contains a reporter gene under control of a normal HMGI protein-regulated promoter; (b) administering to the cell a candidate compound; (c) measuring the levels of reporter gene expression; and (d) determining from the levels of reporter gene expression which candidate compounds inhibit the HMGI biological activity. In another embodiment, the invention pertains to a method for detecting normal HMGI proteins as a diagnostic marker for a tumor using a probe that recognizes normal HMGI proteins, which comprises the steps of (a) contacting normal HMGI proteins from a sample from a patient with a probe which binds to HMGI proteins; and (b) analyzing for normal HMGI proteins by detecting levels of the probe bound to the normal HMGI proteins, wherein the presence of normal HMGI proteins in the sample is positive for a tumor. In another embodiment, the invention pertains to a method for detecting antibodies to normal HMGI proteins using a probe that recognizes antibodies to HMGI normal proteins, which comprises the steps of (a) treating a sample from a patient with a probe which binds to antibodies to normal HMGI proteins; and (b) analyzing for antibodies to HMGI proteins by detecting levels of the probe bound to the antibodies to HMGI proteins, wherein the presence of antibodies to normal HMGI proteins in the sample is positive for a tumor. In another embodiment, the invention pertains to HMGI genes and proteins for use as a starting point to isolate downstream target genes regulated by the HMGI genes and proteins.... The disclosures referred to herein to illustrate the background of the invention and to provide additional detail with respect to its practice are incorporated herein by reference and, for convenience, are referenced in the following text and respectively grouped in the appended bibliography. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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INDOLINE DERIVATIVES AND METHOD OF TREATING OBESITY Inventor(s): Mansell, Howard Langham; (Winnersh, GB), Monck, Nathaniel Julius Thomas; (Winnersh, GB), Davidson, James Edward Paul; (Winnersh, GB), Bentley, Jonathan Mark; (Winnersh, GB) Correspondence: HOFFMANN-LA ROCHE INC. PATENT LAW DEPARTMENT; 340 KINGSLAND STREET; NUTLEY; NJ; 07110 Patent Application Number: 20020183349 Date filed: October 15, 2001 Abstract: The present invention relates to indoline derivatives. These compounds are especially useful for the prevention and treatment of disorders of the central nervous system; damage to the central nervous system; cardiovascular disorders; gastrointestinal disorders; diabetes, sleep apnea, and especially for the treatment and prevention of obesity. Excerpt(s): The present invention relates to indoline derivatives, to processes and intermediates for their preparation, to pharmaceutical compositions comprising them and to their medicinal use. The active compounds of the present invention are useful in treating obesity, diabetes and other disorders.... It has been recognised that obesity is a disease process influenced by environmental factors in which the traditional weight loss methods of dieting and exercise need to be supplemented by therapeutic products (S. Parker, "Obesity: Trends and Treatments", Scrip Reports, PJB Publications Ltd, 1996).... Whether someone is classified as overweight or obese is generally determined on the basis of their body mass index (BMI) which is calculated by dividing body weight (kg) by height squared (m.sup.2). Thus, the units of BMI are kg/m.sup.2 and it is possible to calculate the BMI range associated with minimum mortality in each decade of life. Overweight is defined as a BMI in the range 25-30 kg/m.sup.2, and obesity as a BMI greater than 30 kg/m.sup.2. There are problems with this definition in that it does not take into account the proportion of body mass that is muscle in relation to fat (adipose tissue). To account for this, obesity can also be defined on the basis of body fat content: greater than 25% and 30% in males and females, respectively. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Intragastric device for treating obesity Inventor(s): Surti, Vihar C. (Winston-Salem, NC), Hashiba, Kiyoshi; (Sao Paulo, BR) Correspondence: BRINKS HOFER GILSON & LIONE; P.O. BOX 10395; CHICAGO; IL; 60611; US Patent Application Number: 20030078611 Date filed: May 17, 2002 Abstract: An apparatus and method comprising at least one intragastric member or artificial bezoar made of a digestive-resistant or substantially indigestible material that is introduced into a gastric lumen of a mammal for the treatment of obesity. The intragastric member or artificial bezoar is typically at inserted into the gastric lumen in a partially compacted configuration, whereby it is then manipulated into, or allowed to assume, a second expanded configuration sufficiently large to remain within the reservoir of the stomach during normal activities and not be passed through the pylorus into the intestines. In animals, the present invention has been found to be effective in

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achieving weight loss over a several month period, while being easy to place and retrieve. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/291,790 filed May 17, 2001, and U.S. Provisional Application No. 60/360,353 filed Feb. 27, 2002, both entitled "Intragastric Device For Treating Obesity".... This invention relates to medical devices, and more particularly to obesity treatment devices that can be placed in the stomach of a patient to reduce the size of the stomach reservoir.... It is well known that obesity is a very difficult condition to treat. Methods of treatment are varied, and include drugs, behavior therapy, and physical exercise, or often a combinational approach involving two or more of these methods. Unfortunately, results are seldom long term, with many patients eventually returning to their original weight over time. For that reason, obesity, particularly morbid obesity, is often considered an incurable condition. More invasive approaches have been available which have yielded good results in many patients. These include surgical options such as bypass operations or gastroplasty. However, these procedures carry high risks, and are therefore not appropriate for most patients. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

MCH antagonists and their use in the treatment of obesity Inventor(s): Chan, Tin Yau; (Edison, NJ), Palani, Anandan; (Bridgewater, NJ), Josien, Hubert B. (Hoboken, NJ), Clader, John W. (Cranford, NJ) Correspondence: SCHERING-PLOUGH CORPORATION; PATENT DEPARTMENT (K6-1, 1990); 2000 GALLOPING HILL ROAD; KENILWORTH; NJ; 07033-0530; US Patent Application Number: 20030105094 Date filed: March 19, 2002 Abstract: The present invention discloses compounds which, are novel antagonists for melanin-concentrating hormone (MCH), as well as methods for preparing such compounds. In another embodiment, the invention discloses pharmaceutical compositions comprising such MCH antagonists as well as methods of using them to treat obesity, metabolic disorders, eating disorders such as hyperphagia, and diabetes. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/277,584, filed Mar. 21, 2001.... This invention relates to antagonists for melaninconcentrating hormone (MCH) and their use in the treatment of metabolic and eating disorders.... MCH, a cyclic peptide, was first identified over a decade ago in teleost fish where it appears to regulate color change. More recently, MCH has been the subject of investigation for its possible role as a regulator of eating behavior in mammals. As reported by Shimada et al., Nature, Vol. 396 (Dec. 17, 1998), pp. 670-673, MCH-deficient mice have reduced body weight and leanness due to hypophagia (reduced feeding). In view of their findings, it was suggested that antagonists of MCH action may be effective for the treatment of obesity. U.S. Pat. No. 5,908,830 discloses a combination therapy for the treatment of diabetes or obesity involving the administration of a metabolic rate increasing agent and a feeding behavior modifying agent, an example of the latter being an MCH antagonist. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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MCH antagonists for the treatment of obesity Inventor(s): McBriar, Mark D. (Stewartsville, NJ), Shapiro, Sherry A. (Belford, NJ), Palani, Anandan; (Bridgewater, NJ), Su, Jing; (Scotch Plains, NJ) Correspondence: SCHERING-PLOUGH CORPORATION; PATENT DEPARTMENT (K6-1, 1990); 2000 GALLOPING HILL ROAD; KENILWORTH; NJ; 07033-0530; US Patent Application Number: 20030144261 Date filed: October 23, 2002 Abstract: The present invention discloses compounds, which are novel antagonists for melanin-concentrating hormone (MCH), as well as methods for preparing such compounds. In another embodiment, the invention discloses pharmaceutical compositions comprising such MCH antagonists as well as methods of using them to treat obesity, metabolic disorders, eating disorders such as hyperphagia, and diabetes. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/343,065 filed on Oct. 25, 2001.... This invention relates to antagonists of melaninconcentrating hormone (MCH) and their use in the treatment of obesity, eating disorders and diabetes, pharmaceutical compositions containing the compounds, and methods of treatment using the compounds.... MCH, a cyclic peptide, was first identified over a decade ago in teleost fish where it appears to regulate color change. More recently, MCH has been the subject of investigation for its possible role as a regulator of eating behavior in mammals. As reported by Shimada et al., Nature, Vol. 396 (17 Dec. 1998), pp. 670-673, MCH-deficient mice have reduced body weight and leanness due to hypophagia (reduced feeding). In view of their findings, it was suggested that antagonists of MCH action may be effective for the treatment of obesity. U.S. Pat. No. 5,908,830 discloses a combination therapy for the treatment of diabetes or obesity involving the administration of a metabolic rate increasing agent and a feeding behavior modifying agent, an example of the latter being an MCH antagonist. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Medicament for treating obesity and improving lipid metabolism Inventor(s): Nakata, Tadashi; (Saitama, JP), Shimizu, Takeshi; (Saitama, JP), Suzuki, Kunio; (Saitama, JP) Correspondence: GREENBLUM & BERNSTEIN, P.L.C. 1941 ROLAND CLARKE PLACE; RESTON; VA; 20191; US Patent Application Number: 20020086855 Date filed: January 7, 2002 Abstract: A medicament for preventive and therapeutic treatment of obesity and a disease with abnormal lipid metabolism which comprises a 24-alkylcholest-5-en-3-one as an active ingredient. Excerpt(s): This application is a divisional of application Ser. No. 09/480,892, filed Jan. 11, 2000, which is a continuation-in-part of application Ser. No. 09/186,153, filed Nov. 5, 1998. The entire disclosures of application Ser. Nos. 09/480,892 and 09/186,158 are expressly incorporated by reference herein in their entireties.... The present invention relates to medicaments useful for preventive and/or therapeutic treatment of obesity, and to medicaments of improving lipid metabolism.... Obesity is caused by insufficient exercise of habitual hyperphagia, or by metabolic disturbance due to genetic causes or

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endocrine diseases and other. Obesity may be a risk factor that causes various adult diseases such as myocardial infarct or arterial sclerosis, and it may also be a cause for deteriorating these diseases. Therefore, early therapeutic and preventive treatment of obesity is very important. Diet therapies or exercise therapies have been applied heretofore as the treatment of mild obesity, and drug therapies are sometimes used for serious obesity in combination with these therapies. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method and apparatus for treating obesity and for delivering time-released medicaments Inventor(s): Lloyd, Greg A. (Spokane, WA) Correspondence: WELLS ST. JOHN ROBERTS GREGORY & MATKIN P.S. 601 W. FIRST AVENUE; SUITE 1300; SPOKANE; WA; 99201-3828; US Patent Application Number: 20030021822 Date filed: July 25, 2001 Abstract: An apparatus and method for treating obesity and for delivering time-released medicaments is described and which includes a plurality of space-filling portions which are sized to be received within a human patient's body and which come together in a patient's body to form a structure which provides therapeutic benefit to the patient. In the method of the present invention, the method includes providing a plurality of spacefilling portions which are sized to be received within the patient's body; and inserting the space-filling portions into the body of the patient and wherein the respective spacefilling portions come together following insertion into the body to form a structure providing therapeutic benefit to the patient. Excerpt(s): The present invention relates to a method and apparatus for treating obesity in humans and for delivering time-release medicaments into a patient's stomach and more particularly to a therapeutic structure which includes a plurality of space-filling portions which are sized to be received within the human patient's body and which come together in the patient's body to form a structure which provides therapeutic benefits.... The adverse health consequences of obesity are well known and established. It is clear that many interrelated behavioral and/or metabolic factors are at work. Consequently, it is extremely difficult for many obese people to lose weight on there own volition.... For obese patients at high risk of weight-related illness, and for the morbidly obese, there are a variety of available bariatric treatments. The most aggressive procedures are the various bariatric surgeries for reducing the stomach lumen. These surgeries include gastroplasty, gastric banding, intragastric balloons and gastric stapling. These methods can be highly effective because they severely limit the amount of food a person can ingest at one sitting, and depending upon the procedure, may induce a continual sense of satiety. Unfortunately, these surgical procedures are quite expensive. Further, the general poor health of this class of patient in combination with a major surgical procedure results in a high incidence of complications and mortality. In another approach utilizing minor surgery, an intragastric balloon can be positioned by way of permanently placed, percutaneous endoscopic gastrostomy tube. However, as with any permanent aperture made through the skin, special hygienic practices are required of the patient and complications often arise. Non-surgical bariatric procedures such as the placement of intragastric inflatable balloons via the esophagus, for example, require what is viewed to be an uncomfortable endoscopic procedure. Yet another nonsurgical bariatric procedure entails wiring a patient's jaw shut to limit food intake.

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However, besides being quite embarrassing and physically uncomfortable, this procedure carries an attendant risk of aspiration of vomit so patients must carry scissors or wire cutters at all times. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method for the treatment and prevention of overweight in mammals Inventor(s): Verlaan, George; (Wageningen, NL), Raggers, Rene John; (Amsterdam, NL) Correspondence: YOUNG & THOMPSON; 745 SOUTH 23RD STREET 2ND FLOOR; ARLINGTON; VA; 22202 Patent Application Number: 20030175368 Date filed: March 11, 2003 Abstract: The present invention relates to a method for the prevention and/or treatment of overweight in mammals. More particularly the invention is concerned with such a method comprising the enteral administration to a mammal of a preparation comprising an effective amount of a combination of dill or an isolate thereof and one or more components capable of stimulating in vivo lipolysis. Suitable examples of components capable of stimulating in vivo lipolysis include methylxanthines, adrenergic amines, Paullinia cupana or an isolate thereof, Zingziber officinale or an isolate thereof, Camellia sinensis or an isolate thereof, Ilex paraguayiensis or an isolate thereof.Another aspect of the invention relates to a solid or semi-solid unit dosage, preferably selected from the group consisting of tablets, pills, microparticles, microspheres, suppositories, capsules, caplets and the like, that is suitable for enteral unitary administration to human subjects and other mammals comprising:a. dill or an isolate thereof in an amount equivalent to between 5 mg and 20 g dill andb. a component capable of stimulating in vivo lipolysis. Excerpt(s): The present invention relates to a method for the prevention and/or treatment of overweight comprising the enteral administration of a component capable of stimulating in vivo lipolysis. Additionally the present invention provides unit dosages, which can suitably be used for the prophylactic and curative treatment of overweight.... Obesity is very common in nowadays society. Approximately 25% to 35% of the population of the Western world is overweight. Overweight is associated with considerable morbidity and mortality. Obesity is the second preventable death cause in de US and a major risk factor for coronary heart disease, hypertension and diabetes mellitus type II. A reduction of body weight with 10% has shown to decrease the risk for coronary heart disease with 20%. Besides this, overweight and/or excess body fat is generally considered a problem, influencing social satisfaction and perception of health.... Attempts to combat overweight are often focussed on alteration of the diet or manipulation of the appetite in order to reduce caloric intake. However, there is accumulating evidence that low energy output predisposes individuals to weight gain and obesity, whether the low energy output is caused by low metabolic rate, physical inactivity or both. Increased energy metabolism therefore is an attractive target for treating overweight. Additionally, it allows people to maintain food intake at socially acceptable levels. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

Patents 361

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Method for the treatment of obesity, overweight and fluctuations in blood insuline and/or glucose levels Inventor(s): Nieuwenhuizen, Arie Gijsbert; (Utrecht, NL), Van Laere, Katrien Maria Jozefa; (Heteren, NL) Correspondence: YOUNG & THOMPSON; 745 SOUTH 23RD STREET 2ND FLOOR; ARLINGTON; VA; 22202 Patent Application Number: 20030113310 Date filed: December 17, 2001 Abstract: The present invention relates to a method of treating or preventing obesity, overweight, fluctuations in blood insulin levels and/or fluctuations in blood glucose levels in mammals. The method acording to the invention comprises the enteral administration to a mammal of an effective amount of a preparation containing an enzyme capable of converting an ingested carbohydrate or digestion product thereof into one or more absorbable components, wherein the total metabolic caloric value of the absorbable component(s) is less than the metabolic caloric value of the ingested carbohydrate or digestion product thereof. Thus the present invention effectively provides a method that allows complete digestion of ingested digestible carbohydrates whilst at the same time reducing the actual metabolic caloric value of said ingested carbohydrates.Another aspect of the invention relates to a pill for oral administration provided with an enteric coating and containing 25 to 10.000 IU glucose isomerase per gram. Excerpt(s): The present invention relates to method for the prevention or treatment of overweight, obesity or fluctuations in blood insuline and/or glucose levels in mammals, the method comprising the administration to a mammal of an enzyme capable of converting an ingested carbohydrate or a digestion product thereof into one or more absorbable components, wherein the total metabolic caloric value of the absorbable component(s) is less than the metabolic caloric value of the ingested carbohydrate or digestion product thereof. The invention also provides a preparation useful for such treatment.... Methods for treatment or prevention of obesity, overweight and fluctuations in blood glucose and/or blood insulin levels known in the art often make use of foodstuffs with reduced caloric value; compositions stimulating metabolism, e.g. by inducing in vivo thermogenisis; or compositions providing in vivo inhibition of digestive enzyme activity. Many drawbacks are attached to the methods as described above. Especially low caloric diets are particularly undesirable due to the required change in consumption pattern and the adverse taste of many low caloric foodstuffs. The inhibition of digestive enzyme activity has the disadvantage that it often causes flatulence and that its efficacy is seriously influenced by dietary factors.... Like obese individuals, also subjects who desire to reduce blood glucose and/or blood insulin fluctuations have to carefully control their diet, e.g. by consuming limited amounts of carbohydrates or by consuming foodstuffs with a low carbohydrate content. The downsides are significant as, for example, low carbohydrate compositions often have a bad taste. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Method for treating morbid obesity Inventor(s): Stein, Alan; (Moss Beach, CA), Silverman, David E. (Palo Alto, CA) Correspondence: DORSEY & WHITNEY LLP; INTELLECTUAL PROPERTY DEPARTMENT; 4 EMBARCADERO CENTER; SUITE 3400; SAN FRANCISCO; CA; 94111; US Patent Application Number: 20030158601 Date filed: March 10, 2003 Abstract: A method for treating morbid obesity in a body of a mammal having a gastrointestinal tract extending through a stomach and a pyloric sphincter and a wall forming the stomach and pyloric sphincter. At least one implant is formed in the wall in the vicinity of the pyloric sphincter to inhibit emptying of the stomach. Excerpt(s): This application claims priority to U.S. provisional patent application Serial No. 60/212,072, filed Jun. 15, 2000, the entire contents of which are hereby incorporated herein by reference.... This invention pertains to the treatment of morbid obesity.... Numerous modalities are purported to treat morbid obesity. These include patientspecific dietary restrictions and nutritional supplementation, abdominoplasty or panniculectomy, gastric banding and/or stapling and the more invasive and surgically aggressive gastric bypass. There is a need for a method which is less invasive and more clinically efficacious in treating morbid obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Method for treatment of insulin resistance in obesity and diabetes Inventor(s): Hochgeschwender, Ute; (Oklahoma City, OK), Brennan, Miles B. (Denver, CO) Correspondence: SHERIDAN ROSS PC; 1560 BROADWAY; SUITE 1200; DENVER; CO; 80202 Patent Application Number: 20020099014 Date filed: September 13, 2001 Abstract: Disclosed is a method to identify compounds useful for reducing insulin resistance in a patient, and particularly a patient that has insulin resistance associated with obesity and/or type II diabetes. Also disclosed is a method of reducing insulin resistance in a patient by administering a compound identified using the method of the invention, and particularly, by administering an antagonist of melanocortin stimulating hormone (MSH) biological activity. Excerpt(s): This invention claims priority under 35 U.S.C..sctn.119(e) from U.S. Provisional Application Serial No. 60/232,292, filed Sep. 13, 2000, entitled, "Method for Investigating and Treating Diabetes". The entire disclosure of U.S. Provisional Application Serial No. 60/232,292 is incorporated herein by reference.... The present invention relates to a non-human animal model for obesity and uses of such an animal for studying and developing methods for identifying compounds for use in the regulation of insulin resistance in obesity and type II diabetes, as well as a method of treating insulin resistance in obesity and type II diabetes by administration of such compounds.... Diabetes, and conditions related thereto, are major health concerns throughout the world, and, particularly in the United States, contribute to morbidity and mortality. Non-insulin dependent diabetes mellitus (NIDDM), also known as type II

Patents 363

diabetes, is the major form of diabetes in developed countries. While a large number of environmental and genetic factors contribute to the risk of NIDDM in the United States, prolonged obesity is by far the largest risk factor. The molecular basis of this association, however, is not fully understood. As a consequence, efficient means of therapeutical intervention are lacking. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Method of identifying compounds suitable for treatment and/or prophylaxis of obesity Inventor(s): Preuschoff, Ulf; (Lehrte, DE), Weske, Michael; (Burgdorf, DE), David, Samuel; (Hannover, DE), Antel, Jochen; (Bad Muender, DE), Hebebrand, Johannes; (Marburg, DE), Sann, Holger; (Hannover, DE) Correspondence: CROWELL & MORING LLP; INTELLECTUAL PROPERTY GROUP; P.O. BOX 14300; WASHINGTON; DC; 20044-4300; US Patent Application Number: 20020022245 Date filed: July 18, 2001 Abstract: A method for the discovery of compounds suitable for the treatment and/or prophylaxis of obesity, in which the ability of the test compounds to inhibit de novo lipogenesis in mammals and/or man is determined. The use of compounds which are capable of inhibiting de novo lipogenesis in mammals, and which are substantially free of effects directed towards the CNS, for the preparation of pharmaceutical compositions for the treatment and/or prophylaxis of obesity, as well as for the treatment and/or inhibition of obesity, are also described. Excerpt(s): The present invention relates to a method of identifying compounds suitable for the treatment and/or prophylaxis of obesity. The invention further relates to the use of compounds which are capable of inhibiting de novo lipogenesis in mammals, and which are substantially free of effects directed towards the central nervous system (=CNS), for the preparation of drugs for the treatment and/or prophylaxis of obesity.... Today, especially in the developed industrial nations, obesity is an increasingly serious problem for the health of the population, being caused predominantly by unbalanced and excessively high-fat nutrition. The increase in the percentage of overweight people in the population is being accompanied by an increase in the consequences of obesity, which range from personal discontentment to cardiovascular disease or certain forms of diabetes. There are therefore already a number of therapeutic procedures aimed at the treatment or prophylaxis of obesity. One example which may be mentioned is lipaseinhibitory compounds, which reduce lipolysis in the intestinal tract and thereby cut down the energy yield from the food intake. Thus, in this therapeutic procedure, at least part of the alimentary fats is excreted undecomposed. It is however desirable to have other novel therapeutic procedures for the treatment and/or prophylaxis of obesity which can complement the previously known forms of therapy.... It has now been found, surprisingly, that compounds which are capable of inhibiting de novo lipogenesis in mammals, especially man, are advantageously suitable for the effective treatment and/or prophylaxis of obesity. Particularly good results are achieved by administering the above-mentioned compounds over prolonged periods, for example for periods of several weeks. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Method of treating obesity in adult patients exhibiting primary insulin hypersecretion Inventor(s): Lustig, Robert H. (San Francisco, CA) Correspondence: Michael L. Goldman; NIXON PEABODY LLP; Clinton Square; P.O. Box 31051; Rochester; NY; 14603; US Patent Application Number: 20020156010 Date filed: November 8, 2001 Abstract: Methods of treating obesity in adult patients, reducing the caloric intake in an obese adult patient, and inhibiting insulin hypersecretion in an obese adult patient are disclosed. The methods are practiced by administering to an obese adult patient exhibiting primary insulin hypersecretion an effective amount of somatostatin, a somatostatin receptor agonist or its salt, or combinations thereof, under conditions effective to reduce the weight of the obese adult patient, reduce the caloric intake of the obese adult patient, or inhibit insulin hypersecretion by pancreatic.beta.-cells of the obese adult patient. Excerpt(s): This application claims benefit of U.S. Provisional Patent Application Serial No. 60/252,324, filed Nov. 20, 2000, which is hereby incorporated by reference in its entirety.... The present invention generally relates to method of treating obesity, inhibiting insulin hypersecretion, and reducing the caloric intake in obese adult patients exhibiting primary insulin hypersecretion.... Obesity has reached epidemic proportions throughout the world. The prevalence of obesity (BMI>30 kg/m.sup.2) in the U.S. has risen from 12.8% to 22.5% during the last 20 years (Kuczmarski, et al., "Increasing prevalence of overweight in U.S. adults: The National Health and Nutrition Examination Surveys, 1960 to 1991," JAMA, 272:205-211 (1994); Mokdad, et al., "The spread of the obesity epidemic in the United States, 1991-1998," JAMA, 282:1519-1522 (1999); Bray, et al., "Current and potential drugs for treatment of obesity," Endocrine Rev, 20:805-875 (1999)). Diet and exercise alone are frequently unsuccessful in ameliorating the obesity long-term (Luepker, et al., "Outcomes of a field trial to improve children's dietary patterns and physical activity," JAMA, 275:768-776 (1996); Skender, et al., "Comparison of 2-year weight loss trends in behavioral treatments of obesity: diet, exercise, and combination interventions," J Am Diet Assoc, 96:342-346 (1996); Bray, et al., "Treatment of obesity: an overview," Diab Metab Rev, 4:653-679 (1988)), stressing the importance of metabolic and genetic components to this syndrome. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Methods and therapeutic combinations for the treatment of obesity using sterol absorption inhibitors Inventor(s): Veltri, Enrico P. (Princeton, NJ), Strony, John T. (Lebanon, NJ), Ress, Rudyard J. (Flemington, NJ), Davis, Harry R. (Berkeley Heights, NJ) Correspondence: SCHERING-PLOUGH CORPORATION; PATENT DEPARTMENT (K6-1, 1990); 2000 GALLOPING HILL ROAD; KENILWORTH; NJ; 07033-0530; US Patent Application Number: 20030119428 Date filed: September 19, 2002 Abstract: The present invention provides methods for the treatment of obesity using sterol or 5.alpha.-stanol absorption inhibitors and compositions and therapeutic

Patents 365

combinations including sterol or 5.alpha.-stanol absorption inhibitors and at least one obesity control medication. Excerpt(s): This application claims the benefit of priority from U.S. Provisional Patent Application Serial No. 60/323,840, filed Sep. 21, 2001, and is a continuation-in-part of U.S. patent application Ser. No. 10/166,942, filed Jun. 11, 2002, each incorporated herein by reference.... The present invention relates to compositions and therapeutic combinations for treating obesity in a subject comprising the administration of sterol and/or 5.alpha.-stanol absorption inhibitor(s) or combinations with obesity control medications.... Obesity is one of the most common medical problems in the United States and other developed countries and a risk factor for other illnesses, such as hypertension, diabetes, degenerative arthritis and myocardial infarction. Weight loss medications may be appropriate for use in selected patients who are obese or who are overweight with co-morbid conditions. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Methods for predicting susceptibility to obesity and obesity-associated health problems Inventor(s): Vohl, Marie-Claude; (Cap-Rouge, CA), Williams, Scott M. (Nashville, TN), Gaudet, Daniel; (Chicoutimi, CA), Engert, James C. (Montreal, CA), Hudson, Thomas J. (Montreal, CA), Lepage, Pierre; (Montreal, CA) Correspondence: HAMILTON, BROOK, SMITH & REYNOLDS, P.C. 530 VIRGINIA ROAD; P.O. BOX 9133; CONCORD; MA; 01742-9133; US Patent Application Number: 20030032099 Date filed: April 4, 2002 Abstract: Methods for determining an individual's susceptibility to obesity or to a health disorder associated with obesity, comprising detecting an allele at a polymorphic site genetically linked to the resistin gene locus, wherein the allele is further linked to obesity, and wherein detection of the allele is indicative of the patient's susceptibility to a health disorder associated with obesity are provided. Also included in the present disclosure are nucleic acid molecules containing allelic variants at polymorphic sites. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/281,449, filed Apr. 4, 2001, the entire teachings of which are incorporated herein by reference.... The frequency of obesity is increasing worldwide. Obesity is associated with health disorders such as diabetes mellitus, coronary heart disease, cancer, and sleepbreathing disorders. Indeed, the recent increase in numbers of obese people is cited as a reason for the corresponding rise in the number of cases of Type II diabetes. The documented association of obesity with disorders such as diabetes suggests a need for a better understanding of both the factors that affect obesity and the mechanisms by which obesity is related to other disorders.... Notions of obese individuals as lacking the will power sufficient to curb eating habits are being replaced by theories that obesity has specific genetic and molecular determinants. From genetic evidence, it is becoming clear that factors leading to a predisposition for obesity are heritable, thus implying the existence of one or more genes responsible for causing obesity. Identification of these genes and characterization of their gene products will provide clues to the treatment of obesity and disorders commonly associated with obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Methods for the treatment of metabolic disorders, including obesity and diabetes Inventor(s): Xu, Haiyan; (Weymouth, MA) Correspondence: Jean M. Silveri; Millennium Pharmaceuticals, Inc. 75 Sidney Street; Cambridge; MA; 02139; US Patent Application Number: 20030143610 Date filed: January 8, 2003 Abstract: The invention relates to methods and compositions for the diagnosis and treatment of metabolic disorders, including, but not limited to, obesity, diabetes, overweight, insulin resistance, anorexia, and cachexia. The invention further provides methods for identifying a compound capable of treating a metabolic disorder. The invention also provides methods for identifying a compound capable of modulating a metabolic activity. Yet further, the invention provides a method for modulating a metabolic activity. In addition, the invention provides a method for treating a subject having a metabolic disorder characterized by aberrant SARP3 polypeptide activity or aberrant SARP3 nucleic acid expression. In another aspect, the invention provides methods for modulating lipogenesis in a subject and methods for modulating lipolysis in a subject. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/346,523, filed Jan. 8, 2002, the contents of which are incorporated herein by this reference.... During normal embryonic and adult development of multicellular organisms, cells that are not necessary or deleterious are eliminated by a process referred to as programmed cell death or apoptosis (Ellis R. E. et al. (1991) Annual Rev. Cell Biol. 7:663-698). Programmed cell death occurs in both vertebrate and invertebrate species and is characterized by unique morphological alterations, such as cytoplasmic contraction and chromatin condensation, as well as by specific DNA cleavage into oligonucleosomal fragments. Unlike necrosis, programmed cell death or apoptosis is an irreversible process which in most systems appears to depend on the expression of a specific set of novel "death genes". Deregulation of this process contributes to the pathogenesis of several diseases including cancer, immunodeficiency, autoimmune diseases, and neurodegenerative disorders (Thompson C. B. et al. (1995) Science 267: 1456).... Adipose tissue consists primarily of adipocytes. Vertebrates possess two distinct types of adipose tissue: white adipose tissue (WAT) and brown adipose tissue (BAT). WAT stores and releases fat according to the nutritional needs of the animal. This stored fat is used by the body for (1) heat insulation (e.g., subcutaneous fat), (2) mechanical cushion (e.g., surrounding internal organs), and (3) as a source of energy. BAT burns fat, releasing the energy as heat through thermogenesis. BAT thermogenesis is used both (1) to maintain homeothermy by increasing thermogenesis in response to lower temperatures and (2) to maintain energy balance by increasing energy expenditure in response to increases in caloric intake (Sears, I. B. et al. (1996) Mol. Cell. Biol. 16(7):34103419). BAT is also the major site of thermogenesis in rodents and plays an important role in thermogenesis in human infants. In humans, and to a lesser extend rodents, brown fat diminishes with age, but can be re-activated under certain conditions, such as prolonged exposure to cold, maintenance on a high fat diet and in the presence of noradrenaline producing tumors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

Patents 367

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Methods for the treatment of metabolic disorders, including obesity and diabetes Inventor(s): An, Wenqian Frank; (Framingham, MA), Chen, Hong; (Newton, MA) Correspondence: Jean M. Silveri; Millennium Pharmaceuticals, Inc. 75 Sidney Street; Cambridge; MA; 02139; US Patent Application Number: 20030157110 Date filed: January 7, 2003 Abstract: The invention relates to methods and compositions for the diagnosis and treatment of metabolic disorders, including, but not limited to, obesity, overweight, diabetes, insulin resistance, anorexia, and cachexia. The invention further provides methods for identifying a compound capable of treating a metabolic disorder. The invention also provides methods for identifying a compound capable of modulating a metabolic activity. Yet further, the invention provides a method for modulating a metabolic activity. In addition, the invention provides a method for treating a subject having a metabolic disorder characterized by aberrant MMP-12 polypeptide activity or aberrant MMP-12 nucleic acid expression. In another aspect, the invention provides methods for modulating lipogenesis in a subject and methods for modulating lipolysis in a subject. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/346,354, filed Jan. 7, 2002, the contents of which are incorporated herein by this reference.... The matrix metalloproteinases (MMPs) are a family of structurally related matrix-degrading enzymes produced by macrophages that play important roles in tissue growth and remodeling during normal embryonic development as well as during tissue repair. These zinc-binding endopeptidases are involved in the degradation of extracellular matrix (ECM) components, such as elastin, and function at neutral pH and require Ca.sup.+2 to be active. MMP activitiy is further regulated by tissue inhibitors of metalloproteinases (TIMPs), also produced by macrophages. The MMPs can be divided into four major subfamilies based on sequence homology and domain structures. One subfamily includes matrilysin (also known as MMP-7). It has been attributed with elastolytic activity and is found in peripheral blood monocytes, but not in alveolar macrophages (Busick, et al., (1992) J. Biol. Chem. 267:9087-9092). A second family includes at least three collagenases (MMP-1, MMP-8, and MMP-13), stromelysin (MMP3, MMP-10, and MMP-11), and metalloelastase (MMP-12). The DNA cloning of stromelysin is described in WO 87/07907. The DNA cloning of MMP-12 is described, e.g., in U.S. Pat. No. 6,204,043; and Shapiro, e al., (1992) J. Biol. Chem. 267:4664-4671. A third family includes two type IV-collagenase/gelatinases (MMP-2 and MMP-9), described, e.g., in U.S. Pat. Nos. 4,772,557, 4,923,818, and 4,992,537, respectively. The fourth family includes five members (MMP-14, MMP-15, MMP-16, MMP-17 or MTI-4MMP, and MT5-MMP) that are known as membrane type MMPs.... Given their role in tissue remodeling and repair, aberrant MMP expression or activity is associated with various diseases, such as tumorigenesis, metastasis, and inflammatory disorders such as rheumatoid arthritis, osteoarthritis, atherosclerosis, and pulmonary emphysema. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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METHODS FOR TREATING OBESITY Inventor(s): KOLTERMAN, ORVILLE G. (POWAY, CA), DUFT, BRADFORD J. (SANTE FE, CA) Correspondence: Bradford J Duft Esq; Brobeck Phleger and Harrison LLP; 12390 El Camino Real; San Diego; CA; 92130-2081; US Patent Application Number: 20030026812 Date filed: June 6, 1997 Abstract: Methods for treating obesity are disclosed which comprise administration of a therapeutically effective amount of an amylin or an amylin agonist alone or in conjunction with another obesity relief agent. Excerpt(s): The present invention relates to methods for treating obesity. More particularly, the invention relates to the use of an amylin or agonist of amylin in the treatment of obesity.... The structure and biology of amylin have previously been reviewed. See, for example, Rink et al., Trends in Pharmaceutical Sciences, 14:113-118 (1993); Gaeta and Rink, Med. Chem. Res., 3:483-490 (1994); and, Pittner et al., J. Cell. Biochem., 55S:19-28 (1994). Amylin is a 37 amino acid protein hormone. It was isolated, purified and chemically characterized as the major component of amyloid deposits in the islets of pancreases of deceased human Type 2 diabetics (Cooper et al., Proc. Natl. Acad. Sci. USA, 84:8628-8632 (1987)). The amylin molecule has two important posttranslational modifications: the C-terminus is amidated, and the cysteines in positions 2 and 7 are cross-linked to form an N-terminal loop. The sequence of the open reading frame of the human amylin gene shows the presence of the Lys-Arg dibasic amino acid proteolytic cleavage signal, prior to the N-terminal codon for Lys, and the Gly prior to the Lys-Arg proteolytic signal at the C-terminal position, a typical sequence for amidation by protein amidating enzyme, PAM (Cooper et al., Biochem. Biophys. Acta, 1014:247-258 (1989)). Amylin is the subject of U.S. Pat. No. 5,367,052, issued Nov. 22, 1995.... In Type 1 diabetes, amylin has been shown to be deficient and combined replacement with insulin has been proposed as a preferred treatment over insulin alone in all forms of diabetes. The use of amylin and other amylin agonists for the treatment of diabetes mellitus is the subject of U.S. Pat. No. 5,175,145, issued Dec. 29, 1992. Pharmaceutical compositions containing amylin and amylin plus insulin are described in U.S. Pat. No. 5,124,314, issued Jun. 23, 1992. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Methods for using the obese gene and its gene product to stimulate hematopoietic development Inventor(s): Cioffi, Joseph; (New Albany, OH), Zupancic, Thomas Joel; (Worthington, OH), Snodgrass, H. Ralph; (Powell, OH), Shafer, Alan Wayne; (Lancaster, OH) Correspondence: PENNIE AND EDMONDS; 1155 AVENUE OF THE AMERICAS; NEW YORK; NY; 100362711 Patent Application Number: 20020197232 Date filed: March 12, 2002 Abstract: The present invention relates to methods for using various forms of a novel receptor expressed by hematopoietic and endothelial cells. An additional variant form of this receptor has been detected in brain cells and shown to bind to the obese gene

Patents 369

product, leptin. Therefore, leptin may be used to stimulate the growth and development of receptor-positive hematopoietic and endothelial cells in vitro and in vivo. In addition, this receptor is selectively expressed in hematopoietic progenitor cells with long-term repopulating potential. Thus, agents that specifically bind to this receptor may be used to identify and isolate progenitor cells for a variety of clinical applications. Excerpt(s): The present application is a continuation of co-pending U.S. patent application Ser. No. 08/618,957, filed Mar. 20, 1996, which is a continuation-in-part of U.S. patent application Ser. No. 08/589,915, filed Jan. 23, 1996, (now abandoned) which is a continuation-in-part of U.S. patent application Ser. No. 08/355,888, filed Dec. 14, 1994 (now U.S. Pat. No. 5,763,211), which is a continuation-in-part of U.S. patent application Ser. No. 08/306,231 filed Sep. 14, 1994 (now U.S. Pat. No. 5,643,748), each of which is incorporated by reference herein in its entirety.... The present invention relates to methods for using various forms of a novel receptor expressed by hematopoietic and endothelial cells. An additional variant form of this receptor has been detected in brain cells and shown to bind to the obese gene product, leptin. Therefore, leptin may be used to stimulate the growth and development of receptor-positive hematopoietic and endothelial cells in vitro and in vivo. In addition, this receptor is selectively expressed in hematopoietic progenitor cells with long-term repopulating potential. Thus, agents that specifically bind to this receptor may be used to identify and isolate progenitor cells for a variety of clinical applications.... A variety of diseases, including malignancy and immunodeficiency, are related to malfunction within the lympho-hematopoietic system. Some of these conditions could be alleviated and/or cured by repopulating the hematopoietic system with progenitor cells, which when triggered to differentiate would overcome the patient's deficiency. Therefore, the ability to initiate and regulate hematopoiesis is of great importance (McCune et al., 1988, Science 241:1632). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Methods of treating obesity using a neurotensin receptor ligand Inventor(s): Hadcock, John R. (East Lyme, CT) Correspondence: Gregg C. Benson; Pfizer Inc. Patent Department, MS 4159; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20010046956 Date filed: April 24, 2001 Abstract: The present invention relates to methods of treating obesity, diabetes, sexual dysfunction, atherosclerosis, insulin resistance, impaired glucose tolerance, hypercholesterolemia or hypertrigylceridemia using a neurotensin receptor ligand. The present invention also relates to pharmaceutical compositions and kits that comprise a neurotensin receptor ligand. Excerpt(s): This application claims priority of U.S. provisional application No. 60/199,951, filed Apr. 27, 2000.... The present invention relates to methods of treating obesity, diabetes, sexual dysfunction (including erectile dysfunction), atherosclerosis, insulin resistance, impaired glucose tolerance, hypercholesterolemia, or hypertrigylceridemia using a compound that is a neurotensin receptor ligand. The present invention also relates to compositions and kits that comprise a neurotensin receptor ligand.... Obesity is a devastating disease. In addition to harming physical health, obesity can wreak havoc on mental health because obesity affects self-esteem, which ultimately can affect a person's ability to interact socially with others.

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Unfortunately, obesity is not well understood, and societal stereotypes and presumptions regarding obesity only tend to exacerbate the psychological effects of the disease. Because of the impact of obesity on individuals and society, much effort has been expended to find ways to treat obesity, but little success has been achieved in the long-term treatment and/or prevention of obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Novel genes and their use in the modulation of obesity, diabetes and energy imbalance Inventor(s): McMillan, Janine Susan; (Torquay, AU), Walder, Kenneth Russell; (Ocean Grove, AU), Zimmet, Paul Zev; (Toorak, AU), Collier, Gregory; (Ocean Grove, AU), Windmill, Kelly Fiona; (Newtown, AU) Correspondence: Leopold Presser; Scully, Scott, Murphy & Presser; 400 Garden City Plaza; Garden City; NY; 11530; US Patent Application Number: 20020169287 Date filed: December 31, 2001 Abstract: The present invention relates generally to nucleic acid molecules encoding proteins associated with the modulation of obesity, diabetes and/or metabolic energy levels. More particularly, the present invention is directed to nucleic acid molecules and the recombinant and purified proteins encoded thereby and their use in therapeutic and diagnostic protocols for conditions such as obesity, diabetes and energy imbalance. The subject nucleic acid molecules and proteins and their derivatives, homologs, analogs, chemical equivalents and mimetics are proposed as therapeutic and diagnostic agents for obesity, diabetes and energy imbalance. Excerpt(s): This application a continuation of International Application No. PCT/AU00/00786, filed on Jun. 29, 2000.... The present invention relates generally to nucleic acid molecules encoding proteins associated with the modulation of obesity, diabetes and/or metabolic energy levels. More particularly, the present invention is directed to nucleic acid molecules and the recombinant and purified proteins encoded thereby and their use in therapeutic and diagnostic protocols for conditions such as obesity, diabetes and energy imbalance. The subject nucleic acid molecules and proteins and their derivatives, homologs, analogs, chemical equivalents and mimetics are proposed as therapeutic and diagnostic agents for obesity, diabetes and energy imbalance.... Bibliographic details of the publications referred to by author in this specification are collected at the end of the description. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Novel genes expressed in obese rat hypothalamus Inventor(s): Wu, Linda H. (Woodbridge, CT) Correspondence: BANNER & WITCOFF; 1001 G STREET N W; SUITE 1100; WASHINGTON; DC; 20001; US Patent Application Number: 20020041870 Date filed: July 26, 2001

Patents 371

Abstract: Novel genes expressed in obese rat hypothalamus can be used to provide therapeutic reagents for treating obesity and related disorders. Excerpt(s): This application claims the benefit of and incorporates by reference copending provisional application Ser. No. 60/220,878 filed Jul. 26, 2000.... The invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. See U.S. Pat. No. 6,057,109. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, Essays in Biochem. 20, 110-65, 1985; Himms-Hagen, Prog. Lipid Res. 28, 67-115, 1989). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, Physiol. Rev. 64, 1-64, 1984). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg, Trends Biochem. Sci. 15, 108-12, 1990; Klaus et al., Int. J. Biochem. 23, 791-801, 1991). UCP-mediated uncoupling is not only capable of increasing body temperature in cold-acclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, In BROWN ADIPOSE TISSUE, Trayhurn et al., eds., London, Arnold, p. 269298, 1986; Spiegelman & Flier, Cell 87, 377-89, 1996; Hamann & Flier, Endocrinology 137:2129, 1996). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, Endocrinology 137, 2129, 1996; Lowell et al., Nature 366, 740-42, 1993; Kopecky et al., J. Clin. Invest. 96, 2914-23, 1995; Cunmnings et al., Nature 382, 622-26, 1996). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Ob receptor and methods for the diagnosis and treatment of body weight disorders, including obesity and cachexia Inventor(s): Tepper, Robert I. (Weston, MA), Tartaglia, Louis A. (Watertown, MA), Culpepper, Janice A. (Brookline, MA), White, David W. (Holbrook, MA) Correspondence: ANITA L. MEIKLEJOHN, PH.D. Fish & Richardson P.C. 225 Franklin Street; Boston; MA; 02110-2804; US Patent Application Number: 20020182676 Date filed: February 19, 2002 Abstract: The present invention relates to the discovery, identification and characterization of nucleotides that encode Ob receptor (ObR), a receptor protein that participates in mammalian body weight regulation. The invention encompasses obR nucleotides, host cell expression systems, ObR proteins, fusion proteins, polypeptides and peptides, antibodies to the receptor, transgenic animals that express an obR transgene, or recombinant knock-out animals that do not express the ObR, antagonists and agonists of the receptor, and other compounds that modulate obR gene expression or ObR activity that can be used for diagnosis, drug screening, clinical trial monitoring, and/or the treatment of body weight disorders, including but not limited to obesity, cachexia and anorexia.

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Excerpt(s): This application is a continuation-in-part of application Ser. No. 08/708,123 filed Sep. 3, 1996, which is a continuation-in-part of application Ser. No. 08/638,524 filed Apr. 26, 1996, which is a continuation-in-part of application Ser. No. 08/599,455, filed Jan. 22, 1996, which is a continuation-in-part of application Ser. No. 08/583,153, filed Dec. 28, 1995, which is a continuation-in-part of application Ser. No. 08/570,142, filed Dec. 11, 1995, which is a continuation-in-part of application Ser. No. 08/569,485, filed Dec. 8, 1995, which is a continuation-in-part of application Ser. No. 08/566,622, filed Dec. 4, 1995, which is a continuation-in-part of application Ser. No. 08/562,663, filed Nov. 27, 1995.... The present invention relates to the discovery, identification and characterization of nucleotides that encode Ob receptor (ObR), a receptor protein that participates in mammalian body weight regulation. The invention encompasses obR nucleotides, host cell expression systems, ObR proteins, fusion proteins, polypeptides and peptides, antibodies to the receptor, transgenic animals that express an obR transgene, or recombinant knock-out animals that do not express the ObR, antagonists and agonists of the receptor, and other compounds that modulate obR gene expression or ObR activity that can be used for diagnosis, drug screening, clinical trial monitoring, and/or the treatment of body weight disorders, including but not limited to obesity, cachexia and anorexia.... Obesity represents the most prevalent of body weight disorders, and it is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Obesity inhibitory materials Inventor(s): Takebe, Minoru; (Tokyo, JP) Correspondence: Koda & Androlia; Suite 3850; 2029 Century Park East; Los Angeles; CA; 90067-3024; US Patent Application Number: 20030082247 Date filed: March 6, 2002 Abstract: Anti-obesity material of the present invention is absorbed in vivo by oral ingestion, drops, etc. so as to act against the causes of overeating and control food consumption, and it can thereby promote fat metabolism and control accumulation of body fat while at the same time can inhibit elevation of blood pressure, all without compromising immune system function, thus safely controlling an increase in body weight (obesity). There have previously been no anti-obesity materials like that of the present invention whatsoever. The main characteristic of the present invention is that an anti-obesity material having the above-described excellent effects is obtained since the anti-obesity material has isoflavone aglycone and/or isoflavone glycoside. Excerpt(s): The present invention relates to an anti-obesity material capable of controlling obesity (weight increase) and in particular to an anti-obesity material capable of effectively controlling obesity by controlling an increase in body weight while controlling food consumption and enhancing in vivo immune function as a result of being absorbed in vivo.... Obesity is a cause of development of lifestyle-related disease, including hypertension, diabetes, hyperlipidemia, etc. Moreover, it is reported that, according to epidemiological research, when obese persons lose weight, their average

Patents 373

remaining years are improved. However, it is also a fact that even though obese persons recognize the fact that they are at high risk for lifestyle-related disease, they do not lose weight because it is extremely difficult for them to keep weight off by dietary, etc. methods.... Postmenopausal women in particular develop so-called climacteric symptoms due to a reduction in female hormone (estrogen) secretion. In addition to the climacteric disturbances represented by hot flashes, these symptoms are said to have an effect on general functions of bone metabolism, the cardiovascular system, fat metabolism, the urogenital system, the digestive system, the neurological system, etc. Consequently, hormone-replacement therapy (HRT) whereby female hormones are artificially replenished is being examined as a treatment for the symptoms caused by this loss of estrogen activity. Nevertheless, HRT also poses many problems in that adverse reactions such as uterine bleeding and breast tenderness, etc. readily develop. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Obesity treatment tools and methods Inventor(s): Andreas, Bernard H. (Redwood City, CA), Gifford, Hanson S. III; (Woodside, CA), Deem, Mark E. (Mountain View, CA), Sutton, Douglas S. (Pacifica, CA), French, Ronald G. (Santa Clara, CA) Correspondence: Johney U. Han; Morrison & Foerster LLP; 755 Page Mill Road; Palo Alto; CA; 94304-1018; US Patent Application Number: 20030109892 Date filed: January 14, 2003 Abstract: Various obesity treatment tools and methods are described herein, as well as treatments for other gastric-related diseases, e.g., GERD. Treatment includes reducing the size of the stomach pouch to limit the caloric intake as well as to provide an earlier feeling of satiety. This may be done by creating a smaller gastric pouch within the stomach directly from the interior of the stomach itself. The smaller pouches may be made through the use of individual anchoring devices, rotating probes, or volume reduction devices. A pyloroplasty procedure may also be performed to render the pyloric sphincter incompetent. A gastric bypass procedure may additionally be performed using atraumatic magnetic anastomoses devices so that sugars and fats are passed directly to the bowel while bypassing the stomach. Many of these procedures may be done in a variety of combinations. Treatment may create enforced behavioral modifications by discouraging the ingestion of high-caloric foods. Excerpt(s): This is a continuation of U.S. patent application Ser. No. 09/871,297, filed May 30, 2001, which is incorporated herein by reference in its entirety.... The present invention relates generally to tools and methods for the treatment of obesity. More particularly, the present invention relates to tools and methods for performing less traumatic gastroplasty procedures.... Obesity is considered a major health problem with annual associated costs reaching $100 billion in the U.S. alone. Morbid obesity is a condition of obesity with the presence of a secondary debilitating progressive disease and is generally associated with a body mass index (BMI).gtoreq.40 kg/m.sup.2. While the basic mechanism of obesity is simply an imbalance between caloric intake and burn rate, the underlying factors are varied and complex and conservative attempts at sustained weight loss with this population are almost always unsuccessful. Often, there are genetic and other biological influences that may override environmental causes. Consequently, obesity is a disease that eludes a simple treatment, with a recurrence rate above 90% for those who attempt to lose weight. Moreover, long-term results using

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conservative treatments for morbid obesity are generally unsuccessful and are typically associated with further loss of self-esteem with the regaining of weight. Hypertension, cardiovascular disease, diabetes, along with a host of other comorbidities all make morbid obesity second only to smoking as a preventable cause of death. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Obesity treatment tools and methods Inventor(s): Andreas, Bernard H. (Redwood City, CA), Gifford, Hanson S. III; (Woodside, CA), Sutton, Douglas S. (Pacifica, CA), Deem, Mark E. (Mountain View, CA), French, Ronald G. (Santa Clara, CA) Correspondence: Johney U. Han; Morrison & Foerster LLP; 755 Page Mill Road; Palo Alto; CA; 94304-1018; US Patent Application Number: 20030120265 Date filed: December 5, 2002 Abstract: Various obesity treatment tools and methods are described herein, as well as treatments for other gastric-related diseases, e.g., GERD. Treatment includes reducing the size of the stomach pouch to limit the caloric intake as well as to provide an earlier feeling of satiety. This may be done by creating a smaller gastric pouch within the stomach directly from the interior of the stomach itself. The smaller pouches may be made through the use of individual anchoring devices, rotating probes, or volume reduction devices. A pyloroplasty procedure may also be performed to render the pyloric sphincter incompetent. A gastric bypass procedure may additionally be performed using atraumatic magnetic anastomoses devices so that sugars and fats are passed directly to the bowel while bypassing the stomach. Many of these procedures may be done in a variety of combinations. Treatment may create enforced behavioral modifications by discouraging the ingestion of high-caloric foods. Excerpt(s): This is a divisional of U.S. patent application Ser. No. 09/871,297, filed May 30, 2001, which is incorporated herein by reference in its entirety.... The present invention relates generally to tools and methods for the treatment of obesity. More particularly, the present invention relates to tools and methods for performing less traumatic gastroplasty procedures.... Obesity is considered a major health problem with annual associated costs reaching $100 billion in the U.S. alone. Morbid obesity is a condition of obesity with the presence of a secondary debilitating progressive disease and is generally associated with a body mass index (BMI).gtoreq.40 kg/m.sup.2. While the basic mechanism of obesity is simply an imbalance between caloric intake and bum rate, the underlying factors are varied and complex and conservative attempts at sustained weight loss with this population are almost always unsuccessful. Often, there are genetic and other biological influences that may override environmental causes. Consequently, obesity is a disease that eludes a simple treatment, with a recurrence rate above 90% for those who attempt to lose weight. Moreover, long-term results using conservative treatments for morbid obesity are generally unsuccessful and are typically associated with further loss of self-esteem with the regaining of weight. Hypertension, cardiovascular disease, diabetes, along with a host of other comorbidities all make morbid obesity second only to smoking as a preventable cause of death. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

Patents 375

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Obesity-specific G protein coupled receptors Inventor(s): Wu, Linda H. (Woodbridge, CT) Correspondence: BANNER & WITCOFF; 1001 G STREET N W; SUITE 1100; WASHINGTON; DC; 20001; US Patent Application Number: 20020068306 Date filed: October 17, 2001 Abstract: Novel obesity-specific G protein-coupled receptors can be used to provide therapeutic reagents for treating obesity and related disorders. Excerpt(s): This application incorporates by reference and claims the benefit of copending provisional application Ser. No. 60/240,835 filed Oct. 17, 2000.... The invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. See U.S. Pat. No. 6,057,109. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, Essays in Biochem. 20, 110-65, 1985; Himms-Hagen, Prog. Lipid Res. 28, 67-115, 1989). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, Physiol. Rev. 64, 1-64, 1984). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg, Trends Biochem. Sci. 15, 108-12, 1990; Klaus et al, Int. J. Biochem. 23, 791-801, 1991). UCP-mediated uncoupling is not only capable of increasing body temperature in cold-acclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, In BROWN ADIPOSE TISSUE, Trayhum et al., eds., London, Arnold, p. 269298, 1986; Spiegelman & Flier, Cell 87, 377-89, 1996; Hamann & Flier, Endocrinology 137:2129, 1996). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, Endocrinology 137, 2129, 1996; Lowell et al., Nature 366, 740-42, 1993; Kopecky et al., J. Clin. Invest 96, 2914-23, 1995; Cummings et al., Nature 382, 622-26, 1996). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Percutaneous intragastric balloon catheter for the treatment of obesity Inventor(s): De Hoyos Garza, Andres; (Mexico City, MX) Correspondence: Paul J. Ethington; REISING ,ETHINGTON , BARNES, KISSELLE,; LEARMAN & McCULLOCH, P.C. Post Office Box 4390; Troy; MI; 48099; US Patent Application Number: 20010037127 Date filed: February 23, 2001 Abstract: The present invention relates to a percutaneous intragastric balloon catheter for the treatment of obesity. The invention occupies a portion of the gastric cavity causing a feeling of satiety and decreasing the consumption of food by an obese patient. This invention consists in a percutaneous intragastric balloon that is placed in a nonsurgically form. The percutaneous intragastric balloon catheter is collocated by

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percutaneous endoscopic gastrotomy (PEG). The invention comprises an affixed valve for regulating the amount of fluid introduced or evacuated from the percutaneous intragastric balloon. Excerpt(s): This invention relates to gastrostomy devices for use in the treatment of obesity. More particularly, the invention relates to percutaneous balloon catheters positioned in the stomach for medical treatment of morbid obesity in humans.... Morbid obesity is a chronic medical illness defined as overweight of 50 to 100 percent above the ideal body weight. Obesity is a major medical problem affecting millions of people worldwide. In addition to the phychosocial stigmas associated with the condition or disease, many serious health ramifications may develop. Hypertension, hyperlipidemia, exacerbation of diabetes mellitus, heart disease, degenerative arthritis, and Pickwickian syndrome. Certain types of cancer, gallstones, varicose veins, thromboembolism and hernias are more common among overweight individuals. In addition, morbid obesity can lead to psychosocial difficulties such as depression, loss of self-esteem and decreased employability.... To date, numerous attempts have been made to cause weight loss in morbidly obese patients. None of them have been entirely successful. The weight loss methods can be broadly divided into behavioral modification, vigorous exercise, use of pharmaceuticals, medical diets, surgical procedures and devices. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Pharmaceutical composition for the treatment of obesity or to facilitate or promote weight loss Inventor(s): Dow, Robert L. (Waterford, CT), O'Neill, Brian Thomas; (Old Saybrook, CT), Harrigan, Edmund Patrick; (Old Lyme, CT), Sands, Steven Bradley; (Stonington, CT), Coe, Jotham Wadsworth; (Niantic, CT), Watsky, Eric Jacob; (Stonington, CT) Correspondence: PFIZER INC; 150 EAST 42ND STREET; 5TH FLOOR - STOP 49; NEW YORK; NY; 10017-5612; US Patent Application Number: 20030176457 Date filed: February 13, 2003 Abstract: Pharmaceutical compositions are disclosed for the treatment of obesity, an overweight condition and compulsive overeating. The pharmaceutical compositions are comprised of a therapeutically effective combination of a nicotine receptor partial agonist and an anti-obesity agent or weight loss facilitator or promoter and a pharmaceutically acceptable carrier. The method of using these compounds is also disclosed. Excerpt(s): The present invention relates to pharmaceutical compositions for the treatment of obesity, compulsive overeating; or to facilitate or promote weight loss in a mammal (e.g. human) comprising a nicotine receptor partial agonist (NRPA) and an anti-obesity or weight loss promoting agent. The term NRPA refers to all chemical compounds which bind at neuronal nicotinic acetylcholine specific receptor sites in mammalian tissue and elicit a partial agonist response. A partial agonist response is defined here to mean a partial, or incomplete functional effect in a given functional assay. Additionally, a partial agonist will also exhibit some degree of antagonist activity by its ability to block the action of a full agonist (Feldman, R. S., Meyer, J. S. & Quenzer, L. F. Principles of Neuropsychopharmacology, 1997; Sinauer Assoc. Inc.). The present invention may be used to treat mammals (e.g. humans) for obesity, an overweight condition or compulsive overeating with a decrease in the severity of unwanted side

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effects such as causing nausea and/or stomach upset.... Obesity is a major health risk that leads to increased mortality and incidence of Type 2 diabetes mellitus, hypertension and dyslipidemia. It is the second leading cause of preventable death in the United States, and contributes to>300,000 deaths per year. The estimated direct annual health cost associated with obesity is $70 billion, while the total overall cost to the U.S. economy has been estimated to be over $140 billion. In the U.S., more than 50% of the adult population is overweight, and almost 1/4 of the population is considered to be obese (BMI greater than or equal to 30). Furthermore, the prevalence of obesity in the United States has increased by about 50% in the past 10 years. While the vast majority of obesity occurs in the industrialized world, particularly in U.S. and Europe, the prevalence of obesity is also increasing in Japan. The prevalence of obesity in adults is 10%-25% in most countries of Western Europe. The rise in the incidence of obesity has promoted the WHO to recognize obesity as a significant disease. What is needed are orally active agents that induce sustained weight loss of 10-15% of initial body weight, due to selective loss of body fat in moderately obese patients. These orally active agents should increase energy expenditure, decrease food intake and partition energy away from adipose tissue. This degree of sustained weight loss would then improve comorbidities including hyperglycemia, hypertension and hyperlipidemia, all of which are exacerbated by obesity.... However, even though weight loss agents have therapeutic utility in the treatment of obesity, there are significant liabilities to the use of weight loss compounds. Specifically, many of these compounds that have been tested in humans can cause potentially serious side effects such as gastrointestinal complications including nausea, emesis, ulcers, constipation, flatulence, diarrhea, hypertension, respiratory depression, and psychological and physical dependence. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Pharmaceuticals for treating obesity Inventor(s): Zhang, Bei B. (Edison, NJ), Zhou, Gaochao; (Scotch Plains, NJ), Moller, David E. (Bedminster, NJ), Mosley, Ralph T. (Roselle, NJ), Tolman, Richard L. (Menlo Park, CA), Leibowitz, Mark D. (San Diego, CA), Doebber, Thomas W. (Scotch Plains, NJ), Berger, Joel P. (Hoboken, NJ), Ventre, John; (Nutley, NJ) Correspondence: Merck & Co., Inc. Patent Department; P.O. Box 2000 - RY60-30; Rahway; NJ; 07065-0907; US Patent Application Number: 20030032581 Date filed: September 11, 2002 Abstract: Compounds which are antagonists of strong PPAR-gamma agonists, such as rosiglitazone, and are also partial agonists of the PPAR-gamma receptor, are active agents for correcting or reducing obesity. For example, 1-(p-chlorobenzyl)-5-chloro-3thiophenylindole-2-carboxylic acid, is characterized as being a potent and selective ligand for PPAR-gamma which has partial agonist (<30% maximal effects relative to rosiglitazone) and antagonist activity in cell-free and cell-based assays for the PPARgamma receptor. The compound is a potent agent for reducing obesity and insulin resistance in fat-fed C57BL/6J mice. This compound and other PPAR-gamma antagonists/partial agonists and pharmaceutically acceptable salts are effective in the treatment of obesity and/or diabetes and/or insulin resistance. Excerpt(s): This invention relates to obesity and methods of treating or preventing obesity. In addition, the invention relates to methods for treatment or prevention of insulin resistance, Type II diabetes, and lipid disorders.... Excessive weight, and in

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extreme cases obesity, is a widespread medical problem in the United States and elsewhere as the new millenium approaches. This may be due in part to sedentary life styles and poor diet (high in fats and carbohydrates), as well as to a genetic predisposition in many cases.... Pharmaceuticals have been marketed in the past to help control excessive weight and obesity. These have typically tried to achieve weight loss by reducing the appetite. Drugs used to reduce appetite have not been universally successful. Many are stimulants and have been abused, and others have had unexpected, and sometimes serious side effects (e.g., fen-phen). An approach that has so far not been exploited successfully is the development of pharmaceuticals that control excessive weight and obesity using a metabolic approach by modulation of receptors that can influence weight gain. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Polysubstituted indan-1-ol- systems for the prophylaxis or treatment of obesity Inventor(s): Bickel, Martin; (Bad Homburg, DE), Gossel, Matthias; (Hofheim, DE), Krone, Volker; (Hofheim, DE), Jaehne, Gerhard; (Frankfurt, DE) Correspondence: HELLER EHRMAN WHITE & MCAULIFFE LLP; 1666 K STREET,NW; SUITE 300; WASHINGTON; DC; 20006; US Patent Application Number: 20030130323 Date filed: August 29, 2002 Abstract: Polysubstituted indan-1-ol compounds of formula I, its physiologically acceptable salts and physiologically functional derivatives are disclosed 1Compositions comprising the same, methods of preparation and methods for the prophylaxis or treatment of obesity are also disclosed herein. Excerpt(s): The instant application takes priority from DE 10142659.3 filed Aug. 31, 2001 which is incorporated herein by reference in its entirety.... The invention relates to polysubstituted indan-1-ol compounds and their physiologically acceptable salts and physiologically functional derivatives for the prophylaxis or treatment of obesity.... WO 97/20806 discloses cyclopentyl-substituted indan-1-ol derivatives as antiinflammatory substances. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Preventives or remedies for obesity or fatty liver Inventor(s): Hara, Seijiro; (Toyonaka-shi, JP), Shiomi, Teruo; (Koka-gun, JP) Correspondence: WENDEROTH, LIND & PONACK, L.L.P. 2033 K STREET N. W. SUITE 800; WASHINGTON; DC; 20006-1021; US Patent Application Number: 20030153513 Date filed: January 31, 2003 Abstract: The present invention provides a new use of an agent that inhibits bile acid reabsorption. An agent that inhibits bile acid reabsorption is useful for the prevention or treatment of obesity or fatty liver. Excerpt(s): The invention relates to a pharmaceutical composition for prevention or treatment of obesity or fatty liver, and specifically relates to a pharmaceutical

Patents 379

composition for prevention or treatment of obesity or fatty liver comprising an inhibitor of bile acid reabsorption, to a method for prevention or treatment of obesity or fatty liver comprising using the inhibitor, and to such a new use of the inhibitor.... Since the U.S. LRC-CPPT (Lipid Research Clinics Coronary Primary Prevention Trial) reported in 1984 that the medication of hypercholesterolemia utilizing agents that accelerate bile acid excretion reduced the incidence of ischemic heart diseases, diverse drugs that function through such mechanism have been developed to treat hypercholesterolemia. The drugs include inhibitors of bile acid transport proteins, which have been described, for example, as lignan analogues (JP Publication (kokai) No. 310634/1993, U.S. Pat. No. 5,420,333) and glucuronic acid derivatives thereof (JP Publication (kokai) No. 241206/1997). It has been known that such inhibitors and other compounds that have an activity of inhibiting bile acid reabsorption inhibit the reabsorption of bile acid from the small intestine and thus decrease the LDL-cholesterol level in blood. However, it has never been known that those inhibitors exhibit an anti-obesity effect nor any effect on fatty liver.... The present inventors further studied bile acid reabsorption inhibitors to search for agents that decrease the cholesterol level, and found that such inhibitors exhibit the preventive and therapeutic actions on obesity and fatty liver. The present invention is based on the fact that the inventors found the preventive and therapeutic actions of bile acid reabsorption inhibitors on obesity and fatty liver for the first time. Thus, the present invention aims at providing a pharmaceutical composition for preventing or treating obesity or fatty liver which comprises an inhibitor of bile acid reabsorption; a method for preventing or treating obesity or fatty liver in mammals suffering from obesity or fatty liver, which comprises administrating an inhibitor of bile acid reabsorption in an amount effective for preventing or treating obesity or fatty liver to said mammals; and a use of an inhibitor of bile acid reabsorption for manufacturing a medicament for preventing or treating obesity or fatty liver. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Process for decreasing adiposity using Vitamin A as a dietary supplement Inventor(s): Hayek, Michael G. (Dayton, OH), Sunvold, Gregory D. (Eaton, OH) Correspondence: Killworth, Gottman, Hagan & Schaeff, L.L.P. Suite 500; One Dayton Centre; Dayton; OH; 45402-2023; US Patent Application Number: 20020128324 Date filed: July 23, 2001 Abstract: A process is provided for reducing adiposity in an animal such as a companion animal by feeding the animal an effective amount of Vitamin A for a time sufficient to reduce adiposity in the animal. Preferably, the such effective amount comprises from about 50,000 IU to about 1,000,000 IU of Vitamin A per kilogram of diet. Such an effective amount provides sufficient Vitamin A to decrease accumulation of body fat, increase UCP1 levels, and decrease serum leptin levels in the animal. Excerpt(s): This application claims the benefit of U.S. provisional application Serial No. 60/081,969, filed Apr. 16, 1998.... This invention relates to a pet food supplement and process for decreasing adiposity in animals, and more particular, to a pet food supplement which includes beneficial amounts of Vitamin A in the animal's diet.... Obesity is extremely prevalent in many species including humans, dogs, cats and horses. For example, 20 to 40% of dogs and humans have been estimated to be overweight or obese. Traditionally, high fiber diets have been used to combat obesity. However, high fiber diets are often associated with several undesirable side effects

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including decreased palatability of food, increased stool volume, increased defecation frequency, poor skin and hair, improper mineral balance, and decreased food digestibility. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Product for promoting weight loss in overweight dogs Inventor(s): Davenport, Gary Mitchell; (Dayton, OH), Tetrick, Mark Alan; (Dayton, OH), Sunvold, Gregory Dean; (Eaton, OH) Correspondence: Killworth, Gottman, Hagan & Schaeff, L.L.P. One Dayton Centre, Suite 500; Dayton; OH; 45402-2023; US Patent Application Number: 20010000786 Date filed: December 15, 2000 Abstract: A process for feeding a pet food supplement or diet to an overweight canine for the purpose of promoting weight loss, increasing lean body mass, and enhancing the satiety of the animal is provided. The supplement or diet contains an effective amount of L-carnitine. Excerpt(s): 1. This patent application claims the benefit of U.S. Provisional Patent Application Serial No. 60/090,882, filed Jun. 26, 1998.... 2. The present invention relates to a process and product for promoting weight loss in overweight dogs, and more particularly to a process for supplementing a canine diet with L-carnitine to promote weight loss, improve body composition, and enhance satiety in the animal.... 3. It is estimated that 20 to 40% of the canine population is overweight or obese. This represents a very large number of animals that are in need of a means to lose weight. Obesity and being overweight are conditions associated with several health risks such as diabetes, increased blood pressure, increased blood triglycerides, impaired locomotion, skeletal stress, increased dystocia, thyroid dysfunction, etc. Consequently, ways to help treat these conditions are much needed by this population of animals. Currently, the most common form of treating obesity in dogs is through the use of diets that contain high amounts of fiber to dilute the calories of the diet. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Regulation of transthyretin to treat obesity Inventor(s): Wu, Linda H. (Woodbridge, CT) Correspondence: BANNER & WITCOFF; 1001 G STREET N W; SUITE 1100; WASHINGTON; DC; 20001; US Patent Application Number: 20020160394 Date filed: January 11, 2002 Abstract: Reagents that regulate transthyretin and reagents which bind to transthyretin gene products can play a role in preventing, ameliorating, or correcting obesity and related dysfunctions. Excerpt(s): This application claims the benefit of and incorporates by reference copending provisional application Serial No. 60/263,527 filed Jan. 24, 2001.... The invention relates to the regulation of transthyretin to treat obesity.... Obesity and

Patents 381

overweight are defined as an excess of body fat relative to lean body mass. An increase in caloric intake or a decrease in energy expenditure or both can bring about this imbalance leading to surplus energy being stored as fat. Obesity is associated with important medical morbidities and an increase in mortality. The causes of obesity are poorly understood and may be due to genetic factors, environmental factors or a combination of the two to cause a positive energy balance. In contrast, anorexia and cachexia are characterized by an imbalance in energy intake versus energy expenditure leading to a negative energy balance and weight loss. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Regulators of PPARdelta (beta) and their use in the treatment of obesity and insulin resistance Inventor(s): Hariharan, Narayanan; (Richboro, PA) Correspondence: MARLA J MATHIAS; BRISTOL-MYERS SQUIBB COMPANY; PATENT DEPARTMENT; P O BOX 4000; PRINCETON; NJ; 08543-4000; US Patent Application Number: 20020042359 Date filed: July 19, 2001 Abstract: Obesity is a common clinical problem in most developed nations and is also rapidly becoming a major health concern in developing nations. Overweight individuals frequently suffer from several metabolic disorders such as insulin resistance, type 2 diabetes and dyslipidemia.This invention discloses proof of principle for the role PPAR.delta. (also known as.beta.) plays in the development of diet-induced obesity. In accordance with the present invention, a new method for treating obesity, insulin resistance and hyperlipidemia through administration of a pharmaceutical composition containing a chemical agent that antagonizes the function of PPAR.delta.(.beta.) protein, decreases PPAR.delta.(.beta.) gene expression and or transactivation of PPAR.delta.(.beta.) target gene expression is disclosed. This invention also proposes that obese, insulin resistant hyperlipidemic patients can be effectively treated with a combination of a PPAR.delta.(.beta.) antagonist with either an anti-diabetic agent or a lipid-lowering agent (or both). Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/219,956, filed Jul. 20, 2000.... The present invention relates to a method for treating obesity, insulin resistance and dyslipidemia in mammals including humans through inhibition of PPAR.delta.(.beta.). This invention also relates to methods of screening for chemical entities that act to regulate PPAR.delta.(.beta.) activity. The invention further relates to a method of treatment of obese, insulin resistant and hyperlipidemic patients with one or more combinations of a PPAR.delta.(.beta.) antagonist, an anti-diabetic agent and a lipid-lowering agent.... Obesity is a common clinical problem in most developed nations and is also rapidly becoming a major health concern in developing nations. Overweight individuals frequently suffer from several metabolic disorders such as insulin resistance, type 2 diabetes and dyslipidemia. These individuals also frequently suffer from hypertension, increased risk for cardiovascular diseases such as atherosclerosis and coronary heart disease, and osteoarthritis of the joints. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Substituted 3-phenyl-5-alkoxy-3H(1,3,4)-oxadiazol-2-ones, composition and method for treating obesity thereof

pharmaceutical

Inventor(s): Heuer, Hubert Otto; (Schwabenheim, DE), Bauer, Armin; (Sulzbach, DE), Muller, Gunter; (Sulzbach a. Ts., DE), Schoenafinger, Karl; (Alzenau, DE), Petry, Stefan; (Frankfurt, DE) Correspondence: ROSS J. OEHLER; AVENTIS PHARMACEUTICALS INC. ROUTE 202206; MAIL CODE: D303A; BRIDGEWATER; NJ; 08807; US Patent Application Number: 20030181433 Date filed: February 27, 2003 Abstract: A substituted 3-phenyl-5-alkoxy-3H-(1,3,4)-oxadiazol-2-one, compound of formula 1, 1wherein R.sup.1, R.sup.2, R.sup.3, R.sup.4 and R.sup.5 are as defined herein, pharmaceutical composition comprising the compound and use of the compound for inhibiting pancreatic lipase, or the prophylaxis or treatment of obesity are described. Excerpt(s): The invention relates to substituted 3-phenyl-5-alkoxy-3H-(1,3,4)-o- xadiazol2-ones. The invention further relates to a pharmaceutical composition that comprises a substituted 3-phenyl-5-alkoxy-3H-(1,3,4)-oxa- diazol-2-one. The invention further relates to a method for the prophylaxis or treatment of obesity, or inhibiting pancreatic lipase, PL, in a patient wherein such could be useful comprising administering to the patient a pharmaceutically effective amount of a substituted 3-phenyl-5-alkoxy-3H-(1,3,4)oxadiazol-2-one.... Certain 5-alkoxy-1,3,4-oxadiazol-2-ones with an ortho-substituted phenyl ring as substituent or with fused-on five- or six-membered rings have an anthelmintic (DE-A 26 04 110) and insecticidal action (DE-A 26 03 877, EP-B 0 048 040, EP-B 0 067 471).... Certain 5-phenoxy-1,3,4-oxadiazol-2-ones with an ortho-substituted phenyl ring as substituent show an endoparasiticidal action (EP-A 0 419 918). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Synergistic pharmaceutical combinations for treating obesity with EGCG Inventor(s): Riker, Donald K. (Chattanooga, TN), Law, Michael Y. (Chattanooga, TN) Correspondence: Douglas T. Johnson; Miller & Martin LLP; 1000 Volunteer Building; 832 Georgia Avenue; Chattanooga; TN; 37402; US Patent Application Number: 20030162725 Date filed: February 24, 2003 Abstract: This invention relates to a novel pharmaceutical composition which contains 5-hydroxytryptophan (5-HTP) with or without Vitamin B6 (pyridoxal phosphate) as a cofactor in combination with epigallocatechin gallate (EGCG) and caffeine. This pharmaceutical composition may be used for the treatment of obesity or appetite suppression. Excerpt(s): This application claims priority to provisional application Ser. No. 60/360,199 filed Feb. 25, 2002.... This invention relates to a novel pharmaceutical composition which contains 5-hydroxytryptophan (5-HTP) with or without Vitamin B6 (pyridoxal phosphate) as a cofactor in combination with epigallocatechin gallate (EGCG) and caffeine and a method for the treatment of obesity and appetite suppression.... Studies have documented that medications which increase brain serotonin (5hydroxytryptamine, 5-HT), such as fenfluramine, are effective anorectic agents to help obese patients lose weight and to decrease cravings for sweets and carbohydrates. 5-

Patents 383

Hydroxytryptophan, abbreviated 5-HTP, is the immediate precursor of 5-HT. A goal of treatment with 5-HTP is to increase brain 5-HT. Previous studies in animals and humans have established that oral administration of 5-HTP increases brain 5-HT. It is desirable to have such an anorectic agent for human therapy which does not present the wellknown unwanted and often dangerous effects typical of amphetamine and fenfluramine or their congeners, ranging from nausea and insomnia to hypertension and cardiac arrhythmias. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Therapies for the prevention and treatment of diabetes and obesity Inventor(s): Robinson, Lindsay E. (Guelph, CA), Richter, Erik A. (Gentofte, DK), Graham, Terry E. (Guelph, CA), Thong, Farah S.L. (Guelph, CA) Correspondence: BARBARA KITCHELL; Akerman, Senterfitt Eidson, P.A. Suite 400; 222 Lakeview Avenue; West Palm Beach; FL; 33401; US Patent Application Number: 20030007996 Date filed: May 30, 2002 Abstract: A method for the prevention and treatment of diabetes and obesity by a system of health management promoting a caffeine reduced diet and the use of adenosine analogues and adenosine receptor agonists. Methods for diet plans and labelling are disclosed. Use of decaffeinated coffee is promoted. Excerpt(s): The field of the present invention is human physiology. The present invention relates to the prevention and treatment of diabetes and obesity by a system of health management promoting a reduced caffeine diet and the use of adenosine, adenosine analogues, derivatives, conjugates thereof and adenosine receptor agonists.... Diabetes is a condition characterized by the body's inability to transport glucose from the blood into adipose or skeletal muscle cells. This results in glucose build up in the blood. Insulin is the key hormone that regulates glucose uptake in the body. Type 2 diabetics either do not make enough insulin or their cells are insensitive to it. Type 1 diabetics do not make insulin and have to administer it to their bodies.... It is estimated that at least 120 million people worldwide are suffering from Type 2 diabetes and this is predicted to almost double in our current decade (Shaw et al., 2000). This is attributed to aging populations, increases in obesity together with sedentary lifestyles and poor nutritional habits. As such it is clear that adopting a positive lifestyle would both reduce the probability of developing Type 2 diabetes and/or delay the onset and modify the severity. In Canada by 2000 there are expected to be 2.2 million diabetic patients and this should increase to 3 million by 2010 (Meitzer et al, 1998; Tan and MacLean 1995). About 90% of these patients are expected to be Type 2 diabetics. Diabetes is a major concern not only because of its well known links with cardiovascular disease but also because of its increased risks of blindness, kidney disorders, peripheral neuropathies and vascular disorders. It is believed that only about 50% of Type 2 diabetics are diagnosed; this together with the wide ranging complications make it difficult to establish the total health costs and impact on the quality and quantity of life. The underlying etiology of Type 2 diabetes is not resolved, but it is clear that a negative lifestyle in nutrition and exercise are key factors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Treatment of obesity Inventor(s): Natera, Siria Helens Anna; (Mount Waverly, AU), Jiang, Woei-Jia; (Clayton, AU), Ng, Frank Man-Woon; (Kew, AU) Correspondence: Stephen A. Bent; Foley & Lardner, Washington Harbour; Suite 500; 3000 K Street, N.W. Washington; DC; 20007-5143; US Patent Application Number: 20020142965 Date filed: December 31, 2001 Abstract: A method for the treatment of obesity in an animal such as a human, comprises administering to the animal an effective amount of a peptide which comprises the carboxyl-terminal sequence of a growth hormone, particularly the carboxyl-terminal sequence of human growth hormone containing amine acid residues 177-191. A pharmaceutical composition for use in the treatment of obesity is also disclosed. Excerpt(s): This application is a continuation-in-part of U.S. application Ser. No. 08/340,389, filed Nov. 15, 1994; the contents of which are incorporated herein by reference.... This invention relates to the treatment of obesity in animals. In particular, the invention relates to the treatment of obesity in humans, although it is to be understood that the present invention also extends to the treatment of obesity in nonhuman mammals, for example, for the improvement of meat qualities in farm animals used in food production.... The critical role of human growth hormone (hGH) in postnatal growth in humans is well recognised. Less obvious is the impact of this hormone on the regulation of lipid and carbohydrate metabolism, due to lack of detailed molecular studies. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Treatments for obesity and methods for identifiying compounds useful for treating obesity Inventor(s): Hadcock, John R. (East Lyme, CT), Swick, Andrew G. (East Lyme, CT) Correspondence: PFIZER INC. PATENT DEPARTMENT, MS8260-1611; EASTERN POINT ROAD; GROTON; CT; 06340; US Patent Application Number: 20020198152 Date filed: July 24, 2002 Abstract: The present invention provides a method of treating obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the method comprising the step of administering to a patent having or at risk of having one of the above-mentioned diseases a therapeutically effective amount of a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not attenuate the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors. The present invention also provides a method of identifying a compound that is useful for the treatment or prevention of obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the method

Patents 385

comprising the steps of: 1) determining if a compound affects the binding of agoutirelated protein to melanocortin receptors; 2) determining if a compound affects the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors; and 3) selecting a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not affect the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors. Excerpt(s): This application is a divisional of U.S. patent application Ser. No. 09/761,320, filed Jan. 16, 2001, which claims priority of U.S. Provisional Application Nos. 60/176,508 and 60/206,126, filed Jan. 18, 2000 and May 22, 2000, respectively.... The present invention provides methods of treating obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the methods comprising the step of administering to a patient having or at risk of having one of the above-mentioned diseases or conditions a therapeutically effective amount of a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not attenuate the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors.... The present invention also provides methods of identifying a compound that is useful for the treatment of obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the methods comprising the steps of: 1) determining if a compound affects the binding of agoutirelated protein to melanocortin receptors; 2) determining if a compound affects the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors; and 3) selecting a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not attenuate the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Treatments which elevate functional glycosylated leptin transport factor, for controlling weight and obesity Inventor(s): Qian, Hao; (St. Charles, MO), Gingerich, Ronald; (St. Albans, MO) Correspondence: Patrick D. Kelly; 11939 Manchester #403; St. Louis; MO; 63131; US Patent Application Number: 20020065217 Date filed: August 4, 2001 Abstract: Methods and compounds for treating obesity and inducing weight loss use a functional, glycosylated leptin transport factor (LTF) polypeptide, referred to as fn/glyLTF. An unstable defective version of the LTF protein, referred to herein as def/LTF, is present in freshly-drawn blood from obese animals or people; it is degraded rapidly in circulating blood. In people with normal body weight, fn/glyLTF stabilizes and protects leptin, a hormone with powerful effects on fat metabolism and body mass. LTF apparently is the same protein previously recognized as a soluble truncated fragment of the obesity receptor (Ob-R) protein, referred to in the prior art as Ob-Re, or sOb-R. In humans with normal body weight, fn/glyLYF has a weight of about 145 kD, compared to a polypeptide-only weight of about 93 kD. defLTF has a substantially lower molecular weight, and tests using deglycosylating enzymes indicate that it is not glycosylated to the same level as fn/glyLTF. Treatment methods include: (1) elevating

386 Obesity

concentrations of fn/glyLTF in circulating blood, by means such as intravenous injection or sustained-release implants, or by gene therapy; (2) suppressing enzymatic deglycosylation in circulating blood, such as by extracorporeal removal of deglycosylating enzymes; and, (3) providing "surrogate" forms of fn/glyLTF. Diagnostic kits are also disclosed, for measuring both fn/glyLTF and def/LTF in animals and people suffering from obesity. Excerpt(s): This application claims the benefit under 35 USC 119(e) of provisional application No. 60/222,813, filed Aug. 4, 2000.... This invention is in the fields of medicine and pharmacology, and relates to a natural hormone called leptin, which affects body weight and fat metabolism.... The physiological roles of leptin and leptin receptors are discussed in review articles such as Spiegelman et al 1996, Considine et al 1996, and Friedman et al 1998 (full citations are provided below), and in numerous articles cited therein. Very briefly, leptin is a protein that is encoded by a gene called "ob" (short for "obese"). It was first isolated and identified in 1994, based on genetic analysis of "ob/ob" mice that were grossly overweight due to a mutant ob gene (zhang et al 1994; the double "ob/ob" designation indicates that both chromosomal copies of the ob gene, in the somatic cells of these mice, were mutant forms). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Use of C2-substituted indan-1-ol systems for preparing medicaments for the prophylaxis or treatment of obesity Inventor(s): Gossel, Matthias; (Hofheim, DE), Bickel, Martin; (Bad Homburg, DE), Krone, Volker; (Hofheim, DE), Jaehne, Gerhard; (Frankfurt, DE) Correspondence: Finnegan, Henderson, Farabow,; Garrett & Dunner, L.L.P. 1300 I Street, N.W. Washington; DC; 20005-3315; US Patent Application Number: 20030134879 Date filed: August 30, 2002 Abstract: Embodiments of the invention relate to methods of reducing weight in mammals and for the prophylaxis or treatment of obesity comprising administration of of C2-substituted indan-1-ol systems and their physiologically acceptable salts and physiologically functional derivatives. Compounds for use in the methods of the embodiments of the invention include compounds of the formula (I) 1in which the radicals are as defined, and their physiologically acceptable salts. Excerpt(s): This application claims the benefit of foreign priority under 35 U.S.C..sctn.119 of German patent application no. 10142666.6, filed on Aug. 31, 2001, the contents of which are expressly incorporated by reference herein.... Use of C2substituted indan-1-ol systems for preparing medicaments for the prophylaxis or treatment of obesity. Other applications that describe similar compounds and methods of using these compounds include: 1) "C2-substituted idan-1-ones and their derivatives, processes for their preparation and their use as pharmaceuticals" of Gerhard Jaehne, Volker Krone, Martin Bickel, and Matthias Gossel filed Aug. 31, 2002, Attorney Docket Number 02481.1795; 2) "C2-substituted indan-1-ols and their derivatives, processes for their preparation and their use as pharmaceuticals" of Gerhard Jaehne, Volker Krone, Martin Bickel, and Matthias Gossel filed Aug. 31, 2002, Attorney Docket Number 02481.1799; and 3) "Use of C2-substituted indan-1-one systems for preparing medicaments for the prophylaxis or treatment of obesity" of Gerhard Jaehne, Volker Krone, Martin Bickel, and Matthias Gossel filed Aug. 31, 2002, Attorney Docket Number

Patents 387

02481.1797; all of which are hereby incorporated by reference.... Embodiments of the invention relate to the use of C2-substituted indan-1-ol systems and their physiologically acceptable salts and physiologically functional derivatives for preparing medicaments for reducing weight in mammals and for the prophylaxis or treatment of obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Use of C2-substituted indan-1-one systems for preparing medicaments for the prophylaxis or treatment of obesity Inventor(s): Bickel, Martin; (Bad Homburg, DE), Krone, Volker; (Hofheim, DE), Jaehne, Gerhard; (Frankfurt, DE), Gossel, Matthias; (Hofheim, DE) Correspondence: Finnegan, Henderson, Farabow,; Garrett & Dunner, L.L.P. 1300 I Street, N.W. Washington; DC; 20005-3315; US Patent Application Number: 20030134882 Date filed: August 30, 2002 Abstract: Embodiments of the invention relate to methods of reducing weight in mammals and for the prophylaxis or treatment of obesity comprising administration of C2-substituted indan-1-one systems and their physiologically acceptable salts and physiologically functional derivatives. Compounds for use in methods of embodiments of the invention may include compounds of the formula 1in which the radicals are as defined, and their physiologically acceptable salts. Excerpt(s): This application claims the benefit of foreign priority under 35 U.S.C..sctn.119 of German patent application no.10142668.2, filed on Aug. 31, 2001, the contents of which are expressly incorporated by reference herein.... Use of C2substituted indan-1-one systems for preparing medicaments for the prophylaxis or treatment of obesity.... Other applications that describe similar compounds and methods of using these compounds include: 1) "C2-substituted idan-1-ones and their derivatives, processes for their preparation and their use as pharmaceuticals" of Gerhard Jaehne, Volker Krone, Martin Bickel, and Matthias Gossel filed Aug. 31, 2002, Attorney Docket Number 02481.1795; 2) "C2-substituted indan-1-ols and their derivatives, processes for their preparation and their use as pharmaceuticals" of Gerhard Jaehne, Volker Krone, Martin Bickel, and Matthias Gossel filed Aug. 31, 2002, Attorney Docket Number 02481.1799; and 3) "Use of C2-substituted indan-1-ol systems for preparing medicaments for the prophylaxis or treatment of obesity" of Gerhard Jaehne, Volker Krone, Martin Bickel, and Matthias Gossel filed Aug. 31, 2002, Attorney Docket Number 02481.1800; all of which are hereby incorporated by reference. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Use of CNTF (ciliary neurotrophic factor) receptor activators for the treatment of obesity Inventor(s): Cortese, Riccardo; (Rome, IT), Demartis, Anna; (Rome, IT), Di Marco, Annalise; (Rome, IT), Gloaguen, Isabelle; (Scoppito L'Aquila, IT), Ciliberto, Gennaro; (Rome, IT), Laufer, Ralph; (Rome, IT) Correspondence: MERCK AND CO INC; P O BOX 2000; RAHWAY; NJ; 070650907 Patent Application Number: 20030176346 Date filed: January 31, 2003 Abstract: The present invention refers to the use of hCNTF (human ciliary neurotrophic factor), mutants thereof or other molecules that activate the CNTF receptor, for the preparation of drugs for the treatment of obesity and associated diseases, for example hyperglycemia. FIG. 1 shows the anti-obesity effect of hCNTF and leptin on body weight (left panels) and on food intake (right panels) in genetically obese mice and in mice with diet-induced obesity (DIO). Excerpt(s): The subject of the present invention is the use of molecules that activate the CNTF (ciliary neurotrophic factor) receptor--such as hCNTF (human CNTF) or mutants of hCNTF--as active principles in the formulation of pharmaceutical compositions suitable for the treatment of obesity and of related diseases. The term hCNTF mutant is intended to mean an amino acid sequence that can in theory be derived from hCNTF by substitution of one or more amino acids.... Obesity, which affects >30% of the adult population in the industrial world, is a major public health problem, since it is associated with type II diabetes, hypertension, hyperlipidemia and increased mortality rate. Obesity is the result of a positive energy balance, as a consequence of an increased ratio of caloric intake to energy expenditure. Treatment is generally unsuccessful due to the operation of mechanisms that restore adipose mass after both intentional or unintentional changes (1). The lipostasis theory postulates that the size of the body fat depot is regulated by a feedback loop, constituted by adipocyte-derived circulating molecules that act on the hypothalamus to decrease appetite and increase energy expenditure (2).... The recently identified 16-kilodalton plasma protein leptin (3) fulfills many of the criteria expected from such a lipostatic hormone. It is expressed in adipose tissue, and its plasma levels are highly correlated with body mass index in rodents and humans (4). The absence of leptin in obese (ob/ob) mutant mice leads to a massive increase in body fat, which can be reversed by systemic administration of the recombinant protein (5, 6, 7). However, human obesity does not appear to be due to deficient expression of leptin, since leptin mRNA and plasma protein levels were shown to be increased in obese versus lean subjects (4). Thus, obese humans may be insensitive to the lipostatic effect of leptin, possibly due to a defect at the level of leptin transport, leptin receptor activity, or post-receptorial signalling mechanisms (8). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

Patents 389

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Use of creatine analogues and creatine kinase modulators for the prevention and treatment of obesity and its related disorders Inventor(s): KADDURAH-DAOUK, RIMA; (BELMONT, MA) Correspondence: ELIZABETH A. HANLEY, ESQ. LAHIVE & COCKFIELD, LLP; 28 STATE STREET; BOSTON; MA; 02109 Patent Application Number: 20020035155 Date filed: October 27, 1997 Abstract: The present invention relates to the use of creatine compounds for treating or preventing a metabolic disorder related to body weight control such as obesity, and it's associated diseases in a patient experiencing said disorder. The creatine compounds which can be used in the present method include (1) analogues of creatine which can act as substrates or substrate analogues for the enzyme creatine kinase; (2) compounds which can act as inhibitors of creatine kinase; (3) compounds which can modulate the creatine transporter (4) N-phosphocreatine analogues bearing transferable or nontransferable moieties which mimic the N-phosphoryl group. (5) compounds which modify the association of creatine kinase with other cellular components. Excerpt(s): The present application is a continuation-in-part of and claims priority to Provisional Application U.S. Ser. No. 60/005,882, filed Oct. 26, 1995, the entire disclosure of which is incorporated herein by reference.... The present invention provides for new use for creatine compounds (creatine analogues and compounds which modulate one or more of the structural or functional components of the creatine kinase/creatine phosphate system) as therapeutic agents. More particularly, the present invention provides a method of treating or preventing certain metabolic disorders of human and animal metabolism relating to aberrant body weight regulation as manifested in obesity and it's related disorders.... There are several metabolic diseases of human and animal metabolism, eg., obesity and severe weight loss that relate to energy imbalance--where caloric intake versus energy expenditure--is imbalanced. Obesity, which can be defined as a body weight more than 20% in excess of the ideal body weight, is a major health problem in Western affluent societies. It is associated with an increased risk for cardiovascular disease, hypertension, diabetes, hyperlipidaemia and an increased mortality rate. Obesity is the result of a positive energy balance, as a consequence of an increased ratio of caloric intake to energy expenditure. The molecular factors regulating food intake and body weight balance are incompletely understood. Five single-gene mutations resulting in obesity have been described in mice, implicating genetic factors in the etiology of obesity. (Friedman, j. m., and Leibel, r. l. Cell 69: 217220 (1990)). In the ob mouse a single gene mutation, obese, results in profound obesity, which is accompanied by diabetes (Friedman, J. M., et. al. Genomics 11: 1054-1062 (1991)). Cross-circulation experiments have suggested that the ob mice are deficient of a blood-borne factor regulating nutrient intake and energy metabolism (Coleman, D. L. Diabetologia 14: 141-148 (1978)). Using positional cloning technologies, the mouse ob gene, and subsequently its human homologue, have been recently cloned (Zhang, Y., et. al., Nature 372: 425-432 (1994)). Daily intraperitoneal injections of either mouse or human recombinant OB protein reduced the body weight of obese mice ob/ob by 30% after 2 weeks of injection. The protein reduced food intake and increased energy expenditure in the ob/ob mice (Halaas et. al., Science 269: 543-546 (1995)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Use of histamine H3 receptor inverse agonists for the control of appetite and treatment of obesity Inventor(s): Tedford, Clark E. (South Russell, OH), Yates, Stephen L. (Aurora, OH), Brunden, Kurt R. (Aurora, OH) Correspondence: ROCKEY, MILNAMOW & KATZ, LTD. TWO PRUDENTIAL PLAZA, STE. 4700; 180 NORTH STETSON AVENUE; CHICAGO; IL; 60601; US Patent Application Number: 20030069295 Date filed: August 15, 2001 Abstract: A method for the use of histamine H.sub.3 receptor inverse agonists in the regulation of appetite and treatment of obesity is disclosed. Presently preferred inverse agonists are imidazole derivatives. Excerpt(s): The present invention is directed to a method for the use of histamine H.sub.3 receptor inverse agonists in the regulation of appetite and treatment of obesity. Presently preferred inverse agonists are imidazole derivatives.... Obesity can be described as a state of excessive accumulation of body fat and is widely considered to be a major public health problem, associated with substantially increased morbidity and mortality, as well as psychological problems, reduced economic achievement and discrimination. Examples of health problems thought to be caused or exacerbated by obesity include coronary heart disease, stroke, obstructive sleep apnea, diabetes mellitus, gout, hyperlipidemia, osteoarthritis, reduced fertility, impaired psychosocial function, reduced physical agility and increased risk of accidents, and impaired obstetrical performance.... Causes of obesity remain unclear. However, whether obesity is of genetic origin or is promoted by a genotype-environment interaction, or both, it is evident that energy intake must have exceeded metabolic and physical (work) energy expenditure for there to have been surplus energy available for fat deposition. Considerable uncertainty remains concerning the relative importance of different mechanisms in achieving this positive energy balance. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Use of medium-chain triglycerides for the prevention and therapy of adiposity Inventor(s): Kuzela, Lubomir; (Praha, CZ), Feldheim, Walter; (Kronshagen, DE) Correspondence: BIRCH STEWART KOLASCH & BIRCH; PO BOX 747; FALLS CHURCH; VA; 22040-0747; US Patent Application Number: 20030130346 Date filed: June 25, 2002 Abstract: Use of medium-chain triglycerides for the prevention and therapy of adiposity The use of medium-chain triglycerides or of a composition containing said mediumchain triglycerides for the prevention or therapy of overweight or adiposity is described. Said composition preferably also contains long-chain essential triglycerides, preferably.alpha.-linoleic acid and/or linolenic acid as well as, optionally, further components and/or additives. Excerpt(s): This nonprovisional application claims priority under 35 U.S.C..sctn.119(a) on Patent Application No. DE 101 30 491.9 filed in Germany on Jun. 25, 2001, which is herein incorporated by reference.... The present invention relates to the use of mediumchain triglycerides (MCT) or a composition containing medium-chain triglycerides, for

Patents 391

example a dietetic foodstuff for the prevention or therapy of overweight or adiposity. This composition preferably also contains long-chain essential triglycerides, preferably a-linoleic acid and/or.alpha.-linolenic acid, as well as optionally further components and/or additives.... In the affluent industrial nations, the biggest problem concerning nutrition is overnutrition. The constantly rising number of persons suffering from overweight or adiposity, a considerable share of which are children or adolescents, is problematic due to its consequence, namely the increase in nutrition-related diseases. Overweight is a risk factor for diseases of the skeletal and musculoskeletal system, hypertension (4-fold risk), type 2 diabetes mellitus (6-fold risk), heart attack (4-fold risk), breast cancer (3-fold risk), biliary stones (10-fold risk), gout etc. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •

Use of pyridoxamine for the treatment and inhibition of obesity-related complications Inventor(s): Baynes, John; (Columbia, SC) Correspondence: MCDONNELL BOEHNEN HULBERT & BERGHOFF; 300 SOUTH WACKER DRIVE; SUITE 3200; CHICAGO; IL; 60606; US Patent Application Number: 20020128295 Date filed: November 2, 2001 Abstract: The present invention provides methods and pharmaceutical compositions for treating or inhibiting obesity-related complications that comprise administering to an obese subject an amount effective of pyridoxamine to treat or inhibit obesity-related complications selected from the group consisting of hyperlipidemia, renal disease, proliferation or smooth muscle cells in the aorta, coronary artery occlusion, atherosclerosis, hypertension, advanced glycation end-product formation and advanced lipoxidation end-product formation. Excerpt(s): This application claims priority form U.S. Provisional Patent Application Ser. No. 60/245,630, filed Nov. 2, 2000, and Ser. No. 60/315,789 filed Aug. 29, 2001.... The invention is related to the fields of obesity and obesity complications.... Obesity is generally defined as a body mass index (BMI) of greater than 30 kg/m.sup.2 (m.sup.2=the square of height measured in meters) while morbid or extreme obesity is generally defined as a BMI of greater than 40 kg/m.sup.2. Both types of obesity represent a health hazard, and are associated with a host of other disorders, including but not limited to hypertension, dyslipidemia, and insulin resistance and/or hyperinsulinemia. Normal treatment for morbid obesity is surgery to remove part of the stomach or intestine. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Use of sterols as active ingredient in a cosmetic composition against adiposity Inventor(s): Morvan, Pierre-Yves; (Rennes, FR), Vallee, Romuald; (St Meloir Des Ondes, FR), Gedouin, Antoine; (Saint Vincent, FR) Correspondence: ARMSTRONG,WESTERMAN & HATTORI, LLP; 1725 K STREET, NW. SUITE 1000; WASHINGTON; DC; 20006; US Patent Application Number: 20020106389 Date filed: November 30, 2001 Abstract: The present invention relates to the use of sterols derived from a plant or algae extract as the active principle of a cosmetic composition for combating adiposity. Said sterols are, for example, at least one of the three following sterols: campesterol, betasitosterol or stigmasterol. Excerpt(s): The present invention relates to a use of sterols as active principle in a cosmetic composition to combat adiposity and thus refine the silhouette.... Sterols are known for their use as active substance in anti-inflammatory medications in which they act as inhibitors of lipoxygenase. One may refer to the patent document FR-A-2 705 030 which shows such an activity.... They are also known for cosmetic compositions for treatment of the skin in which they act as emollients by presenting good properties of moisturizing and barrier. Document U.S. Pat. No. 4,604,281 shows such a use. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

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Use of the Peg3 gene in assays and products relating to obesity, thermoregulation and behavioral disorders Inventor(s): Surani, Azim; (Cambridge, GB) Correspondence: ROYLANCE, ABRAMS, BERDO & GOODMAN, L.L.P. 1300 19TH STREET, N.W. SUITE 600; WASHINGTON,; DC; 20036; US Patent Application Number: 20030018987 Date filed: August 15, 2002 Abstract: The invention relates to the finding that animals deficient in the Peg3 gene suffer from a number of phenotypic traits, including obesity, aberrant thermoregulation and behavioral defects, including impaired maternal behavior. The invention provides a transgenic non-human animal which comprises an inactive copy for the Peg3 gene, and the use of such animals as model systems in assays for novel therapies in the treatment of conditions such as those mentioned above. Excerpt(s): The present invention relates to the Peg3 gene and the finding that it is involved in thermoregulation, obesity and maternal behaviour, olfaction, male behaviour, apoptosis, cell survival and degeneration, and infectious diseases.... The Peg3 gene was identified in a screen for expression of imprinted genes in mice. Imprinted genes show an unusual pattern of expression as their expression is determined strictly by their parental origin. Peg3 shows imprinting, with the paternal copy of the gene being expressed in offspring while the maternal copy is silent. The gene expresses an mRNA of about 9 kb in size which encodes an unusual zinc finger protein with eleven widely spaced "C2H2" motifs and two groups of amino acid repeats. The predicted size of the protein is 1,572 amino acids. See Kuroiwa et al, (1996), Nature Genetics 12; 186189. The sequence of Peg3 can be found in GenBank, accession number AF038939 (NCBI--REF 363877).... Peg3 is expressed early in development in somites, branchial

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arches and other mesodermal tissue. In adults it is expressed predominantly in the brain including the hypothalamus medial preoptic area, amygdala as well as the olfactory bulb. It is also expressed in few other adult tissues such as the adrenal gland. The function of the gene is unknown, although in Kuroiwa et al, ibid, it is noted that the gene maps to a region of murine chromosome 7 which is syntenic with the human chromosomal location for genes associated with myotonic dystrophy and tumour suppression. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html

Keeping Current In order to stay informed about patents and patent applications dealing with obesity, you can access the U.S. Patent Office archive via the Internet at the following Web address: http://www.uspto.gov/patft/index.html. You will see two broad options: (1) Issued Patent, and (2) Published Applications. To see a list of issued patents, perform the following steps: Under “Issued Patents,” click “Quick Search.” Then, type “obesity” (or synonyms) into the “Term 1” box. After clicking on the search button, scroll down to see the various patents which have been granted to date on obesity. You can also use this procedure to view pending patent applications concerning obesity. Simply go back to http://www.uspto.gov/patft/index.html. Select “Quick Search” under “Published Applications.” Then proceed with the steps listed above.

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CHAPTER 7. BOOKS ON OBESITY Overview This chapter provides bibliographic book references relating to obesity. In addition to online booksellers such as www.amazon.com and www.bn.com, excellent sources for book titles on obesity include the Combined Health Information Database and the National Library of Medicine. Your local medical library also may have these titles available for loan.

Book Summaries: Federal Agencies The Combined Health Information Database collects various book abstracts from a variety of healthcare institutions and federal agencies. To access these summaries, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. You will need to use the “Detailed Search” option. To find book summaries, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer. For the format option, select “Monograph/Book.” Now type “obesity” (or synonyms) into the “For these words:” box. You should check back periodically with this database which is updated every three months. The following is a typical result when searching for books on obesity: •

Origins and Consequences of Obesity Source: Somerset, NJ: John Wiley and Sons, Inc. 1996. 278 p. Contact: Available from John Wiley and Sons, Inc. One Wiley Drive, Somerset, NJ 08875. (800) 225-5945 or (732) 469-4400. Fax (732) 302-2300. Website: www.wiley.com. PRICE: $90.00 plus shipping and handling. ISBN: 0471965065. Summary: This book presents the papers given at a symposium that brought together an international and interdisciplinary group of experts on all aspects of the origins, consequences, and treatment of obesity. The health consequences of being obese or overweight, which include diabetes, hypertension, and hyperlipidemia, are among the most common health problems in industrialized nations. Speakers discussed the epidemiology of obesity, obesity among people living in Caribbean nations, and obesity in peoples of the African diaspora. Other presenters focused on the metabolic consequences of obesity and body fat pattern, diabetes, obesity and cardiovascular

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disease, the genetics of obesity in humans, and early-life nutritional influences upon obesity and body proportions. The presentation on diabetes examined the relationship between obesity and type 2 diabetes. It also reviewed clinical and epidemiological studies on insulin resistance in central obesity, addressed pathogenetic considerations, and discussed endocrine regulation of body fat distribution and endocrine regulation of insulin sensitivity. The presentation also examined evidence for the view that endocrine abnormalities may be diabetogenic via the induction of insulin resistance. Remaining speakers provided information on behavioral physiological interactions in the control of food intake, obesity and metabolic efficiency, socioeconomic status and obesity, the economic and psychosocial consequences of obesity, obesity and physical activity, and preventive and management strategies for obesity. A discussion followed each presentation, and two general discussion sessions were conducted. The book concludes with an index of contributors and a subject index. 1 appendix. 38 figures. 26 tables. Numerous references. •

From Obesity to Diabetes Source: New York, NY: John Wiley and Sons. 1993. 310 p. Contact: Available from John Wiley and Sons. Distribution Center, 1 Wiley Drive, Somerset, NJ 08875-1272. (800) 225-5945 or (732) 469-4400. Fax (732) 302-2300. PRICE: $170. ISBN: 0471927651. Summary: This book introduces a metabolic approach to the study of noninsulindependent diabetes mellitus (NIDDM or type II) and obesity. The authors concentrate in particular on the metabolic effects of obesity on glucose metabolism and the progressive development of impaired glucose tolerance and diabetes. The book highlights the frequent progressive development of impaired glucose tolerance and diabetes and demonstrates continuity in both cross-over and longitudinal studies. The reversibility of the phenomena, as well as prevention and therapy, are presented in relation to physiopathological observations. The authors cite epidemiological studies which relate the progressive occurrence of diabetes to obesity in populations where the lifestyle has changed with richer food and decreased exercise. Fifteen chapters cover topics including epidemiology; methods for the study of human metabolism in vivo; insulin secretion; insulin resistance; energy metabolism; endogenous glucose production in obesity and NIDDM; evolution from obesity to diabetes; associated cardiovascular morbidity; and prevention and therapeutics. Each chapter includes figures, tables, and references; a subject index concludes the volume. 683 references. (AA-M).

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Health Risks of Obesity: Special Report. 2nd ed Source: Hettinger, ND: Obesity and Health, Healthy Living Institute. 1993. 190 p. Contact: Available from Obesity and Health. 402 South 14th Street, Hettinger, ND 58639. (701) 567-2845. Fax (701) 567-2443. PRICE: $65. Summary: This report sets forth current information on the health risks of obesity. The report is intended to help educators, policy makers, and health care providers deal more effectively with the complexities and dilemmas of obesity. Eleven chapters address the following topics: the health risks of obesity in the areas of heart disease, stroke, cancer, diabetes, and other related diseases; fat distribution; obesity in ethnic populations, notably the high risk of diabetes in the Native American population; early puberty; leanness and aging; the risks of losing weight; effectiveness of treatment; weight cycling; mortality and weight loss; treatment decisions; and challenges for the future. Numerous

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appendices present information about measuring and defining obesity and two NIH conferences. •

Obesity Source: Hagerstown, MD: J.B. Lippincott Company. 1992. 805 p. Contact: Available from J.B. Lippincott Company. P.O. Box 1580, Hagerstown, MD 21741. (800) 777-2295. PRICE: $79.50; plus shipping and handling. ISBN: 0397509995. Summary: This book provides an overview of fundamental research and clinical aspects of obesity. The 66 chapters of the book, each written by preeminent scientists and clinicians, are presented in 11 sections: fat metabolism; assessment of body composition; energy metabolism; animal models of obesity; general aspects of human obesity; hunger satiety and mood; associated health impairments; health impairments associated with abdominal distribution of adipose tissue; special forms of obesity; nonpharmacologic treatment of obesity; and the pharmacologic treatment of obesity. Chapters related to diabetes include a chapter on glucose metabolism in obesity and Type II diabetes and chapters discussing hyperlipidemia, cardiovascular disease, and hypertension. Each chapter includes numerous references to primary sources, and a subject index concludes the volume.

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Obesity in Primary Health Care: A Literature Review Source: London, England, Health Education Authority, 62 p., 1995. Contact: Health Education Authority, Hamilton House, Mabledon Place, London WC1H 9TX, England. Summary: Obesity in Primary Health Care: A Literature Review presents a body of knowledge to help health professionals meet the compelling problem of obesity, with particular emphasis on opportunities for the primary health care team in the United Kingdom. The monograph has seven sections: (1) Defining the Issues in Prevention and Management discusses the increased prevalence of overweight and obesity, overweight and obesity as a public health risk, and the use of waist-hip ratios to define overweight and obesity; (2) What Seems to Be Important in Designing Treatments for Overweight and Obesity? addresses issues of screening and creating risk profiles, understanding how people change, self-efficacy theory and the Weight Efficacy Lifestyle Questionnaire, characteristics of people who lose weight and keep it off, perceptions of people who are overweight or obese, and implications of attrition for screening; (3) Issues in Program Design: A Long-Term Perspective discusses understanding the impact of diet, behavior modification, and exercise; group versus individual treatment; and partner weight status and spousal involvement in treatment; (4) Preventing Relapse: Strategies for Improving Maintenance of Weight Loss discusses characteristics of those who relapse and presents a continuous care model of obesity management that involves extensive posttreatment support; (5) Is There a Single Best Practice for the Treatment of Obesity and Overweight? describes the Dietary Intervention: Evaluation of Technology (DIET) study, a multidisciplinary approach to weight control, a weight reduction program in Finnish primary health care, the Harrow Slimming Club, GutBusters (a weight control program for men), and the Pawtucket Weigh-In; (6) Community-based Approaches to Weight Loss addresses worksite interventions, weight-loss competitions at the worksite, weight loss programs by mail, and community programs; and (7) Opportunities for the Prevention of Overweight and Obesity describes public health policy strategies, the identification of at-risk groups, and a study on weight gain prevention for adults. The

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author concludes that the health professional must become better informed about the outcomes of interventions in both the short-term and the longer-term. •

Special Report: Health Risks of Obesity. Second Edition Source: Hettinger, ND, Obesity and Health, 190 p., 1993. Contact: Obesity and Health, Route 2, Box 905, Hettinger, ND 58639. (701) 567-2840. Summary: Special Report: Health Risks of Obesity helps educators, policymakers, and health care providers deal more effectively with the complexities and dilemmas of obesity by generating discussion that can lead to effective preventive action. The monograph presents information on the health risks and treatment of obesity. There are two sections. Section one, Risks of Obesity, examines (1) Health Risks of Obesity: Heart Disease and Stroke, Cancer Risk, Diabetes Risk, and Other Related Diseases; (2) Fat Distribution: Ethnic Differences; (3) Ethnic Populations: Diabetes is High Risk for Native Americans; (4) Early Puberty; and (5) Leanness and Aging: Elderly Research is Critical. Part two, Risks of Intervention, examines (1) Risks of Losing Weight: Potential Side Effects of Very Low Calorie Diets and The Biology of Human Starvation, (2) Effectiveness of Treatment, (3) Weight Cycling, (4) Mortality Increase With Weight Loss, (5) To Treat or Not to Treat, and (6) Challenges for the Future. Five appendixes present statistics, information, and research on (1) a definition of obesity, (2) how to measure obesity, (3) prevalence of obesity, (4) risks of obesity, and (5) risks of intervention.

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New multidisciplinary strategies in obesity management Source: Reno, NV: Nutrition Education and Research Program, University of Nevada School of Medicine. 1997. 24 pp. Contact: Available from Nutrition Education and Research Program, University of Nevada School of Medicine, Reno, NV. Summary: This monograph presents the findings of a multidisciplinary symposium on the treatment of obesity. It includes a definition of obesity, its incidence and prevalence, and criteria for measuring successful treatment outcomes. Clinical success in the management of obesity and the role of the dietitian are defined in terms of new clinical guidelines and current concepts of obesity. New approaches to lifestyle modification based on physical activity and nutrition management are described. The adjunctive role of pharmacotherapy with newly available and investigational drugs also is discussed.

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Obesity assessment: Tools, methods, interpretations: A reference case: The RENO diet-heart study Source: New York, NY: Chapman and Hall. 1997. 932 pp. Contact: Available from International Thomson Publishing, Chapman and Hall, 7625 Empire Drive, Florence, KY 41042. Telephone: (800) 842-3636 or (606) 525-6600 / fax: (606) 525-7778 / e-mail: [email protected] / Gopher: gopher.thomson.com / ftp: ftp.thomson.com / Web site: http://www.thomson.com. $74.95 plus $3.00 shipping and handling for first book, $1.50 for each additional book; prepayment required. Summary: This book examines the interrelated variables that can contribute to the development of obesity based upon data derived from the RENO (Relationships of Energy and Nutrition to Obesity) Diet-Heart Study. The book presents tools and methods that can be used for obesity assessment. For each, it includes a description of the tool or method; describes its uses and limitations; methods of application; data by

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weight status, gender, and age; analysis of the results; suggested future applications; and brief annotated reference lists. The book includes ten sections covering background information on the original study; anthropometric measurements; physiological and genetic measurements; physical activity and energy expenditure measurements; dietary intake assessments; assessments of attitude, eating, and dieting behaviors; personality and psychological assessments; assessments of emotions and stress; assessments of interpersonal relationships; and assessing change. •

Contemporary Diagnosis and Management of Obesity Source: Newtown, PA: Handbooks in Health Care, Co., 289p., 1998. Contact: Handbooks in Health Care, Inc., 3 Terry Dr., Suite 201, Newtown, PA, 18940. (215) 860- 9600. Summary: This is a comprehensive discussion of obesity. Chapter topics include the epidemiology of obesity, possible causes of obesity, health hazards, evaluation and treatment, behavior modification, nutrition and diet, drug therapy, and surgical treatment. Appendices offer a testing method for diet readiness, a guide for improving eating and nutrition, and a discussion of energy metabolism. Each chapter is illustrated with tables and charts, and references are included at the end of each chapter.

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Guidance for Treatment of Adult Obesity Source: Bethesda MD: ShapeUp America!, 101p., 1997. Contact: ShapeUp America!, 67-7 Democracy Blvd., Suite 107, Bethesda, MD 20817. http://www.shapeup.org/sua. Summary: This publication offers suggestions to health professionals regarding diagnosis and treatment of overweight patients. The reader is urged to intervene when an obese patient is seen and to offer guidelines on weight loss. A variety of technical aids are included, such as a Body Mass Index chart, the formula for energy deficit calculation, anthropometric measurement protocols, and so on. Appendices list weight loss programs, obesity resources, and weight management information sources.

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Body Image, Eating Disorders, and Obesity: An Integrative Guide for Assessment and Treatment Source: Carlsbad, CA : Guerze Books, 515p., 1996. Contact: Guerze Books, P.O. Box 2238 Carlsbad, CA 92018. (800) 756-7533. www.guerze.com. Summary: The book helps practitioners to distinguish individuals with healthy appearance-related concerns from those who suffer disturbances of body image. The 19 chapters cover physical and psychological diagnoses, treatment planning, and protocols for interventions. Also included is an extensive review of the literature.

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Full Figure Fitness: A Program for Teaching Overweight Adults Source: Champaign, IL, Life Enhancement Publications, 80 p., 1988. Contact: Human Kinetics, Box 5076, Champaign, IL 61825. (800) 747-4457. Summary: Full Figure Fitness: A Program for Teaching Overweight Adults presents a fitness program that is geared toward people who are in need of exercise but are less likely to take advantage of standardized exercise programs because of their weight. Full

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Figure Fitness offers a comprehensive program of fitness in the company of others who share similar concerns. The book (1) teaches fitness instructors how to offer a quality exercise program to overweight and obese individuals; (2) gives practical advice from experts in the fields of psychology, eating disorders, physical therapy, and nutrition; (3) discusses theories regarding the causes and complex nature of obesity; (4) explains how an instructor can successfully market and promote an exercise program for overweight individuals; and (5) describes what exercise techniques are most appropriate for an overweight population. Chapters include (1) The Whys and Wherefores of Full Figure Fitness, (2) Understanding the Full Figure Participant, (3) Broad Scope Program Development, (4) The Full Figure Fitness Exercise Program, and (5) FFF: FYI Instructor's Concerns. There are five appendixes: (1) Sample Flyers to Advertise Your Program, (2) Full Figure Fitness Participant Forms, (3) Welcome to the Program, (4) Calculating and Monitoring the Exercise Heart Rate, and (5) Evaluating New Reducing Diets. •

Beyond Dieting: Psychoeducational Interventions for Chronically Obese Women: A Non-dieting Approach Source: New York, NY, Brunner/Mazel, Inc., 176 p., 1990. Contact: Brunner/Mazel, Inc., 19 Union Square West, New York, NY 10003. Summary: Beyond Dieting: Psychoeducational Interventions for Chronically Obese Women: A Non-dieting Approach addresses eating disorders and their prevention and offers an alternative to dieting for healthy, chronically obese women. Chapter one contains an overview of dieting and its relationship to self esteem and body image and explores the negative and destructive side effects frequently experienced by obese women as a result of dieting. Chapter two discusses the etiology of obesity, provides a definition and measurement of obesity, and explores alternate interventions to dieting. Chapter three describes the weekly Beyond Dieting program, with weekly objectives, group exercises, content, resources, expected reactions, and a list of recommended readings from background literature. Chapter four presents an evaluation of two related non-dieting interventions: Education alone and a more intense psychoeducational approach. The randomized controlled trial involved 142 obese adult female volunteers and evaluated the effects of group interventions for clinically obese women on self esteem, body satisfaction, restrained eating, social adjustment, symptoms of depression, scores on bulimia and drive for thinness scales, weight, blood pressure, and serum levels of glucose and lipids. Researchers collected data at pretest, posttest, and 6 and 12 months after program completion. Chapter five provides general discussion of the intervention and implications for future research. 141 references.

Book Summaries: Online Booksellers Commercial Internet-based booksellers, such as Amazon.com and Barnes&Noble.com, offer summaries which have been supplied by each title’s publisher. Some summaries also include customer reviews. Your local bookseller may have access to in-house and commercial databases that index all published books (e.g. Books in Print). IMPORTANT NOTE: Online booksellers typically produce search results for medical and non-medical books. When searching for “obesity” at online booksellers’ Web sites, you may discover nonmedical books that use the generic term “obesity” (or a synonym) in their titles. The following is indicative of the results you might find when searching for “obesity” (sorted alphabetically by title; follow the hyperlink to view more details at Amazon.com):

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10th International Symposium on Endocrinology and Development: Growth and Metabolism: Obesity, Insulin Action and Use of Anthropometry by A. Attanasio (Editor) (1993); ISBN: 3805558848; http://www.amazon.com/exec/obidos/ASIN/3805558848/icongroupinterna

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21st Century Collection Centers for Disease Control (CDC) Morbidity and Mortality Weekly Report (MMWR) - Comprehensive Collection from 1982 through 2002 with Reports on Diseases, Environmental Hazards, Disasters, Occupational Diseases, Injuries, Influenza, HIV, AIDS, Malaria, TB, Lyme Disease, Suicide, Cancer, Alcohol Use, Immunization, Toy Injuries, Infant Mortality, Homicides, Smoking, Nutrition, Obesity, Pollution (Core Federal Information Series) by U.S. Government; ISBN: 159248073X; http://www.amazon.com/exec/obidos/ASIN/159248073X/icongroupinterna

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5-Htp: The Natural Way to Overcome Depression, Obesity, and Insomnia by Michael T. Murray; ISBN: 0553379461; http://www.amazon.com/exec/obidos/ASIN/0553379461/icongroupinterna

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7 Steps to Overcoming Obesity : A Practical Guide to Mental, Physical, and Spiritual Needs by Gary Null (Author) (2005); ISBN: 0743479858; http://www.amazon.com/exec/obidos/ASIN/0743479858/icongroupinterna

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A Color Atlas of Obesity by Roland T. Jung; ISBN: 0801662966; http://www.amazon.com/exec/obidos/ASIN/0801662966/icongroupinterna

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A Colour Atlas of Obesity by Ronald T. Jung MA MD FRCP FRCPE; ISBN: 0723415773; http://www.amazon.com/exec/obidos/ASIN/0723415773/icongroupinterna

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A Complete Guide to Obesity Surgery: Everything You Need to Know About Weight Loss Surgery and How to Succeed by Bryan G. Woodward (2001); ISBN: 1552126641; http://www.amazon.com/exec/obidos/ASIN/1552126641/icongroupinterna

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A Hundred Pounds Thinner: Life After Obesity Surgery by Linda Algazi; ISBN: 1930807023; http://www.amazon.com/exec/obidos/ASIN/1930807023/icongroupinterna

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A Parent's Guide to Eating Disorders and Obesity (The Children's Hospital of Philadelphia Series) by Martha Moraghan Jablow, C. Everett Koop (1993); ISBN: 044050645X; http://www.amazon.com/exec/obidos/ASIN/044050645X/icongroupinterna

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Adipocyte and Obesity: Cellular and Molecular Mechanisms by Aubie Angel (Editor); ISBN: 0890049467; http://www.amazon.com/exec/obidos/ASIN/0890049467/icongroupinterna

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Adult Obesity Therapy by Michael D. LeBow (1989); ISBN: 0080355560; http://www.amazon.com/exec/obidos/ASIN/0080355560/icongroupinterna

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Adult Obesity: A Paediatric Challenge by Terry Wilkin (Editor), et al (2003); ISBN: 0415300150; http://www.amazon.com/exec/obidos/ASIN/0415300150/icongroupinterna

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Advances in Eating Disorders: A Research Annual: Treating and Preventing Obesity, 1987 by William G. Johnson (Editor) (1987); ISBN: 0892328142; http://www.amazon.com/exec/obidos/ASIN/0892328142/icongroupinterna

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Advances in Modern Human Nutrition: Role of Nutrition in Obesity and Disease by Richard B., M.D. Tobin, Myron A. Mehlman (Editor) (1992); ISBN: 0930376072; http://www.amazon.com/exec/obidos/ASIN/0930376072/icongroupinterna

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An Atlas of Obesity and Weight Control by G. A. Bray, C. A. Bray; ISBN: 1842140493; http://www.amazon.com/exec/obidos/ASIN/1842140493/icongroupinterna

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Animal Models of Obesity by Shlomo Giora Shoham (Editor), Francis Rosenstiel (Editor); ISBN: 0333253396; http://www.amazon.com/exec/obidos/ASIN/0333253396/icongroupinterna

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Appetite and Obesity: Disorders of Over and Under-eating by Peter Kopelman (Editor); ISBN: 1860160840; http://www.amazon.com/exec/obidos/ASIN/1860160840/icongroupinterna

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Aspects of Surgical Treatment of Morbid Obesity (Comprehensive Summaries of Uppsala Dissertations from the Faculty of mediciNe, 1029) by Agneta Westling (2001); ISBN: 9155450032; http://www.amazon.com/exec/obidos/ASIN/9155450032/icongroupinterna

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Assessment of Eating Disorders: Obesity, Anorexia, and Bulimia Nervosa by Donald A. Williamson (1990); ISBN: 0080364527; http://www.amazon.com/exec/obidos/ASIN/0080364527/icongroupinterna

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Behavioral Management of Obesity (Lacrosse Exercise and Health Series) by Jean Storlie, Henry A. Jordan (Editor); ISBN: 0873229088; http://www.amazon.com/exec/obidos/ASIN/0873229088/icongroupinterna

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Behavioral Treatments of Obesity by J. Foreyt; ISBN: 008019902X; http://www.amazon.com/exec/obidos/ASIN/008019902X/icongroupinterna

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Black Health Library Guide: Obesity: Vital Health Information for African Americans by Mavis Thompson, et al (2000); ISBN: 1575664852; http://www.amazon.com/exec/obidos/ASIN/1575664852/icongroupinterna

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Body Image, Eating Disorders, and Obesity in Youth: Assessment, Prevention, and Treatment by J. Kevin Thompson (Editor), Linda Smolak (Editor) (2001); ISBN: 1557987580; http://www.amazon.com/exec/obidos/ASIN/1557987580/icongroupinterna

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Body Image, Eating Disorders, and Obesity: An Integrative Guide for Assessment by J. Kevin Thompson (Editor) (2003); ISBN: 1557987262; http://www.amazon.com/exec/obidos/ASIN/1557987262/icongroupinterna

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Body Image, Eating Disorders, and Obesity: An Integrative Guide for Assessment and Treatment by J. Kevin Thompson (Editor) (1996); ISBN: 1557983240; http://www.amazon.com/exec/obidos/ASIN/1557983240/icongroupinterna

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Body Weight Control: The Physiology, Clinical Treatment and Prevention of Obesity by A.E. Bender, L.J. Brookes (Editor); ISBN: 0443036888; http://www.amazon.com/exec/obidos/ASIN/0443036888/icongroupinterna

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Child and Adolescent Obesity: Causes and Consequences, Prevention and Management by Walter Burniat (Editor), et al; ISBN: 0521652375; http://www.amazon.com/exec/obidos/ASIN/0521652375/icongroupinterna

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Child Obesity: A New Frontier of Behavior Therapy (Springer Series on Behavior Therapy and Behavioral Medicine; V. 12) by Michael D. Lebow; ISBN: 0826137806; http://www.amazon.com/exec/obidos/ASIN/0826137806/icongroupinterna

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Childhood Obesity by Platon J Collipp (Author); ISBN: 0884160165; http://www.amazon.com/exec/obidos/ASIN/0884160165/icongroupinterna

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Childhood Obesity by Myron. Winick; ISBN: 0471954411; http://www.amazon.com/exec/obidos/ASIN/0471954411/icongroupinterna

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Childhood Obesity 2002: How obesity is shaping the U.S. food and beverage markets [DOWNLOAD: PDF] by Datamonitor (Author); ISBN: B00008R3YD; http://www.amazon.com/exec/obidos/ASIN/B00008R3YD/icongroupinterna

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Childhood Obesity: A Biobehavioral Perspective by Norman A. Krasnegor; ISBN: 0936923040; http://www.amazon.com/exec/obidos/ASIN/0936923040/icongroupinterna

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Childhood Obesity: Prevention and Treatment by Jana Parizkova, Andrew P. Hills; ISBN: 0849387361; http://www.amazon.com/exec/obidos/ASIN/0849387361/icongroupinterna

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Chromium: A Remarkable Micro-Nutrient Which May Protect Against Cardiovascular Disease, Diabetes, and Obesity (Woodland Health Ser) by Rita Elkins, Woodland Publishing (1999); ISBN: 1885670214; http://www.amazon.com/exec/obidos/ASIN/1885670214/icongroupinterna

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Cider Vinegar: Nature's Great Health-Promoter and Safest Treatment of Obesity by Cyril Scott, Thorsons; ISBN: 0722518765; http://www.amazon.com/exec/obidos/ASIN/0722518765/icongroupinterna

•

Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults (2003); ISBN: 1588080021; http://www.amazon.com/exec/obidos/ASIN/1588080021/icongroupinterna

•

Clinical Research in Diabetes and Obesity, Vol Ii: Diabetes and Obesity by Boris Draznin (Editor), Robert Rizza (Editor); ISBN: 0896034925; http://www.amazon.com/exec/obidos/ASIN/0896034925/icongroupinterna

•

Clinical Research in Diabetes and Obesity, Volume I: Methods, Assessment, and Metabolic Regulation by Boris Draznin (Editor), Robert Rizza (Editor); ISBN: 0896033503; http://www.amazon.com/exec/obidos/ASIN/0896033503/icongroupinterna

•

Cognitive-Behavioral Treatment of Obesity: A Clinician's Guide by Zafra Cooper, et al (2003); ISBN: 1572308885; http://www.amazon.com/exec/obidos/ASIN/1572308885/icongroupinterna

•

Contemporary Diagnosis and Management of Obesity by George A. Bray; ISBN: 1884065597; http://www.amazon.com/exec/obidos/ASIN/1884065597/icongroupinterna

•

Controversies in Obesity (1983); ISBN: 003063007X; http://www.amazon.com/exec/obidos/ASIN/003063007X/icongroupinterna

•

Cumulus the Puffy Cloud: A Story About Dealing With Childhood Obesity by Benny Hardouin (Illustrator) (1998); ISBN: 0966473108; http://www.amazon.com/exec/obidos/ASIN/0966473108/icongroupinterna

•

Diabetes and Obesity - Complete Medical Guides with Authoritative Federal Government Documents and Clinical References for Patients and Physicians with Practical Information on Diagnosis and Treatment Options (Two CD-ROM Set) by PM Medical Health News; ISBN: 1931828954; http://www.amazon.com/exec/obidos/ASIN/1931828954/icongroupinterna

404 Obesity

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Diabetes and obesity : proceedings of the Vth International Meeting of Endocrinology, Marseilles, June 19-21, 1978; ISBN: 0444900586; http://www.amazon.com/exec/obidos/ASIN/0444900586/icongroupinterna

•

Diabetes, Obesity and Hyperlipidemias: 5: Plurimetabolic Syndrome by Gaetano Crepaldi, et al; ISBN: 0444816399; http://www.amazon.com/exec/obidos/ASIN/0444816399/icongroupinterna

•

Diabetes, Obesity and Hyperlipidemias-III: Proceedings of the 4th European Symposium on Metabolism (International Congress Series, No 681) by Gaetano Crepaldi, et al; ISBN: 0444807314; http://www.amazon.com/exec/obidos/ASIN/0444807314/icongroupinterna

•

Diabetes, Obesity, and Hyperlipidemias-IV: Proceedings of the 5th European Symposium on Metabolism, Padova, 15-17 May 1989 (International Congress Series, No. 872) by Gaetano/ Tiengo, Antonio/ Enzi, G. European Symposium on Metabolism 1989 Padua Italy)/ Crepaldi; ISBN: 0444811516; http://www.amazon.com/exec/obidos/ASIN/0444811516/icongroupinterna

•

Diabetes, Obesity, and Vascular Disease: Metabolic and Molecular Interrelationships by Hem, et al; ISBN: 0470262869; http://www.amazon.com/exec/obidos/ASIN/0470262869/icongroupinterna

•

Diet and Obesity; ISBN: 476222572X; http://www.amazon.com/exec/obidos/ASIN/476222572X/icongroupinterna

•

Diet and Obesity by George A. Bray, et al; ISBN: 3805549806; http://www.amazon.com/exec/obidos/ASIN/3805549806/icongroupinterna

•

Diet, Obesity, and Cardiovascular Disease by MD, PhD Steven H. Zeisel; ISBN: 1892483025; http://www.amazon.com/exec/obidos/ASIN/1892483025/icongroupinterna

•

Eating Disorders and Obesity, Second Edition: A Comprehensive Handbook by Christopher G. Fairburn (Editor), Kelly D. Brownell (Editor); ISBN: 1572306882; http://www.amazon.com/exec/obidos/ASIN/1572306882/icongroupinterna

•

Eating Disorders: Management of Obesity, Bulimia, and Anorexia Nervosa by Stewart Agras, W. Stewart Agras (1987); ISBN: 0080336450; http://www.amazon.com/exec/obidos/ASIN/0080336450/icongroupinterna

•

Eating Disorders: Obesity, Anorexia Nervosa, and Bulimia in Childhood and Adolescence by D.W. Kaplan (Editor); ISBN: 3805542690; http://www.amazon.com/exec/obidos/ASIN/3805542690/icongroupinterna

•

Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within by Hilda Bruch, Hilde Bruch (1985); ISBN: 0465017827; http://www.amazon.com/exec/obidos/ASIN/0465017827/icongroupinterna

•

Emotion, Obesity, and Crime by Stanley Schachter; ISBN: 012621350X; http://www.amazon.com/exec/obidos/ASIN/012621350X/icongroupinterna

•

Energy balance and obesity in man by J. S. Garrow; ISBN: 0444105417; http://www.amazon.com/exec/obidos/ASIN/0444105417/icongroupinterna

•

Evaluation & Management of Obesity by Daniel H. Bessesen (Editor), et al; ISBN: 1560534699; http://www.amazon.com/exec/obidos/ASIN/1560534699/icongroupinterna

Books 405

•

Evaluation and Management of Eating Disorders: Anorexia, Bulimia, and Obesity (Lacrosse Exercise and Health Series) by Richard B. Parr, et al; ISBN: 0873229118; http://www.amazon.com/exec/obidos/ASIN/0873229118/icongroupinterna

•

Evaluation and Treatment of Obesity: Sports Medicine and Health Science by Jean Storlie, Henry A. Jordan (Editor); ISBN: 0893352063; http://www.amazon.com/exec/obidos/ASIN/0893352063/icongroupinterna

•

Exercise and obesity; ISBN: 1854630865; http://www.amazon.com/exec/obidos/ASIN/1854630865/icongroupinterna

•

Fat : Fighting the Obesity Epidemic by Robert Pool (2001); ISBN: 0195118537; http://www.amazon.com/exec/obidos/ASIN/0195118537/icongroupinterna

•

Fat and Thin: A Natural History of Obesity by Anne Scott Beller; ISBN: 0070044139; http://www.amazon.com/exec/obidos/ASIN/0070044139/icongroupinterna

•

Food Fight : The Inside Story of the Food Industry, America's Obesity Crisis, and What We Can Do About It by Kelly D. Brownell, Katherine Battle Horgen; ISBN: 0071402500; http://www.amazon.com/exec/obidos/ASIN/0071402500/icongroupinterna

•

Food for Thought: The Sourcebook for Obesity and Eating Disorders by Dana K. Cassell, David H. Gleaves (2000); ISBN: 0816041474; http://www.amazon.com/exec/obidos/ASIN/0816041474/icongroupinterna

•

Food, Eating and Obesity: The Psychological Basis of Appetite and Weight Control by David J. Mela, Peter J. Rogers (1998); ISBN: 0412719207; http://www.amazon.com/exec/obidos/ASIN/0412719207/icongroupinterna

•

Growth and its disorders : basics and standards, approach and classifications, growth deficiency disorders, growth excess disorders, obesity by David W. Smith; ISBN: 0721683789; http://www.amazon.com/exec/obidos/ASIN/0721683789/icongroupinterna

•

Handbook of Eating Disorders and Obesity by Joel Kevin Thompson (Editor) (2003); ISBN: 0471230731; http://www.amazon.com/exec/obidos/ASIN/0471230731/icongroupinterna

•

Handbook of Eating Disorders, Part 2: Obesity by Graham D. Burrows, et al; ISBN: 0444809643; http://www.amazon.com/exec/obidos/ASIN/0444809643/icongroupinterna

•

Handbook of Eating Disorders: Physiology, Psychology, and Treatment of Obesity, Anorexia, and Bulimia by Kelly D. Brownell (Editor), et al; ISBN: 0465028624; http://www.amazon.com/exec/obidos/ASIN/0465028624/icongroupinterna

•

Handbook of Obesity by C. Bouchard, George A. Bray (2004); ISBN: 0824709691; http://www.amazon.com/exec/obidos/ASIN/0824709691/icongroupinterna

•

Handbook of Obesity Treatment by Thomas A. Wadden (Editor), Albert J. Stunkard (Editor); ISBN: 1572307226; http://www.amazon.com/exec/obidos/ASIN/1572307226/icongroupinterna

•

Hand-Me-Down Genes and Second-Hand Emotions: You Can Overcome the Genetic and Family Factors That Can Lead to Depression, Alcoholism, Obesity, and S by Stephen Arterburn; ISBN: 0671897187; http://www.amazon.com/exec/obidos/ASIN/0671897187/icongroupinterna

406 Obesity

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Health and Obesity by Hadley Conn (Editor), et al; ISBN: 0890048096; http://www.amazon.com/exec/obidos/ASIN/0890048096/icongroupinterna

•

Histophysiology of the Obesity-Diabetes Syndrome in Sand Rats (Advances in Anatomy, Embryology, and Cell Biology; V. 130) by Herwig Hahn Von Dorsche, et al; ISBN: 0387579133; http://www.amazon.com/exec/obidos/ASIN/0387579133/icongroupinterna

•

Hormones and Nutrition in Obesity and Cachexia by M. J. Muller, et al; ISBN: 0387516379; http://www.amazon.com/exec/obidos/ASIN/0387516379/icongroupinterna

•

Hormones and Nutrition in Obesity and Cachexia (1990); ISBN: 3540516379; http://www.amazon.com/exec/obidos/ASIN/3540516379/icongroupinterna

•

Hormones, Thermogenesis, and Obesity: Proceedings by Henry Lardy, Frederick Stratman (Editor); ISBN: 0444014764; http://www.amazon.com/exec/obidos/ASIN/0444014764/icongroupinterna

•

Human obesity; ISBN: 0897663942; http://www.amazon.com/exec/obidos/ASIN/0897663942/icongroupinterna

•

Human Obesity - Treatment & Therapy: Index of Authors and Subjects by Georgette R., Dr Darvonne (1993); ISBN: 1559149477; http://www.amazon.com/exec/obidos/ASIN/1559149477/icongroupinterna

•

Human Obesity (Annals of the New York Academy of Sciences, Vol 499) by Richard J. Wurtman, Judith J. Wurtman (Editor) (1987); ISBN: 0897663934; http://www.amazon.com/exec/obidos/ASIN/0897663934/icongroupinterna

•

Human Obesity-- Treatment & Therapy: Index of Author and Subjects by Georgette Rose Darvonne (1995); ISBN: 0788306707; http://www.amazon.com/exec/obidos/ASIN/0788306707/icongroupinterna

•

Human Obesity-Treatment and Therapy: Index of New Information With Authors and Subjects by Georgette R. Darvonne (1993); ISBN: 1559149469; http://www.amazon.com/exec/obidos/ASIN/1559149469/icongroupinterna

•

Hungry Mind-Hungry Body: Childhood Obesity (Real Life Storybooks) by Illana Katz, et al; ISBN: 1882388127; http://www.amazon.com/exec/obidos/ASIN/1882388127/icongroupinterna

•

Improving the Long-Term Management of Obesity: Theory, Research, and Clinical Guidelines by Michael G. Perri (Author), et al; ISBN: 0471528994; http://www.amazon.com/exec/obidos/ASIN/0471528994/icongroupinterna

•

Interior Passages: Obesity and Transformation by Francine Saillant, Myriam Jarsky (Translator) (1997); ISBN: 092900504X; http://www.amazon.com/exec/obidos/ASIN/092900504X/icongroupinterna

•

International Textbook of Obesity by Per Björntorp (Editor); ISBN: 0471988707; http://www.amazon.com/exec/obidos/ASIN/0471988707/icongroupinterna

•

Just For Kids! (Obesity Prevention Workbook) by Susan Johnson, Laurel Mellin; ISBN: 0935902341; http://www.amazon.com/exec/obidos/ASIN/0935902341/icongroupinterna

•

Laparoscopic Surgery for Morbid Obesity (CD-ROM) by Medascend (2002); ISBN: 1888829273; http://www.amazon.com/exec/obidos/ASIN/1888829273/icongroupinterna

Books 407

•

Lifestyle Drugs: Obesity [DOWNLOAD: PDF] by Nicholas Hall & Company (Author); ISBN: B00005TYE1; http://www.amazon.com/exec/obidos/ASIN/B00005TYE1/icongroupinterna

•

Lifestyle Drugs: Patient-Initiated Prescribing: New Opportunities in Sexual Dysfunction, Obesity and Rejuvenation [DOWNLOAD: PDF] by Nicholas Hall & Company (Author); ISBN: B00005RQ8S; http://www.amazon.com/exec/obidos/ASIN/B00005RQ8S/icongroupinterna

•

Lifestyle Obesity Management by John Paul Foreyt (Editor), et al (2003); ISBN: 1405103442; http://www.amazon.com/exec/obidos/ASIN/1405103442/icongroupinterna

•

Lipid metabolism, obesity, and diabetes mellitus : impact upon atherosclerosis : international symposium, Arpil 1972; ISBN: 3135076016; http://www.amazon.com/exec/obidos/ASIN/3135076016/icongroupinterna

•

Livin' Large: African American Sisters Confront Obesity by Stacy Ann, MD Mitchell, et al; ISBN: 0971606749; http://www.amazon.com/exec/obidos/ASIN/0971606749/icongroupinterna

•

Love, Honor, and Obesity by Allison. Hughes; ISBN: 0310263301; http://www.amazon.com/exec/obidos/ASIN/0310263301/icongroupinterna

•

Macrosomy, Obesity and Cancer by Lev M. Berstein (1997); ISBN: 1560722029; http://www.amazon.com/exec/obidos/ASIN/1560722029/icongroupinterna

•

Management of Obesity by Severe Caloric Restriction by George L. Blackburn, George A. Bray (Editor); ISBN: 0884164950; http://www.amazon.com/exec/obidos/ASIN/0884164950/icongroupinterna

•

Managing Obesity by Gordon Mallarkey (Editor) (1999); ISBN: 0864710682; http://www.amazon.com/exec/obidos/ASIN/0864710682/icongroupinterna

•

Managing Obesity and Cardiovascular Disease by James Shepherd (2002); ISBN: 1858739136; http://www.amazon.com/exec/obidos/ASIN/1858739136/icongroupinterna

•

Managing Obesity and Eating Disorders (Nursing CEU Course) by Nancy Gustafson; ISBN: 1578010071; http://www.amazon.com/exec/obidos/ASIN/1578010071/icongroupinterna

•

Managing Obesity: A Clinical Guide by Gary D. Foster (2003); ISBN: 0880913347; http://www.amazon.com/exec/obidos/ASIN/0880913347/icongroupinterna

•

Metabolic Control of Eating, Energy Expenditure and the Bioenergetics of Obesity (World Review of Nutrition and Dietetics, Vol 70) by Artemis P. Simopoulos (Editor) (1992); ISBN: 3805555954; http://www.amazon.com/exec/obidos/ASIN/3805555954/icongroupinterna

•

New Directions in Research and Clinical Works for Obesity and Diabetes Mellitus: Proceedings (International Congress Series, No 963) by Nobuo Sakamoto, et al; ISBN: 0444814396; http://www.amazon.com/exec/obidos/ASIN/0444814396/icongroupinterna

•

Nutrition, Genetics, and Obesity (Pennington Center Nutrition Series, Vol 9) by George A. Bray (Editor), et al (1999); ISBN: 0807124079; http://www.amazon.com/exec/obidos/ASIN/0807124079/icongroupinterna

408 Obesity

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Nutritional, Psychological and Social Aspects of Obesity =: Diatetische, Psychologische Und Soziale Aspekte Des Ubergewichts by Johann Carl Somogyi (1978); ISBN: 3805527640; http://www.amazon.com/exec/obidos/ASIN/3805527640/icongroupinterna

•

Obesity by Barry Gumbiner (Editor), et al; ISBN: 1930513127; http://www.amazon.com/exec/obidos/ASIN/1930513127/icongroupinterna

•

Obesity by Albert J. Stunkard; ISBN: 0721686354; http://www.amazon.com/exec/obidos/ASIN/0721686354/icongroupinterna

•

Obesity by Finer, et al; ISBN: 1899541667; http://www.amazon.com/exec/obidos/ASIN/1899541667/icongroupinterna

•

Obesity by Per Bjorntorp, Bernard N. Brodoff (Editor); ISBN: 0397509995; http://www.amazon.com/exec/obidos/ASIN/0397509995/icongroupinterna

•

Obesity by M.R.C. Greenwood (Editor); ISBN: 0443081867; http://www.amazon.com/exec/obidos/ASIN/0443081867/icongroupinterna

•

Obesity; ISBN: 1853348880; http://www.amazon.com/exec/obidos/ASIN/1853348880/icongroupinterna

•

Obesity by George L. Blackburn, Beatrice S. Kanders (1994); ISBN: 0442013434; http://www.amazon.com/exec/obidos/ASIN/0442013434/icongroupinterna

•

Obesity (A Venture Book) by Daniel McMillan, Daniel MacMillan; ISBN: 0531112012; http://www.amazon.com/exec/obidos/ASIN/0531112012/icongroupinterna

•

Obesity (Lucent Overview Series) by Charlene Akers (2000); ISBN: 1560066628; http://www.amazon.com/exec/obidos/ASIN/1560066628/icongroupinterna

•

Obesity : a bibliography, 1974-1979 by Anne Smith; ISBN: 0904147177; http://www.amazon.com/exec/obidos/ASIN/0904147177/icongroupinterna

•

Obesity : dietary factors and control; ISBN: 3805554796; http://www.amazon.com/exec/obidos/ASIN/3805554796/icongroupinterna

•

Obesity : its pathogenesis and management; ISBN: 0852000871; http://www.amazon.com/exec/obidos/ASIN/0852000871/icongroupinterna

•

Obesity and Anorexia Nervosa: a Question of Shape by Peter Dally, Joan Gomez; ISBN: 0571114725; http://www.amazon.com/exec/obidos/ASIN/0571114725/icongroupinterna

•

Obesity and Anti-Obesity Agents: Index of New Information for Consumers, Reference and Research by Joseph R., Dr Richie (2002); ISBN: 0788324322; http://www.amazon.com/exec/obidos/ASIN/0788324322/icongroupinterna

•

Obesity and CV disease [DOWNLOAD: PDF] by Datamonitor (Author); ISBN: B00008R3MP; http://www.amazon.com/exec/obidos/ASIN/B00008R3MP/icongroupinterna

•

Obesity and Depression in the Enlightenment: The Life and Times of George Cheyne (Series for Science and Culture, Vol 3) by Anita Guerrini (2000); ISBN: 0806132019; http://www.amazon.com/exec/obidos/ASIN/0806132019/icongroupinterna

•

Obesity and Diabetes Mellitus by E. I. Sokolov (1997); ISBN: 9067642126; http://www.amazon.com/exec/obidos/ASIN/9067642126/icongroupinterna

•

Obesity and its management by Denis Craddock; ISBN: 044301017X; http://www.amazon.com/exec/obidos/ASIN/044301017X/icongroupinterna

Books 409

•

Obesity and Its Treatment (ARR) by J E Blundell; ISBN: 0443018553; http://www.amazon.com/exec/obidos/ASIN/0443018553/icongroupinterna

•

Obesity and Leanness: Basic Aspects by Nancy Rothwell, Michael J. Stock; ISBN: 0471898570; http://www.amazon.com/exec/obidos/ASIN/0471898570/icongroupinterna

•

Obesity and Medical Student Education by Walter Futterweit (Editor) (1999); ISBN: 0930194896; http://www.amazon.com/exec/obidos/ASIN/0930194896/icongroupinterna

•

Obesity and NIDDM by Kenji Shima (Editor); ISBN: 0444501126; http://www.amazon.com/exec/obidos/ASIN/0444501126/icongroupinterna

•

Obesity and Overweight; ISBN: 1854482734; http://www.amazon.com/exec/obidos/ASIN/1854482734/icongroupinterna

•

Obesity and Overweight Matters in Primary Care by Ruth Chambers, et al; ISBN: 1857755146; http://www.amazon.com/exec/obidos/ASIN/1857755146/icongroupinterna

•

Obesity and Poverty: A New Public Health Challenge; ISBN: 9275115761; http://www.amazon.com/exec/obidos/ASIN/9275115761/icongroupinterna

•

Obesity and Related Disease by J.S. Garrow (1988); ISBN: 0443037981; http://www.amazon.com/exec/obidos/ASIN/0443037981/icongroupinterna

•

Obesity and the Family by David D. Kallen (1984); ISBN: 0866561625; http://www.amazon.com/exec/obidos/ASIN/0866561625/icongroupinterna

•

Obesity and Weight Control: The Health Professional's Guide to Understanding and Treatment by Reva T. Frankle, Mei-Uih Yang (Editor); ISBN: 0871898691; http://www.amazon.com/exec/obidos/ASIN/0871898691/icongroupinterna

•

Obesity and Weight Management in Primary Care by Colin Waine, et al (2002); ISBN: 0632065141; http://www.amazon.com/exec/obidos/ASIN/0632065141/icongroupinterna

•

Obesity Assessment: Tools, Methods, Interpretations: A Reference Case: The Reno Diet-Heart Study (Chapman & Hall Series in Clinical Nutrition) by Sachiko T. St. Jeor (Editor), et al (1997); ISBN: 0412072416; http://www.amazon.com/exec/obidos/ASIN/0412072416/icongroupinterna

•

Obesity Epidemic : The Marshall Plan Natural Diet-free Solution by Colin S Marshall (Author) (2003); ISBN: 0595657516; http://www.amazon.com/exec/obidos/ASIN/0595657516/icongroupinterna

•

Obesity in Childhood and Adolescence by Chunming Chen (Editor), William H. Dietz (Editor); ISBN: 0781741327; http://www.amazon.com/exec/obidos/ASIN/0781741327/icongroupinterna

•

Obesity in Children and Youth: Measurement, Characteristics, Causes and Treatment by Anthony F. Rotatori, Robert A. Fox; ISBN: 0398055947; http://www.amazon.com/exec/obidos/ASIN/0398055947/icongroupinterna

•

Obesity Management and Redux by Stylianos Nicolaidis (Editor) (1996); ISBN: 0125181701; http://www.amazon.com/exec/obidos/ASIN/0125181701/icongroupinterna

410 Obesity

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Obesity medical and scientific aspects; proceedings of the first symposium of the Obesity Association of Great Britain held in London, October 1968; ISBN: 0443006520; http://www.amazon.com/exec/obidos/ASIN/0443006520/icongroupinterna

•

Obesity Sourcebook: Basic Consumer Health Information About Diseases and Other Problems Associated With Obesity, and Including Facts About Risk Factors, Prevention (Health Reference Series) by Wilma Caldwell (Editor), Chad T. Kimball (Editor) (2001); ISBN: 0780803337; http://www.amazon.com/exec/obidos/ASIN/0780803337/icongroupinterna

•

Obesity Surgery by Louis F. Martin, Louis Martin; ISBN: 0071406409; http://www.amazon.com/exec/obidos/ASIN/0071406409/icongroupinterna

•

Obesity symposium : proceedings of a Servier Research Institute symposium held in December 1973; ISBN: 0443012148; http://www.amazon.com/exec/obidos/ASIN/0443012148/icongroupinterna

•

Obesity Update: Can Scientific Advances Overcome Marketing Hurdles? [DOWNLOAD: PDF] by Datamonitor (Author); ISBN: B00008R3W4; http://www.amazon.com/exec/obidos/ASIN/B00008R3W4/icongroupinterna

•

Obesity, Diabetes, & How To Eat To Live by Kevin A Muhammad; ISBN: 0965886409; http://www.amazon.com/exec/obidos/ASIN/0965886409/icongroupinterna

•

Obesity, Growth and Development by F.E. Johnston (Editor) (2001); ISBN: 1854632175; http://www.amazon.com/exec/obidos/ASIN/1854632175/icongroupinterna

•

Obesity, Towards a Molecular Approach: Proceedings of a UCLA Symposium Held at Keystone, Colorado, April 17-23, 1989 (UCLA Symposia on Molecular and by George A. Bray (Editor), et al; ISBN: 0471567558; http://www.amazon.com/exec/obidos/ASIN/0471567558/icongroupinterna

•

Obesity, Weight Loss and Eating Disorders: Cooking for Health (Macrobiotic Food and Cooking Series) by Aveline Kushi, Helaine Honig (Editor); ISBN: 0870406426; http://www.amazon.com/exec/obidos/ASIN/0870406426/icongroupinterna

•

Obesity: a Clinical Issue by M. Lean; ISBN: 1858731488; http://www.amazon.com/exec/obidos/ASIN/1858731488/icongroupinterna

•

Obesity: A Disease of the Mind (Book and Cassette) by Michael S. Beaulieu; ISBN: 0961686707; http://www.amazon.com/exec/obidos/ASIN/0961686707/icongroupinterna

•

Obesity: Basic Concepts and Clinical Aspects: Proceedings (Frontiers in Diabetes, Vol. 11) by F. Belfiore, et al (1992); ISBN: 3805554052; http://www.amazon.com/exec/obidos/ASIN/3805554052/icongroupinterna

•

Obesity: Behavioral Approaches to Dietary Management by Ben J. Williams; ISBN: 0876301154; http://www.amazon.com/exec/obidos/ASIN/0876301154/icongroupinterna

•

Obesity: Behavioral, Medical and Surgical Management by Margaret Bischel; ISBN: 1893826287; http://www.amazon.com/exec/obidos/ASIN/1893826287/icongroupinterna

•

Obesity: Behavioral, Medical and Surgical Management [DOWNLOAD: PDF] by Apollo Managed Care Consultants (Author); ISBN: B00005V83Y; http://www.amazon.com/exec/obidos/ASIN/B00005V83Y/icongroupinterna

Books 411

•

Obesity: Comparative Methods of Weight Control by Bray; ISBN: 0877622612; http://www.amazon.com/exec/obidos/ASIN/0877622612/icongroupinterna

•

Obesity: Etiology, Assessment, Treatment, and Prevention by Jennifer Weinberg, Ross E. Andersen (2003); ISBN: 0736003282; http://www.amazon.com/exec/obidos/ASIN/0736003282/icongroupinterna

•

Obesity: Etiology, Treatment, and Management by Milton V., Comp. Kline (1976); ISBN: 0398033692; http://www.amazon.com/exec/obidos/ASIN/0398033692/icongroupinterna

•

Obesity: Impact on Cardiovascular Disease (American Heart Association Monograph Series) by Gerald F. Fletcher (Editor), et al (1999); ISBN: 0879934182; http://www.amazon.com/exec/obidos/ASIN/0879934182/icongroupinterna

•

Obesity: Mechanisms and Clinical Management by Robert H. Eckel (Editor), Robert H. Eckel MD (Editor) (2003); ISBN: 0781728444; http://www.amazon.com/exec/obidos/ASIN/0781728444/icongroupinterna

•

Obesity: Medical Subject Analysis With Bibliography by Charlotte J. Kowalski (1987); ISBN: 0881645230; http://www.amazon.com/exec/obidos/ASIN/0881645230/icongroupinterna

•

Obesity: New Directions in Assessment and Management by Theodore B. Van Itallie (Editor), et al (1995); ISBN: 0914783742; http://www.amazon.com/exec/obidos/ASIN/0914783742/icongroupinterna

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Obesity: Pathology and Therapy (Handbook of Experimental Pharmacology, 149) by D. H. Lockwood (Editor), et al; ISBN: 3540661336; http://www.amazon.com/exec/obidos/ASIN/3540661336/icongroupinterna

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Obesity: Pathophysiology, Psychology, and Treatment (Chapman & Hall Series in Clinical Nutrition) by George L. Blackburn, Beatrice S. Kanders (Editor) (1994); ISBN: 041298461X; http://www.amazon.com/exec/obidos/ASIN/041298461X/icongroupinterna

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Obesity: Preventing and Managing the Global Epidemic: Report of a WHO Consultation (WHO Technical Series) (2001); ISBN: 9241208945; http://www.amazon.com/exec/obidos/ASIN/9241208945/icongroupinterna

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Obesity: The Regulation of Weight by Pauline S. Powers; ISBN: 0683069535; http://www.amazon.com/exec/obidos/ASIN/0683069535/icongroupinterna

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Obesity: The Report of the British Nutrition Foundation Task Force by British Nutrition Foundation Obesity Task Force, British Nutrition Foundation (2000); ISBN: 0632052988; http://www.amazon.com/exec/obidos/ASIN/0632052988/icongroupinterna

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Office Management of Obesity by George A. Bray, et al; ISBN: 0721606474; http://www.amazon.com/exec/obidos/ASIN/0721606474/icongroupinterna

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Overcoming Childhood Obesity by Colleen Thompson, Ellen Shanley (2003); ISBN: 092352178X; http://www.amazon.com/exec/obidos/ASIN/092352178X/icongroupinterna

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Overweight, Obesity and Health: Web Resource Guide for Consumers, Healthcare Providers, Patients, and Physicians by Eugene A. Defelice (2002); ISBN: 0595262406; http://www.amazon.com/exec/obidos/ASIN/0595262406/icongroupinterna

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Owl Was a Baker's Daughter: Obesity, Anorexia Nervosa, and the Repressed Feminine--A Psychological Study (139P) by Marion Woodman (1985); ISBN: 0919123031; http://www.amazon.com/exec/obidos/ASIN/0919123031/icongroupinterna

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Passing the OBESITY & NUTRITION Exam in Primary Care by Southland, Southland Tutorials; ISBN: 1888628227; http://www.amazon.com/exec/obidos/ASIN/1888628227/icongroupinterna

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Physical Activity and Obesity by Claude Bouchard (Editor) (2000); ISBN: 0880119098; http://www.amazon.com/exec/obidos/ASIN/0880119098/icongroupinterna

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Prader-Willi Syndrome As a Model for Obesity: International Symposium, Zurich, October 18-19, 2002 by Urs Eiholzer (Editor), et al (2003); ISBN: 3805575742; http://www.amazon.com/exec/obidos/ASIN/3805575742/icongroupinterna

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Prevention and Treatment of Childhood Obesity (Annals of the New York Academy of Sciences, V. 699) by Christine L. Williams, Sue Y. S. Kimm; ISBN: 0897668324; http://www.amazon.com/exec/obidos/ASIN/0897668324/icongroupinterna

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Progress in Obesity by Bernard Guy-Grand (Editor), et al (1996); ISBN: 0861965329; http://www.amazon.com/exec/obidos/ASIN/0861965329/icongroupinterna

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Protein-Sparing Diets: A Special Issue of Journal of Obesity and Weight Regulation by Jonathan Wise (Editor) (1984); ISBN: 089885220X; http://www.amazon.com/exec/obidos/ASIN/089885220X/icongroupinterna

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Psychological Aspects of Obesity: A Handbook by Wolman; ISBN: 0442226098; http://www.amazon.com/exec/obidos/ASIN/0442226098/icongroupinterna

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Recent Advances in Obesity and Diabetes Research by N. Melchionda; ISBN: 0890049696; http://www.amazon.com/exec/obidos/ASIN/0890049696/icongroupinterna

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Recent Advances in Obesity Research, IV by T.B. Van Itallie (Editor), Jules Hirsch (Editor) (1985); ISBN: 0861960491; http://www.amazon.com/exec/obidos/ASIN/0861960491/icongroupinterna

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Recent Advances in Obesity Research, V by E. Berry (Editor), et al (1987); ISBN: 0917678222; http://www.amazon.com/exec/obidos/ASIN/0917678222/icongroupinterna

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Relation Between Qualitative Changes in High- And Low-Density Lipoproteins & Their (Anti) Atherogenic Potential in Obesity (Acta Biomedica lovaniensia by Ann Mertens (2002); ISBN: 9058672743; http://www.amazon.com/exec/obidos/ASIN/9058672743/icongroupinterna

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Slim Chance in a Fat World: Behavioral Control on Obesity by Richard B. Stuart, Barbara Davis; ISBN: 0878220607; http://www.amazon.com/exec/obidos/ASIN/0878220607/icongroupinterna

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Slim Down : Fighting Childhood Obesity with Healthy Habits by Pierpaolo R. Palmieri (2000); ISBN: 1581127448; http://www.amazon.com/exec/obidos/ASIN/1581127448/icongroupinterna

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So You Think You're Fat?: All About Obesity, Anorexia Nervosa, Bulimia Nervosa, and Other Eating Disorders by Alvin Silverstein (Contributor), et al; ISBN: 0060216425; http://www.amazon.com/exec/obidos/ASIN/0060216425/icongroupinterna

Books 413

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Social Aspects of Obesity (Culture and Ecology of Food and Nutrition) by I. De Garine (Editor), et al (1995); ISBN: 2884491856; http://www.amazon.com/exec/obidos/ASIN/2884491856/icongroupinterna

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Surgery for Morbid Obesity by John H. Linner (Editor); ISBN: 0387908889; http://www.amazon.com/exec/obidos/ASIN/0387908889/icongroupinterna

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Surgical Treatment of Obesity by Edward Eaton Mason; ISBN: 0721661416; http://www.amazon.com/exec/obidos/ASIN/0721661416/icongroupinterna

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Tackling Obesity in England; ISBN: 0102814015; http://www.amazon.com/exec/obidos/ASIN/0102814015/icongroupinterna

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The 2002 Official Patient's Sourcebook on Obesity by Icon Health Publications, et al (2002); ISBN: 0597831823; http://www.amazon.com/exec/obidos/ASIN/0597831823/icongroupinterna

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The 21st Century Complete Medical Guide to Obesity and Weight Control, Dieting, Nutrition, Fat, Meal Plans and Activities: Authoritative Federal Government Documents, Clinical References, and Practical Information for Patients and Physicians by PM Medical Health News; ISBN: 1931828180; http://www.amazon.com/exec/obidos/ASIN/1931828180/icongroupinterna

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The 3-Week Family Fat Cure: The Revolutionary Family Fit Program That Breaks the Cycle of Obesity for Good by John Mayer, John E. Mayer (2003); ISBN: 1931412022; http://www.amazon.com/exec/obidos/ASIN/1931412022/icongroupinterna

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The Addictive Behaviors: Treatment of Alcoholism, Drug Abuse, Smoking, and Obesity by William R. Miller (Editor); ISBN: 0080308376; http://www.amazon.com/exec/obidos/ASIN/0080308376/icongroupinterna

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The Black Health Library Guide to Obesity (The Black Health Library) by Mavis Thompson, et al; ISBN: 0805022872; http://www.amazon.com/exec/obidos/ASIN/0805022872/icongroupinterna

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The Encyclopedia of Obesity and Eating Disorders by Dana K. Cassell, Felix E. F. Larocca (Contributor) (1994); ISBN: 0816019851; http://www.amazon.com/exec/obidos/ASIN/0816019851/icongroupinterna

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The End of Obesity by Samuel N. Grief, et al (1998); ISBN: 0966056302; http://www.amazon.com/exec/obidos/ASIN/0966056302/icongroupinterna

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The Food Allergy Cure: A New Solution to Food Cravings, Obesity, Depression, Headaches, Arthritis and Fatigue by Ellen Dr Cutler, Ellen W. Cutler (2003); ISBN: 0609809008; http://www.amazon.com/exec/obidos/ASIN/0609809008/icongroupinterna

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The Genetics of Obesity by Claude Bouchard (Editor), et al; ISBN: 0849348803; http://www.amazon.com/exec/obidos/ASIN/0849348803/icongroupinterna

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The Heart and Lung in Obesity by Martin A. Alpert (Editor), James K. Alexander (Editor) (1998); ISBN: 0879936851; http://www.amazon.com/exec/obidos/ASIN/0879936851/icongroupinterna

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The Management of Eating Disorders and Obesity by David J. Goldstein (Editor); ISBN: 0896034070; http://www.amazon.com/exec/obidos/ASIN/0896034070/icongroupinterna

414 Obesity

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The Management of Obesity and Related Disorders by Peter G. Kopelman (Editor); ISBN: 1853179140; http://www.amazon.com/exec/obidos/ASIN/1853179140/icongroupinterna

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The Metabolic Syndrome X: Convergence of Insulin Resistance, Glucose Intolerance, Hypertension, Obesity, and Dyslipidemias-Searching for the Underlying Defeats (Annals of the New York Academy of Sciences (Cloth), Vol 892) by Barbara Caleen Hansen (Editor), et al; ISBN: 157331207X; http://www.amazon.com/exec/obidos/ASIN/157331207X/icongroupinterna

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The Modern Nutritional Diseases: And How to Prevent Them: Heart Disease, Stroke, Type-2 Diabetes, Obesity, Cancer by Fred Ottoboni, et al (2002); ISBN: 091524103X; http://www.amazon.com/exec/obidos/ASIN/091524103X/icongroupinterna

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The owl was a baker's daughter : obesity, anorexia nervosa and the repressed feminine : a psychological study by Marion Woodman (Author); ISBN: B00005WJW0; http://www.amazon.com/exec/obidos/ASIN/B00005WJW0/icongroupinterna

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The Pain of Obesity by Albert J. Stunkard; ISBN: 0915950464; http://www.amazon.com/exec/obidos/ASIN/0915950464/icongroupinterna

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The Pain of Obesity (1980); ISBN: 0915950057; http://www.amazon.com/exec/obidos/ASIN/0915950057/icongroupinterna

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The Psychology of Obesity: Dynamics and Treatment by Norman Kiell; ISBN: 0398026858; http://www.amazon.com/exec/obidos/ASIN/0398026858/icongroupinterna

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The punishment cure : how aversion therapy is being used to eliminate smoking, drinking, obesity, homosexuality... and practically anything else by Stephen J. Sansweet; ISBN: 0884051188; http://www.amazon.com/exec/obidos/ASIN/0884051188/icongroupinterna

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The Use of Very Low Calorie Diets in Obesity: Report of the Working Group on Very Low Calorie Diets, Committee on Medical Aspects of Food Policy (Report on Health and Social Subjects) by H. Keen; ISBN: 0113211236; http://www.amazon.com/exec/obidos/ASIN/0113211236/icongroupinterna

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Therapeutic approaches to the treatment of obesity by Cynthia Marie Arbeeny; ISBN: 1579360629; http://www.amazon.com/exec/obidos/ASIN/1579360629/icongroupinterna

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Treating Childhood and Adolescent Obesity by William G. Johnson, et al (1987); ISBN: 0080324134; http://www.amazon.com/exec/obidos/ASIN/0080324134/icongroupinterna

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Treating Eating Disorders: Obesity, Anorexia Nervosa, and Bulimia by Gloria Rakita Leon; ISBN: 0866160264; http://www.amazon.com/exec/obidos/ASIN/0866160264/icongroupinterna

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Underage and Overweight: America's Childhood Obesity Epidemic--What Every Parent Needs to Know by Frances M. Berg, Andrew Flach; ISBN: 1578261201; http://www.amazon.com/exec/obidos/ASIN/1578261201/icongroupinterna

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Understanding Anorexia Nervosa and Obesity: A Sense of Proportion by Peter Dally, Joan Gomez (Editor); ISBN: 0571154735; http://www.amazon.com/exec/obidos/ASIN/0571154735/icongroupinterna

Books 415

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Understanding Childhood Obesity (Understanding Health and Sickness Series) by J. Clinton Smith (1999); ISBN: 1578061342; http://www.amazon.com/exec/obidos/ASIN/1578061342/icongroupinterna

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Understanding Eating Disorders: Anorexia Nervosa, Bulimia Nervosa and Obesity by Leeann Alexander-Mott, et al (1994); ISBN: 1560322942; http://www.amazon.com/exec/obidos/ASIN/1560322942/icongroupinterna

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Understanding Obesity: The Five Medical Causes (Your Personal Health) by Lance, Dr. Levy; ISBN: 1552094790; http://www.amazon.com/exec/obidos/ASIN/1552094790/icongroupinterna

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Weight Loss Surgery : Understanding & Overcoming Morbid Obesity - Life Before, During & After Surgery by Michelle Boasten; ISBN: 1931033013; http://www.amazon.com/exec/obidos/ASIN/1931033013/icongroupinterna

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When food is a four-letter word : programs for recovery from anorexia, bulimia, bulimarexia, obesity, and other appetite disorders by Paul Haskew; ISBN: 0139561110; http://www.amazon.com/exec/obidos/ASIN/0139561110/icongroupinterna

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World Data Book of Obesity: Published in Conjunction With the 6th International Congress on Obesity, Kobe, Japan, 21-26 October 1990 (International) by Shigeaki Baba, Paul Zimmet (Editor); ISBN: 0444814337; http://www.amazon.com/exec/obidos/ASIN/0444814337/icongroupinterna

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Zinc and Eating Disorders: Discover the Fascinating Role of a Mineral Nutrient in Anorexia Nervosa Bulimia Obesity and Pica by Alexander Schauss, Carolyn Costin (Contributor); ISBN: 0879835079; http://www.amazon.com/exec/obidos/ASIN/0879835079/icongroupinterna

The National Library of Medicine Book Index The National Library of Medicine at the National Institutes of Health has a massive database of books published on healthcare and biomedicine. Go to the following Internet site, http://locatorplus.gov/, and then select “Search LOCATORplus.” Once you are in the search area, simply type “obesity” (or synonyms) into the search box, and select “books only.” From there, results can be sorted by publication date, author, or relevance. The following was recently catalogued by the National Library of Medicine:11 •

Anorexia and obesity. Edited by Christopher V. Rowland, Jr. Author: Rowland, Christopher V.,; Year: 1967; Boston, Little, Brown [c1970]; ISBN: 700001654

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Aspects of steroid metabolism in obese subjects under various nutritional conditions. Author: Hendrikx, Achiel.; Year: 1966; Brussel, Arscia, 1968

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Obesity and disease. Author: Office of Health Economics (London, England); Year: 1966; London [1969]

11

In addition to LOCATORPlus, in collaboration with authors and publishers, the National Center for Biotechnology Information (NCBI) is currently adapting biomedical books for the Web. The books may be accessed in two ways: (1) by searching directly using any search term or phrase (in the same way as the bibliographic database PubMed), or (2) by following the links to PubMed abstracts. Each PubMed abstract has a "Books" button that displays a facsimile of the abstract in which some phrases are hypertext links. These phrases are also found in the books available at NCBI. Click on hyperlinked results in the list of books in which the phrase is found. Currently, the majority of the links are between the books and PubMed. In the future, more links will be created between the books and other types of information, such as gene and protein sequences and macromolecular structures. See http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Books.

416 Obesity

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Obesity and health; a source book of current information for professional health personnel. Author: United States. Public Health Service. Division of Chronic Diseases.; Year: 1960; Washington [1966]

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Obesity, by M. N. Yegorov and L. M. Levitskiy. Author: Egorov, M. N. (Mikhail Nikolaevich); Year: 1963; Washington, U. S. Office of Technical Services, Joint Publications Research Service, 1964

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Obesity: medical and scientific aspects. Proceedings of the first symposium of the Obesity Association of Great Britain. Edited... by I. McLean Baird & Alan N. Howard. Author: Baird, I. McLean.; Year: 1968; Edinburgh, Livingstone, 1969; ISBN: 443006520

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Overweight; causes, cost, and control. Author: Mayer, Jean,; Year: 1965; Englewood Cliffs, N. J., Prentice-Hall [1968]

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Secrets of an obesity specialist. Author: Theberge, Lawrence L.; Year: 1963; New York, Vantage Press [c1966]

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Serum cholesterol, parental longevity, overweight, and hypertension in the old; a factorial study by Anni Seppänen [et al.]. Author: Seppänen, Anni.; Year: 1966; Helsinki, 1963

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Symposium on the prevention of obesity, sponsored by the American Heart Association held at the New York Academy of Medicine, May 26, 1959. Presiding: Herbert Pollack. Ed. by Robert L. Craig. Author: American Heart Association.; Year: 1965; [New York, 1960]

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The overweight society; an authoritative entertaining investigation into the facts and follies of girth control. Author: Wyden, Peter.; Year: 1965; New York, Morrow, 1965

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Treatment of obesity; guest editor: Charles H. Hollenberg. Treatment of burns; guest editor: Charles L. Fox. Author: Hollenberg, Charles H.,; Year: 1966; [New York] Hoeber, 1967

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Your overweight child, by Milton I. Levine and Jean H. Seligmann. Author: Levine, Milton I. (Milton Isra),; Year: 1965; New York, World Pub. Co. [c1970]

Chapters on Obesity In order to find chapters that specifically relate to obesity, an excellent source of abstracts is the Combined Health Information Database. You will need to limit your search to book chapters and obesity using the “Detailed Search” option. Go to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find book chapters, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Book Chapter.” Type “obesity” (or synonyms) into the “For these words:” box. The following is a typical result when searching for book chapters on obesity: •

Obesity and the Professional Voice User Source: in Sataloff, R.T., ed. Professional Voice: The Science and Art of Clinical Care. 2nd ed. San Diego, CA: Singular Publishing Group, Inc. 1997. p. 335-336. Contact: Available from Singular Publishing Group, Inc. 401 West 'A' Street, Suite 325, San Diego, CA 92101-7904. (800) 521-8545 or (619) 238-6777. Fax (800) 774-8398 or (619) 238-6789. E-mail: [email protected]. Website: www.singpub.com. PRICE: $325.00 plus shipping and handling. ISBN: 1565937287.

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Summary: This short chapter on obesity and the professional voice user is from a book on the clinical care of the professional voice. Today, most people involved in voice education and singing recognize that singing is athletic. As such, it requires good abdominal and respiratory conditioning, physical strength, and endurance. All of these are undermined by significant obesity. The authors list the adverse effects of obesity on health and longevity and stress that the best treatment for obesity is avoidance of the problem. Early in training, singers should learn the importance of good physical and aerobic conditioning. This is important to the singer's general health, vocal health, and art. In the overweight singer, weight should be lost slowly through modification of eating and lifestyle habits. Rapid loss of weight causes fluid shifts that may result in changes in vocal quality and endurance. In training, singers should be encouraged to treat their entire bodies with the same reverence with which they regard their vocal cords. 1 table. 1 reference. •

Creating Social and Public Health Environments to Sustain Behavior Change: Lessons From Obesity Research Source: in Integrating Behavioral and Social Sciences With Public Health. Schneiderman, N. Speers, M.A. Silva, J.M. Tomes, H. Gentry, J.H. eds. Washington, DC, American Psychological Association, pp. 31-50, 2001. Contact: American Psychological Association, 750 First Street, NE., Washington, DC 20002. Summary: Creating Social and Public Health Environments to Sustain Behavior Change: Lessons From Obesity Research, a chapter in Integrating Behavioral and Social Sciences With Public Health, uses obesity as an example to highlight how individual risk factors are influenced by multiple levels of intervention. The authors suggest that the success of previous efforts to address obesity has been limited by too much focus on individual behavioral and psychological levels, looking at eating patterns and psychological factors related to habits and appetite. The paper reviews the influence of these, and biological, social, and environmental levels, suggesting that to be effective, interventions related to obesity require a transdisciplinary, multilevel perspective that takes into account (1) biological factors, such as genetic susceptibilities; (2) psychological factors, such as negative affect; (3) social factors, such as familial and group norms; and (4) environmental factors, such as availability of healthy food alternatives.

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What Can Be Done to Prevent Childhood Obesity? Source: in Understanding Childhood Obesity. Smith, J.C. Jackson, MS, University Press of Mississippi, pp. 81-98, 1999. Contact: University Press of Mississippi, 3825 Ridgewood Road, Jackson, MS 392116492. (800) 737-7788; (601) 432-6246; (601) 432-6205. FAX: (601) 432-6217. INTERNET/EMAIL: http://www.upress.state.ms.us. Summary: What Can Be Done to Prevent Childhood Obesity?, a chapter in Understanding Childhood Obesity, discusses efforts to prevent childhood obesity. National surveys have shown that estimated total energy intakes of children age 1 to 19 years remained almost constant between 1970 and 1991, and only since 1991 has total energy actually increased. However, obesity has increased among this population during that time. One possible explanation for this is that total fat consumption during this time probably exceeded 30 percent of total energy intake. In recent years, children have eaten more fat-containing snacks and fast food meals than in the 1960's. This trend will likely continue with 75 percent of American women working outside of the home.

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In addition, food manufacturers will continue to make the high-fat foods that the American population craves. The hope for obesity prevention is that as more Americans get the message that eating excessive amounts of food, especially fatty foods, can result in obesity, people's buying habits will be less responsive to advertising of high-fat highcalorie foods. Another factor in the increase in obesity among American children is that they decrease their physical activity as they get older, and physical education enrollment has decreased from 42 percent in 1991 to 25 percent in 1995. Schools are the likely place to undertake obesity prevention, but schools have competing requirements that make this difficult. The federal government has made and will continue to make tremendous contributions to the health of the nation. Parents have an important role to play in helping children assume responsibility for their own healthy nutrition choices and physical activity by teaching them to link nutrition to their physical functioning and well-being. Certain subgroups tend to be heavier than others, but if preventive interventions are to be carried out among particular groups of people at high risk for obesity, close attention must be paid to the cultural and social characteristics of those groups. •

Obesity, Hypertension, and the Heart Source: in Heart and Lung in Obesity. Alpert, M.A. Alexander, J.K. eds. Armonk, NY, Futura Publishing, pp. 95-108, 1998. Contact: Futura Publishing Company, Inc., 135 Bedford Road, P.O. Box 418, Armonk, NY 10504-0418. INTERNET/EMAIL: www.futuraco.com. Summary: Obesity, Hypertension, and the Heart, a chapter in Heart and Lung in Obesity, considers links between obesity and underlying mechanism abnormalities. Topics include (1) epidemiology and heredity; (2) mechanisms in obesity-hypertension, insulin resistance, and hyperinsulinemia; (3) the renin-angiotensin-aldosterone system; (4) sodium, sympathetic activity, and Na-K-ATPase activity; (5) plasma, total blood volume, and systemic hemodynamics; and (6) the effect of obesity-hypertension on the heart. Epidemiological studies have indicated a direct link between obesity and hypertension, particularly between upper body obesity and hypertension. Central adiposity is an important risk factor for death from coronary heart disease. The development of obesity-hypertension has been associated with endocrine, adrenergic, and metabolic mechanisms including insulin resistance; hyperinsulinemia; increases in adrenergic activity; and increases in aldosterone levels. These mechanisms induce sodium and water retention and hypervolemia. Such changes affect the hemodynamic characteristics of obese-hypertensive patients, including absolute total blood volume, with higher redistribution to the cardiopulmonary volume, which enhances venous return. Also affected are cardiac output stroke volume and left ventricular (LV) wall thickness, with peripheral resistance that is not appropriate given increased cardiac output. All these changes in hemodynamics enhance the preload to the LV, inducing eccentric LV hypertrophy. Hypertension increases the afterload which induces concentric LV hypertrophy. It is the coexistence of obesity and hypertension that induces eccentric-concentric LV hypertrophy, increasing the risk of congestive heart failure.

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Obesity and Coronary Heart Disease Source: in Heart and Lung in Obesity. Alpert, M.A. Alexander, J.K. eds. Armonk, NY, Futura publishing, pp. 213-238, 1998.

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Contact: Futura Publishing Company, Inc., 135 Bedford Road, P.O. Box 418, Armonk, NY 10504-0418. INTERNET/EMAIL: www.futuraco.com. Summary: Obesity and Coronary Heart Disease, a chapter in Heart and Lung in Obesity, reviews epidemiological studies concerning the relationship between obesity and coronary heart disease (CHD) mortality and morbidity. Estimates indicate that one-third of the adult population and one-quarter of children and adolescents in the United States are overweight. Study results have been complicated by imprecise measures of fatness, small cohort size, short-term followup, not controlling for smoking, preexisting disease, and inappropriate control for intermediate risk factors. A major problem is trying to relate a single entity, conditioned by complex interaction of factors, to a complex set of interactions conditioning CHD mortality and morbidity. Large cohort population studies or those with longer followup reveal a predictive power for CHD mortality with maintenance body mass indices of more than 30 kilograms per square meter for men and greater than 27 kilograms per square meter for women; this is less apparent in older persons. Autopsy studies generally do not indicate a correlation between obesity indices and extent and degree of coronary atheromatous disease. Cross-sectional anatomic studies offer no support for an independent effect of excess total fat mass on the development or progression of the atheromatous process. Considerable proof does exist for an association between excess abdominal visceral fat and increased CHD mortality and morbidity. Established CHD risk factors seen more frequently in obese subjects include dyslipidemia, diabetes, hypertension, and hyperuricemia. Evidence indicates that the effects of excess total and abdominal fat in relation to CHD are mediated through enhanced atherogenic factors. Sustained weight loss in obese subjects has been associated with significant reductions in plasma triglyceride levels, elevations in high density lipoprotein levels, augmented low density lipoprotein size, enhanced glucose oxidation, lower fasting insulin levels, and increased insulin sensitivity, as well as lowered blood pressure. Although the impact of weight loss in obese subjects on CHD risk factors is unclear with respect to mortality and morbidity, evidence does suggest a beneficial effect in those with pre-existing CHD. •

Prevention of Pediatric Obesity: Examining the Issues and Forecasting Research Directions Source: in Preventive Nutrition: The Comprehensive Guide for Health Professionals. Bendich, A. Deckelbaum, R.J. eds. Totowa, NJ, Humana Press, pp. 471-486, 1997. Contact: Humana Press Inc., 999 Riverview Drive, Suite 208, Totowa, NJ 07512. (201) 256-1699. FAX: (201) 256-8241. INTERNET/EMAIL: [email protected]. Summary: Prevention of Pediatric Obesity: Examining the Issues and Forecasting Research Directions, a chapter in Preventive Nutrition: The Comprehensive Guide for Health Professionals, examines issues in the prevention of childhood obesity. The chapter is divided into four sections. The first section discusses why the prevention of childhood obesity is a high priority. The second section reviews causal mechanisms of childhood obesity considering the role of genetic and environmental factors as well as their implications for the design and implementation of prevention programs. In the third section, existing programs for the prevention of childhood obesity and their clinical efficacy are reviewed. Finally, more fundamental theoretical issues for future prevention research with children and adolescents are examined. Interest has grown in prevention due to the mounting number of studies documenting the health risks of pediatric obesity, including elevated blood pressure, glucose intolerance, hyperinsulinemia, and dyslipidemias. Approaches to prevention include targeting, philosophy, punitiveness, and timing. The target audience can be either broad or aimed

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more specifically at those deemed to be at risk. Philosophically, prevention strategies can be directed at changing the child or changing the environment. Children can be taught to avoid overeating, to select low-fat foods, and to devote more time to exercise. Environmental manipulations include the taxation of fattening foods, installing signs in public settings to promote activity over sedentary behaviors, prompts in super markets to guide food selection, and providing additional campaigns designed to heighten awareness. Four recommendations are offered for the prevention and treatment of pediatric obesity: (1) Increase and sustain the child's overall activity level, (2) involve the parents in treatment, (3) change the environment surrounding the child, and (4) consult a health professional when considering more substantial dietary modification. •

Obesity Epidemic: Nutrition Policy and Public Health Imperatives Source: in Nutrition Policy in Public Health. Bronner, F. ed. New York, NY, Springer Publishing Company, Inc., pp. 138-156, 1997. Contact: Springer Publishing Company, Inc., 536 Broadway, New York, NY 10012-3955. Summary: Obesity Epidemic: Nutrition Policy and Public Health Imperatives, a chapter in Nutrition Policy in Public Health, addresses the key issues related to obesity, and provides public policy recommendations and health-promoting activities for the nutrition officer in a public health setting. Obesity is linked to heart disease, adult-onset diabetes, hypertension, atherosclerosis, stroke, and certain types of cancer. The estimated costs associated with obesity-related diseases represent a major drain on the United States economy. Factors related to obesity include (1) female gender; (2) black, Hispanic, Pacific Islander, and Native American ethnicity; and (3) low income and socioeconomic status. Factors to consider when choosing a weight-loss strategy include (1) inclusion of physical activity, portion control, and a weight-maintenance strategy; (2) basis on the Dietary Guidelines or the Food Guide Pyramid; (3) focus on slow, steady weight loss; and (4) focus on psychological, social, and environmental factors that may impede commitment. Public policy recommendations include (1) making public education about the prevention and treatment of obesity a national priority; (2) creating new economic and workplace incentives for weight-reduction efforts; (3) generating public support for increased funding and availability of school and community-based physical activity and nutrition programs; (4) mobilizing the nation's physicians and other health care workers to fight obesity; (5) putting development and approval of drugs to treat obesity on a fast track; and (6) expanding research efforts into the prevention, causes, and treatment of obesity. The authors urge nutrition officers in public health settings to (1) promote nutrition and physical activity programs for adults and children; (2) include healthy food at school and community functions; (3) encourage employment of teachers trained in physical education, health education, and nutrition; (4) teach parents not to use food as a tool to reward or punish; and (5) encourage school officials and parents to provide input to school food service programs.

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Obesity and Evaluation of Weight Control Programs Source: in Nutritional Concerns of Women. Wolinski, I. Klimis-Tavantzis, D; eds. Boca Raton, FL, CRC Press, pp. 89-109, 1996. Contact: CRC Press LLC, 2000 Corporate Blvd., NW., Boca Raton, FL 33431. Summary: Obesity and Evaluation of Weight Control Programs, a chapter in Nutritional Concerns of Women, notes that obesity is one of the most important nutrition-related diseases in the United States. A more aggressive policy is needed to inform the public and health care providers about the nature of obesity, the difficulties inherent in treating

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this disease and achieving permanent weight management, and the need for susceptible individuals to take steps to prevent its occurrence or minimize its development. One of the more common techniques for assessing overweight is to use the body mass index (BMI). The health risks associated with obesity are related to the amount of body fat and its distribution. Increased BMI is associated with increased risk for certain diseases such as diabetes and hypertension. Body fat distribution is crudely assessed by several measures. Computed tomography scanning, magnetic resonance imaging, and ultrasound are more precise and are strong predictors of health risk. Health risks are increased in women with abdominal obesity. There are also economic, social, and psychological consequences of being obese. Overweight women completed fewer years of schooling, were less likely to be married, and had lower household incomes. The vast majority of weight control programs available use one or more of the following approaches: diet, physical activity, behavior modification, drug therapy, and gastric surgery. There are do it yourself programs as well as nonclinical and clinical approaches. The New York City Department of Consumer Affairs issued a Truth-in Dieting regulation in 1992, as a result of an investigation of deceptive practices used by rapid-weight-loss centers. In 1990 a task force of the Michigan Department of Public Health developed guidelines for the conduct of adult weight loss programs in that state. They are quite detailed and apply to both nonclinical and clinical programs, calling for providers to screen prospective clients and assess their level of health risk and recommend appropriate action. Guidelines for evaluating weight loss methods and programs were developed by the National Institutes of Health as a result of a Technology Assessment Conference on methods of voluntary weight loss and control. The Federal Trade Commission efforts in regard to the weight loss industry address one specific challenge, allegedly deceptive advertising claims that companies have made to promote their programs and diet aids. The Food and Drug Administration is the government agency responsible for approving drugs for use in the United States. Few antiobesity drugs are available to physicians, and no new drugs have been approved to treat obesity since 1973. Current standards for antiobesity drugs appear unreasonable, given the growing acceptance of obesity as a chronic degenerative disease that contributes substantially to the burden of disease and death in the United States. In December of 1994, the Institute of Medicine released a report that proposed criteria for evaluating weight control programs in a consistent and comprehensive manner. The report emphasizes that weight management requires a lifelong plan, with the individual at the center of decision making about how to proceed. Unfortunately, the lay public, health care providers, and regulatory agencies often view obesity as a problem of willful misconduct, eating too much and exercising too little. 3 figures, 3 tables, 56 references. •

Childhood Obesity Source: in Child Health, Nutrition, and Physical Activity. Cheung, L. Richmond, J.B. eds. Champaign, IL, Human Kinetics, pp. 155-169, 1995. Contact: Human Kinetics, P.O. Box 5076, Champaign, IL 61825-5076. (800)747-4457. INTERNET/EMAIL: http:/www.humankinetics.com; [email protected]. Summary: Childhood Obesity, a chapter in Child Health, Nutrition, and Physical Activity, reviews the prevalence, causes, and consequences of childhood obesity. The chapter emphasizes (1) the factors that identify children at risk for the development of obesity and (2) the particular behaviors that may serve as a logical focus for programs directed at prevention of obesity or treatment of established disease. Most variables that affect the prevalence of childhood obesity can be found within the family. The link between parental obesity and obesity in offspring may be attributable to a shared

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environment as well as a shared genetic inheritance. Among the most important consequences of the awareness of childhood obesity is the preoccupation with fatness among preadolescent and adolescent girls. The major consequences of obesity in children include (1) growth changes, (2) psychosocial consequences, (3) orthopedic problems, (4) respiratory difficulties, (5) abnormal glucose metabolism, (6) hypertension, (7) hyperlipidemia, and (8) persistence of obesity into adulthood. The first step in the prevention of obesity is the identification of high-risk cohorts. Steps to maintain an appropriate weight from early childhood on should be the focus of counseling by pediatricians. Preventive counseling should also focus on behaviors that will increase energy expenditure. The dietary guidelines for Americans should offer several directives for promoting dietary practices that will prevent or decrease the prevalence of obesity. The process of maintaining ideal weight should begin in early childhood. The dietary guidelines state that Americans should (1) eat a variety of foods; (2) maintain a healthy weight; (3) choose a lowfat, low saturated fat, low cholesterol diet; (4) increase consumption of vegetables, fruits, and grains; and (5) consume sugar, sodium, and alcohol only in moderation. Three major difficulties confront health care providers who attempt to treat childhood obesity: (1) Limited reimbursement for therapeutic interventions; (2) differences in the way patients, families, and providers perceive the problem; and (3) the need to develop skills for altering eating and activity behaviors. •

School-based Interventions for Childhood Obesity Source: in Child Health, Nutrition, and Physical Activity. Cheung, L. Richmond, J.B. eds. Champaign, IL, Human Kinetics, pp. 179-203, 1995. Contact: Human Kinetics, P.O. Box 5076, Champaign, IL 61825-5076. (800) 747-4457. INTERNET/EMAIL: http:/www.humankinetics.com; [email protected]. Summary: School-Based Interventions for Childhood Obesity, a chapter in Child Health, Nutrition, and Physical Activity, considers the rationale for school-based treatments and interventions. An estimated 95 percent of all children in the United States aged 5 through 18 years are enrolled in school. Opportunities for school-based obesity interventions can be found on many levels and categorized into two types: (1) Secondary prevention interventions that target high-risk children who are already overweight or obese, and (2) primary prevention interventions that reduce the risk factor distribution in entire populations by changing eating and physical activity behaviors in all students. The authors reviewed 11 school-based treatment studies for obese children and adolescents. The studies included 508 children and 443 adolescents. Treatment lengths ranged from 9 weeks to 6 months, with session frequencies ranging from 1 a week to 5 times a week to 2 times daily. Interventions included modified physical education, diet and nutrition education, modified lunch, and parental involvement. The results of treatment of obesity in childhood were promising, while the results obtained among adolescents were much less encouraging. Overall, the studies support the use of multi-component obesity treatments in a school setting. A review was also made of 11 school-based obesity prevention interventions for children and adolescents. Intervention components included physical activity education, modified physical education, diet and nutrition education, modified school lunch, parental involvement, and behavior modification. Despite the effectiveness of the school-based programs for reducing some health risk factors, they were generally ineffective for body fat and body mass.

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Weight-Loss Treatments for Overweight Individuals with Type 2 Diabetes Source: in Franz, M.J. and Bantle, J.P., eds. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes. Alexandria, VA: American Diabetes Association. 1999. p. 69-82. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $39.95 for members; $49.95 for nonmembers; plus shipping and handling. ISBN: 158040006X. Order number 561601. Summary: This chapter focuses on weight loss treatments for overweight people who have diabetes. Most people with type 2 diabetes are overweight, and this aggravates insulin resistance and impairs glucose disposal. Long term weight loss is difficult because energy intake, energy balance, and therefore body weight are controlled by the central nervous system. Available evidence suggests that obesity is caused by a defect in the hypothalamic control center or its biochemical signals, caloric intake in excess of that for which the control center can compensate, or some combination of these factors. Although standard weight reduction diets that restrict caloric intake are usually not effective, some people may achieve long term weight loss with them. Very low calorie diets (VLCDs) which provide 800 or fewer calories daily can produce substantial weight loss and rapid improvements in glycemia and lipemia in patients with type 2 diabetes; however, most people who follow VLCDs are not able to maintain long term weight loss. Although gastric reduction surgery is the most effective weight loss treatment for obese people with type 2 diabetes, data defining the benefits and risks are lacking. Studies have shown that fenfluramine and phentermine produce significant weight loss, but fenfluramine and dexfenfluramine have been withdrawn from the U.S. market. Phentermine continues to be available, but as a single agent it appears to have limited efficacy. Other available pharmacologic weight loss agents include sibutramine and orlistat. Although available data suggest that weight loss drugs are an important approach to the treatment of overweight patients with type 2 diabetes, they also suggest that the drugs work only as long as they are taken. In addition, limited data on the efficacy and safety of phentermine, sibutramine, and orlistat are available. 1 figure. 4 tables. 47 references.

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Nutrition and Overweight Source: in Healthy People 2010 (Conference Edition), Volume II. U.S. Department of Health and Human Services, Washington, DC, pp. 19-1-19-52, January 2000. Contact: U.S. Government Printing Office, Superintendent of Documents, P.O. Box 371954, Pittsburgh, PA 15250-7954. (202) 512-1800. Stock No. 017-001-00547-9. INTERNET/EMAIL: www.health.gov/healthypeople. Summary: Nutrition and Overweight, a chapter in Healthy People 2010 (Conference Edition), notes that the goal is to promote health and reduce chronic disease associated with diet and weight. Many dietary components are involved in the relationship between nutrition and health. A primary concern is consuming too much saturated fat and too few vegetables, fruits, and grain products that are high in complex carbohydrates, dietary fiber, vitamins and minerals, and other substances conducive to health. Specific objectives are to (1) increase the proportion of adults who are at a healthy weight; (2) reduce the proportion of adults who are obese; (3) reduce the proportion of children and adolescents who are overweight or obese; (4) reduce the growth retardation among low-income children under age 5 years; (5) increase the proportion of persons age 21 and older who consume at least two daily servings of fruit;

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(6) increase the proportion of persons age 2 years and older who consume at least three daily servings of vegetables with at least one third being dark green or deep yellow vegetables; (7) increase the proportion of persons age 2 years and older who consume at last six daily servings of grain products with at least three being whole grains; (8) increase the proportion of persons age 2 years and older who consume less than 10 percent of calories from saturated fat; (9) increase the proportion of persons age 2 years and older who consume no more than 30 percent of calories from fat; (10) increase the proportion of persons age 2 years and older who consume 2,400 milligrams or less of sodium daily; (11) increase the proportion of persons age 2 years and older who meet dietary recommendations for calcium; (12) reduce iron deficiency among young children and females of childbearing age; (13) reduce anemia among low-income pregnant females in their third trimester; (14) reduce iron deficiency among pregnant females; (15) increase the proportion of children and adolescents age 6 to 19 years whose intake of meals and snacks at school contributes proportionally to good overall dietary equality; (16) increase the proportion of worksites that offer nutrition or weight management classes or counseling; (17) increase the proportion of physician office visits made by patients with a diagnosis of cardiovascular disease, diabetes, or hyperlipidemia that include counseling or education related to diet and nutrition; and (18) increase food security among households in the United States and in so doing reduce hunger. •

Target Population for Diabetes Prevention: The Metabolically Obese, Normal-Weight Individual Source: in Devlin, J.T. and Schneider, S.H., eds. Handbook of Exercise in Diabetes. Alexandria, VA: American Diabetes Association. 2002. p. 235-249. Contact: Available from American Diabetes Association (ADA). Order Fulfillment Department, P.O. Box 930850, Atlanta, GA 31193-0850. (800) 232-6733. Fax (770) 4429742. Website: www.diabetes.org. PRICE: $69.95 plus shipping and handling. ISBN: 1580400191. Summary: Epidemiological evidence suggests that regular physical activity may prevent, or at least retard, the development of type 2 diabetes and coronary heart disease. This benefit of exercise is likely to be most prominent in individuals predisposed to the insulin resistance syndrome. Individuals with insulin resistance often have generalized obesity; however, they also may not be obese or even overweight by present standards. The latter have been referred to as metabolically obese, normalweight (MONW) individuals. This chapter is from a book that provides a practical, comprehensive guide to diabetes and exercise for health care professionals involved in patient care. In this chapter, the author considers the MONW group as a target population for diabetes prevention. Exercise may be therapeutically more efficacious in MONW individuals than in patients with established type 2 diabetes and overt obesity. People at risk for type 2 diabetes and the insulin resistance syndrome, including MONW individuals, may be identified early by such factors as family history, birth weight, and the presence of gestational diabetes (a type of diabetes that occurs during pregnancy), polycystic ovarian syndrome, and central adiposity (the tendency to add fat in the middle of the body). Whether lifestyle modification programs of diet and exercise should be targeted specifically at these high risk individuals or aimed at the general population is a major public health issue. 2 figures. 6 tables. 37 references.

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Attaining Nutrition Goals for Hyperlipidemic and Obese Renal Patients Source: in American Dietetic Association. Clinical Guide to Nutrition Care in End-Stage Renal Disease. Chicago, IL: American Dietetic Association. 1994. p. 171-176.

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Contact: Available from American Dietetic Association. 216 West Jackson Boulevard Chicago, IL 60606-6995. (312) 899-0040. PRICE: $24 for members; $28 for non-members; plus shipping and handling. ISBN: 0880911247. Summary: This chapter, from a manual that provides guidelines for the clinical nutrition care of patients with end-stage renal disease (ESRD), discusses attaining nutrition goals for hyperlipidemic and obese renal patients. Topics include hyperlipidemia in renal disease; predialysis and hemodialysis patients; patients utilizing continuous ambulatory peritoneal dialysis (CAPD); and considerations for patients following kidney transplantation. The author stresses that since atherosclerotic plaque develops over many years, risk factors for atherogenesis should be modified early in the course of chronic renal failure (CRF); the cornerstone of therapy remains diet modifications. 25 references.

Directories In addition to the references and resources discussed earlier in this chapter, a number of directories relating to obesity have been published that consolidate information across various sources. The Combined Health Information Database lists the following, which you may wish to consult in your local medical library:12 •

Directory of Cardiovascular Resources for Minority Populations Source: Bethesda, MD, US Department of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute, 122 p., January 1989. Contact: US Department of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute Education Programs Information Center, 4733 Bethesda Avenue, Suite 530, Bethesda, MD 20814. (301) 9513260. Summary: The Directory of Cardiovascular Resources for Minority Populations contains detailed information on printed and audiovisual materials for cardiovascular education specifically designed for the four major minority populations of the U.S.: Blacks, Hispanics, American Indians, and Asians/Pacific Islanders. Materials were selected on the basis of suitability for public education; therefore, scholarly publications have not been included. The directory is designed for use by health professionals who provide services to minority populations but can also be used by health care providers serving the general public. The directory describes leaflets, pamphlets, booklets, books, posters, wallet cards, films, and videotapes that address high blood pressure, high blood cholesterol, and cigarette smoking, as well as other risk factors such as obesity,

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You will need to limit your search to “Directory” and “obesity” using the "Detailed Search" option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find directories, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Select your preferred language and the format option “Directory.” Type “obesity” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months.

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nutrition, and sedentary lifestyle. Each entry includes information on the language, target audience, grade level, producer, publication date, reproduction restrictions, format, content description, availability, and cost of the materials.

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CHAPTER 8. MULTIMEDIA ON OBESITY Overview In this chapter, we show you how to keep current on multimedia sources of information on obesity. We start with sources that have been summarized by federal agencies, and then show you how to find bibliographic information catalogued by the National Library of Medicine.

Video Recordings An excellent source of multimedia information on obesity is the Combined Health Information Database. You will need to limit your search to “Videorecording” and “obesity” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find video productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Videorecording (videotape, videocassette, etc.).” Type “obesity” (or synonyms) into the “For these words:” box. The following is a typical result when searching for video recordings on obesity: •

Obesity and Type II Diabetes Source: Los Angeles, CA: National Health Video, Inc. 2000. (videocassette). Contact: Available from National Health Video, Inc. 12021 Wilshire Boulevard, Suite 550, Los Angeles, CA 90025. (800) 543-6803. Fax (310) 477-8198. E-mail: [email protected]. PRICE: $89.00 plus shipping and handling. Summary: This videotape discusses the relationship between type 2 diabetes and obesity. Obesity presents special problems for people who have diabetes because excess body fat decreases the body's ability to use insulin, strains the pancreas, and makes the body less able to use the insulin it produces. Although the causes of obesity are not well understood, factors such as age, heredity, and gender have been associated with weight gain. A weight loss of just 10 to 20 pounds can improve blood glucose levels, blood pressure, and cholesterol. Methods of losing weight include eating a variety of foods in moderation, incorporating moderate activity into a daily schedule, undergoing stomach restrictive and intestinal bypass procedures (recommended only for people who are

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severely obese), using diet medications, and enrolling in a weight loss program. Other topics include the role of obesity in diseases other than diabetes and the growing problem of childhood obesity. The videotape is accompanied by a teaching resource guide and a transcript of the tape. •

Behavioral Approaches to the Treatment of Obesity and Type II Diabetes Source: Bethesda, MD: Weight-Control Information Network. 1993. (videorecording). Contact: Available from Weight-Control Information Network. 1 WIN Way, Bethesda, MD 20892-3665. (800) 946-8098 or (301) 984-7378. Fax (301) 984-7196. E-mail: [email protected]. PRICE: $5.00. Summary: This video, from a lecture series on clinical obesity, addresses behavioral approaches to the treatment of obesity and type 2 diabetes. The speaker, Rena R. Wing from the University of Pittsburgh, examines changes in behavioral approaches to obesity between the 1980s and the 1990s. In the 1980s, researchers considered antecedents and consequences of obesity and believed that a change in environment would lead to a change in behavior. In the 1990s, issues of food provision are being emphasized. Researchers are also stressing the importance of followup visits, since people enrolled in twenty week programs, for example, often gained weight after therapy ended. Studies have also shown that restricting both fat and caloric intake, as opposed to focusing on just one, has been effective in the treatment of type 2 diabetes. In addition, the combination of diet and exercise appears to be effective for long-term weight loss. People who are asked to diet and exercise, as opposed to just exercise, seem to be more successful. The speaker concludes that obesity should continue to be considered a chronic disease and treated with structured exercise programs and lowfat diets. The speaker entertains numerous questions at the end of her lecture. (AA-M).

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Visceral Obesity: More Than a Weight Problem Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: In this lecture, Dr. Despres discusses visceral obesity and its relations as an indicator for obesity complications and cardiovascular diseases (CVD). Dr. Despres reviews the results of several studies, including the Quebec Cardiovascular Study that indicates that neither the waist-to-hip ratio nor a high body mass index are dependable indicators of increased risk for CVD or other obesity complications. However, he notes that recent analyses from epidemiological studies clearly show that a high accumulation of abdominal adipose tissue is associated with an increased risk of developing CVD; this association is independent of the level of obesity. A study of 187 women and 173 men found that visceral adipose tissue, as measured by computer tomography, tends to be lower in pre-menopausal women than in men, but increases in post-menopausal women. There seems to be a progressive accumulation of visceral adipose tissue, they were found to have the same glycemic response. Abdominal obesity is associated with an excess if visceral adipose tissue accumulation, and is further associated the insulinresistant hyperinsulenemic state, low HDL-cholesterol levels, and with a higher concentration and proportion of small LDL particles, which indicate increased risk of CVD. Dr. Despres notes that the hip-to-waist ratio may not be a good indicator of increased risk of developing CVD and metabolic complications; waist circumference is a better indicator. The threshold waist circumference is 95 cm for women and 100 cm for men. Furthermore, he believes the risk associated with having a high waist

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circumference should be publicized as a risk factor for developing CVD. The lecture concludes with Dr. Despres recommendations that viscerally obese individuals should reduce fat intake to less than 30 percent calories from fat, increase activity level with regular, low-level exercise (1 hour a day, 5 or 6 days a week), increase intake of complex carbohydrates, and moderately reduce calorie intake. Failing these, a pharmacological approach should be considered. •

Severe Obesity, the New Epidemic: Surgical Update Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: In this lecture, Dr. Pories discusses how morbid obesity can be controlled through improved gastric bypass surgical procedures and how morbidly obese patients who also had insulin-treated noninsulin-dependent diabetes mellitus (NIDDM) were able to stop or greatly reduce their daily insulin dosage as a co-result of the surgery. More than 2 percent (5 million) of the U.S. population is morbidly obese, which Dr. Pories defines as being more than 100 pounds over ideal body weight, or a body mass index (BMI) of greater than 40. Dr. Pories notes that morbid obesity is a major cause of illnesses such as hypertension, diabetes, and arthritis and often is a cause of premature death. Dr. Pories recommends that morbidly obese patients with diabetes should be recommended for surgery.

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Physical Activity, Diet Composition, and Obesity Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: Dr. Hill's research involves manipulating diet composition and physical activity and observing the effect on body composition and body weight. In this lecture, Dr. Hill discusses recent research results and their implications for the prevention and treatment of obesity. Dr. Hill describes his laboratory's "whole room calorimeter," which provides a controlled environment for the accurate measure of energy intake and expenditure in human subjects. A limitation of the calorimeter is that most study subjects do not attain their usual levels of energy expenditure while confined to the room. Subjects nonetheless show wide variation in energy expenditure, from a low of 200 kcal/day to a high of 1,000kcal/day. This suggests, according to Dr. Hill, that differences in the amount of energy expended in exercise are very important in body weight regulation. More research is needed to identify why some people engage in more physical activity that others and whether some people are more efficient exercisers than others. Dr. Hill goes on to discuss studies on the effect of exercise on body composition. He notes that in short-term studies (less than 20 weeks), the effect of exercise as a treatment for obesity is modest. However, in studies where the subjects were followed up a year later, exercise was the best predictor of successful weight loss. Also discussed is a recent diet composition study conducted in Dr. Hill's laboratory. Investigators manipulated subjects' intake of fats and carbohydrates to observe the effect on body composition and energy expenditure. More than 80 percent of the excess fat consumed was stored as adipose (fat) tissue, and less than 5 percent was burned through increased energy expenditure. Excess carbohydrate was directed more into energy expenditure and less into storage; however, over time, the amount of excess carbohydrate stored as adipose tissue increased. There were striking differences between individuals' responses

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to this dietary manipulation. Dr. Hill concludes that, calorie for calorie, while dietary fat is more likely to lead to obesity than carbohydrate, some people remain susceptible to obesity even on a high-carbohydrate diet. "The idea that all obesity is due to a high-fat diet is probably naive," he says. He further concludes that a low-fat diet and increased physical activity may be an effective strategy for preventing or treating obesity in some subjects, and that more research is needed to identify subjects who will respond to this regimen. •

Human Studies on Obesity Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: In this lecture, Dr. Hirsch describes how his interest in obesity research developed from studies on the composition of human adipose (fat) tissue, which he conducted early in his career. He began offering weight loss treatment to his obese patients in return for their participation in these studies. Dr. Hirsch believed obesity was caused by overeating and inactivity, and could be successfully treated by diet and counseling. He found, however, that many patients felt worse, both physically and emotionally, after weight loss and quickly regained all the lost weight. Studies of growth-stunted and genetically obese rats led him to theorize that genetic predisposition played a crucial role in the development of obesity. Since then, his work has focused on developing a better understanding of the genetics and biology of obesity. Dr. Hirsch briefly describes the work of Max Kleiber, who found a direct relationship between an animal's body size and its caloric intake. This relationship is generally referred to as "Kleiber's line." Dr. Hirsch discusses human studies that suggest some people are genetically predisposed to store more than the usual amount of body fat. When these individuals lose weight, their bodies are "out of balance" relative to Kleiber's line; balance is restored when they return to the obese state. This theory may explain why many obese people feel unwell when they lose weight and quickly return to their previous weight. However, Dr. Hirsch notes that genetic factors alone do not cause obesity; a complex interplay of genetics, psychosocial factors, and food availability is likely to be involved. Dr. Hirsch outlines current work in his laboratory aimed at understanding genetic mechanisms in rodent obesity and discusses questions that future research needs to address on human obesity. He observes that answers to these questions may be important in the study of other behavioral disorders that, like obesity, have biologic roots, but depend on developmental and psychosocial events for their full display. The lecture includes a question-and-answer session and a tribute to the late W. Henry Sebrell, a former director of the NIDDK and the National Institutes of Health, who died in September 1992.

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Critical Periods in the Development of Childhood Obesity Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: Dr. Dietz begins his lecture by noting that health surveys show that the prevalence of childhood and adolescent obesity in the United States is increasing rapidly. Surveys also show that obesity present in adolescence has an 80 percent chance of persisting into adulthood. For these reasons, it is important to identify periods critical to the development of childhood and adolescent obesity. Dr. Dietz believes that three

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such "critical periods" may exist; as a fetus in the third trimester of pregnancy and the immediate postnatal period; ages four to seven; and adolescence. He discusses a number of studies that have linked maternal nutrition in the third trimester of pregnancy with the child's predisposition to leanness or obesity in later life. Some studies have also shown that an infant's growth in the first year may predispose him or her to later obesity; however, this association is less well established. Data that support the existence of a second "critical period" at ages 4 to 7 are also less well established. In typical childhood growth patterns, there is an increase in fatness from birth up to the preschool years, when fatness begins to decrease or stabilize. This is then followed by a second period of fat increase after age 7 called "adiposity rebound." Dr. Dietz says there is some evidence that early adiposity rebound, occurring between ages 4 to 7, may be a risk factor for the early development of obesity. Dr. Dietz discusses studies that have shown a strong link between adolescent obesity, adult obesity, and the complications of obesity during the third critical period, adolescence. Other topics discussed in the lecture include the mechanisms that may promote the development of obesity, the results of weight reduction programs in children, and the possible role of brown adipose tissue as a regulator of satiety in rats. •

Gender, Genetics, and Obesity Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665. Summary: In this lecture, Dr. Greenwood discusses current understanding of the impact of gender and genetics on obesity and describes animal and human studies that offer clues about why it is so difficult to treat obesity. Data strongly suggest that increased incidence and prevalence of obesity in the United States is not caused solely by increased caloric intake. Dr. Greenwood describes the different patterns of obesity that tend to occur in men and in women and evidence from various studies suggesting that fat distribution may be the factor contributing most to the health risk of obesity. The lecture goes on to discuss animal models that suggest the vulnerability to obesity may be the result of aberrant nutrition partitioning, whereby a higher than normal proportion of nutrients are deposited in fatty tissue, leaving other tissues (notably skeletal muscle) relatively deprived. Dr. Greenwood and her colleagues propose that overeating is an adaptive response to this process, which they believe may be regulated by lipoprotein lipase, an enzyme manufactured by fat cells. Dr. Greenwood also examines research on weight cycling, a phenomenon in which an individual loses weight, gains it back, loses it again, and so on. Evidence gleaned from studies in both rats and humans suggests that weight cycling may be an independent risk factor for increased morbidity and mortality, and may also be associated with the decreased effectiveness of weight loss methods. However, Dr. Greenwood notes that no long-term studies have been conducted on the effects of weight cycling, and that this is an important area for future research. The lecture concludes with the observation that weight loss advice should address the need for physical fitness and permanent lifestyle change and diet composition over caloric restriction.

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The Biologic Basis of Obesity Source: Bethesda, MD: National Institute of Diabetes and Digestive and Kidney Diseases, 1992, 60 minutes. Contact: WIN, 1 WIN WAY, Bethesda, MD 20892-3665.

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Summary: In this lecture, Dr. Leibel describes the two types of studies he and his colleagues are conducting on defining the biologic basis of obesity: long-term studies of obesity in humans, and studies of the molecular genetics of rodent obesity. Results of long-term studies of obesity in humans have shown that body composition remains remarkably constant. This suggests, according to Dr. Leibel, that energy intake and output are regulated to maintain stored energy close to a "set point." However, the nature and origin of the regulatory "signal" are as yet unknown. The regulatory process is a fine one, since small imbalances in intake and output can have a significant impact on body weight. For example, a 3 to 4 percent excess of caloric intake over expenditure will result in weight gain of 6 to 8 pounds over 1 year. The hypothesis of a strong genetic component in obesity is supported by studies of monozygotic (identical) and dizygotic (fraternal) twins. Monozygotic twins demonstrate much lower inter-twin difference in body weight than do dizygotic pairs. Dr. Leibel goes on to describe a series of experiments involving mice and rats that become obese following removal of a section of the hypothalamus. The lesions cause alterations in both food intake and energy efficiency, which suggests that these regions of the brain affect the set point function. Several single gene mutations in mice result in an obese/diabetic phenotype. Efforts are underway to clone several of these genes and to examine their possible role in human obesity and diabetes.

Audio Recordings The Combined Health Information Database contains abstracts on audio productions. To search CHID, go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find audio productions, use the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Sound Recordings.” Type “obesity” (or synonyms) into the “For these words:” box. The following is a typical result when searching for sound recordings on obesity: •

[Digestive Disease Week 1992 Sessions Audiocassettes] Source: Timonium, MD: Milner-Fenwick, Inc. 1992. (audiocassettes). Contact: Available from AGA Audiovisual Materials in Gastroenterology and Liver Disease. c/o Milner Fenwick, Inc., 2125 Greenspring Drive, Timonium, MD 21093-3100. PRICE: $15 per cassette; discount available for series purchase. Summary: These audiocassettes reproduce clinical symposia, research forums, and lectures sponsored by Digestive Disease Week (DDW). Topics available include the pathogenesis, diagnosis, and treatment of gastroesophageal reflux disease (GERD); controversial issues in acute pancreatitis; the epidemiology, pathogenetic mechanisms, and molecular biology of Helicobacter pylori; the physiological and psychological basis for functional gastrointestinal pain; the management of esophageal varices; obesity, weight loss, and gallstones; therapy of inflammatory bowel disease (IBD); and clinical management strategies for anemia, colon polyps, dyspepsia of unknown cause, dysphagia, achalasia, motility disorders, and liver enzyme abnormalities. Topics in lectures include: alcoholic hepatitis; vitamin status and the elderly; erythromycin, macrolides and motilin as prokinetic agents; gallbladder mucosal function; Crohn's disease; and antibiotic selection for gastroenterology practice.

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Bernstein Plan: Type II Source: Van Nuys, CA: Prana Publications. 1995. (audiocassettes). Contact: Available from Prana Publications. 5623 Matilija Avenue, Van Nuys, CA 91401. (800) 735-7726 or (818) 780-1308. Fax (818) 786-7359. E-Mail [email protected]. PRICE: $22.95 plus $3.25 shipping and handling (as of 1995). Order Number A05. Summary: These audiocassette tapes familiarize listeners with Dr. R.K. Bernstein's method of diabetes control for noninsulin-dependent diabetes. Dr. Bernstein, who has had insulin-dependent diabetes for 49 years, believes high blood sugar causes diabetes complications and that complications can be prevented and at times reversed by normalizing blood sugar. Topics on the tapes include the low carbohydrate diet; muscle building; blood glucose tests; the use of metformin and/or insulin; and how to break the obesity cycle by cutting carbohydrates to reduce hunger, blood sugar, and weight. (AAM).

Bibliography: Multimedia on Obesity The National Library of Medicine is a rich source of information on healthcare-related multimedia productions including slides, computer software, and databases. To access the multimedia database, go to the following Web site: http://locatorplus.gov/. Select “Search LOCATORplus.” Once in the search area, simply type in obesity (or synonyms). Then, in the option box provided below the search box, select “Audiovisuals and Computer Files.” From there, you can choose to sort results by publication date, author, or relevance. The following multimedia has been indexed on obesity: •

All about obesity [slide] Source: David J. Gerrick; Year: 1980; Format: Slide; Lorain, OH: Dayton Lab, c1980

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Behavior modification component in the treatment of obesity [slide] Source: Western New York Dietetic Association, with the cooperation of the New York State Dept. of Health, and the Lakes Area Regional Medical Program; Year: 1975; Format: Slide; [Buffalo]: Communications in Learning, 1975

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Behavior modification for obesity [videorecording] Source: [presented by] American Dietetic Association; Year: 1979; Format: Videorecording; [Chicago]: The Association, c1979

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Being obese [videorecording] Source: produced by Grandview Hospital, Audiovisual Department; Year: 1984; Format: Videorecording; Dayton, Ohio: The Hospital, c1984

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CRC forum on obesity [sound recording] Source: chaired by John R. K. Robson; produced by CRC Forums; Year: 1977; Format: Sound recording; Cleveland: CRC Forums; [Boca Raton, Fla.: for sale by CRC Press], c1977

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How to help the obese patient [videorecording] Source: Department of Medicine, Emory University, School of Medicine; Year: 1980; Format: Videorecording; Atlanta: Emory Medical Television Network: [for loan or sale by A. W. Calhoun Medical Library], 1980

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Hypertension in the obese and the old [videorecording] Source: presented by the Department of Medicine, Emory University, School of Medicine; Year: 1985; Format: Videorecording; Atlanta, Ga.: The University, 1985

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Jejunoileal bypass for morbid obesity [sound recording] Source: American College of Surgeons; Year: 1977; Format: Sound recording; [Chicago]: The College, [1977]

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Nutritional needs and obesity in the adolescent [videorecording]: nursing implications Source: Intercollegiate Center for Nursing Education; Year: 1984; Format: Videorecording; Spokane, Wash.: I.C.N.E., c1984

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Obesity: are diet changes needed [videorecording] Source: University of Texas System Cancer Center M. D. Anderson Hospital and Tumor Institute; Year: 1973; Format: Videorecording; Houston: The Center, 1973

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Obesity [slide] Source: University of Washington; Year: 1973; Format: Slide; [Seattle]: The University: [for sale by its Health Sciences Center for Educational Resources], 1973

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Obesity and energy metabolism [videorecording] Source: presented by the Clinical Center, National Institutes of Health, Public Health Service, U.S. Department of Health, Education, and Welfare; Year: 1979; Format: Videorecording; [Bethesda, Md.]: The Center, [1979]

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Obesity and metabolic adaptation [slide] Source: sponsored by Department of Biochemistry, School of Medicine, State University of New York at Buffalo; Year: 1979; Format: Slide; [Buffalo, N.Y.]: The Department, 1979

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Obesity and overweight [videorecording] Source: [presented by] American Medical Association; Year: 1982; Format: Videorecording; Chicago, Ill.: The Association, c1982

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Obesity in adolescence [sound recording] Source: Bernard Eisenberg; [produced by] Dept. of Continuing Medical Education, School of Medicine, State University of New York at Buffalo, in cooperation with Lakes Area Regional Medical Program; Year: 1975; Format: Sound recording; Buffalo, N. Y.: Communications in Learning, 1975

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Obesity, effective management [videorecording] Source: Biomedical Media Production Unit, the University of Michigan Medical Center, Office of Educational Resources & Research; Year: 1981; Format: Videorecording; Ann Arbor, Mich.: The University, c1981

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Problems in obesity surgery [sound recording] Source: American College of Surgeons; Year: 1986; Format: Sound recording; [Chicago, Ill.]: The College, [1986]

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Psychosomatic conditions [motion picture]: obesity Source: produced by Robert Anderson Associates Limited; Year: 1963; Format: Motion picture; Canada: [s.n., 1963]

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The Obesity problem [videorecording] Source: Frances Stern Nutrition Center, Tufts New England Medical Center; Year: 1976; Format: Videorecording; [Boston]: The Nutrition Center: [for sale by its Educational Media Center, 1976]

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The Role of body contouring after reduction of obesity [sound recording] Source: American College Surgeons; Year: 1978; Format: Sound recording; [Chicago]: The College, [1978]

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CHAPTER 9. PERIODICALS AND NEWS ON OBESITY Overview In this chapter, we suggest a number of news sources and present various periodicals that cover obesity.

News Services and Press Releases One of the simplest ways of tracking press releases on obesity is to search the news wires. In the following sample of sources, we will briefly describe how to access each service. These services only post recent news intended for public viewing. PR Newswire To access the PR Newswire archive, simply go to http://www.prnewswire.com/. Select your country. Type “obesity” (or synonyms) into the search box. You will automatically receive information on relevant news releases posted within the last 30 days. The search results are shown by order of relevance. Reuters Health The Reuters’ Medical News and Health eLine databases can be very useful in exploring news archives relating to obesity. While some of the listed articles are free to view, others are available for purchase for a nominal fee. To access this archive, go to http://www.reutershealth.com/en/index.html and search by “obesity” (or synonyms). The following was recently listed in this archive for obesity: •

Surgery can reduce breathing problems in obese kids Source: Reuters Health eLine Date: September 19, 2003 http://www.reutershealth.com/archive/2003/09/19/eline/links/20030919elin014.htm l

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Obesity in children linked with asthma risk Source: Reuters Health eLine Date: September 19, 2003

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Alizyme shares surge as obesity drug shows promise Source: Reuters Industry Breifing Date: September 19, 2003

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Germany's Evotec signs obesity, diabetes drug deal Source: Reuters Industry Breifing Date: September 10, 2003

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Judge throws out obesity suit against McDonalds Source: Reuters Health eLine Date: September 04, 2003

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Gut hormone could help treat obesity Source: Reuters Health eLine Date: September 03, 2003

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Ireland mulls 'fat tax' to curb obesity levels Source: Reuters Health eLine Date: August 26, 2003

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Obesity doesn't hinder pregnancy with donated eggs Source: Reuters Health eLine Date: August 19, 2003

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Obesity may increase mountain sickness risk Source: Reuters Health eLine Date: August 18, 2003

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Parents blame selves for children's obesity Source: Reuters Health eLine Date: August 11, 2003

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Obesity takes emotional toll on teens Source: Reuters Health eLine Date: August 11, 2003

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Obesity increases risk of pregnancy complications Source: Reuters Health eLine Date: August 11, 2003

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Low-carb better than low-fat diet for obese teens Source: Reuters Health eLine Date: August 11, 2003

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Alizyme shares jump on obesity drug deal. Source: Reuters Industry Breifing Date: August 08, 2003

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Pediatricians enlisted to combat childhood obesity Source: Reuters Health eLine Date: August 04, 2003

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EU commission loses court fight on obesity drugs Source: Reuters Industry Breifing Date: July 24, 2003

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Death risk higher in obese women with colon cancer Source: Reuters Health eLine Date: July 17, 2003

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Obesity hikes risk of acid reflux, study finds Source: Reuters Health eLine Date: July 01, 2003

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Pre-diabetic condition more common in obese girls Source: Reuters Health eLine Date: June 30, 2003

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Obesity in British males approaching U.S. levels Source: Reuters Health eLine Date: June 25, 2003

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Low-dose GH with diet and exercise may boost weight loss in obese adults Source: Reuters Industry Breifing Date: June 23, 2003

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Tobacco foes ready legal assault over obesity Source: Reuters Health eLine Date: June 20, 2003

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Gene mutation may play a role in child obesity Source: Reuters Health eLine Date: June 20, 2003

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U.S. employers point to obesity as big cost driver Source: Reuters Industry Breifing Date: June 17, 2003

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U.S. employers point to cost of obesity Source: Reuters Health eLine Date: June 17, 2003

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Obese people do OK after surgery: report Source: Reuters Health eLine Date: June 13, 2003

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Obesity epidemic sweeping U.S., Harvard forum told Source: Reuters Health eLine Date: June 12, 2003

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Britain helps U.S. investigate childhood obesity Source: Reuters Health eLine Date: June 10, 2003

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Obesity may worsen eye disease common in old age Source: Reuters Health eLine Date: June 09, 2003

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Obese young adults more likely to have gum disease Source: Reuters Health eLine Date: June 05, 2003

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CDC: obesity fastest growing health threat in U.S. Source: Reuters Health eLine Date: June 05, 2003

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Roche's Xenical obesity drug cuts risk factors for heart disease Source: Reuters Industry Breifing Date: May 30, 2003

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Obesity drug cuts risk factors for heart disease Source: Reuters Health eLine Date: May 30, 2003

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Genes seen as key to understanding obesity Source: Reuters Health eLine Date: May 30, 2003

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European nations failing obese patients -- survey Source: Reuters Health eLine Date: May 30, 2003

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Obesity epidemic set to get worse Source: Reuters Health eLine Date: May 29, 2003

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European initiative launched to tackle obesity Source: Reuters Health eLine Date: May 29, 2003

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Obesity surgery success depends on surgeon Source: Reuters Health eLine Date: May 26, 2003

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Even short walk reduces deadly clot risk in obese Source: Reuters Health eLine Date: May 14, 2003

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Anti-obesity medication use on the rise in the U.S. Source: Reuters Industry Breifing Date: May 12, 2003

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Obesity before pregnancy ups risk of birth defects Source: Reuters Health eLine Date: May 05, 2003

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Lactation hormone lower in new moms who are obese Source: Reuters Health eLine Date: May 05, 2003

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Even toddlers are obese, study shows Source: Reuters Health eLine Date: May 05, 2003

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Obesity behind 90,000 cancer deaths each year Source: Reuters Health eLine Date: April 23, 2003

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Children's obesity rates may be worse than thought Source: Reuters Health eLine Date: April 18, 2003

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Obesity surgery may lead to weakened bones Source: Reuters Health eLine Date: April 14, 2003

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Americans fear obesity raging out of control: poll Source: Reuters Health eLine Date: April 10, 2003

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Two drugs show early promise for obesity Source: Reuters Health eLine Date: April 08, 2003

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Too much TV ups obesity, diabetes risk in women Source: Reuters Health eLine Date: April 08, 2003

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Obesity severely impacts children's quality of life, but sibutramine may help Source: Reuters Industry Breifing Date: April 08, 2003 The NIH

Within MEDLINEplus, the NIH has made an agreement with the New York Times Syndicate, the AP News Service, and Reuters to deliver news that can be browsed by the public. Search news releases at http://www.nlm.nih.gov/medlineplus/alphanews_a.html. MEDLINEplus allows you to browse across an alphabetical index. Or you can search by date at the following Web page: http://www.nlm.nih.gov/medlineplus/newsbydate.html. Often, news items are indexed by MEDLINEplus within its search engine. Business Wire Business Wire is similar to PR Newswire. To access this archive, simply go to http://www.businesswire.com/. You can scan the news by industry category or company name. Market Wire Market Wire is more focused on technology than the other wires. To browse the latest press releases by topic, such as alternative medicine, biotechnology, fitness, healthcare, legal, nutrition, and pharmaceuticals, access Market Wire’s Medical/Health channel at http://www.marketwire.com/mw/release_index?channel=MedicalHealth. Or simply go to Market Wire’s home page at http://www.marketwire.com/mw/home, type “obesity” (or synonyms) into the search box, and click on “Search News.” As this service is technology oriented, you may wish to use it when searching for press releases covering diagnostic procedures or tests.

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Search Engines Medical news is also available in the news sections of commercial Internet search engines. See the health news page at Yahoo (http://dir.yahoo.com/Health/News_and_Media/), or you can use this Web site’s general news search page at http://news.yahoo.com/. Type in “obesity” (or synonyms). If you know the name of a company that is relevant to obesity, you can go to any stock trading Web site (such as http://www.etrade.com/) and search for the company name there. News items across various news sources are reported on indicated hyperlinks. Google offers a similar service at http://news.google.com/. BBC Covering news from a more European perspective, the British Broadcasting Corporation (BBC) allows the public free access to their news archive located at http://www.bbc.co.uk/. Search by “obesity” (or synonyms).

Newsletters on Obesity Find newsletters on obesity using the Combined Health Information Database (CHID). You will need to use the “Detailed Search” option. To access CHID, go to the following hyperlink: http://chid.nih.gov/detail/detail.html. Limit your search to “Newsletter” and “obesity.” Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter.” Type “obesity” (or synonyms) into the “For these words:” box. The following list was generated using the options described above: •

Obesity: A modern epidemic Source: Novartis Nutrition. Contact: Novartis Nutrition Corporation, Minneapolis, MN, 55440-0370. 1-800-662-2540. Summary: As a major contributor to preventable death and disease in the United States, overweight and obesity pose a significant public health challenge. At present, 97 million American adults are overweight or obese. The causes of obesity are complex, involving social, behavioral, cultural, physiological, metabolic, and genetic factors. This newsletter claims that long-tem change in lifestyle is the only safe and effective treatment.

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Medical Update on Obesity Source: Minneapolis, MN: Sandoz Nutrition, Issue XVII, 4p, Spring 1996. Contact: Sandoz Nutrition, 5320 West 23rd Street, Minneapolis, MN 55416. Summary: This newsletter updates medical professionals about obesity research and treatment. This issue considers the benefits of physical activity following weight loss, and the relationship between weight loss and increased metabolic efficiency.

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Newsletter Articles Use the Combined Health Information Database, and limit your search criteria to “newsletter articles.” Again, you will need to use the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. Go to the bottom of the search page where “You may refine your search by.” Select the dates and language that you prefer. For the format option, select “Newsletter Article.” Type “obesity” (or synonyms) into the “For these words:” box. You should check back periodically with this database as it is updated every three months. The following is a typical result when searching for newsletter articles on obesity: •

Childhood Obesity and the Emerging Epidemic of Type 2 Diabetes in Youth Source: On the Cutting Edge. 22(6):4-9. Winter 2001. Contact: Available from American Dietetic Association. 216 West Jackson Boulevard, Suite 800, Chicago, IL 60606-6995. (800) 877-4746. Summary: This article discusses the phenomenon of early onset of type 2 diabetes in children and adolescents, a condition that is increasing in prevalence. This observed increase is thought to be caused by societal factors that lead to sedentary lifestyles and increased prevalence of obesity. Metabolic and cardiovascular complications often associated with adult obesity have their onset in childhood. Hyperglycemia (high levels of blood glucose) can exist for years before diagnosis of type 2 diabetes is made and treatment is initiated. Children with type 2 diabetes are often asymptomatic at the time of diagnosis; therefore screening for this disorder in this high risk population is very important. The author addresses the metabolic effects of obesity in children, criteria for diagnosis of type 2 diabetes in youth, and treatment strategies. One sidebar describes the use of body mass index (BMI) and revised United States growth charts. 2 tables. 14 references.

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Obesity: Trying to Figure it All Out Source: Fit Society Page. p. 3, 8-9. Winter 2003. Contact: American College of Sports Medicine. P.O. Box 1440, Indianapolis, IN 462061440. www.acsm.org. Summary: This article reviews the health risks of obesity and contributing factors. Weight gain and obesity may be due to a combination of factors including environmental factors, genetic factors, and individual behavior, such as the choices a person makes in eating and physical activity. The article notes that treating obesity is challenging because the causes may include one or more of these factors. As the longterm management of obesity and associated health problems is challenging and costly, the article recommends increased emphasis on obesity prevention.

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When Might Obesity Surgery be Right? Source: University of California, Berkeley Wellness Letter. 21(2):1, 4-5. April 2003. Contact: Health Letter Associates, P.O. Box 412, Prince Street Station, New York, New York. 10012-0007. www.wellnessletter.com. Summary: This article reviews the benefits, side effects, and risks of surgery for the treatment of obesity. More than 63,000 operations were performed in 2002. This surgery is a possible treatment for the 10 to 14 million Americans who are morbidly obese,

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generally defined as being at least 100 pounds overweight or having a body mass index (BMI) of 40 or more. In the surgery, staples or a plastic band are used to close off most of the stomach. The smaller stomach pouch can accommodate only tiny, well-chewed bites eaten very slowly. Another type of surgery, a Roux-en-Y, combines stomach reduction with a closing off of part of the small intestine. The post-operative lifestyle changes that must be made permanently are described. The long-term weight loss and health results of the surgery are reviewed. Guidelines for choosing a treatment program and surgeon conclude the article. •

Obesity: Childhood Epidemic Source: Nutrition Action Healthletter. 29(2):8. March 2002. Contact: Center for Science in the Public Interest. 1875 Connecticut Ave., NW, Suite 300, Washington, DC 20009-5728. www.cspinet.org. Summary: According to an article originally published in the Journal of the American Medical Association, the number of overweight children increased by more than 50 percent among whites and more than 120 percent among African Americans and Hispanics between 1986 and 1999. In 1998, one out of five African-American and Hispanic children were overweight. In contrast, one out of eight white children were overweight. One of 6 children living in the South was overweight compared to 1 of 10 from the West. The article recommends ensuring that children participate in a sport or other physical activity they enjoy and serving them healthy foods, including fruits and vegetables.

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Childhood Obesity and CVD Risk Source: Nutrition Close up. 19(1):1-2. Spring 2002. Contact: Egg Nutrition Center. 1050 17th Street, NW. Suite 560, Washington, DC 20036. 202/833-8850. [email protected]. Summary: Data from the National Longitudinal Survey of Youth (NLSY) revealed that one in five African-American and Hispanic-American children, and one in eight Caucasian children were obese. Obesity was defined as a Body Mass Index (BMI) greater than 95 percent for age and sex. Overweight children were heavier in 1998 than in 1986 and were more likely to become overweight adults. Southern states also had a higher incidence of childhood obesity compared with other regions of the country. One finding of the study indicated that childhood BMI does not raise cardiovascular disease risk factors, but suggests an inverse effect.

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FDA Approves Adjustable Stomach Band to Treat Severe Obesity Source: WIN Notes. p. 7. Winter 2001/2002. Contact: Weight-control Information Network, 1 WIN Way, Bethesda, MD 20992-3665. (202) 828-1025. [email protected]. Summary: In June 2001, the United States Food and Drug Administration (FDA) approved a new surgical device for the treatment of severe obesity. The device, called the Lap-Band Adjustable Gastric Banding System, provides some advantages over traditional gastric bypass surgery, but may not be as effective. The Lap-Band is inserted via laparoscopy, a procedure less invasive than some types of obesity surgeries. Researchers at the Medical College of Virginia of the Virginia Commonwealth University (VCU) in Richmond, one of eight centers performing the procedure during

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FDA's clinical trial, did not find the Lap-Band to be effective for the surgical treatment of morbid obesity and recommended further studies to determine its long-term efficacy. VCU patients lost an average of 38 percent of their excess weight over 3 years, which is about half the amount of weight usually lost after more traditional gastric bypass surgery. •

Researchers Investigate New Obesity-related Disease Source: WIN Notes. p. 4, 10. Summer 2002. Contact: Weight-control Information Network, 1 WIN Way, Bethesda, MD 20992-3665. (202) 828-1025. Summary: Nonalcoholic steatohepatitis (NASH) is a liver disease that occurs most often in adults over the age of 40 who are overweight or have diabetes, insulin resistance, or hyperlipidemia. NASH resembles alcoholic liver disease, however, people with NASH drink little or no alcohol. Although most people with NASH are middle-aged, obese, and diabetic, the disease may also strike children and normal-weight adults without diabetes. The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) is funding a 5-year study of NASH in hopes of finding prevention and treatment approaches. Scientists are uncertain about what causes NASH, but believe it is a combination of insulin resistance and oxidative stress. NIDDK plans to establish a NASH Clinical Research Network to study this poorly understood disease. Researchers will investigate NASH's origin, contributing factors, natural history, and complications. They hope to identify safe and effective methods to prevent and treat this increasingly common disease.

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Soft Drinks and Obesity Source: Nutrition Action Healthletter. 28(4): 9. May 2001. Contact: Center for Science in the Public Interest. 1875 Connecticut Avenue NW, Suite 300, Washington, DC 20009-5728. Summary: A 2-year study published in the journal Lancet found that in 500 sixth and seventh grade students, those who increased their consumption of sweetened soft drinks, fruit drinks, and iced tea were most likely to become obese. Co- author David Ludwig of the Harvard School of Public Health notes that 'sugar- sweetened drinks could lead to obesity because people may not compensate well for calories consumed in liquid form' by eating fewer calories later. The article recommends limiting intake of sweetened soft drinks and fruit drinks to help prevent obesity or to lose weight.

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New Obesity Gene Discovered Source: WIN Notes. p. 2. Summer 2001. Contact: Weight-control Information Network. 1-877-WIN-4627. Summary: A gene that produces a protein called 'beacon' plays an important role in the development of obesity and diabetes, according to Greg Collier from Deakin University in Melbourne, Australia. The protein increases appetite, body weight, and the incidence of type 2 diabetes in desert rats. Since beacon is identical in rats and humans, the beacon gene represents a potential target for the development of anti-obesity drugs, says the Deakin University research team. To test their theory that the beacon gene contributes to the regulation of energy balance, the researchers administered beacon via pumps directly into the brains of lean rats for 7 days. Rats receiving the highest dose increased

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their body weight by 5 percent by the end of the week. Those receiving higher doses of beacon showed a greater increase in food intake. To find how beacon worked to increase food intake and body weight, the researchers looked at the expression of the protein neuropeptide Y (NPY) in beacon-treated rats. The levels of NPY, known to stimulate appetite, doubled in the rats receiving high doses of beacon. One way beacon increases body weight may be to stimulate the activity of NPY. The researchers conclude that beacon may be a new target for the development of therapeutic agents for obesity and anorexia nervosa. The full report of this research appears in the November 2000 issue of Diabetes. •

Preventing Childhood Obesity: a Multipronged Approach Source: WIN Notes. pp. 4-5. Summer 2001. Contact: Weight-control Information Network. 1-877-WIN-4627. Summary: At the 2000 annual meeting of the American Obesity Association (AOA), many experts expressed concern about the rise in childhood obesity. The percentage of overweight and obese children aged 6 to 17 has doubled in the past 30 years, with a corresponding rise in the incidence of type 2 diabetes, hypertension, cardiovascular disease, hyperlipidemia, and psychosocial disorders among these children. Many of those who spoke at the AOA meeting stressed the need to develop effective strategies to reverse the rise in childhood obesity. William Dietz, M.D., Ph.D., at the Centers for Disease Control and Prevention (CDC), described how family, community, health care providers, and media influence could all help increase physical activity and support good nutrition among children. Howell Wechsler, Ed.D., M.P.H., a CDC scientist, outlined strategies for shaping the psychosocial environment of a school to support physical activity and healthy eating. Morgan Downey, J.D., AOA's executive director, suggested that health care professionals speak with local PTAs and school boards to 'connect the dots' between fast food lunches, fewer physical education classes, and high rates of childhood obesity with the accompanying chronic health problems. Marc Jacobson, M.D., Director of the Center for Atherosclerosis Prevention at Schneider Children's Hospital in New York, spoke about the pediatrician's role in obesity prevention. For children 2 to 7 years old, weight maintenance is the goal, unless other health complications exist. For those children age 8 and older, weight loss is targeted only for those children whose BMI is above the 95th percentile, unless complications are present in those above the 85th percentile.

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Obesity: The Overlooked Cancer Risk Source: American Institute for Cancer Research Newsletter. Issue 74, p. 5. Winter 2002. Summary: Research indicates that obesity is a risk factor for cancer. Fat tissue produces a variety of hormones and proteins that encourage cells to grow and divide more rapidly, increasing the chance of spontaneous mutations that can lead to cancer. Obesity may also increase the body's vulnerability to cancer-causing substances found in food or the environment because these materials can be stored in body fat. Cancers that have been associated with obesity include breast, colon, endometrium, esophagus, kidney, prostate, and gallbladder. Individuals can reduce cancer risks associated with obesity by decreasing serving sizes and increasing physical activity levels to reduce or prevent obesity and its effects.

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Poor Parental Eating Habits Raise Obesity Risk in Children Source: WIN Notes. pp. 3, 5. Fall 2001.

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Contact: Weight-control Information Network. 1-877-WIN-4627. Summary: A study published in the September 2000 issue of the International Journal of Obesity found that parents who alternate between restrictive and impulsive eating behaviors are sending their children mixed messages. These mixed messages may increase the risk of childhood obesity according to a 6-year study conducted at the Boston University School of Medicine. Ninety-two children ages 3 to 5 participated in the Framingham Children's Study. Those children whose parents reported high levels of both dietary restraint and disinhibition had the greatest increases in body mass and skinfold thickness by the end of the study. 'These results may help parents to become more aware of their own eating behaviors and attitudes, and the impact their behaviors may unconsciously be having on their children,' said Maggie Y. Hood, M.P.H., lead study author. •

Study Links Soft Drink Consumption to Childhood Obesity Source: WIN Notes. pp. 4, 5. Fall 2001. Contact: Weight-control Information Network. 1-877-WIN-4627. Summary: The results of a study led by Davis S. Ludwig, M.D., Ph.D., director of the obesity program at Children's Hospital in Boston, suggested that the link between soft drink consumption and obesity is independent of food intake, television viewing, and physical activity. Sixty-five percent of girls and 74 percent of boys consume soft drinks. Dr. Ludwig notes that 'consumption rates among children have doubled in the past decade.' The researchers hypothesized that this could be one factor contributing to the 100 percent increase in the prevalence of childhood obesity in the United States between 1980 and 1994. The prospective study followed 548 children ages 11 to 12 in the Boston area from October 1995 to May 1997. Fifty-seven percent of the children increased their daily sugar-sweetened drink consumption over the 19-month period, with a quarter drinking more than one extra can or glass per day. After making adjustments for other factors that might affect body weight, the researchers found that body mass index (BMI) increased with each additional serving. Thirty-seven children who were not obese at baseline were obese by the end of the study. Dr. Ludwig explains that the 'data suggest that people are not compensating' for excess energy intake in liquid form by eating less at meals. The study's authors conclude that this physiological mechanism is a viable explanation for their findings that sugar-sweetened drinks contribute to childhood obesity.

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Obesity and Chronic Health Problems Source: AICR Science News. Issue 22. p. 2. December 2001. Contact: American Institute for Cancer Research. 1759 R Street NW, Washington, DC 20009. 202-328-7744. www.aicr.org. Summary: In a study initially published in the Journal of Public Health, researchers gathered data from 9,585 American adults about their height, weight, smoking and drinking habits, income, quality of life, and incidence of 17 chronic health problems. Obese adults experienced more chronic health problems than smokers, heavy drinkers, and individuals below the poverty line. Additionally, obese individuals in the study reported nearly twice as many chronic health problems as individuals of normal weight.

•

Dramatic Increase in Obesity and Diabetes in Past Decade Source: Nutrition Close-Up. 18(4): 4. Winter 2001.

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Contact: Egg Nutrition Center. 1050 17th Street NW. Suite 560. Washington, DC 20036. 202-833-8850. Summary: Based on the extrapolation of the 2000 Behavioral Risk Factor Surveillance System (BRFSS), which randomly phoned 184,450 adults age 18 or older, 19.6 million men and 19.2 million women were obese in 2000, a 61 percent increase since 1991. The prevalence of diabetes also increased from 4.9 percent in 1990 to 7.3 percent in 2000. The BRFSS data showed that African-Americans were more likely to be obese and have diabetes compared with other ethnic groups. Education levels were inversely associated with diabetes. The prevalence of those with both obesity and diabetes doubled from 1990 to 2000, from 1.4 percent to 2.9 percent. The authors conclude that 'innovative interventions aimed at weight control, healthy eating, and physical activity that consumers will follow are needed to counter this trend.' •

Management of Obesity Using the Mayo Clinic Healthy Weight Pyramid Source: SCAN's Pulse. 20(1):7-9. Winter 2001. Contact: Sports, Cardiovascular, and Wellness Nutritionists, HOD/Practice Operations Team, the American Dietetic Association, 216 W. Jackson Blvd., Suite 800, Chicago, IL 60606-6995. Summary: This article describes the approach used to treat obesity at the Mayo Clinic. The approach promotes lifestyle changes in eating patterns, physical activity habits, and other weight-related behaviors. Mayo Clinic health practitioners individualize the approach according to the factors contributing to each patient's increased weight. The Mayo Clinic Healthy Weight Pyramid is the tool used to counsel patients about healthy eating. The pyramid emphasizes healthy food choices within each category. The author contrasts the Healthy Weight Pyramid with the Food Guide Pyramid from the United States Department of Agriculture (USDA). Vegetables and fruits appear at the base of the Healthy Weight Pyramid, and eating unlimited amounts is encouraged. For the other food groups, the number of servings is specified within a range. Within each food group of the Healthy Weight Pyramid, a 'best foods' list promotes foods associated with the greatest health benefits. By following the eating plan of the Healthy Weight Pyramid, women will consume about 1,200 calories a day and men will consume about 1,400 calories a day. Since fruits and vegetables are unlimited, actual caloric intake may be higher but still remain low enough to promote weight loss. The article includes an image of the Healthy Weight Pyramid, along with a description of the various food groups and the number of recommended servings for each group.

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Genes Play Key Role in Childhood Obesity Source: WIN Notes. p.3. Spring 2000. Contact: Weight-Control Information Network. 1 WIN WAY, Bethesda, MD 20892-3665, USA. (877) 946-4627. [email protected]. Summary: Researchers at Columbia University, led by David B. Allison, found that there seems to be a substantial (75-80 percent) genetic contribution to fat mass over and above that measured by body mass index (BMI) in children and adolescents. They studied 66 pairs of twins, ages 3 through 17. Their findings indicate that "BMI alone may be a useful but insufficient measure of fat mass for gene-mapping studies using pediatric samples".

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•

Conference Highlights Obesity as a Public Health Crisis Source: WIN Notes. p.5,7. Spring 2000. Contact: Weight Control Information Network. 1 WIN WAY, Bethesda, MD 20892-3665, USA. (877) 946-4627. [email protected]. Summary: The American Obesity Association (AOA) hosted a conference in September of 1999 to present the latest scientific and clinical findings on obesity and to outline the directions of future prevention and intervention strategies. Participants discussed medical and psychological problems stemming from obesity, as well as economic, social, research, and educational issues. Dr. Richard Atkinson, Professor of Medicine and Nutritional Sciences at the University of Wisconsin and co-founder and president of AOA, presented an action plan for the U.S. Government to address in the next year.

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Childhood Obesity Growing Dramatically in Korea: ILSI Korea Responds Source: ILSI News. p.4. January-March 2000. Contact: International Life Sciences Institute. 1126 16th St., NW, Suite 110, Washington, DC 20036-4810. (202) 659-0074. [email protected]. www.ilsi.org. Summary: This article discusses the International Life Sciences Institute's October 1999 seminar in Seoul addressing the increased rate of childhood obesity in the last few decades in Korea. According to Dr. Kim Eun Kyung from Kangnung National University, the prevalence of childhood obesity over the last 18 years has increased 4.6 times in males and 3.2 times in females in Seoul. The ILSI seminar participants discussed causes for this increase, such as decreased opportunity for physical activity and increased abundance of food. The seminar also addressed ways to prevent and treat obesity in children and adolescents. These strategies include the use of school- and community-linked interventions to promote physical activity and proper nutrition.

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Holiday Weight Gain May Contribute to Overweight and Obesity Source: WIN Notes. p. 1, 4. Fall 2000. Contact: Weight-control Information Network. 1-877-WIN-4627. Summary: According to a study from the National Institutes of Health (NIH), the weight Americans gain over the winter holidays may be a major contributor to the increase in body weight that often occurs during adulthood. Researchers from the National Institute of Child Health and Human Development (NICHD) and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) measured actual seasonal weight changes in 195 adults from September through March with followup measurements of 165 subjects in June and September/October. Participants' average net weight gain between September and March was 1.06 pounds, with 75 percent of that gain occurring during the holiday period from mid-November to mid-January. For the 165 participants who returned in June and either September or October, the average weight gain for the full year was 1.36 pounds, leading researchers to conclude that weight gained during the winter holidays is not lost during the warmer months. The research team concluded that promotion of weight stability during the fall and winter months may be a useful strategy for preventing the weight gain that occurs during adulthood. The finding that participants who reported more physical activity had less weight gain points to the need for more research into increased physical activity as a means for preventing holiday weight gain among persons at risk. This study appears in the March 23, 2000, issue of The New England Journal of Medicine.

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The Obesity Factor: Excessive Weight Has Strong Cancer Links Source: AICR Newsletter. Issue 62, p.11. Winter 1999. Contact: AICR, 1759 R Street NW, Washington, DC. (202) 328-7744. Summary: This article discusses the link between obesity and cancer risk. According to two recent studies, obese individuals are at increased risk for certain kinds of cancer, especially if they have excess abdominal fat. The author suggests that this may be caused by increased levels of estrogen in the blood, or by an increased gut transit time (the time it takes for substances to pass through the large intestine). The article recommends weight control and exercise. A formula for calculating body mass index is provided.

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Needs assessment identifies barriers to treating obesity in children Source: International Life Sciences Institute (ILSI) Newsletter. September 1999. Contact: ILSI Center for Health Promotion, 2900 Chamblee-Tucker Road, Building 2, Atlanta, GA 30341-4128. Summary: The key to addressing childhood obesity is preventing it. This article gives suggestions made for ways to help pediatric practitioners improve management of childhood obesity.

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International Life Sciences Institute (ILSI) meeting sets research agenda to address childhood obesity Source: International Life Sciences Institute (ILSI) Newsletter. September 1999. Contact: ILSI Center for Health Promotion, 2900 Chamblee-Tucker Road, Building 2, Atlanta, GA 30341-4128. Summary: Something has changed to make the present generation of children more obese than their parents. Experts do not always agree on why obesity is so much more prevalent today than it was only a couple of decades ago, but they do agree on the urgent need for treatment and prevention. This article discusses ILSI's Center for Health Promotion's research agenda to address childhood obesity.

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Fat Intake: Is It Responsible for Rising Obesity Rates? Source: Healthy Weight Journal. 12(4):52-57. July/August 1998. Contact: Healthy Living Institute, 402 S. 14th St., Hettinger, ND 58639. (701) 567-2645. Summary: Berg reports on a symposium held at the University of Texas in April 1996 on `Fats and oil consumption to combat metabolic complications and obesity.' According to Berg, consumption of fat in America is declining while obesity rates are rising. The results from scientific studies have been mixed, with some studies showing that a diet high in fat results in weight gain and obesity and other studies showing that some subjects gain weight without regard to the fat or carbohydrate content of their diet.

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First Federal Obesity Guidelines Released Source: News from ASBP. p.4-6. July/August 1998. Contact: American Society of Bariatric Physicians, 5600 South Quebec, Suite 160-D, Englewood, CO 80111. (303) 770-2526.

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Summary: This article discusses the guidelines for obesity released in June 1998 by the National Heart, Lung, and Blood Institute of the National Institutes of Health. According to the author, the guidelines do not present new information for bariatric physicians, although they are potentially useful to those who do not normally treat overweight patients. The guidelines include three measures in their assessment of overweight-body mass index, waist circumference, and risk factors for diseases and conditions associated with obesity. The authors of the guidelines state that all three measures should be used in conjunction. Suggestions offered by the guidelines for weight loss include physical activity, reduction of dietary fat, controlled and slow weight loss, and weight maintenance. According to the author of this article, the guidelines also warn that lifestyle changes such as exercise and diet should be attempted for at least six months before medications are tried. Finally, the guidelines state that obesity surgery should be a last resort for patients with clinically severe obesity when less invasive methods have failed and the patient is at high risk for obesity- related illnesses. •

New Obesity Guidelines: Minority Women at Risk Source: Closing the Gap. p.6-7. June/July, 1998. Contact: Office of Minority Health Resource Center, P.O. Box 37337, Washington, DC 20013-7337. (800) 444-6472. Web Site: http://www.omhrc.gov. Summary: Urgo reviews the National Heart, Lung, and Blood Institute's clinical guidelines on obesity. She finds that, according to the Institute's statistics, AfricanAmerican, Native-American and Native-Hawaiian women are overweight at higher rates than any other group of women. Urgo says that women in these minority groups also tend to feel less social pressure to be thin, higher self-esteem, and greater acceptance of overweight than white women. According to Byllye Avery, president of the National Black Women's Health Project, any campaign to increase physical activity among these populations will require a holistic approach, one incorporating the community and the culture, if it is to be successful.

•

Media Coverage of New BMI Obesity Standard Adds Fuel to Billion Dollar Diet Industry Source: EDAP Matters. p.1,6-7. Summer/Fall, 1998. Contact: Eating Disorders Awareness and Prevention, Inc., 603 Stewart St., Suite 803, Seattle, WA 98101. (206) 382-3587. http://www.members.aol.com/edapinc. Summary: The author examines the National Heart, Lung, and Blood Institute's report on weight in Americans, with its new guidelines on body mass index (BMI). Biely is concerned that the stricter guidelines on obesity may induce some individuals to begin dangerous dieting habits or cause those already dieting to attempt life- threatening weight-loss maneuvers. She discusses BMI measurement and says that BMI alone does not indicate cardiac or respiratory health. Biely also claims that the emphasis in the governmental report is on the very high BMIs, not the very low ones, which are also unhealthy. Finally, she raises the issue of continued weight cycling; weight loss and regain followed by loss and regain again.

•

Childhood Obesity: Healthier Lifestyles Needed to Treat This Growing Problem Source: Mayo Clinic Health Letter. May 1997.

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Contact: Mayo Clinic Health Letter, 200 First St., SW, Rochester, MN 55905. (800) 3339038. Summary: The author discusses the incidence, causes, and treatment of childhood obesity. The third National Health and Nutrition Examination Survey (NHANES III) showed that about one in five American children are overweight. According to the author, this is significant because overweight children may suffer from weight-related illnesses such as heart disease, diabetes, and arthritis, as well as psychological stress from peer attitudes towards overweight. These children often become overweight adults, and overweight adults often suffer from the same illnesses. Several causes of obesity are suggested, including poor dietary habits, lack of physical activity, family lifestyle, genetics, and ethnicity. The author suggests a family approach to weight loss, with increased physical activity as a part of family outings, improved eating habits, and a supportive attitude towards the overweight child. •

Exercise, Obesity, and Weight Control Source: Physical Activity and Fitness Research Digest. 1(6):1-8, May 1994. Contact: U.S. Department of Health and Human Services, President's Council on Physical Fitness and Sports, Room 250, 701 Pennsylvania Avenue, NW, Washington, DC 20004. Summary: This newsletter issue is devoted to the subject of overweight and obesity and explains how they are affected by physical activity. First the author defines overweight, obesity, and how they are assessed in the medical setting. The prevalence of obesity and overweight in the United States is addressed. The author provides basic information on how body weight is controlled or regulated in order to better understand how one becomes obese. The article covers the etiology of obesity, the health implications of overweight and obesity, and general treatment of each. The role that physical activity plays in weight control and reduction is also addressed. (25 refs).

•

Efforts in Obesity Research Take New Directions Source: NAASO Notes and Notices. 3(1):1, 6; Winter 1994. Summary: This newsletter article summarizes developments within the Federal government that are highly relevant to the activities of the North American Association for the Study of Obesity (NAASO). This includes the move of the Nutrition Coordinating Committee of the National Institutes of Health (NIH) from the Office of the Director to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). NIDDK's interest in obesity favor the research agenda of the NAASO. The author recently testified to the Subcommittee on Department Operations and Nutrition of the House Agriculture Committee on the importance of alterations in the school lunch programs. The hearings were prompted by a recent USDA survey that found that almost all of the school lunches exceeded dietary guidelines for fat. Efforts to correct this situation are addressed.

•

Childhood Obesity: Etiology and Treatment Source: Healthy Weight Journal. 8(5):89-90; September/October 1994. Contact: Healthy Living Institute, 402 S. 14th St., Hettinger, ND 58639. (701) 567-2645. Summary: This article addresses the etiology of childhood obesity. The causes of childhood obesity include television viewing and sedentary lifestyle. Changes in the

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American family system have also had a detrimental effect on obese children. Since childhood obesity is a disorder affecting a specialized and specific population, the treatment needs to be individualized by a team of health professionals. Restricting calories in children can be dangerous, and researchers agree that diets alone are ineffective. While it is agreed that preventing and treating obesity properly is important, preoccupation with weight can lead to serious consequences. The article concludes with suggestions for a safe program of behavior therapy. •

Obesity is Not an Eating Disorder Source: The Harvard Mental Health Letter. 8(4):4-6; October 1991. Summary: The author presents three theories that can account for the relationship between eating and obesity: overeating, the pica hypothesis, and the fat-stat, or set-point theory. The author believes that research has proven that the setpoint theory is becoming progressively more plausible, and the overeating hypothesis has less and less to recommend it. The salient research on each of these theories is summarized.

•

Low-income Mothers Unconcerned About Children's Overweight Source: WIN Notes. p. 4. Winter 2001/2002. Contact: Weight-control Information Network, 1 WIN Way, Bethesda, MD 20992-3665. (202) 828-1025. [email protected]. Summary: Researchers from the University of Chicago Department of Pediatrics and University of Cincinnati College of Medicine conducted focus groups with 18 lowincome mothers of preschool children at risk for later obesity. According to Centers for Disease Control and Prevention (CDC) definitions, 14 of the 18 children enrolled at a clinic of the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) were overweight, and three were at risk for overweight. Among the mothers of overweight children, only two were concerned about their child's present weight and only five were concerned about their child's weight in the future. Researchers found that mothers do not rely on measurements or standardized growth charts to determine a healthy weight. The mothers worried about children's weight only if they were inactive, 'lazy,' or teased about their weight. The focus group findings suggest that health professionals and low-income mothers view the definition and causes of overweight differently. Both agree that children should be physically active and follow healthy eating patterns. The researchers conclude that using growth charts when counseling low-income mothers of overweight children may not be helpful. Focusing on shared goals may have a greater impact on preventing childhood obesity in this population. This study was initially published in the May 5, 2001 issue of Pediatrics.

•

Primary Care Intervention Helps Overweight Adolescents Source: WIN Notes. p. 3. Summer 2002. Contact: Weight-control Information Network, 1 WIN Way, Bethesda, MD 20992-3665. (202) 828-1025. Summary: This article reviews a study initially published in the January 1, 2002 issue of 'Obesity Research.' It found that overweight adolescents enrolled in a behavioral weightcontrol program begun in a primary care setting and continued through telephone and mail contacts have better outcomes than those receiving single-session physician counseling. Researchers from the Children's Hospital Medical Center in Cincinnati, OH randomly assigned 44 overweight adolescents between 12 and 16 years of age to either a

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4-month multi-component Healthy Habits (HH) intervention or single-session Typical Care (TC). At the end of 4 months, HH adolescents showed a decrease in body mass index (BMI) of 0.2 units, whereas the TC group showed an average 1.1 unit increase. Both HH adolescents and their parents reported greater use of behavioral skills than TC adolescents. The article concludes that the multi-component approach shows promise in treating overweight adolescents. •

Dieting Not Linked to Eating Disorders in Overweight Adults Source: WIN Notes. pp. 1, 8. Fall 2001. Contact: Weight-control Information Network. 1-877-WIN-4627. Summary: The National Task Force on Prevention and Treatment of Obesity conducted a literature review and concluded that dieting, the intentional and sustained restriction of caloric intake to reduce body weight or change body shape, does not appear to cause eating disorders or other psychological dysfunction in overweight and obese adults. Reporting in the September 25, 2000, Archives of Internal Medicine, the task force found that weight-loss treatment, very low calorie diets (VLCDs), weight cycling, prescription medications, and 'nondieting' approaches do not support concerns that dieting may lead to or worsen eating disorders in overweight and obese adults. The task force also found that such concerns should not discourage overweight adults from eating fewer calories and being more active to lose a moderate amount of weight or to prevent additional weight gain.

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Overweight People More Prone to Vitamin D Shortfall Source: Tufts University Health and Nutrition Letter. 18(9):6. November 2000. Contact: 10 High Street, Suite 706, Boston, MA 02110. [email protected]. www.healthletter.tufts.edu. Summary: The more overweight someone is, the lower the level of vitamin D in the bloodstream. Less vitamin D means the body is less capable of absorbing calcium. Researchers have found that the vitamin D that overweight people produce, as well as the vitamin D they eat in food, is less likely to make it to their blood. When exposed to sunlight, overweight men produce the same amount as thinner men, but rather than flowing from tiny capillaries in the skin into the main pathways of the bloodstream, the vitamin moves to the fat cells beneath the skin's surface. The researchers also believe that when vitamin D is eaten in foods, and after it is absorbed into the bloodstream from the gastrointestinal tract, it ends up "sequestered" in the large pool of body fat. The chance of a vitamin D deficiency is not high in an overweight person not attempting to lose weight. However, once an overweight person, especially a very overweight person, starts a weight-loss diet, then a marginal deficiency can become a definite vitamin D deficiency. Many low-fat, low-calorie diets are low in vitamin D. Researchers recommend a supplement containing vitamin D for overweight people attempting to lose weight. The more a person weighs, the more important a supplement becomes because more fat cells mean less vitamin D ends up in the bloodstream.

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When Your Child Is Overweight Source: Diabetes Self-Management. p.60,62,65-66. July/August 1998. Summary: Schreiner and Phillips discuss some of the factors contributing to overweight in children, including lack of physical activity, readily available snack foods of low nutritional value, and heredity. They say that obesity in childhood and adolescence

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often means obesity as an adult, with the resulting risk factors for stroke, diabetes, and heart disease. The authors explain how to determine if a child is overweight and offer a variety of strategies for weight loss and nutritional education. They list alternative snacks, include healthful recipes, and illustrate the suggested levels of activity with an activity pyramid patterned after the Food Guide Pyramid. •

Care of Obese Patients Challenges Health Care Providers Source: WIN Notes. p. 1-2. Summer 2002. Contact: Weight-control Information Network, 1 WIN Way, Bethesda, MD 20992-3665. (202) 828-1025. Summary: The January 1, 2002 issue of the 'American Family Physician' offers recommendations on the medical care of obese patients from the National Task Force on Prevention and Treatment of Obesity. Patients who are obese have special health care needs and physicians and medical staff face challenges in providing routine preventive care. To increase patients' access to quality care, health care providers should educate staff about treating patients with respect regardless of weight, not overlook preventive care for patients who are obese, and encourage behaviors such as healthy eating and physical activity for health and weight. A sidebar lists appropriate equipment and supplies for the health care of obese patients.

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Lighten Up for Health: One in Three Americans is Obese Source: American Institute for Cancer Research Newsletter. 47:4-5; Spring 1995. Contact: The American Institute for Cancer Research Newsletter, 1759 R Street, NW, Washington, DC 20009. (202) 328-7744. Summary: This brief article describes recent trends in the eating habits of Americans. While Americans are making progress towards eating less dietary fat, people are consuming more calories and gaining weight in the process. According to statistics from the Centers for Disease Control and Prevention, one in three Americans is classified as obese. The article offers possible reasons for the overweight trend.

Academic Periodicals covering Obesity Numerous periodicals are currently indexed within the National Library of Medicine’s PubMed database that are known to publish articles relating to obesity. In addition to these sources, you can search for articles covering obesity that have been published by any of the periodicals listed in previous chapters. To find the latest studies published, go to http://www.ncbi.nlm.nih.gov/pubmed, type the name of the periodical into the search box, and click “Go.” If you want complete details about the historical contents of a journal, you can also visit the following Web site: http://www.ncbi.nlm.nih.gov/entrez/jrbrowser.cgi. Here, type in the name of the journal or its abbreviation, and you will receive an index of published articles. At http://locatorplus.gov/, you can retrieve more indexing information on medical periodicals (e.g. the name of the publisher). Select the button “Search LOCATORplus.” Then type in the name of the journal and select the advanced search option “Journal Title Search.”

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APPENDICES

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APPENDIX A. PHYSICIAN RESOURCES Overview In this chapter, we focus on databases and Internet-based guidelines and information resources created or written for a professional audience.

NIH Guidelines Commonly referred to as “clinical” or “professional” guidelines, the National Institutes of Health publish physician guidelines for the most common diseases. Publications are available at the following by relevant Institute13: •

Office of the Director (OD); guidelines consolidated across agencies available at http://www.nih.gov/health/consumer/conkey.htm

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National Institute of General Medical Sciences (NIGMS); fact sheets available at http://www.nigms.nih.gov/news/facts/

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National Library of Medicine (NLM); extensive encyclopedia (A.D.A.M., Inc.) with guidelines: http://www.nlm.nih.gov/medlineplus/healthtopics.html

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National Cancer Institute (NCI); guidelines available at http://www.cancer.gov/cancerinfo/list.aspx?viewid=5f35036e-5497-4d86-8c2c714a9f7c8d25

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National Eye Institute (NEI); guidelines available at http://www.nei.nih.gov/order/index.htm

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National Heart, Lung, and Blood Institute (NHLBI); guidelines available at http://www.nhlbi.nih.gov/guidelines/index.htm

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National Human Genome Research Institute (NHGRI); research available at http://www.genome.gov/page.cfm?pageID=10000375

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National Institute on Aging (NIA); guidelines available at http://www.nia.nih.gov/health/

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These publications are typically written by one or more of the various NIH Institutes.

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National Institute on Alcohol Abuse and Alcoholism (NIAAA); guidelines available at http://www.niaaa.nih.gov/publications/publications.htm

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National Institute of Allergy and Infectious Diseases (NIAID); guidelines available at http://www.niaid.nih.gov/publications/

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National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS); fact sheets and guidelines available at http://www.niams.nih.gov/hi/index.htm

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National Institute of Child Health and Human Development (NICHD); guidelines available at http://www.nichd.nih.gov/publications/pubskey.cfm

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National Institute on Deafness and Other Communication Disorders (NIDCD); fact sheets and guidelines at http://www.nidcd.nih.gov/health/

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National Institute of Dental and Craniofacial Research (NIDCR); guidelines available at http://www.nidr.nih.gov/health/

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National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK); guidelines available at http://www.niddk.nih.gov/health/health.htm

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National Institute on Drug Abuse (NIDA); guidelines available at http://www.nida.nih.gov/DrugAbuse.html

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National Institute of Environmental Health Sciences (NIEHS); environmental health information available at http://www.niehs.nih.gov/external/facts.htm

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National Institute of Mental Health (NIMH); guidelines available at http://www.nimh.nih.gov/practitioners/index.cfm

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National Institute of Neurological Disorders and Stroke (NINDS); neurological disorder information pages available at http://www.ninds.nih.gov/health_and_medical/disorder_index.htm

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National Institute of Nursing Research (NINR); publications on selected illnesses at http://www.nih.gov/ninr/news-info/publications.html

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National Institute of Biomedical Imaging and Bioengineering; general information at http://grants.nih.gov/grants/becon/becon_info.htm

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Center for Information Technology (CIT); referrals to other agencies based on keyword searches available at http://kb.nih.gov/www_query_main.asp

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National Center for Complementary and Alternative Medicine (NCCAM); health information available at http://nccam.nih.gov/health/

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National Center for Research Resources (NCRR); various information directories available at http://www.ncrr.nih.gov/publications.asp

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Office of Rare Diseases; various fact sheets available at http://rarediseases.info.nih.gov/html/resources/rep_pubs.html

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Centers for Disease Control and Prevention; various fact sheets on infectious diseases available at http://www.cdc.gov/publications.htm

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NIH Databases In addition to the various Institutes of Health that publish professional guidelines, the NIH has designed a number of databases for professionals.14 Physician-oriented resources provide a wide variety of information related to the biomedical and health sciences, both past and present. The format of these resources varies. Searchable databases, bibliographic citations, full-text articles (when available), archival collections, and images are all available. The following are referenced by the National Library of Medicine:15 •

Bioethics: Access to published literature on the ethical, legal, and public policy issues surrounding healthcare and biomedical research. This information is provided in conjunction with the Kennedy Institute of Ethics located at Georgetown University, Washington, D.C.: http://www.nlm.nih.gov/databases/databases_bioethics.html

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HIV/AIDS Resources: Describes various links and databases dedicated to HIV/AIDS research: http://www.nlm.nih.gov/pubs/factsheets/aidsinfs.html

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NLM Online Exhibitions: Describes “Exhibitions in the History of Medicine”: http://www.nlm.nih.gov/exhibition/exhibition.html. Additional resources for historical scholarship in medicine: http://www.nlm.nih.gov/hmd/hmd.html

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Biotechnology Information: Access to public databases. The National Center for Biotechnology Information conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information for the better understanding of molecular processes affecting human health and disease: http://www.ncbi.nlm.nih.gov/

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Population Information: The National Library of Medicine provides access to worldwide coverage of population, family planning, and related health issues, including family planning technology and programs, fertility, and population law and policy: http://www.nlm.nih.gov/databases/databases_population.html

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Cancer Information: Access to cancer-oriented databases: http://www.nlm.nih.gov/databases/databases_cancer.html

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Profiles in Science: Offering the archival collections of prominent twentieth-century biomedical scientists to the public through modern digital technology: http://www.profiles.nlm.nih.gov/

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Chemical Information: Provides links to various chemical databases and references: http://sis.nlm.nih.gov/Chem/ChemMain.html

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Clinical Alerts: Reports the release of findings from the NIH-funded clinical trials where such release could significantly affect morbidity and mortality: http://www.nlm.nih.gov/databases/alerts/clinical_alerts.html

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Space Life Sciences: Provides links and information to space-based research (including NASA): http://www.nlm.nih.gov/databases/databases_space.html

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MEDLINE: Bibliographic database covering the fields of medicine, nursing, dentistry, veterinary medicine, the healthcare system, and the pre-clinical sciences: http://www.nlm.nih.gov/databases/databases_medline.html

14

Remember, for the general public, the National Library of Medicine recommends the databases referenced in MEDLINEplus (http://medlineplus.gov/ or http://www.nlm.nih.gov/medlineplus/databases.html). 15 See http://www.nlm.nih.gov/databases/databases.html.

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•

Toxicology and Environmental Health Information (TOXNET): Databases covering toxicology and environmental health: http://sis.nlm.nih.gov/Tox/ToxMain.html

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Visible Human Interface: Anatomically detailed, three-dimensional representations of normal male and female human bodies: http://www.nlm.nih.gov/research/visible/visible_human.html The Combined Health Information Database

A comprehensive source of information on clinical guidelines written for professionals is the Combined Health Information Database. You will need to limit your search to one of the following: Brochure/Pamphlet, Fact Sheet, or Information Package, and “obesity” using the “Detailed Search” option. Go directly to the following hyperlink: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For the publication date, select “All Years.” Select your preferred language and the format option “Fact Sheet.” Type “obesity” (or synonyms) into the “For these words:” box. The following is a sample result: •

Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report Source: Obesity Research. 6(Supplement 2): 51S-209S. September 1998. Contact: Available from North American Association for the Study of Obesity (NAASO). 8630 Fenton Street, Suite 412, Silver Spring, MD 20910. (301) 563-6526. Fax (301) 587-2365. Summary: This journal provides clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. The guidelines offer a state of the art review of the scientific basis of the relationship between obesity and major disease endpoints and of the scientific rationale for the management of overweight and obese patients. Section one presents the rationale for guidelines development, the objectives of the guidelines, guidelines development methodology, and a statement of assumptions. Intended users of the guidelines are also identified. Section two provides background information on overweight and obesity, focusing on the health and economic costs of overweight and obesity, the prevention of overweight and obesity, the health risks of overweight and obesity, weight loss and mortality, and environmental and genetic influences on the development of overweight and obesity. Section three examines randomized controlled trial evidence demonstrating the effect of weight loss on blood pressure, serum and plasma lipids and lipoproteins, fasting blood glucose and fasting insulin, and abdominal fat. This section also reviews evidence on the effectiveness of dietary therapy, physical therapy, combined diet and physical therapy, behavior therapy, pharmacotherapy, surgery, and other interventions for overweight and obesity treatment. Section four presents treatment guidelines. Topics include assessment and classification of overweight and obesity, assessment of risk status, evaluation of treatment strategy, exclusion from weight loss therapy, patient motivation, goals of weight loss and management, strategies for weight loss and management, smoking cessation, and the role of health professionals in weight loss therapy. Section five presents a summary of recommendations. Section six addresses the issue of future research, focusing on intervention approaches; causes and mechanisms of overweight and obesity; abdominal fat, body weight, and disease risk; and assessment methods. Section seven presents appendices. The journal also includes evidence report endorsements, a reference list, North American Association for the Study of Obesity

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(NAASO) standards of conducts, and NAASO policies and procedures for membership discipline. 8 appendices. 7 figures. 17 tables. 769 references. •

Report on the NIH Workshop on Pharmacologic Treatment of Obesity Source: American Journal of Clinical Nutrition. 60: 153-156. 1994. Contact: Reprint available from Weight-Control Information Network. 1 WIN Way, Bethesda, MD 20892-3665. (800) 946-8098 or (301) 984-7378. Fax (301) 984-7196. E-mail: [email protected]. PRICE: Single copy free. Summary: This article reports on a National Institutes of Health workshop on the pharmacologic treatment of obesity, which was held on September 1, 1992, in Atlanta. The article includes a summary of the workshop's presentations, discussions, recommendations, and conclusions. The summary was reviewed by members of the National Task Force on Prevention and Treatment of Obesity. The authors point out that although most other chronic diseases are treated with long term drug therapy, drugs have not played a large role in the treatment of obesity in America. The workshop concluded that pharmacologic agents may be effective in reducing body weight over a long period of time, but that drugs should be used as only one component of a comprehensive, long term weight-loss program. Additional research is needed on the long term effectiveness and safety of drugs for obesity. An appendix lists symposium participants. 33 references. (AA-M).

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Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity, 2001 Source: Rockville, MD, U.S. Department of Health and Human Services, Public Health Service, Office of the Surgeon General, 75 p., 2001. Contact: Superintendent of Documents, U.S. Government Printing Office, Mail Stop SSOP, Washington, DC 20402-0001. (866) 512-1800; (202) 512-1800. FAX: (202) 512-2250. INTERNET/EMAIL: http://www.bookstore.GPO.gov; http://surgeongeneral.gov/topics/obesity/calltoaction/CalltoAction.pdf. Summary: Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity, 2001 represents an opportunity for people to make healthy lifestyle choices for themselves and their families. It encourages health care providers to help people prevent and treat the new health care challenges of overweight and obesity. Goals are to (1) promote the recognition of overweight and obesity as a major public health problem, (2) help Americans balance healthful eating with regular physical activity, (3) identify effective and culturally appropriate interventions, (4) encourage environmental changes to help prevent overweight and obesity, and (5) develop and enhance public-private partnerships to help implement this vision. Section 1, Overweight and Obesity as Public Health Problems in America, includes information on measuring overweight and obesity, health risks, economic consequences, epidemiology, disparities in prevalence, and health benefits of weight loss. Section 2, Posing Questions and Developing Strategies, focuses on developing a public health response, and communication, action, research, and evaluation to address overweight and obesity in various settings (families and communities, schools, health care, media and communications, and worksites). Section 3, The Power of People and Ideas, focuses on creating and sustaining national action. Section 4, Vision for the Future, discusses the Surgeon General's priorities for action in the areas of communication, action, research, and evaluation. Appendixes present examples of federal programs and initiatives and a federal program resource list.

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Burden of Cardiovascular Disease and Obesity in the State of Illinois Source: Springfield, IL, Illinois Department of Public Health, Office of Health Promotion, 6 p., June 30, 2000. Contact: Illinois Department of Public Health, Office of Health Promotion, 535 West Jefferson Street, 2nd floor, Springfield, IL 62761. (217) 785-4093. FAX: (217) 524-2831. Summary: Burden of Cardiovascular Disease and Obesity in the State of Illinois is a report to the Governor of Illinois and the Illinois General Assembly. The Illinois Cardiovascular Disease (CVD) Prevention Task Force was tasked with (1) examining the incidence of, and cause of, heart disease and stroke; (2) developing a profile of the heart disease and stroke burden in Illinois; and (3) recommending changes needed in laws, regulations, programs, policies, and services to enhance the prevention of heart disease and stroke. The task force found that (1) CVD is the leading cause of death in Illinois; (2) more than 42,000 Illinoisans die from CVD each year; (3) CVD death rates are high for all Illinoisans, but the rates for nonwhites exceed those for whites; (4) total health care costs for heart disease and stroke in Illinois approach $4 billion annually; (5) more than 3.6 million adults in Illinois are obese; (6) 88 percent of all Illinoisans have at least one risk factor for CVD; and (7) health care costs attributable to obesity approach $700 million annually. The task force generated 14 recommendations based on these facts. These recommendations focus on (1) education, (2) physical activity, (3) secondary prevention, (4) data management and surveillance, (5) nutrition, (6) advocacy, and (7) tobacco. The task force calls upon the Illinois General Assembly to fund five first-steps to address the CVD problem in the state: (1) Pilot a program to develop motor skills and to increase nutrition awareness and knowledge within the state's six Head Start program sites; (2) implement the Coordinated Approach to Child Health (CATCH) program in 14 elementary schools; (3) fund the deployment of the Take Charge Challenge, a worksite-based physical activity and nutrition program, at six employers in Illinois; (4) establish Project Active programs to bring about community-wide changes in the physical activity status of Illinoisans in six communities; and (5) fund a multidisciplinary program designed to teach congestive heart failure patients to participate in and manage their conditions more successfully.

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Status of Obesity in Georgia, 2000 Source: Georgia Department of Human Resources, Division of Public Health, Nutrition Section, 15 p., 2000. Contact: Georgia Department of Human Resources, Division of Public Health, Family Health Branch, Nutrition Section, Two Peachtree Street, Suite 11-222, Atlanta, GA 303033142. (404) 657-2884. FAX: (404) 657-2886. INTERNET/EMAIL: http://health.state.ga.us/programs/nutrition; http:/www.ph.dhr.state.ga.us/programs/nutrition/pdfs/obesity2000.pdf. Publication no. DPH01.15HW. Summary: Status of Obesity in Georgia, 2000 reports on the problem of obesity in Georgia and approaches for addressing the problem. The report (1) presents background information on obesity among Georgia residents; (2) summarizes obesityrelated diseases; (3) describes specific populations in Georgia toward which obesity prevention initiatives should be directed; (4) discusses barriers to obesity control and prevention, including physical inactivity, environmental barriers to exercise, television viewing, commercial food marketing practices, and children's eating behaviors; (5) discusses the results of a 1996 survey of perceived barriers to physical activity conducted by the Office of Nutrition, Georgia Department of Health; (6) discusses

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initiatives aimed at preventing and managing obesity implemented by Georgia organizations in 2000; (7) describes the Take Charge of Your Health Campaign, designed to motivate Georgia residents to accept personal responsibility for their own and their family's health; and (8) presents recommendations for halting the epidemic of obesity. The Take Charge program focuses on three behaviors to reduce the risk of chronic diseases associated with obesity using social marketing techniques: (1) Eating five servings of fruits and vegetables daily, (2) eating less fatty foods, and (3) being more physically active. •

Obesity and Overweight in Maryland Source: Baltimore, MD, Division of Cardiovascular Health and Nutrition, Maryland Department of Health and Mental Hygiene, 9 p., November 1999. Contact: Division of Cardiovascular Health and Nutrition, Maryland Department of Health and Mental Hygiene, 6 St. Paul Street, Suite 1202, Baltimore, MD 21202. (410) 767-6778. FAX: (410) 333-8926. INTERNET/EMAIL: http://www.fha.state.md.us/ocd/cardio/pdf/obesity.pdf. Summary: Obesity and Overweight in Maryland provides information on the prevalence of overweight and obesity in Maryland, the effects on health, guidelines for treatment and prevention, and current activities in Maryland to reduce the prevalence of overweight and obesity. Disease burdens associated with overweight and obesity include cardiovascular disease, diabetes (type II), hypertension, arthritis, and cancer. In Maryland, the prevalence of obesity increased by 75.8 percent between 1991 and 1998. By 1998, 20.5 percent of adult Marylanders were obese. Over the past 30 years the prevalence of childhood obesity increased by about 50 percent nationally. Childhood and adolescent obesity is more prevalent in African American and Hispanic populations. The report lists current guidelines in the treatment and prevention of overweight and obesity. Current activities to reduce the prevalence of these conditions in Maryland include (1) Move It Maryland, (2) a conference on addressing childhood obesity through schools, (3) a community nutrition education exposition, (4) partnerships with local health departments, (5) the National Partnership for Healthy Weight Management, and (6) the Maryland State Advisory Council on Physical Fitness. The report offers recommendations for weight control. 6 figures, 6 references.

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Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report: Executive Summary Source: Bethesda, MD, National Institutes of Health, National Heart, Lung, and Blood Institute, 21 p., June 1998. Contact: National Heart, Lung, and Blood Institute (NHLBI) Health Information Network, P.O. Box 30105, Bethesda, MD 20824-0105. (301) 592-8573. FAX: (301) 592-8563. INTERNET/EMAIL: http://www.nhlbi.nih.gov/guidelines/obesity/ob_xsum.htm. Summary: Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report: Executive Summary summarizes the evidence used in developing clinical guidelines for identifying, evaluating, and treating overweight and obesity in adults. The guidelines were developed by an expert panel convened in May 1995 by the National Heart, Lung, and Blood Institute's Obesity Education Initiative in cooperation with the National Institute of Diabetes and Digestive and Kidney Diseases. The guidelines are based on a systematic review of the published scientific literature found in MEDLINE from January 1980 to September 1997 dealing with overweight and obesity issues. The guidelines

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contain evidence-based recommendations that address the following issues and topics: (1) Advantages of weight loss on blood pressure and hypertension, serum/plasma lipid concentrations, and fasting blood glucose and insulin; (2) measurement of the degree of overweight and obesity; (3) goals for weight loss and weight management; (4) strategies for achieving weight loss; (5) goals for weight loss maintenance; and (6) special treatment groups, such as smokers and older adults. There is evidence that the body mass index can be used to assess overweight and obesity, and body weight alone can be used to follow weight loss and evaluate the effectiveness of weight loss programs. •

Obesity: Reversing the Increasing Problem of Obesity in England: A Report From the Nutrition and Physical Activity Task Forces Source: London, England, Great Britain Department of Health, 34 p., October 1995. Contact: Great Britain Department of Health, P.O. Box 410, Wetherby LS23 7LN, England. Summary: Obesity: Reversing the Increasing Problem of Obesity in England: A Report From the Nutrition and Physical Activity Task Forces charts the increase in the levels of obesity in the United Kingdom over the last 15 years and discusses possible reasons for the increase in and the risks associated with obesity. The prevalence of obesity in England has increased from 6 percent of men and 8 percent of women in 1980 to 13 percent of men and 16 percent of women in 1993. The Health of the Nation target is to reduce the prevalence of obesity to the levels seen in 1980. Chapters include (1) an introduction; (2) the problem of obesity, including the measurement of obesity, obesity as a risk factor for chronic disease, blood pressure and cholesterol levels, individual factors, smoking, and fat distribution; (3) the extent of the problem of obesity in the United Kingdom; (4) factors that might explain the increase in body mass index; (5) factors controlling energy balance; (6) dietary factors contributing to obesity; (7) physical activity; (8) addressing the problem of obesity; and (9) conclusion. Task force members recommend (1) that actions be taken by the National Health Service, local authorities, schools, employers, and industry to address the problem of obesity; (2) the development and evaluation of new approaches to helping individuals achieve and maintain a healthy weight; and (3) the establishment of an Obesity Focus Group to assess current evidence of the effectiveness of weight loss strategies, advise on the best means of improving the delivery of appropriate weight loss services to those needing to lose weight, identify and prioritize specific areas for further research into effective strategies for the prevention of obesity, and advise on the development and evaluation of new approaches to helping individuals achieve and maintain a healthy weight. Appendixes include (1) a list of task force members, (2) the report of an obesity symposium, and (3) a list of background papers.

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Maternal Obesity and Excess Risk of Perinatal Mortality: Evidence From a Large Biracial Population Source: Raleigh, NC, State Center for Health and Environmental Statistics, 11 p., March 1994. Contact: State Center for Health and Environmental Statistics, P.O. Box 29538, Raleigh, NC 27626. Summary: Maternal Obesity and Excess Risk of Perinatal Mortality: Evidence From a Large Biracial Population reports on results of retrospective research conducted in North Carolina during 1988-1990. To investigate the risk of perinatal death associated with maternal obesity, a cohort of low-income women (45,651 African Americans and

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40,929 whites) who participated in the North Carolina Special Supplemental Food Program for Women, Infants and Children (WIC) program during 1988-1990 was evaluated retrospectively. WIC provides food and nutrition education to low-income pregnant, postpartum, and breast feeding women, infants, and children under age 5. Data sources included WIC certification records and vital records (i.e., birth certificates, fetal death reports, and infant death reports). Perinatal mortality rate ratios for moderate overweight and obesity were calculated using normal weight women as the referent group. A logistic regression analysis provided adjusted estimates of the relative risks of perinatal mortality associated with maternal overweight and obesity. Maternal obesity was associated with an excess risk of perinatal death among both African-American (RR = 1.4) and white (RR = 1.6) women, after adjustment for maternal age, education, parity, cigarette smoking, gestational weight gain, diabetes, and hypertension. The excess risk of perinatal mortality among infants of obese women corresponded to 5.4 and 6.7 excess deaths per 1,000, respectively. There was no overall elevated risk of perinatal death among infants of moderately overweight women for either race. For both AfricanAmerican and white women, stronger associations of maternal obesity with perinatal mortality were observed among women under age 18, women over age 35, and women with adequate or excessive gestational weight gain. Results confirm that obesity is a major risk factor for perinatal mortality, not solely due to risk factors associated with obesity, such as diabetes and hypertension. The high prevalence of obesity among lowincome women, which leads to high rates of chronic disease in later life, adversely affects reproductive outcomes as well. 6 tables, 36 references. •

Behavioral Risk Factor Surveillance System: Overweight in New York State Source: BRFSS-Summary Report. 3(1): 4 p., Summer 1996. Contact: New York State Department of Health, Bureau of Chronic Disease Epidemiology and Surveillance, Empire State Plaza, Room 557, Corning Tower, Albany, NY 12237-0679. (518) 474-2460. Summary: The authors provide data on overweight in New York residents, based on data from various sources, including the 1996 New York Behavioral Risk Factor Surveillance System (BRFSS), the National Health Interview Survey, the Pediatric Nutrition Surveillance System, and surveys of school children across the state. From 1989 to 1991, 25.4 to 25.9 percent of adults in New York State were considered obese. Obesity ranged from 23.8 percent in white women to 39.7 percent in black women. The prevalence of overweight among school children in New York City was 34.5 percent, while the prevalence among children from the rest of the state was 27.9 percent. The prevalence of overweight among preschool children in New York State was 10.7 percent. Hispanic American preschool children were more likely to be overweight. The public health response to these data should be to (1) emphasize the importance of improving eating habits and increasing physical activity; (2) emphasize the prevention of overweight, especially in children; and (3) implement environmental and policy initiatives that make it easier for people to eat better and be more active.

The NLM Gateway16

16

Adapted from NLM: http://gateway.nlm.nih.gov/gw/Cmd?Overview.x.

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The NLM (National Library of Medicine) Gateway is a Web-based system that lets users search simultaneously in multiple retrieval systems at the U.S. National Library of Medicine (NLM). It allows users of NLM services to initiate searches from one Web interface, providing one-stop searching for many of NLM’s information resources or databases.17 To use the NLM Gateway, simply go to the search site at http://gateway.nlm.nih.gov/gw/Cmd. Type “obesity” (or synonyms) into the search box and click “Search.” The results will be presented in a tabular form, indicating the number of references in each database category. Results Summary Category Journal Articles Books / Periodicals / Audio Visual Consumer Health Meeting Abstracts Other Collections Total

Items Found 68450 1540 309 201 52 70552

HSTAT18 HSTAT is a free, Web-based resource that provides access to full-text documents used in healthcare decision-making.19 These documents include clinical practice guidelines, quickreference guides for clinicians, consumer health brochures, evidence reports and technology assessments from the Agency for Healthcare Research and Quality (AHRQ), as well as AHRQ’s Put Prevention Into Practice.20 Simply search by “obesity” (or synonyms) at the following Web site: http://text.nlm.nih.gov.

Coffee Break: Tutorials for Biologists21 Coffee Break is a general healthcare site that takes a scientific view of the news and covers recent breakthroughs in biology that may one day assist physicians in developing treatments. Here you will find a collection of short reports on recent biological discoveries. Each report incorporates interactive tutorials that demonstrate how bioinformatics tools are used as a part of the research process. Currently, all Coffee Breaks are written by NCBI staff.22 Each report is about 400 words and is usually based on a discovery reported in one or 17

The NLM Gateway is currently being developed by the Lister Hill National Center for Biomedical Communications (LHNCBC) at the National Library of Medicine (NLM) of the National Institutes of Health (NIH). 18 Adapted from HSTAT: http://www.nlm.nih.gov/pubs/factsheets/hstat.html. 19

The HSTAT URL is http://hstat.nlm.nih.gov/.

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Other important documents in HSTAT include: the National Institutes of Health (NIH) Consensus Conference Reports and Technology Assessment Reports; the HIV/AIDS Treatment Information Service (ATIS) resource documents; the Substance Abuse and Mental Health Services Administration's Center for Substance Abuse Treatment (SAMHSA/CSAT) Treatment Improvement Protocols (TIP) and Center for Substance Abuse Prevention (SAMHSA/CSAP) Prevention Enhancement Protocols System (PEPS); the Public Health Service (PHS) Preventive Services Task Force's Guide to Clinical Preventive Services; the independent, nonfederal Task Force on Community Services’ Guide to Community Preventive Services; and the Health Technology Advisory Committee (HTAC) of the Minnesota Health Care Commission (MHCC) health technology evaluations. 21 Adapted from http://www.ncbi.nlm.nih.gov/Coffeebreak/Archive/FAQ.html. 22

The figure that accompanies each article is frequently supplied by an expert external to NCBI, in which case the source of the figure is cited. The result is an interactive tutorial that tells a biological story.

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more articles from recently published, peer-reviewed literature.23 This site has new articles every few weeks, so it can be considered an online magazine of sorts. It is intended for general background information. You can access the Coffee Break Web site at the following hyperlink: http://www.ncbi.nlm.nih.gov/Coffeebreak/.

Other Commercial Databases In addition to resources maintained by official agencies, other databases exist that are commercial ventures addressing medical professionals. Here are some examples that may interest you: •

CliniWeb International: Index and table of contents to selected clinical information on the Internet; see http://www.ohsu.edu/cliniweb/.

•

Medical World Search: Searches full text from thousands of selected medical sites on the Internet; see http://www.mwsearch.com/.

The Genome Project and Obesity In the following section, we will discuss databases and references which relate to the Genome Project and obesity. Online Mendelian Inheritance in Man (OMIM) The Online Mendelian Inheritance in Man (OMIM) database is a catalog of human genes and genetic disorders authored and edited by Dr. Victor A. McKusick and his colleagues at Johns Hopkins and elsewhere. OMIM was developed for the World Wide Web by the National Center for Biotechnology Information (NCBI).24 The database contains textual information, pictures, and reference information. It also contains copious links to NCBI’s Entrez database of MEDLINE articles and sequence information. To search the database, go to http://www.ncbi.nlm.nih.gov/Omim/searchomim.html. Type “obesity” (or synonyms) into the search box, and click “Submit Search.” If too many results appear, you can narrow the search by adding the word “clinical.” Each report will have additional links to related research and databases. In particular, the option “Database Links” will search across technical databases that offer an abundance of information. The following is an example of the results you can obtain from the OMIM for obesity: •

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Abdominal Obesity-metabolic Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605552

After a brief introduction that sets the work described into a broader context, the report focuses on how a molecular understanding can provide explanations of observed biology and lead to therapies for diseases. Each vignette is accompanied by a figure and hypertext links that lead to a series of pages that interactively show how NCBI tools and resources are used in the research process. 24 Adapted from http://www.ncbi.nlm.nih.gov/. Established in 1988 as a national resource for molecular biology information, NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing genome data, and disseminates biomedical information--all for the better understanding of molecular processes affecting human health and disease.

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Abdominal Obesity-metabolic Syndrome Qtl2 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?605572

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Adiposis Dolorosa Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?103200

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Choroideremia with Deafness and Obesity Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?303110

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Coloboma-obesity-hypogenitalism-mental Retardation Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601794

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Mental Retardation with Distinctive Mouth, Obesity, and Hypogonadism Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?309490

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Mental Retardation, Epileptic Seizures, Hypogonadism and Hypogenitalism, Microcephaly, and Obesity Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?300148

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Mental Retardation, Obesity, Mandibular Prognathism, and Eye and Skin Anomalies Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?606772

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Obesity Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?601665

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Obesity and Endocrinopathy due to Impaired Processing of Prohormones Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?600955

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Obesity Quantitative Trait Locus on Chromosome 20 Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?602025

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Obesity Quantitative Trait Locus on Chromosome X Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?300306

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Obesity, Susceptibility To, on Chromosome 10p Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?603188

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Obesity, Susceptibility To, on Chromosome 10q Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?607514

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Obesity-hypoventilation Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?257500

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Prolactin Deficiency with Obesity and Enlarged Testes Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?264120

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Short Stature-obesity Syndrome Web site: http://www.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?269870 Genes and Disease (NCBI - Map)

The Genes and Disease database is produced by the National Center for Biotechnology Information of the National Library of Medicine at the National Institutes of Health. This Web site categorizes each disorder by system of the body. Go to http://www.ncbi.nlm.nih.gov/disease/, and browse the system pages to have a full view of important conditions linked to human genes. Since this site is regularly updated, you may wish to revisit it from time to time. The following systems and associated disorders are addressed:

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•

Cancer: Uncontrolled cell division. Examples: Breast and ovarian cancer, Burkitt lymphoma, chronic myeloid leukemia, colon cancer, lung cancer, malignant melanoma, multiple endocrine neoplasia, neurofibromatosis, p53 tumor suppressor, pancreatic cancer, prostate cancer, Ras oncogene, RB: retinoblastoma, von Hippel-Lindau syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Cancer.html

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Immune System: Fights invaders. Examples: Asthma, autoimmune polyglandular syndrome, Crohn’s disease, DiGeorge syndrome, familial Mediterranean fever, immunodeficiency with Hyper-IgM, severe combined immunodeficiency. Web site: http://www.ncbi.nlm.nih.gov/disease/Immune.html

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Metabolism: Food and energy. Examples: Adreno-leukodystrophy, atherosclerosis, Best disease, Gaucher disease, glucose galactose malabsorption, gyrate atrophy, juvenile-onset diabetes, obesity, paroxysmal nocturnal hemoglobinuria, phenylketonuria, Refsum disease, Tangier disease, Tay-Sachs disease. Web site: http://www.ncbi.nlm.nih.gov/disease/Metabolism.html

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Muscle and Bone: Movement and growth. Examples: Duchenne muscular dystrophy, Ellis-van Creveld syndrome, Marfan syndrome, myotonic dystrophy, spinal muscular atrophy. Web site: http://www.ncbi.nlm.nih.gov/disease/Muscle.html

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Nervous System: Mind and body. Examples: Alzheimer disease, amyotrophic lateral sclerosis, Angelman syndrome, Charcot-Marie-Tooth disease, epilepsy, essential tremor, fragile X syndrome, Friedreich’s ataxia, Huntington disease, Niemann-Pick disease, Parkinson disease, Prader-Willi syndrome, Rett syndrome, spinocerebellar atrophy, Williams syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Brain.html

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Signals: Cellular messages. Examples: Ataxia telangiectasia, Cockayne syndrome, glaucoma, male-patterned baldness, SRY: sex determination, tuberous sclerosis, Waardenburg syndrome, Werner syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Signals.html

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Transporters: Pumps and channels. Examples: Cystic fibrosis, deafness, diastrophic dysplasia, Hemophilia A, long-QT syndrome, Menkes syndrome, Pendred syndrome, polycystic kidney disease, sickle cell anemia, Wilson’s disease, Zellweger syndrome. Web site: http://www.ncbi.nlm.nih.gov/disease/Transporters.html Entrez

Entrez is a search and retrieval system that integrates several linked databases at the National Center for Biotechnology Information (NCBI). These databases include nucleotide sequences, protein sequences, macromolecular structures, whole genomes, and MEDLINE through PubMed. Entrez provides access to the following databases: •

3D Domains: Domains from Entrez Structure, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo

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Books: Online books, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=books

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Genome: Complete genome assemblies, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Genome

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NCBI’s Protein Sequence Information Survey Results: Web site: http://www.ncbi.nlm.nih.gov/About/proteinsurvey/

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Nucleotide Sequence Database (Genbank): Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Nucleotide

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OMIM: Online Mendelian Inheritance in Man, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=OMIM

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PopSet: Population study data sets, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Popset

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ProbeSet: Gene Expression Omnibus (GEO), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=geo

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Protein Sequence Database: Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Protein

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PubMed: Biomedical literature (PubMed), Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed

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Structure: Three-dimensional macromolecular structures, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Structure

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Taxonomy: Organisms in GenBank, Web site: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Taxonomy

To access the Entrez system at the National Center for Biotechnology Information, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=genome, and then select the database that you would like to search. The databases available are listed in the drop box next to “Search.” Enter “obesity” (or synonyms) into the search box and click “Go.” Jablonski’s Multiple Congenital Anomaly/Mental Retardation (MCA/MR) Syndromes Database25 This online resource has been developed to facilitate the identification and differentiation of syndromic entities. Special attention is given to the type of information that is usually limited or completely omitted in existing reference sources due to space limitations of the printed form. At http://www.nlm.nih.gov/mesh/jablonski/syndrome_toc/toc_a.html, you can search across syndromes using an alphabetical index. Search by keywords at http://www.nlm.nih.gov/mesh/jablonski/syndrome_db.html.

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Adapted from the National Library of Medicine: http://www.nlm.nih.gov/mesh/jablonski/about_syndrome.html.

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The Genome Database26 Established at Johns Hopkins University in Baltimore, Maryland in 1990, the Genome Database (GDB) is the official central repository for genomic mapping data resulting from the Human Genome Initiative. In the spring of 1999, the Bioinformatics Supercomputing Centre (BiSC) at the Hospital for Sick Children in Toronto, Ontario assumed the management of GDB. The Human Genome Initiative is a worldwide research effort focusing on structural analysis of human DNA to determine the location and sequence of the estimated 100,000 human genes. In support of this project, GDB stores and curates data generated by researchers worldwide who are engaged in the mapping effort of the Human Genome Project (HGP). GDB’s mission is to provide scientists with an encyclopedia of the human genome which is continually revised and updated to reflect the current state of scientific knowledge. Although GDB has historically focused on gene mapping, its focus will broaden as the Genome Project moves from mapping to sequence, and finally, to functional analysis. To access the GDB, simply go to the following hyperlink: http://www.gdb.org/. Search “All Biological Data” by “Keyword.” Type “obesity” (or synonyms) into the search box, and review the results. If more than one word is used in the search box, then separate each one with the word “and” or “or” (using “or” might be useful when using synonyms).

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Adapted from the Genome Database: http://gdbwww.gdb.org/gdb/aboutGDB.html - mission.

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APPENDIX B. PATIENT RESOURCES Overview Official agencies, as well as federally funded institutions supported by national grants, frequently publish a variety of guidelines written with the patient in mind. These are typically called “Fact Sheets” or “Guidelines.” They can take the form of a brochure, information kit, pamphlet, or flyer. Often they are only a few pages in length. Since new guidelines on obesity can appear at any moment and be published by a number of sources, the best approach to finding guidelines is to systematically scan the Internet-based services that post them.

Patient Guideline Sources The remainder of this chapter directs you to sources which either publish or can help you find additional guidelines on topics related to obesity. Due to space limitations, these sources are listed in a concise manner. Do not hesitate to consult the following sources by either using the Internet hyperlink provided, or, in cases where the contact information is provided, contacting the publisher or author directly. The National Institutes of Health The NIH gateway to patients is located at http://health.nih.gov/. From this site, you can search across various sources and institutes, a number of which are summarized below. Topic Pages: MEDLINEplus The National Library of Medicine has created a vast and patient-oriented healthcare information portal called MEDLINEplus. Within this Internet-based system are “health topic pages” which list links to available materials relevant to obesity. To access this system, log on to http://www.nlm.nih.gov/medlineplus/healthtopics.html. From there you can either search using the alphabetical index or browse by broad topic areas. Recently, MEDLINEplus listed the following when searched for “obesity”:

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Other Guides Diabetes http://www.nlm.nih.gov/medlineplus/diabetes.html Heart Diseases http://www.nlm.nih.gov/medlineplus/heartdiseasesgeneral.html Metabolic Syndrome X http://www.nlm.nih.gov/medlineplus/metabolicsyndromex.html Weight Loss Surgery http://www.nlm.nih.gov/medlineplus/weightlosssurgery.html

Within the health topic page dedicated to obesity, the following was listed: •

General/Overviews Defining Overweight and Obesity Source: National Center for Chronic Disease Prevention and Health Promotion http://www.cdc.gov/nccdphp/dnpa/obesity/defining.htm JAMA Patient Page: Are You Obese? Source: American Medical Association http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZ805URJAC&s ub_cat=382 Obesity http://www.4woman.gov/faq/Easyread/obesity-etr.htm Overweight and Obesity: Frequently Asked Questions Source: National Center for Chronic Disease Prevention and Health Promotion http://www.cdc.gov/nccdphp/dnpa/obesity/faq.htm

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Diagnosis/Symptoms Body Mass Index Chart Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/guidelines/obesity/bmi_tbl.htm Calculate Your Body Mass Index Source: National Heart, Lung, and Blood Institute http://www.nhlbisupport.com/bmi/

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Treatment MEDLINEplus: Weight Loss Surgery Source: National Library of Medicine http://www.nlm.nih.gov/medlineplus/weightlosssurgery.html Prescription Medications for the Treatment of Obesity Source: Weight-control Information Network http://www.niddk.nih.gov/health/nutrit/pubs/presmeds.htm Questions and Answers About Safety of Phenylpropanolamine Source: Center for Drug Evaluation and Research http://www.fda.gov/cder/drug/infopage/ppa/qa.htm

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Very Low-Calorie Diets Source: Weight-control Information Network http://www.niddk.nih.gov/health/nutrit/pubs/vlcd.htm •

Nutrition Eating Healthy Starts with Healthy Food Shopping Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/heart/obesity/lose_wt/shop.htm Eating Healthy with Ethnic Food Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/heart/obesity/lose_wt/eth_dine.htm Weight Control: Eating Right and Keeping Fit Source: American College of Obstetricians and Gynecologists http://www.medem.com/medlb/article_detaillb.cfm?article_ID=ZZZOFUWF97C &sub_cat=382

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Specific Conditions/Aspects Active at Any Size Source: Weight-control Information Network http://www.niddk.nih.gov/health/nutrit/activeatanysize/active.html American Diabetes Association Survey Finds Overweight & Obese Americans Don't Believe They Are At Risk for Diabetes Source: American Diabetes Association http://ada.yellowbrix.com/pages/ada/Story.nsp?story_id=41504111&ID=ada Factors Contributing to Obesity Source: National Center for Chronic Disease Prevention and Health Promotion http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm Losing Weight: More Than Counting Calories Source: Food and Drug Administration http://www.fda.gov/fdac/features/2002/102_fat.html Obesity and Cancer Source: National Cancer Institute http://cis.nci.nih.gov/fact/3_70.htm Overweight, Obesity Threaten U.S. Health Gains Source: Food and Drug Administration http://www.fda.gov/fdac/features/2002/202_fat.html

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Children Body Mass Index-for-Age (Children) Source: National Center for Chronic Disease Prevention and Health Promotion http://www.cdc.gov/nccdphp/dnpa/bmi/bmi-for-age.htm Childhood Obesity on the Rise Source: National Institutes of Health http://www.nih.gov/news/WordonHealth/jun2002/childhoodobesity.htm

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Childhood Obesity: Parenting Advice Source: Mayo Foundation for Medical Education and Research http://www.mayoclinic.com/invoke.cfm?id=FL00058 •

From the National Institutes of Health Aim for a Healthy Weight: Key Recommendations Source: National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/health/public/heart/obesity/lose_wt/recommen.htm Do You Know the Health Risks of Being Overweight? Source: Weight-control Information Network http://www.niddk.nih.gov/health/nutrit/pubs/health.htm Understanding Adult Obesity Source: Weight-control Information Network http://www.niddk.nih.gov/health/nutrit/pubs/unders.htm

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Journals/Newsletters WIN Notes Source: Weight-control Information Network http://www.niddk.nih.gov/health/nutrit/winnotes/wnotes.htm

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Latest News American Diabetes Association Survey Finds Overweight & Obese Americans Don't Believe They Are At Risk for Diabetes Source: 09/09/2003, American Diabetes Association http://ada.yellowbrix.com/pages/ada/Story.nsp?story_id=41504111&ID=ada Experts Say 'Portion Distortion' Raises Cancer Risk Source: 09/17/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14028 .html Metabolic Syndrome Puts Some Teens At Risk Source: 09/09/2003, American Diabetes Association http://ada.yellowbrix.com/pages/ada/Story.nsp?story_id=41504351&ID=ada More News on Obesity http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/alphanews_o.html#O besity Obesity in Children Linked with Asthma Risk Source: 09/19/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14034 .html Surgery Can Reduce Breathing Problems in Obese Kids Source: 09/19/2003, Reuters Health http://www.nlm.nih.gov//www.nlm.nih.gov/medlineplus/news/fullstory_14032 .html

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Law and Policy Disability Due to Obesity Source: American Obesity Association http://www.obesity.org/subs/disability/ Discrimination: Employment Source: American Obesity Association http://www.obesity.org/discrimination/employment.shtml Health Insurance Coverage for Obesity Source: American Obesity Association http://www.obesity.org/treatment/health.shtml Tax Breaks for Obesity Source: American Obesity Association http://www.obesity.org/subs/tax/taxbreak.shtml

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Lists of Print Publications Weight Control and Obesity Source: Food and Nutrition Information Center http://www.nal.usda.gov/fnic/pubs/bibs/topics/weight/consumer.html

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Organizations American Obesity Association http://www.obesity.org/ National Heart, Lung, and Blood Institute http://www.nhlbi.nih.gov/ National Institute of Diabetes and Digestive and Kidney Diseases http://www.niddk.nih.gov/ Weight-control Information Network Source: National Institute of Diabetes and Digestive and Kidney Diseases http://www.niddk.nih.gov/health/nutrit/win.htm

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Prevention/Screening Physical Activity and Good Nutrition: Essential Elements to Prevent Chronic Diseases and Obesity Source: Centers for Disease Control and Prevention http://www.cdc.gov/nccdphp/aag/aag_dnpa.htm

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Research Designer Mice Eat More, Weigh Less Source: National Institute of General Medical Sciences http://www.nigms.nih.gov/news/releases/brief_wakil.html Drug Targets Brain Circuits That Drive Appetite and Body Weight Source: National Institute of Mental Health http://www.nih.gov/news/pr/jul2002/nimh-25.htm

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Elevated Leptin in Teens Linked with Dangerous Artery Changes Source: American Heart Association http://www.americanheart.org/presenter.jhtml%3Bjsessionid=FTFPLYDILVGP3W FZOAGSCZQ?identifier=3005364 Journal of the American Medical Association Study: Efficacy and Safety of LowCarbohydrate Diets Source: American Heart Association http://www.americanheart.org/presenter.jhtml?identifier=3010801 Many Obese Youth Have Condition That Precedes Type 2 Diabetes Source: National Institute of Child Health and Human Development http://www.nih.gov/news/pr/mar2002/nichd-13.htm Maternal Obesity and Risk for Birth Defects http://www.cdc.gov/ncbddd/factsheets/pediatrics/Pediatrics_maternal_obesity.p df Metabolic Syndrome Puts Some Teens At Risk Source: American Diabetes Association http://ada.yellowbrix.com/pages/ada/Story.nsp?story_id=41504351&ID=ada NHLBI's Framingham Heart Study Finds Overweight/Obesity and Risk for Heart Failure Source: National Heart, Lung, and Blood Institute http://www.nih.gov/news/pr/jul2002/nhlbi-31.htm

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Obesity and Acute Mountain Sickness Source: American College of Physicians http://www.annals.org/cgi/content/full/139/4/I-41 Overweight and Obesity by Middle Age Are Associated with Shortened Lifespan Source: American College of Physicians http://www.annals.org/cgi/content/full/138/1/I-44 Pathological Obesity and Drug Addiction Share Common Brain Characteristics Source: National Institute on Drug Abuse http://www.nida.nih.gov/NIDA_Notes/NNVol16N4/pathological.html •

Statistics FASTATS: Overweight Prevalence Source: National Center for Health Statistics http://www.cdc.gov/nchs/fastats/overwt.htm Improving Nutrition and Increasing Physical Activity Source: National Center for Chronic Disease Prevention and Health Promotion http://www.cdc.gov/nccdphp/bb_nutrition/index.htm National Health and Nutrition Examination Survey: Healthy Weight, Overweight, and Obesity Among U.S. Adults http://www.cdc.gov/nchs/data/nhanes/databriefs/adultweight.pdf New State Data Show Obesity and Diabetes Still On the Rise Source: Centers for Disease Control and Prevention http://www.cdc.gov/od/oc/media/pressrel/r021231.htm

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Obesity Still on the Rise, New Data Show Source: National Center for Health Statistics http://www.cdc.gov/nchs/releases/02news/obesityonrise.htm Obesity Trends: Prevalence of Obesity Among U.S. Adults, Region and State Source: National Center for Chronic Disease Prevention and Health Promotion http://www.cdc.gov/nccdphp/dnpa/obesity/trend/prev_reg.htm Prevalence among U.S. Adults of a Metabolic Syndrome Associated with Obesity Source: Centers for Disease Control and Prevention http://www.cdc.gov/nccdphp/dnpa/obesity/trend/metabolic.htm Prevalence of Obesity Among Adults Aged 20 Years and Over: United States, 1997 - 2002 Source: National Center for Health Statistics http://www.cdc.gov/nchs/about/major/nhis/released200212/figures06_16_3.htm Preventing Obesity and Chronic Diseases Through Good Nutrition and Physical Activity Source: National Center for Chronic Disease Prevention and Health Promotion http://www.cdc.gov/nccdphp/pe_factsheets/pe_pa.htm Statistics Related to Overweight and Obesity Source: Weight-control Information Network http://www.niddk.nih.gov/health/nutrit/pubs/statobes.htm You may also choose to use the search utility provided by MEDLINEplus at the following Web address: http://www.nlm.nih.gov/medlineplus/. Simply type a keyword into the search box and click “Search.” This utility is similar to the NIH search utility, with the exception that it only includes materials that are linked within the MEDLINEplus system (mostly patient-oriented information). It also has the disadvantage of generating unstructured results. We recommend, therefore, that you use this method only if you have a very targeted search. The Combined Health Information Database (CHID) CHID Online is a reference tool that maintains a database directory of thousands of journal articles and patient education guidelines on obesity. CHID offers summaries that describe the guidelines available, including contact information and pricing. CHID’s general Web site is http://chid.nih.gov/. To search this database, go to http://chid.nih.gov/detail/detail.html. In particular, you can use the advanced search options to look up pamphlets, reports, brochures, and information kits. The following was recently posted in this archive: •

Gastrointestinal Surgery for Severe Obesity Source: Bethesda, MD: National Institutes of Health. 1991. 22 p. Contact: Available from National Institutes of Health. Office of Medical Applications of Research, Building 1, Room 260, Bethesda, MD 20892. (301) 496-1144. Summary: The National Institutes of Health Consensus Development Conference on Gastrointestinal Surgery for Severe Obesity brought together surgeons, gastroenterologists, endocrinologists, psychiatrists, nutritionists, and other health care professionals as well as the public in March of 1991. The conference addressed the

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nonsurgical treatment options for severe obesity, the surgical treatments for severe obesity and the criteria for selection, the efficacy and risks of surgical treatments for severe obesity, and the need for future research on and epidemiological evaluation of these therapies. This brochure reprints the full text of the consensus panel's statement. Among their findings, the panel recommended that patients seeking therapy for severe obesity for the first time should be considered for treatment in a nonsurgical program with integrated components of a dietary regimen, appropriate exercise, and behavioral modification and support; gastric restrictive or bypass procedures could be considered for well-informed and motivated patients with acceptable operative risks; patients who are candidates for surgical procedures should be selected carefully after evaluation by a multidisciplinary team; the operation should be performed by a surgeon with substantial experience with the appropriate procedures and working in a clinical setting with adequate support for all aspects of management and assessment; and lifelong medical surveillance after surgical therapy is a necessity. •

Issues in Weight Control: Causes of Obesity Source: Battle Creek, MI: Kellogg Company Food and Nutrition Communications, 6 p., N.D. Contact: Kellogg Company Food and Nutrition Communications, PO Box 3447, Department B-2, Battle Creek, MI 49016-3447. Summary: This promotional brochure reviews research into the causes and treatment of obesity. Research suggests that there are many different reasons for obesity, such as social, genetic, dietary, metabolic, and psychological factors. These are discussed along with dietary fiber and its effect on weight loss. This publication suggests ways to lose weight, including physical activity, support from family and friends, internal motivation, focusing on positive changes, and cutting out fat from diets. Inserted in this pamphlet is an article by John P. Foreyt, Ph.D., on predictors of success and failure for long-term weight maintenance. A list of selected sources is provided.

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Guidelines for Patient Selection and Postoperative Follow-up Care in Surgical Treatment of Obesity Source: San Francisco, CA: The American Society for Bariatric Surgery, 6 p., May 1994. Contact: American Society for Bariatric Surgery, 140 NW 75th Drive, Suite C., Gainesville, FL. 32607 (U.S.A.). (352) 331-4900. FAX (352) 331-4975. Website: http://www.asbs.org. Summary: This brochure outlines the guidelines for operative treatment of obesity. The patient should be 100 pounds overweight according to the 1983 Metropolitan Height and Weight Tables, or have a serious medical problem that requires weight reduction and warrants the risk of the proposed operation. The guidelines for postoperative, follow-up care are also outlined. These include the frequency of the postoperative follow-up examination, physical examination, and radiographic or endoscopic studies.

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Surgery for Severe Obesity: What Patients Should Know Source: San Francisco, CA: American Society for Bariatric Surgery, 28 p., 1994. Contact: American Society for Bariatric Surgery, 140 NW 75th Drive, Suite C., Gainesville, FL. 32607 (U.S.A.). (352) 331-4900. FAX (352) 331-4975. Website: http://www.asbs.org.

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Summary: This booklet provides patients and their families with basic information on the surgical treatment of severe obesity. A patient should be at least 100 pounds overweight or have sufficient medical need for weight reduction to qualify for surgical treatment. The ways in which the surgery will control obesity are described; these are restriction of food intake and malabsorption of ingested foods. The anatomy and functions involved with the process are also outlined. The risks and benefits of gastric banding, vertical banded gastroplasty, gastric bypass, and biliopancreatic diversion are considered. The booklet also discusses the risks and benefits over the patient's lifetime. •

Understanding Adult Obesity Source: Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 6 p., 1993. Contact: Weight-Control Information Network, 1 WIN WAY, BETHESDA, MD 208923665. (301) 570 2178 OR (800)946-8098. Summary: This fact sheet provides basic information about obesity. It defines obesity and explains the different ways it is measured including body mass index (BMI), weight-for-height tables, body fat distribution, and the waist-to-hip ratio. The factors that contribute to obesity including genetic, environmental, and psychological, are considered. The health, social, and psychological effects of obesity are also described.

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Women's Health: Obesity and Your Health Source: Washington, DC: American College of Obstetricians and Gynecologists, 12 p., 1991. Contact: American College of Obstetricians and Gynecologists, 409 12th Street, NW, Washington, DC 20024-2188. Summary: This patient education brochure focuses on the health problems related to obesity and provides information on how to control weight. The brochure includes a height and weight table for women, and discusses some of the basic causes of obesity, such as excess calorie intake and sedentary lifestyle. The health risks associated with obesity are outlined, especially as they pertain to women: these include menstrual problems and infertility, cancer, complications during pregnancy and childbirth, heart disease, and diabetes. The brochure provides suggestions for proper diet and an exercise program that can help the reader achieve and maintain a healthy lifestyle. A glossary of terms is included.

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Dopamine Receptors Implicated in Obesity Source: National Institute On Drug Abuse. February 1, 2001. Contact: 6001 Executive Boulevard, Bethesda, MD 20892. (301) 443-6245. Summary: This press release by the National Institute on Drug Abuse (NIDA), discusses an article in the medical journal, Lancet. The study found that a deficiency of dopamine in the brain may explain why some individuals engage in pathological overeating, resulting in severe obesity. Dopamine, a neurotransmitter in the brain, helps to regulate feelings of pleasure and modulates the rewarding properties of food. Dr. Jean-Jack Wang, leader of the study and the research team, believes that individuals deficient in dopamine receptors may need to eat more than people with higher dopamine levels to induce feelings of satisfaction and gratification. Dr. Wang notes that findings from the

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study 'suggest that developing a way to improve dopamine receptor function might lead to better treatment of obesity.' Presently, the 'most appropriate practical application of this finding is to urge overweight individuals to exercise,' according to Dr. Wang. The study also found that dopamine receptor availability was lower in obese than in control individuals and that body mass index (BMI) correlated negatively with the measure of dopamine receptors. Individuals with the lowest dopamine receptor values had the largest BMI. •

Obesity - A global epidemic Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: This fact sheet discusses the increase in the prevalence of overweight and obesity worldwide in both developing and developed countries. Environmental and behavioral changes brought about by economic development, modernization, and urbanization have been linked to a rise in global obesity. Obesity is increasing in children and adults, and true health consequences may become fully apparent in the near future.

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Obesity in the US Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: This fact sheet states that obesity is a complex, multi-factorial chronic disease involving environmental, genetic, physiological, metabolic, behavioral, and psychological components. Poor diet and inactivity, which contribute to obesity, is estimated to be the second leading cause of preventable death in the U.S. This fact sheet demonstrates the impact of overweight and obesity on millions of individuals of all ages and socioeconomic groups, both genders, and populations of various racial-ethnic backgrounds.

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Obesity in minority populations Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: This fact sheet claims overweight and obesity occur at higher rates in racialethnic minority populations compared with white Americans in the U.S. Cultural factors that influence dietary and exercise behaviors are reported to play a major role in the development of excess weight in minority groups.

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Women and obesity Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: This fact sheet states that obesity plays a significant role in causing poor health in women, negatively affecting quality of life and shortening quantity of life.

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More than half of adult U.S. women are overweight, and nearly one quarter are obese. The AOA claims that prevention and early treatment of obesity are crucial to ensuring a healthy population of women of all ages. •

Obesity and youth Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: This fact sheet claims that diabetes, hypertension and other obesity-related chronic diseases that are prevalent among adults are becoming more common in youngsters. The percentage of children and adolescents who are overweight and obese are now at its highest. Poor dietary habits and inactivity are reported to contribute to the increase of obesity in youth. As the most inactive generation ever in history, today's youth are at a disadvantage of having less physical education programs in schools as well as recreational facilities that are unsafe. This fact sheet outlines many factors related to obesity in youth that make it a major health care challenge for the 21st century.

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Physical Activity and Good Nutrition: Essential Elements to Prevent Chronic Diseases and Obesity: At-a-Glance 2002 Source: Atlanta, GA, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 4 p., 2002. Contact: National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Mail Stop K-46, 4770 Buford Highway NE., Atlanta, GA 30341-3717. (770) 488-5820. FAX: (770) 488-6000. INTERNET/EMAIL: [email protected]; http://www.cdc.gov/nccdphp/dnpa; http://www.cdc.gov/nccdphp/dnpa/pdf/dnpaaag.pdf. Summary: Physical Activity and Good Nutrition: Essential Elements to Prevent Chronic Diseases and Obesity: At-a-Glance 2002 describes efforts to promote physical activity and good nutrition to prevent chronic diseases and obesity. Chronic diseases account for seven of every ten deaths in the United States and for more than 60 percent of medical care expenditures. The prolonged illness and disability associated with many chronic diseases decrease quality of life for millions of Americans. Obesity has reached epidemic proportions in this country. People who are overweight are at increased risk for heart disease, high blood pressure, diabetes, arthritis-related disabilities and some cancers. Regular physical activity substantially reduces the risk of dying of coronary heart disease and decreases the risk for colon cancer, diabetes, and high blood pressure. It also helps control weight, contributes to healthy bones as well as muscles and joints, reduces falls among the elderly, helps relieve pain of arthritis, reduces symptoms of anxiety and depression, is associated with fewer doctor and hospital visits and fewer needs for medication. Good nutrition lowers the risk of many chronic diseases. Poor eating habits are often established during childhood. The fact sheet describes steps for reaching young people through the school systems in the United States, as well as efforts being made to promote healthy lifestyles among adults.

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Physical Activity and Good Nutrition: Essential Elements to Prevent Chronic Diseases and Obesity: At-a-Glance 2001 Source: Atlanta, GA, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 4 p., 2001.

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Contact: National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Mail Stop K-46, 4770 Buford Highway NE, Atlanta, GA 30341-3717. (770) 488-5820. FAX: (770) 488-5020. INTERNET/EMAIL: http://www.cdc.gov/nccdphp/dnpa; [email protected]. Summary: Physical Activity and Good Nutrition: Essential Elements to Prevent Chronic Diseases and Obesity: At-a-Glance, 2001 describes efforts to promote physical activity and good nutrition to prevent chronic diseases and obesity. Chronic diseases account for 7 out of every 10 United States deaths and for More than 60 percent of medical care expenditures. Much of the chronic disease burden is preventable. Physical inactivity and unhealthy eating contribute to obesity, cancer, cardiovascular disease, and diabetes. More than 60 percent of adults in the United States are overweight or obese. Promoting regular physical activity and healthy eating and creating an environment that supports these behaviors are essential to reducing this epidemic. In 2000, Congress provided the first-ever funding for the Centers for Disease Control and Prevention (CDC) to work with states and conduct applied research to address escalating obesity rates. Through the CDC's Prevention Research Centers network, better methods are being developed to measure physical activity levels focusing on African American, American Indian, Hispanic, and low-income white women older than age 40 years. CDC is collecting information to better understand how policies and environmental conditions determine levels of walking and cycling. The CDC is also engaged in efforts to reach young people through schools, to promote healthy lifestyles, to develop growth charts, and to provide training. •

Facts About Obesity in the U.S Source: Washington, DC, American Obesity Association, National Campaign of Obesity Education, 2 p., September 2000. Contact: American Obesity Association, 1250 24th Street, NW., Suite 300, Washington, DC 20037. (800) 986-2373. (202) 776-7711. FAX: (202) 776-7712. INTERNET/EMAIL: http://www.obesity.org. Summary: The Facts About Obesity in the U.S. provides facts and figures depicting the problem of obesity in the United States. Obesity is the second leading cause of preventable death in the United States. Overweight and obesity have steadily moved away from their targets for improvement as established by the U.S. Department of Health and Human Services. Overall, an estimated 58 million Americans are overweight and 39 million are obese, and the numbers are increasing. About 25 percent of children and adolescents are obese. Obesity increases the risk of illness from about 30 serious medical conditions. Obesity is associated with increases in deaths from all causes. Overweight increases steadily with age. People age 60 to 69 years have the highest prevalence of overweight. People age 50 to 59 years have the highest prevalence of obesity. The prevalence of overweight is 59.4 percent for men and 50.7 percent for women, while the prevalence of obesity is 25.0 percent for women and 19.5 percent for men. Obesity prevalence has increased across all educational levels, but is higher for persons with less education. The incidence of obesity ranges from 14.1 percent in the Mountain region to 20.0 percent in the east south central region.

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Obesity in Children Source: Research File, no. 97-07, 1 p., 1997.

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Contact: Canadian Fitness and Lifestyle Research Institute, 201-185 Somerset Street West, Ottawa, Ontario K2P 0J2, Canada. (613) 233-5528. FAX: (613) 233-5536. INTERNET/EMAIL: http://www.cflri.ca/cflri/resources/pub_rf.php. [email protected]. Summary: This article, one of a series providing fitness professionals with information from the Canadian Fitness and Lifestyle Research Institute, focuses on the results of several studies addressing physical activity and obesity in children. The 1981 Canada Fitness Survey and the 1988 Campbell Survey on Well-being in Canada found that childhood obesity increased by more than 50 percent between 1981 and 1988, as measured by skinfold thicknesses. Obesity in children is an important cause of childhood hypertension as well as a risk factor for psychosocial, orthopedic, and respiratory disorders. Carried into adulthood, obesity is associated with a higher risk of morbidity and mortality from chronic diseases, in part due to the added risk of lipid abnormalities, elevated blood pressure, and noninsulin dependent diabetes. A number of studies have shown that excess body fat which develops in childhood tends to persist throughout childhood and into adulthood. Most cross-sectional studies have found that obese individuals are less active than those who are not obese, and in adolescents, as weight increases the tendency to be active decreases. The Framingham Children's Study, a longitudinal study of children age 3 to 5 years, examined changes in body fatness over time, paying special attention to the effect of preschool activities on children's body fat from preschool to fifth grade. Results showed that from the start of the study to entry into the first grade (1) inactive girls gained 1.75 millimeters (mm) in their triceps skinfolds, compared with 1.0 mm for active girls; (2) inactive boys gained 0.25 mm in their triceps while active boys lost 0.75 mm; (3) inactive preschoolers were almost four times as likely to have larger triceps during followup; and (4) inactive preschoolers who were fatter to begin with fared the worst, being nearly six times as likely to have larger triceps during followup. In order to slow the increase in obesity in children, it is crucial to foster early development of an active lifestyle. •

Research File: Information for Professionals from the Canadian Fitness and Lifestyle Research Institute: The Obesity-inactivity Connection Source: Canadian Fitness and Lifestyle Research Institute, 1 p., (n.d.). Contact: Canadian Fitness and Lifestyle Research Institute. Reference no. 00-02. Summary: The Obesity-inactivity Connection, a fact sheet from The Research File: Information for Professionals from the Canadian Fitness and Lifestyle Research Institute, discusses costs of obesity and how to prevent it. Overweight is defined as a body mass index (BMI) over 27, and 29 percent of Canadians age 20 to 64 are overweight. Obesity is defined as a BMI over 30, and 12 percent of Canadians age 20 to 64 are obese. Obesity is a problem of excess and is generally centered in developed countries. Obesity is a comorbidity for (1) type 2 diabetes; (2) hypertension; (3) coronary heart disease; (4) gallbladder disease; (5) osteoarthritis; and (6) cancer of the breast, colon, and endometrium. Obesity may also be related to asthma. Researchers in Minnesota examined the short-term costs of overweight and obesity in more than 5,000 people age 40 and older. Results showed that (1) overweight and obesity accounted for 1.9 percent higher health plan charges per unit BMI; and (2) controlling for other factors, an obese individual would have health care charges about 19 percent higher than a health plan member with a normal BMI. The direct health care costs of obesity are estimated at $70 billion annually, or 7 percent of total health care costs. Solving the obesity problem requires a greater emphasis on primary prevention, particularly physical activity. Ordering information is provided for (1) Canada's Food Guide to

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Healthy Living, and (2) Canada's Physical Activity Guide to Healthy Living. 3 references. •

Health effects of obesity Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: This fact sheet states that persons with obesity are at risk of developing one or more serious medical conditions, which can cause poor health and premature death. Obesity is associated with more than 30 medical conditions. Scientific evidence has established a strong relationship between obesity and at least 15 conditions, and preliminary data show the impact of obesity on numerous other conditions. Weight loss of at least 5 to 10 percent of body weight, for persons with overweight or obesity, can improve various obesity-related medical conditions, including diabetes and hypertension.

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The facts about obesity as a medical deduction Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: The Internal Revenue Service (IRS) has declared that treatments for obesity are not eligible for a tax deduction. Deductibility is already allowed for preventable causes of death such as alcohol treatment, drug addiction treatment, and smoking cessation programs. This fact sheet states that the behavioral and environmental components of obesity, involving poor diet and inactivity, have made it the second leading cause of preventable death.

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The facts about obesity research Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: This fact sheet discusses the past four decades of obesity research and the progress that has been made in identifying causes and treatment. Research has provided a greater understanding of obesity as a chronic disease caused by a complex interaction of genetic, metabolic, behavioral, psychological and environmental factors. However, despite the advances in research, children, adolescents and adults are continuing to become overweight and obese in record high numbers. The American Obesity Association states that due to the complexity of obesity, more research is needed in a variety of areas, particularly in prevention to control the spread of the epidemic.

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The facts about obesity and health insurance Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: Many insurance plans do not provide reimbursement for weight loss treatment. The countless number of available insurance plans and ever changing

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policies have made it difficult to assess the extent to which obesity treatment and prevention services are covered by third party insurers. This fact sheet discusses the need for more data and better tracking to determine the health needs of persons with obesity. •

The facts about obesity as a disability Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: The dictionary definition of disable is to weaken, incapacitate, cripple or immobilize. Persons with sever obesity report bodily pain that affects normal daily activities. Obesity would be considered a disability when applying to the dictionary definition. Legal definitions of disability, and obesity as a disability are much more complex. The Social Security Administration (SSA) and the Department of Justice (DOJ), which handles legal cases involving the American with Disabilities Act (ADA), use legal definitions to define disability. This fact sheet explains how the SSA and the ADA interpret obesity and disability.

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The facts about obesity, Medicaid and Medicare Source: American Obesity Association. Contact: American Obesity Association, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98-OBESE. Summary: This fact sheet states that Medicaid does not cover obesity, and under Medicare, hospital and physician services for obesity are clearly excluded. Recipients of Medicaid are primary women and children who are poor and members of minority groups. Given the high prevalence of obesity among those populations, it is presumed that many Medicaid recipients are likely to have obesity.

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Obesity surgery Source: American Obesity Association (AOA). Contact: AOA, 1250 24th Street, N.W., Suite 300, Washington, DC 20037. 1-800-98OBESE. Summary: Surgery is a treatment option suitable for some persons with obesity. This fact sheet discusses the risks and benefits of the surgery and the commitment involved to make a lifestyle change. This fact sheet also discusses the health risks of being severely obese, and the health benefits gained from losing excess weight.

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Pharmacotherapy for the management of obesity Source: Novartis Nutrition Corporation. Contact: Novartis Nutrition Corporation, P.O. Box 370, Minneapolis, MN 55440-0370. 1800-662-2540. Summary: The dangers inherent to the rising level of obesity in the U.S. have prompted aggressive research on new pharmacotherapies for weight management. Recognition for the need for long-term, perhaps lifelong treatment, has led many to embrace the concept of long-term drug therapy, as used in other chronic diseases. Research conducted on weight loss drugs shows the potential to enhance long-term maintenance of weight loss

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when combined with nutrition, exercise, and behavior therapy. This fact sheet focuses on current pharmacotherapy options for weight management. •

Do You Know the Health Risks of Being Overweight? Source: Bethesda, MD: Weight-Control Information Network. 1999. 10 p. Contact: Available from Weight-Control Information Network. 1 WIN Way, Bethesda, MD 20892-3665. (800) 946-8098 or (301) 984-7378. Fax (301) 984-7196. E-mail: [email protected]. Website: www.niddk.nih.gov/health/nutrit/nutrit.htm. PRICE: Full-text available online at no charge; single copy free. Summary: This brochure discusses the health risks of being overweight. It uses a question and answer format to help people determine whether they are overweight, whether their waist measurement indicates a risk for health problems, and what health problems overweight people may experience. Health risks associated with being overweight include heart disease and stroke, type 2 diabetes, various cancers, sleep apnea, osteoarthritis, gout, and gallbladder disease. The brochure suggests that even a small weight loss can improve one's health. It recommends that people make long-term changes in eating habits and physical activity to lose weight and keep it off over time. In addition, the brochure provides a list of additional reading materials and identifies organizations that have information and educational materials available to the public on health problems associated with being overweight. 1 figure.

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Helping Your Overweight Child Source: Bethesda, MD: Weight-Control Information Network. 1997. 14 p. Contact: Available from National Diabetes Information Clearinghouse (NDIC). 1 Information Way, Bethesda, MD 20892-3560. (800) 860-8747 or (301) 654-3327. Fax (301) 634-0716. E-mail: [email protected]. Also available at http://www.niddk.nih.gov/. PRICE: Full-text available online at no charge; single copy free; bulk orders availabl. Summary: This booklet uses a question and answer format to provide parents with guidelines on helping their overweight child. The booklet identifies the reasons children become overweight, including genetic factors, lack of physical activity, unhealthy eating patterns, or a combination of these factors. The booklet explains how physicians determine whether a child is overweight and offers suggestions on helping an overweight child. Parents should be supportive and focus on increasing the physical activity of all family members, as well as teaching family members healthy eating habits. In addition, the booklet presents ways to help a child develop good attitudes about eating, such as not placing a child on a restrictive diet or overly restricting sweets and treats, reducing dietary fat, making a variety of foods available in the house, encouraging a child to eat slowly, and eating meals together as a family. Other suggestions include involving children in food shopping and meal preparation, planning for snacks, discouraging meals or snacks while watching television, trying not to use food as a punishment or reward, and making sure a child's meals outside the home are well balanced. The booklet concludes by outlining the characteristics of a good weight-control program, providing information on the Weight-Control Information Network, and identifying additional resources. 1 figure.

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If your child is overweight: A guide for parents Source: Chicago, IL: American Dietetic Association. 1993. 32 pp.

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Contact: Available from Customer Service, American Dietetic Association, 216 West Jackson Boulevard, Suite 800, Chicago, IL 60606-6995. Telephone: (312) 899-0040 or (800) 877-1600 or (800) 366-1655 or (800) 225-5267 / fax: (312) 899-1758 / Web site: http://www.eatright.org. $4.20 ADA members; $4.95 nonmembers; prepayment required; make checks payable to ADA. Summary: This booklet provides general information for the parents of children between the ages of 6 and 12 who are concerned that their children may have a weight problem. It discusses ways to determine if a child is overweight, causal factors, whether diets are dangerous for the child, steps to take to develop nutritious eating patterns for the whole family, meal planning, and planning for special events. The booklet includes suggestions for obtaining additional help and lists cookbooks and other resources. •

If My Child is Overweight, What Should I Do About It? Source: Oakland, CA: University of California, Division of Agriculture and Natural Resources, 16 p., 1998. Contact: University of California, Division of Agriculture and Natural Resources, Communication Services Publications, 701 San Pablo Ave., 2nd Floor, Oakland, CA 94608-1239. (800) 994-849. (510) 642-2431. FAX (510) 643-5470. E-mail: [email protected]. Website: http://danrcs.ucdavis.edu. Summary: Using a question and answer format, this booklet discusses the overweight child from a parent's perspective. Parents are advised to check with a health care provider if they think their child is overweight, and to structure the child's food intake if the child is overweight, rather than restrict food intake. The need for increased activity is stressed, and suggestions are offered on ensuring activity for the child. Some of these include participating in organized sports, utilizing an after-school program that includes activity, encouraging family activities that include physical activities, and having toys at home that encourage activity, such as balls, bats, roller skates, Frisbees, and bicycles.

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Food insufficiency and prevalence of overweight among adult women Source: Alexandria, VA: Center for Nutrition Policy and Promotion, U.S. Department of Agriculture. 2002. 2 pp. Contact: Available from U.S. Center for Nutrition Policy and Promotion, U.S. Department of Agriculture, 3101 Park Center Drive, Room 1034, Alexandria, VA 223021594. Telephone: (703) 305-7400 / fax: (703) 305-43400 / e- mail: [email protected] / Web site: http://www.usda.gov/cnpp/. Available at no charge; also available from the Web site at no charge. Summary: This fact sheet describes a study conducted to examine the association between food insufficiency and overweight by adult women. The authors of the study used data from the 1988-94 National Health and Nutrition Examination Survey (NHANES III) and also examined women's overall diet quality as gauged by the Healthy Eating Index and its components. The fact sheet concludes with references.

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Physical Activity for Sedentary, Overweight Women Source: Research File, Reference no. 98-05, 1 p., 1998. Contact: Canadian Fitness and Lifestyle Research Institute, 201-185 Somerset Street West, Ottawa, Ontario K2P 0J2, Canada. (613) 233-5528. FAX: (613) 233-5536. INTERNET/EMAIL: http://www.cflri.ca/cflri/resources/pub_rf.php. [email protected].

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Summary: Physical Activity for Sedentary, Overweight Women discusses studies that investigated the physiological effects of physical activity programs and factors influencing adherence in sedentary, overweight women. One such study compared the effects of endurance training and resistance training on resting energy expenditure (REE), body composition (sum of skinfolds and fat-free mass (FFM)), and aerobic fitness in three groups of women: (1) An endurance group that pursued an aggressive walking program; (2) a resistance-training group which used light weights, gradually increasing the demands of their routine; and (3) a control group. Neither type of activity had an effect on REE, while both the endurance and resistance training had a significant effect on body composition, as shown by decreases in skinfold thicknesses and increases in FFM. Aerobic fitness increased in both groups. Self-report data indicated that the main factors influencing completion of the program were (1) the instructor, (2) personal reasons, (3) timing/convenience of the classes, (4) commitment to a goal and the project, and (5) group dynamics/camaraderie. An enthusiastic, encouraging instructor with the sensitivity to provide a program that suited the needs of the participants was a key factor promoting adherence identified by the participants. Adherence was greatest in the endurance (walking) group. This was most apparent for unsupervised activity. Fitness professionals can use the findings of this study as a guide to review their own efforts for promoting physical activity among sedentary, overweight women.

The National Guideline Clearinghouse™ The National Guideline Clearinghouse™ offers hundreds of evidence-based clinical practice guidelines published in the United States and other countries. You can search this site located at http://www.guideline.gov/ by using the keyword “obesity” (or synonyms). The following was recently posted: •

AACE/ACE position statement on the prevention, diagnosis and treatment of obesity Source: American Association of Clinical Endocrinologists - Medical Specialty Society; 1997 (revised 1998); 35 pages http://www.guideline.gov/summary/summary.aspx?doc_id=1750&nbr=976&am p;string=obesity

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American Gastroenterological Association medical position statement on obesity Source: American Gastroenterological Association - Medical Specialty Society; 2002 September; 3 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3490&nbr=2716&a mp;string=obesity

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Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Source: National Heart, Lung, and Blood Institute (U.S.) - Federal Government Agency [U.S.]; 1998 June; 228 pages http://www.guideline.gov/summary/summary.aspx?doc_id=1402&nbr=660&am p;string=obesity

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Periodic health examination, 1999 update: 1. Detection, prevention and treatment of obesity Source: Canadian Task Force on Preventive Health Care - National Government Agency [Non-U.S.]; 1999; 12 pages http://www.guideline.gov/summary/summary.aspx?doc_id=2054&nbr=1280&a mp;string=obesity

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Weight management counseling of overweight adults Source: American College of Preventive Medicine - Medical Specialty Society; 2001 July; 6 pages http://www.guideline.gov/summary/summary.aspx?doc_id=3154&nbr=2380&a mp;string=obesity Healthfinder™

Healthfinder™ is sponsored by the U.S. Department of Health and Human Services and offers links to hundreds of other sites that contain healthcare information. This Web site is located at http://www.healthfinder.gov. Again, keyword searches can be used to find guidelines. The following was recently found in this database: •

Aim for A Healthy Weight!: Information for Health Professionals Summary: Health professionals working in the field of bariatrics and related fields can access the Federal government's practice guidelines on the identification, evaluation, and treatment of overweight and Source: National Heart, Lung, and Blood Institute Information Center http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6087

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Aim for A Healthy Weight!: Information for Patients and the Public Summary: These guidelines from the National Heart, Lung, and Blood Institute present a new approach for the assessment of overweight and obesity and establish principles of safe and effective weight loss. Source: National Heart, Lung, and Blood Institute, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4330

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Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults Summary: A guideline for physicians that presents a new approach for the assessment of overweight and obesity and establish principles of safe and effective weight loss. Source: National Heart, Lung, and Blood Institute, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2814

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Do You Know the Health Risks of Being Overweight? Summary: This guide can help you lose weight safely and develop a healthier lifestyle that will reduce your chances of developing serious health problems -- like heart disease, diabetes, or cancer. Source: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=5974

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healthfinder® just for you: Blacks or African Americans Summary: healthfinder®'s just for you: Blacks or African Americans section features topics such as diabetes, high blood pressure, and obesity Source: U.S. Department of Health and Human Services http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7021

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Information about Losing Weight and Maintaining a Healthy Weight Summary: This web site provides links to information about obesity and weight loss provided by CFSAN, other Federal government agencies and non-government agencies. Source: Center for Food Safety and Applied Nutrition http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=3632

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NHLBI Obesity Education Initiative: Guide to Behavior Change Summary: If you are overweight, these behavioral changes from the National Heart, Lung, and Blood Institute will reduce your risk for some health problems that affect the heart, lungs and joints, as well as Source: National Heart, Lung, and Blood Institute, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4332

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NHLBI Obesity Education Initiative: Guide to Physical Activity Summary: The National Heart, Lung, and Blood Institute provides advice on how to adapt a regime of daily physical activity that complements your lifestyle and provides maximum health benefit. Source: National Heart, Lung, and Blood Institute, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=4331

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Obesity and Cancer Summary: A fact sheet that summarizes research on the potential link between obesity and cancer risk. Source: Cancer Information Service, National Cancer Institute http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=7077

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Obesity Education Initiative (OEI) Summary: The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) launched the Obesity Education Initiative (OEI) in January 1991. Source: National Heart, Lung, and Blood Institute, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=728

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Palm OS Applications--National Heart, Lung, and Blood Institute Summary: Palm OS applications from NHLBI for the following: asthma treatment, BMI calculations, obesity treatment, and cholesterol management. Source: National Heart, Lung, and Blood Institute, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6391

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Prescription Medications for the Treatment of Obesity Summary: Visit this site for information about medications prescribed for the treatment of obesity, their application, benefits and side effects. Source: Weight-Control Information Network, National Institute of Diabetes and Digestive and Kidney Diseases http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2535

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Surgeon General's Call To Action To Prevent and Decrease Overweight and Obesity Summary: This report outlines strategies that communities can use in helping to address the problems of overweight and obesity. Source: U.S. Department of Health and Human Services http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6401

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The Pima Indians: Pathfinders for Health Summary: By studying Pima Indian volunteers, researchers have determined that diabetes runs in families, as does insulin resistance, and obesity. Source: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=2624

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Ways to Win at Weight Loss Summary: This article discusses obesity in the United States and effective methods for weight loss success and for keeping weight off. Source: U.S. Food and Drug Administration http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=6088

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Weight Loss and Control Summary: The Weight-Control Information Network (WIN) is a national source of information on weight control, obesity, and weight-related nutritional disorders for health professionals and the public. Source: National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health http://www.healthfinder.gov/scripts/recordpass.asp?RecordType=0&RecordID=707 The NIH Search Utility

The NIH search utility allows you to search for documents on over 100 selected Web sites that comprise the NIH-WEB-SPACE. Each of these servers is “crawled” and indexed on an ongoing basis. Your search will produce a list of various documents, all of which will relate in some way to obesity. The drawbacks of this approach are that the information is not organized by theme and that the references are often a mix of information for professionals and patients. Nevertheless, a large number of the listed Web sites provide useful background information. We can only recommend this route, therefore, for relatively rare or specific disorders, or when using highly targeted searches. To use the NIH search utility, visit the following Web page: http://search.nih.gov/index.html. Additional Web Sources

A number of Web sites are available to the public that often link to government sites. These can also point you in the direction of essential information. The following is a representative sample: •

AOL: http://search.aol.com/cat.adp?id=168&layer=&from=subcats

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Family Village: http://www.familyvillage.wisc.edu/specific.htm

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Google: http://directory.google.com/Top/Health/Conditions_and_Diseases/

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Med Help International: http://www.medhelp.org/HealthTopics/A.html

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Open Directory Project: http://dmoz.org/Health/Conditions_and_Diseases/

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Yahoo.com: http://dir.yahoo.com/Health/Diseases_and_Conditions/

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WebMDHealth: http://my.webmd.com/health_topics

Associations and Obesity The following is a list of associations that provide information on and resources relating to obesity: •

American Lung Association Telephone: (212) 315-8700 Toll-free: (800) 586-4872 Fax: (212) 265-5642 Email: [email protected] Web Site: http://www.lungusa.org

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Background: The American Lung Association (ALA) is a national not-for-profit voluntary health organization dedicated to the prevention, cure, and control of all types of lung disease such as asthma, emphysema, tuberculosis, and lung cancer. This is accomplished through programs of community service, public health education, advocacy, and research. The ALA was established in 1904 as the National Association for the Study and Prevention of Tuberculosis. As the number of tuberculosis cases declined over the years, the association widened its focus to include other forms of lung disease and, in 1973, changed its name to the American Lung Association. The Association offers assistance through support groups, genetic counseling, patient networking, referrals, and the development and dissemination of educational materials. Such materials include reports, brochures, audiovisual aids, and Spanish language materials. Relevant area(s) of interest: Asthma •

Asthma and Allergy Foundation of America, Inc Telephone: (202) 466-7643 Toll-free: (800) 727-8462 Fax: (202) 466-8940 Email: [email protected] Web Site: http://www.aafa.org Background: The Asthma and Allergy Foundation of America, Inc. (AAFA) is a private, not-for-profit organization dedicated to finding a cure for and controlling asthma and allergic diseases. AAFA serves the estimated 50 million individuals with asthma and allergic disorders through the support of research, patient and public education programs, public and governmental advocacy, and a nationwide network of chapters and education/support groups. Educational materials include a bi-monthly newsletter 'ADVANCE,' a support group newsletter, and a resource list brochure. Relevant area(s) of interest: Asthma

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Asthma Society of Canada Telephone: (416) 787-4050 Toll-free: (800) 787-3880 Fax: (416) 787-5807 Email: [email protected] Web Site: http://www.asthmasociety.com Background: The Asthma Society of Canada (ASC) is a national not-for-profit volunteerbased organization dedicated to enhancing the quality of life of people living with asthma and eliminating the disorder. Asthma is a chronic disease characterized by recurrent attacks of breathlessness and wheezing due to narrowing of small airways in the lungs (bronchioles). The Society, which was established in 1973, offers a toll-free helpline with trained health professionals to answer questions; develops and distributes print materials on asthma; facilitates support groups that enable affected individuals and family members to share information and mutual support; and runs camps for affected children. In addition, the Society promotes and funds asthma research, publishes a quarterly newsletter, and maintains a web site on the Internet. The Society's web site discusses the organization's history, mission, and goals; includes fact sheets such as those entitled 'Asthma,' 'Asthma and Exercise,' 'What to Do About Asthma,' and 'Asthma at School'; and provides links to additional sources of information and support.

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Fundaci n Alfa-1 de Puerto Rico Telephone: (787) 743-0268 Fax: (787) 743-0268 Email: [email protected] Web Site: http://www.alfal.org Background: The Puerto Rico Alpha 1 Support Group (Grupo de Apoyo Alfa 1 de Puerto Rico) is an international, nonprofit organization dedicated to providing support to individuals and families affected by alpha 1-antitrypsin deficiency through programs of education, advocacy, and support of research. Alpha 1-antitrypsin deficiency is a rare hereditary metabolic disease characterized by low levels of the enzyme alpha 1antitrypsin and progressive degenerative and destructive changes in the lungs. The organization s main goal to increase awareness and knowledge about alpha 1antitrypsin deficiency among the general public and healthcare professionals. Established in 1997, the organization also encourages early detection and treatment of this disorder. The organization produces educational materials including a brochure entitled 'Enfisema Ocasionado por la Deficiencia de AAT' as well as translations of brochures published by the Alpha-1-Antitrypsin Deficiency Association. La Fundaci n Alfa-1 de Puerto Rico es una organizaci n cuya misi n es educar y dar apoyo a las personas que padecen de la Deficiencia de Alfa-1 Antitripsina (Alfa-1) y sus familiares, concienciar al p blico en general y a los profesionales de la salud sobre este trastorno y la importancia de la detecci n temprana; y apoyar la investigaci n dirigida a encontrar una cura y mejores tratamientos para el Alfa-1.

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Second Wind Lung Transplant Association, Inc Telephone: Toll-free: (888) 222-2690 Fax: (727) 442-9762 Email: [email protected] Web Site: http://www.2ndwind.org Background: Second Wind Lung Transplant Association, Inc. is a not-for-profit organization dedicated to improving the quality of life for lung transplant recipients, lung surgery candidates, people with related pulmonary concerns, and their families. The Association provides support, advocacy, education, information, and guidance through a spirit of service, 'adding years to their lives and life to their years.' Established in 1995 by a group of lung transplant recipients, candidates, and their families, Second Wind has quarterly support group meetings to provide educational programs (e.g., on nutrition, effects of medications and exercise, physical therapy) for both lung transplant candidates and recipients; to share experiences; and to enjoy social activities. In addition, the organization provides educational programs; seeks to increase Organ Donor Awareness; and provides a quarterly newsletter entitled 'AirWays' to its members. Relevant area(s) of interest: Asthma

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Finding Associations There are several Internet directories that provide lists of medical associations with information on or resources relating to obesity. By consulting all of associations listed in this chapter, you will have nearly exhausted all sources for patient associations concerned with obesity. The National Health Information Center (NHIC) The National Health Information Center (NHIC) offers a free referral service to help people find organizations that provide information about obesity. For more information, see the NHIC’s Web site at http://www.health.gov/NHIC/ or contact an information specialist by calling 1-800-336-4797. Directory of Health Organizations The Directory of Health Organizations, provided by the National Library of Medicine Specialized Information Services, is a comprehensive source of information on associations. The Directory of Health Organizations database can be accessed via the Internet at http://www.sis.nlm.nih.gov/Dir/DirMain.html. It is composed of two parts: DIRLINE and Health Hotlines. The DIRLINE database comprises some 10,000 records of organizations, research centers, and government institutes and associations that primarily focus on health and biomedicine. To access DIRLINE directly, go to the following Web site: http://dirline.nlm.nih.gov/. Simply type in “obesity” (or a synonym), and you will receive information on all relevant organizations listed in the database. Health Hotlines directs you to toll-free numbers to over 300 organizations. You can access this database directly at http://www.sis.nlm.nih.gov/hotlines/. On this page, you are given the option to search by keyword or by browsing the subject list. When you have received your search results, click on the name of the organization for its description and contact information. The Combined Health Information Database Another comprehensive source of information on healthcare associations is the Combined Health Information Database. Using the “Detailed Search” option, you will need to limit your search to “Organizations” and “obesity”. Type the following hyperlink into your Web browser: http://chid.nih.gov/detail/detail.html. To find associations, use the drop boxes at the bottom of the search page where “You may refine your search by.” For publication date, select “All Years.” Then, select your preferred language and the format option “Organization Resource Sheet.” Type “obesity” (or synonyms) into the “For these words:” box. You should check back periodically with this database since it is updated every three months.

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The National Organization for Rare Disorders, Inc. The National Organization for Rare Disorders, Inc. has prepared a Web site that provides, at no charge, lists of associations organized by health topic. You can access this database at the following Web site: http://www.rarediseases.org/search/orgsearch.html. Type “obesity” (or a synonym) into the search box, and click “Submit Query.”

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APPENDIX C. FINDING MEDICAL LIBRARIES Overview In this Appendix, we show you how to quickly find a medical library in your area.

Preparation Your local public library and medical libraries have interlibrary loan programs with the National Library of Medicine (NLM), one of the largest medical collections in the world. According to the NLM, most of the literature in the general and historical collections of the National Library of Medicine is available on interlibrary loan to any library. If you would like to access NLM medical literature, then visit a library in your area that can request the publications for you.27

Finding a Local Medical Library The quickest method to locate medical libraries is to use the Internet-based directory published by the National Network of Libraries of Medicine (NN/LM). This network includes 4626 members and affiliates that provide many services to librarians, health professionals, and the public. To find a library in your area, simply visit http://nnlm.gov/members/adv.html or call 1-800-338-7657.

Medical Libraries in the U.S. and Canada In addition to the NN/LM, the National Library of Medicine (NLM) lists a number of libraries with reference facilities that are open to the public. The following is the NLM’s list and includes hyperlinks to each library’s Web site. These Web pages can provide information on hours of operation and other restrictions. The list below is a small sample of

27

Adapted from the NLM: http://www.nlm.nih.gov/psd/cas/interlibrary.html.

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libraries recommended by the National Library of Medicine (sorted alphabetically by name of the U.S. state or Canadian province where the library is located)28: •

Alabama: Health InfoNet of Jefferson County (Jefferson County Library Cooperative, Lister Hill Library of the Health Sciences), http://www.uab.edu/infonet/

•

Alabama: Richard M. Scrushy Library (American Sports Medicine Institute)

•

Arizona: Samaritan Regional Medical Center: The Learning Center (Samaritan Health System, Phoenix, Arizona), http://www.samaritan.edu/library/bannerlibs.htm

•

California: Kris Kelly Health Information Center (St. Joseph Health System, Humboldt), http://www.humboldt1.com/~kkhic/index.html

•

California: Community Health Library of Los Gatos, http://www.healthlib.org/orgresources.html

•

California: Consumer Health Program and Services (CHIPS) (County of Los Angeles Public Library, Los Angeles County Harbor-UCLA Medical Center Library) - Carson, CA, http://www.colapublib.org/services/chips.html

•

California: Gateway Health Library (Sutter Gould Medical Foundation)

•

California: Health Library (Stanford University Medical Center), http://wwwmed.stanford.edu/healthlibrary/

•

California: Patient Education Resource Center - Health Information and Resources (University of California, San Francisco), http://sfghdean.ucsf.edu/barnett/PERC/default.asp

•

California: Redwood Health Library (Petaluma Health Care District), http://www.phcd.org/rdwdlib.html

•

California: Los Gatos PlaneTree Health Library, http://planetreesanjose.org/

•

California: Sutter Resource Library (Sutter Hospitals Foundation, Sacramento), http://suttermedicalcenter.org/library/

•

California: Health Sciences Libraries (University of California, Davis), http://www.lib.ucdavis.edu/healthsci/

•

California: ValleyCare Health Library & Ryan Comer Cancer Resource Center (ValleyCare Health System, Pleasanton), http://gaelnet.stmarysca.edu/other.libs/gbal/east/vchl.html

•

California: Washington Community Health Resource Library (Fremont), http://www.healthlibrary.org/

•

Colorado: William V. Gervasini Memorial Library (Exempla Healthcare), http://www.saintjosephdenver.org/yourhealth/libraries/

•

Connecticut: Hartford Hospital Health Science Libraries (Hartford Hospital), http://www.harthosp.org/library/

•

Connecticut: Healthnet: Connecticut Consumer Health Information Center (University of Connecticut Health Center, Lyman Maynard Stowe Library), http://library.uchc.edu/departm/hnet/

28

Abstracted from http://www.nlm.nih.gov/medlineplus/libraries.html.

Finding Medical Libraries 501

•

Connecticut: Waterbury Hospital Health Center Library (Waterbury Hospital, Waterbury), http://www.waterburyhospital.com/library/consumer.shtml

•

Delaware: Consumer Health Library (Christiana Care Health System, Eugene du Pont Preventive Medicine & Rehabilitation Institute, Wilmington), http://www.christianacare.org/health_guide/health_guide_pmri_health_info.cfm

•

Delaware: Lewis B. Flinn Library (Delaware Academy of Medicine, Wilmington), http://www.delamed.org/chls.html

•

Georgia: Family Resource Library (Medical College of Georgia, Augusta), http://cmc.mcg.edu/kids_families/fam_resources/fam_res_lib/frl.htm

•

Georgia: Health Resource Center (Medical Center of Central Georgia, Macon), http://www.mccg.org/hrc/hrchome.asp

•

Hawaii: Hawaii Medical Library: Consumer Health Information Service (Hawaii Medical Library, Honolulu), http://hml.org/CHIS/

•

Idaho: DeArmond Consumer Health Library (Kootenai Medical Center, Coeur d’Alene), http://www.nicon.org/DeArmond/index.htm

•

Illinois: Health Learning Center of Northwestern Memorial Hospital (Chicago), http://www.nmh.org/health_info/hlc.html

•

Illinois: Medical Library (OSF Saint Francis Medical Center, Peoria), http://www.osfsaintfrancis.org/general/library/

•

Kentucky: Medical Library - Services for Patients, Families, Students & the Public (Central Baptist Hospital, Lexington), http://www.centralbap.com/education/community/library.cfm

•

Kentucky: University of Kentucky - Health Information Library (Chandler Medical Center, Lexington), http://www.mc.uky.edu/PatientEd/

•

Louisiana: Alton Ochsner Medical Foundation Library (Alton Ochsner Medical Foundation, New Orleans), http://www.ochsner.org/library/

•

Louisiana: Louisiana State University Health Sciences Center Medical LibraryShreveport, http://lib-sh.lsuhsc.edu/

•

Maine: Franklin Memorial Hospital Medical Library (Franklin Memorial Hospital, Farmington), http://www.fchn.org/fmh/lib.htm

•

Maine: Gerrish-True Health Sciences Library (Central Maine Medical Center, Lewiston), http://www.cmmc.org/library/library.html

•

Maine: Hadley Parrot Health Science Library (Eastern Maine Healthcare, Bangor), http://www.emh.org/hll/hpl/guide.htm

•

Maine: Maine Medical Center Library (Maine Medical Center, Portland), http://www.mmc.org/library/

•

Maine: Parkview Hospital (Brunswick), http://www.parkviewhospital.org/

•

Maine: Southern Maine Medical Center Health Sciences Library (Southern Maine Medical Center, Biddeford), http://www.smmc.org/services/service.php3?choice=10

•

Maine: Stephens Memorial Hospital’s Health Information Library (Western Maine Health, Norway), http://www.wmhcc.org/Library/

502 Obesity

•

Manitoba, Canada: Consumer & Patient Health Information Service (University of Manitoba Libraries), http://www.umanitoba.ca/libraries/units/health/reference/chis.html

•

Manitoba, Canada: J.W. Crane Memorial Library (Deer Lodge Centre, Winnipeg), http://www.deerlodge.mb.ca/crane_library/about.asp

•

Maryland: Health Information Center at the Wheaton Regional Library (Montgomery County, Dept. of Public Libraries, Wheaton Regional Library), http://www.mont.lib.md.us/healthinfo/hic.asp

•

Massachusetts: Baystate Medical Center Library (Baystate Health System), http://www.baystatehealth.com/1024/

•

Massachusetts: Boston University Medical Center Alumni Medical Library (Boston University Medical Center), http://med-libwww.bu.edu/library/lib.html

•

Massachusetts: Lowell General Hospital Health Sciences Library (Lowell General Hospital, Lowell), http://www.lowellgeneral.org/library/HomePageLinks/WWW.htm

•

Massachusetts: Paul E. Woodard Health Sciences Library (New England Baptist Hospital, Boston), http://www.nebh.org/health_lib.asp

•

Massachusetts: St. Luke’s Hospital Health Sciences Library (St. Luke’s Hospital, Southcoast Health System, New Bedford), http://www.southcoast.org/library/

•

Massachusetts: Treadwell Library Consumer Health Reference Center (Massachusetts General Hospital), http://www.mgh.harvard.edu/library/chrcindex.html

•

Massachusetts: UMass HealthNet (University of Massachusetts Medical School, Worchester), http://healthnet.umassmed.edu/

•

Michigan: Botsford General Hospital Library - Consumer Health (Botsford General Hospital, Library & Internet Services), http://www.botsfordlibrary.org/consumer.htm

•

Michigan: Helen DeRoy Medical Library (Providence Hospital and Medical Centers), http://www.providence-hospital.org/library/

•

Michigan: Marquette General Hospital - Consumer Health Library (Marquette General Hospital, Health Information Center), http://www.mgh.org/center.html

•

Michigan: Patient Education Resouce Center - University of Michigan Cancer Center (University of Michigan Comprehensive Cancer Center, Ann Arbor), http://www.cancer.med.umich.edu/learn/leares.htm

•

Michigan: Sladen Library & Center for Health Information Resources - Consumer Health Information (Detroit), http://www.henryford.com/body.cfm?id=39330

•

Montana: Center for Health Information (St. Patrick Hospital and Health Sciences Center, Missoula)

•

National: Consumer Health Library Directory (Medical Library Association, Consumer and Patient Health Information Section), http://caphis.mlanet.org/directory/index.html

•

National: National Network of Libraries of Medicine (National Library of Medicine) provides library services for health professionals in the United States who do not have access to a medical library, http://nnlm.gov/

•

National: NN/LM List of Libraries Serving the Public (National Network of Libraries of Medicine), http://nnlm.gov/members/

Finding Medical Libraries 503

•

Nevada: Health Science Library, West Charleston Library (Las Vegas-Clark County Library District, Las Vegas), http://www.lvccld.org/special_collections/medical/index.htm

•

New Hampshire: Dartmouth Biomedical Libraries (Dartmouth College Library, Hanover), http://www.dartmouth.edu/~biomed/resources.htmld/conshealth.htmld/

•

New Jersey: Consumer Health Library (Rahway Hospital, Rahway), http://www.rahwayhospital.com/library.htm

•

New Jersey: Dr. Walter Phillips Health Sciences Library (Englewood Hospital and Medical Center, Englewood), http://www.englewoodhospital.com/links/index.htm

•

New Jersey: Meland Foundation (Englewood Hospital and Medical Center, Englewood), http://www.geocities.com/ResearchTriangle/9360/

•

New York: Choices in Health Information (New York Public Library) - NLM Consumer Pilot Project participant, http://www.nypl.org/branch/health/links.html

•

New York: Health Information Center (Upstate Medical University, State University of New York, Syracuse), http://www.upstate.edu/library/hic/

•

New York: Health Sciences Library (Long Island Jewish Medical Center, New Hyde Park), http://www.lij.edu/library/library.html

•

New York: ViaHealth Medical Library (Rochester General Hospital), http://www.nyam.org/library/

•

Ohio: Consumer Health Library (Akron General Medical Center, Medical & Consumer Health Library), http://www.akrongeneral.org/hwlibrary.htm

•

Oklahoma: The Health Information Center at Saint Francis Hospital (Saint Francis Health System, Tulsa), http://www.sfh-tulsa.com/services/healthinfo.asp

•

Oregon: Planetree Health Resource Center (Mid-Columbia Medical Center, The Dalles), http://www.mcmc.net/phrc/

•

Pennsylvania: Community Health Information Library (Milton S. Hershey Medical Center, Hershey), http://www.hmc.psu.edu/commhealth/

•

Pennsylvania: Community Health Resource Library (Geisinger Medical Center, Danville), http://www.geisinger.edu/education/commlib.shtml

•

Pennsylvania: HealthInfo Library (Moses Taylor Hospital, Scranton), http://www.mth.org/healthwellness.html

•

Pennsylvania: Hopwood Library (University of Pittsburgh, Health Sciences Library System, Pittsburgh), http://www.hsls.pitt.edu/guides/chi/hopwood/index_html

•

Pennsylvania: Koop Community Health Information Center (College of Physicians of Philadelphia), http://www.collphyphil.org/kooppg1.shtml

•

Pennsylvania: Learning Resources Center - Medical Library (Susquehanna Health System, Williamsport), http://www.shscares.org/services/lrc/index.asp

•

Pennsylvania: Medical Library (UPMC Health System, Pittsburgh), http://www.upmc.edu/passavant/library.htm

•

Quebec, Canada: Medical Library (Montreal General Hospital), http://www.mghlib.mcgill.ca/

504 Obesity

•

South Dakota: Rapid City Regional Hospital Medical Library (Rapid City Regional Hospital), http://www.rcrh.org/Services/Library/Default.asp

•

Texas: Houston HealthWays (Houston Academy of Medicine-Texas Medical Center Library), http://hhw.library.tmc.edu/

•

Washington: Community Health Library (Kittitas Valley Community Hospital), http://www.kvch.com/

•

Washington: Southwest Washington Medical Center Library (Southwest Washington Medical Center, Vancouver), http://www.swmedicalcenter.com/body.cfm?id=72

505

ONLINE GLOSSARIES The Internet provides access to a number of free-to-use medical dictionaries. The National Library of Medicine has compiled the following list of online dictionaries: •

ADAM Medical Encyclopedia (A.D.A.M., Inc.), comprehensive medical reference: http://www.nlm.nih.gov/medlineplus/encyclopedia.html

•

MedicineNet.com Medical Dictionary (MedicineNet, Inc.): http://www.medterms.com/Script/Main/hp.asp

•

Merriam-Webster Medical Dictionary (Inteli-Health, Inc.): http://www.intelihealth.com/IH/

•

Multilingual Glossary of Technical and Popular Medical Terms in Eight European Languages (European Commission) - Danish, Dutch, English, French, German, Italian, Portuguese, and Spanish: http://allserv.rug.ac.be/~rvdstich/eugloss/welcome.html

•

On-line Medical Dictionary (CancerWEB): http://cancerweb.ncl.ac.uk/omd/

•

Rare Diseases Terms (Office of Rare Diseases): http://ord.aspensys.com/asp/diseases/diseases.asp

•

Technology Glossary (National Library of Medicine) - Health Care Technology: http://www.nlm.nih.gov/nichsr/ta101/ta10108.htm

Beyond these, MEDLINEplus contains a very patient-friendly encyclopedia covering every aspect of medicine (licensed from A.D.A.M., Inc.). The ADAM Medical Encyclopedia can be accessed at http://www.nlm.nih.gov/medlineplus/encyclopedia.html. ADAM is also available on commercial Web sites such as drkoop.com (http://www.drkoop.com/) and Web MD (http://my.webmd.com/adam/asset/adam_disease_articles/a_to_z/a). The NIH suggests the following Web sites in the ADAM Medical Encyclopedia when searching for information on obesity: •

Basic Guidelines for Obesity Obesity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003101.htm Obesity hypoventilation syndrome (Pickwickian syndrome) Web site: http://www.nlm.nih.gov/medlineplus/ency/article/000085.htm

•

Signs & Symptoms for Obesity Apnea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003069.htm Depression Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003213.htm Dyspnea Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003075.htm

506 Obesity

Flushed face Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003241.htm Hypoxia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003215.htm Joint pain Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003261.htm Morbid obesity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003102.htm Obesity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003101.htm Polydipsia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003085.htm Polyuria Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003146.htm Stress Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003211.htm Swelling Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm Weight loss Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003107.htm •

Diagnostics and Tests for Obesity Hyperplasia Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003441.htm T4 Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003517.htm Thyroid function tests Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003444.htm X-ray Web site: http://www.nlm.nih.gov/medlineplus/ency/article/003337.htm

•

Nutrition for Obesity Carbohydrates Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002469.htm Diet and calories Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002457.htm

Online Glossaries 507

Fat Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002468.htm Protein Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002467.htm •

Surgery and Procedures for Obesity Liposuction Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002985.htm Tummy tuck Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002978.htm

•

Background Topics for Obesity Chronic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002312.htm Eating disorders - support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002171.htm Endocrine Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002351.htm Exercise Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Hypothalamic Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002380.htm Incidence Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002387.htm Intentional weight loss Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001940.htm Metabolism Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002257.htm Physical activity Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001941.htm Physical examination Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002274.htm Support group Web site: http://www.nlm.nih.gov/medlineplus/ency/article/002150.htm Weight reduction Web site: http://www.nlm.nih.gov/medlineplus/ency/article/001940.htm

508 Obesity

Online Dictionary Directories The following are additional online directories compiled by the National Library of Medicine, including a number of specialized medical dictionaries: •

Medical Dictionaries: Medical & Biological (World Health Organization): http://www.who.int/hlt/virtuallibrary/English/diction.htm#Medical

•

MEL-Michigan Electronic Library List of Online Health and Medical Dictionaries (Michigan Electronic Library): http://mel.lib.mi.us/health/health-dictionaries.html

•

Patient Education: Glossaries (DMOZ Open Directory Project): http://dmoz.org/Health/Education/Patient_Education/Glossaries/

•

Web of Online Dictionaries (Bucknell University): http://www.yourdictionary.com/diction5.html#medicine

509

OBESITY DICTIONARY The definitions below are derived from official public sources, including the National Institutes of Health [NIH] and the European Union [EU]. 5-Hydroxytryptophan: Precursor of serotonin used as antiepileptic and antidepressant. [NIH]

Abdomen: That portion of the body that lies between the thorax and the pelvis. [NIH] Abdominal: Having to do with the abdomen, which is the part of the body between the chest and the hips that contains the pancreas, stomach, intestines, liver, gallbladder, and other organs. [NIH] Abdominal fat: Fat (adipose tissue) that is centrally distributed between the thorax and pelvis and that induces greater health risk. [NIH] Aberrant: Wandering or deviating from the usual or normal course. [EU] Ablation: The removal of an organ by surgery. [NIH] Abortion: 1. The premature expulsion from the uterus of the products of conception - of the embryo, or of a nonviable fetus. The four classic symptoms, usually present in each type of abortion, are uterine contractions, uterine haemorrhage, softening and dilatation of the cervix, and presentation or expulsion of all or part of the products of conception. 2. Premature stoppage of a natural or a pathological process. [EU] Acanthosis Nigricans: A circumscribed melanosis consisting of a brown-pigmented, velvety verrucosity or fine papillomatosis appearing in the axillae and other body folds. It occurs in association with endocrine disorders, underlying malignancy, administration of certain drugs, or as in inherited disorder. [NIH] Acceptor: A substance which, while normally not oxidized by oxygen or reduced by hydrogen, can be oxidized or reduced in presence of a substance which is itself undergoing oxidation or reduction. [NIH] Acculturation: Process of cultural change in which one group or members of a group assimilates various cultural patterns from another. [NIH] ACE: Angiotensin-coverting enzyme. A drug used to decrease pressure inside blood vessels. [NIH] Acetone: A colorless liquid used as a solvent and an antiseptic. It is one of the ketone bodies produced during ketoacidosis. [NIH] Acetylcholine: A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. [NIH] Acidity: The quality of being acid or sour; containing acid (hydrogen ions). [EU] Acidosis: A pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, and characterized by an increase in hydrogen ion concentration. [EU] Activities of Daily Living: The performance of the basic activities of self care, such as dressing, ambulation, eating, etc., in rehabilitation. [NIH]

510 Obesity

Acute lymphoblastic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphocytic leukemia. [NIH] Acute lymphocytic leukemia: ALL. A quickly progressing disease in which too many immature white blood cells called lymphoblasts are found in the blood and bone marrow. Also called acute lymphoblastic leukemia. [NIH] Acyl: Chemical signal used by bacteria to communicate. [NIH] Adaptability: Ability to develop some form of tolerance to conditions extremely different from those under which a living organism evolved. [NIH] Adaptation: 1. The adjustment of an organism to its environment, or the process by which it enhances such fitness. 2. The normal ability of the eye to adjust itself to variations in the intensity of light; the adjustment to such variations. 3. The decline in the frequency of firing of a neuron, particularly of a receptor, under conditions of constant stimulation. 4. In dentistry, (a) the proper fitting of a denture, (b) the degree of proximity and interlocking of restorative material to a tooth preparation, (c) the exact adjustment of bands to teeth. 5. In microbiology, the adjustment of bacterial physiology to a new environment. [EU] Adenine: A purine base and a fundamental unit of adenine nucleotides. [NIH] Adenocarcinoma: A malignant epithelial tumor with a glandular organization. [NIH] Adenoma: A benign epithelial tumor with a glandular organization. [NIH] Adenosine: A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. [NIH] Adenovirus: A group of viruses that cause respiratory tract and eye infections. Adenoviruses used in gene therapy are altered to carry a specific tumor-fighting gene. [NIH] Adipocytes: Fat-storing cells found mostly in the abdominal cavity and subcutaneous tissue. Fat is usually stored in the form of tryglycerides. [NIH] Adipose Tissue: Connective tissue composed of fat cells lodged in the meshes of areolar tissue. [NIH] Adjustment: The dynamic process wherein the thoughts, feelings, behavior, and biophysiological mechanisms of the individual continually change to adjust to the environment. [NIH] Adjuvant: A substance which aids another, such as an auxiliary remedy; in immunology, nonspecific stimulator (e.g., BCG vaccine) of the immune response. [EU] Adolescence: The period of life beginning with the appearance of secondary sex characteristics and terminating with the cessation of somatic growth. The years usually referred to as adolescence lie between 13 and 18 years of age. [NIH] Adrenal Cortex: The outer layer of the adrenal gland. It secretes mineralocorticoids, androgens, and glucocorticoids. [NIH] Adrenal Medulla: The inner part of the adrenal gland; it synthesizes, stores and releases catecholamines. [NIH] Adrenergic: Activated by, characteristic of, or secreting epinephrine or substances with similar activity; the term is applied to those nerve fibres that liberate norepinephrine at a synapse when a nerve impulse passes, i.e., the sympathetic fibres. [EU] Adrenergic Agents: Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.

Dictionary 511

[NIH]

Adsorption: The condensation of gases, liquids, or dissolved substances on the surfaces of solids. It includes adsorptive phenomena of bacteria and viruses as well as of tissues treated with exogenous drugs and chemicals. [NIH] Adsorptive: It captures volatile compounds by binding them to agents such as activated carbon or adsorptive resins. [NIH] Adult-Onset Diabetes: Former term for noninsulin-dependent or type II diabetes. [NIH] Adverse Effect: An unwanted side effect of treatment. [NIH] Aerobic: In biochemistry, reactions that need oxygen to happen or happen when oxygen is present. [NIH] Aerobic Exercise: A type of physical activity that includes walking, jogging, running, and dancing. Aerobic training improves the efficiency of the aerobic energy-producing systems that can improve cardiorespiratory endurance. [NIH] Aetiology: Study of the causes of disease. [EU] Afferent: Concerned with the transmission of neural impulse toward the central part of the nervous system. [NIH] Affinity: 1. Inherent likeness or relationship. 2. A special attraction for a specific element, organ, or structure. 3. Chemical affinity; the force that binds atoms in molecules; the tendency of substances to combine by chemical reaction. 4. The strength of noncovalent chemical binding between two substances as measured by the dissociation constant of the complex. 5. In immunology, a thermodynamic expression of the strength of interaction between a single antigen-binding site and a single antigenic determinant (and thus of the stereochemical compatibility between them), most accurately applied to interactions among simple, uniform antigenic determinants such as haptens. Expressed as the association constant (K litres mole -1), which, owing to the heterogeneity of affinities in a population of antibody molecules of a given specificity, actually represents an average value (mean intrinsic association constant). 6. The reciprocal of the dissociation constant. [EU] Afterload: The tension produced by the heart muscle after contraction. [EU] Agar: A complex sulfated polymer of galactose units, extracted from Gelidium cartilagineum, Gracilaria confervoides, and related red algae. It is used as a gel in the preparation of solid culture media for microorganisms, as a bulk laxative, in making emulsions, and as a supporting medium for immunodiffusion and immunoelectrophoresis. [NIH]

Age Groups: Persons classified by age from birth (infant, newborn) to octogenarians and older (aged, 80 and over). [NIH] Age of Onset: The age or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual. [NIH] Aged, 80 and Over: A person 80 years of age and older. [NIH] Agonist: In anatomy, a prime mover. In pharmacology, a drug that has affinity for and stimulates physiologic activity at cell receptors normally stimulated by naturally occurring substances. [EU] Airway: A device for securing unobstructed passage of air into and out of the lungs during general anesthesia. [NIH] Akathisia: 1. A condition of motor restlessness in which there is a feeling of muscular quivering, an urge to move about constantly, and an inability to sit still, a common extrapyramidal side effect of neuroleptic drugs. 2. An inability to sit down because of intense anxiety at the thought of doing so. [EU]

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Albumin: 1. Any protein that is soluble in water and moderately concentrated salt solutions and is coagulable by heat. 2. Serum albumin; the major plasma protein (approximately 60 per cent of the total), which is responsible for much of the plasma colloidal osmotic pressure and serves as a transport protein carrying large organic anions, such as fatty acids, bilirubin, and many drugs, and also carrying certain hormones, such as cortisol and thyroxine, when their specific binding globulins are saturated. Albumin is synthesized in the liver. Low serum levels occur in protein malnutrition, active inflammation and serious hepatic and renal disease. [EU] Aldosterone: (11 beta)-11,21-Dihydroxy-3,20-dioxopregn-4-en-18-al. A hormone secreted by the adrenal cortex that functions in the regulation of electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium. [NIH] Alertness: A state of readiness to detect and respond to certain specified small changes occurring at random intervals in the environment. [NIH] Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task. [NIH] Alimentary: Pertaining to food or nutritive material, or to the organs of digestion. [EU] Alkaline: Having the reactions of an alkali. [EU] Alkaloid: A member of a large group of chemicals that are made by plants and have nitrogen in them. Some alkaloids have been shown to work against cancer. [NIH] Alleles: Mutually exclusive forms of the same gene, occupying the same locus on homologous chromosomes, and governing the same biochemical and developmental process. [NIH] Allografts: A graft of tissue obtained from the body of another animal of the same species but with genotype differing from that of the recipient; tissue graft from a donor of one genotype to a host of another genotype with host and donor being members of the same species. [NIH] Alloys: A mixture of metallic elements or compounds with other metallic or metalloid elements in varying proportions. [NIH] Allylamine: Possesses an unusual and selective cytotoxicity for vascular smooth muscle cells in dogs and rats. Useful for experiments dealing with arterial injury, myocardial fibrosis or cardiac decompensation. [NIH] Alpha 1-Antitrypsin: Plasma glycoprotein member of the serpin superfamily which inhibits trypsin, neutrophil elastase, and other proteolytic enzymes. Commonly referred to as alpha 1-proteinase inhibitor (A1PI), it exists in over 30 different biochemical variant forms known collectively as the PI (protease inhibitor) system. Hereditary A1PI deficiency is associated with pulmonary emphysema. [NIH] Alpha 1-Antitrypsin Deficiency: A disease caused by single gene defects. [NIH] Alpha-Linolenic Acid: A fatty acid that is found in plants and involved in the formation of prostaglandins. [NIH] Alternative medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used instead of standard treatments. Alternative medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Alveoli: Tiny air sacs at the end of the bronchioles in the lungs. [NIH] Ameliorating: A changeable condition which prevents the consequence of a failure or

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accident from becoming as bad as it otherwise would. [NIH] Amenorrhea: Absence of menstruation. [NIH] Amine: An organic compound containing nitrogen; any member of a group of chemical compounds formed from ammonia by replacement of one or more of the hydrogen atoms by organic (hydrocarbon) radicals. The amines are distinguished as primary, secondary, and tertiary, according to whether one, two, or three hydrogen atoms are replaced. The amines include allylamine, amylamine, ethylamine, methylamine, phenylamine, propylamine, and many other compounds. [EU] Amino acid: Any organic compound containing an amino (-NH2 and a carboxyl (- COOH) group. The 20 a-amino acids listed in the accompanying table are the amino acids from which proteins are synthesized by formation of peptide bonds during ribosomal translation of messenger RNA; all except glycine, which is not optically active, have the L configuration. Other amino acids occurring in proteins, such as hydroxyproline in collagen, are formed by posttranslational enzymatic modification of amino acids residues in polypeptide chains. There are also several important amino acids, such as the neurotransmitter y-aminobutyric acid, that have no relation to proteins. Abbreviated AA. [EU] Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining protein conformation. [NIH] Aminoethyl: A protease inhibitor. [NIH] Ammonia: A colorless alkaline gas. It is formed in the body during decomposition of organic materials during a large number of metabolically important reactions. [NIH] Amnestic: Nominal aphasia; a difficulty in finding the right name for an object. [NIH] Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is dextroamphetamine. [NIH] Amplification: The production of additional copies of a chromosomal DNA sequence, found as either intrachromosomal or extrachromosomal DNA. [NIH] Ampulla: A sac-like enlargement of a canal or duct. [NIH] Amygdala: Almond-shaped group of basal nuclei anterior to the inferior horn of the lateral ventricle of the brain, within the temporal lobe. The amygdala is part of the limbic system. [NIH]

Amyloid: A general term for a variety of different proteins that accumulate as extracellular fibrils of 7-10 nm and have common structural features, including a beta-pleated sheet conformation and the ability to bind such dyes as Congo red and thioflavine (Kandel, Schwartz, and Jessel, Principles of Neural Science, 3rd ed). [NIH] Anabolic: Relating to, characterized by, or promoting anabolism. [EU] Anaerobic: 1. Lacking molecular oxygen. 2. Growing, living, or occurring in the absence of molecular oxygen; pertaining to an anaerobe. [EU] Anaesthesia: Loss of feeling or sensation. Although the term is used for loss of tactile sensibility, or of any of the other senses, it is applied especially to loss of the sensation of pain, as it is induced to permit performance of surgery or other painful procedures. [EU] Anal: Having to do with the anus, which is the posterior opening of the large bowel. [NIH]

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Analgesics: Compounds capable of relieving pain without the loss of consciousness or without producing anesthesia. [NIH] Analog: In chemistry, a substance that is similar, but not identical, to another. [NIH] Analogous: Resembling or similar in some respects, as in function or appearance, but not in origin or development;. [EU] Anaphylatoxins: The family of peptides C3a, C4a, C5a, and C5a des-arginine produced in the serum during complement activation. They produce smooth muscle contraction, mast cell histamine release, affect platelet aggregation, and act as mediators of the local inflammatory process. The order of anaphylatoxin activity from strongest to weakest is C5a, C3a, C4a, and C5a des-arginine. The latter is the so-called "classical" anaphylatoxin but shows no spasmogenic activity though it contains some chemotactic ability. [NIH] Anastomosis: A procedure to connect healthy sections of tubular structures in the body after the diseased portion has been surgically removed. [NIH] Anatomical: Pertaining to anatomy, or to the structure of the organism. [EU] Androgens: A class of sex hormones associated with the development and maintenance of the secondary male sex characteristics, sperm induction, and sexual differentiation. In addition to increasing virility and libido, they also increase nitrogen and water retention and stimulate skeletal growth. [NIH] Anemia: A reduction in the number of circulating erythrocytes or in the quantity of hemoglobin. [NIH] Anesthesia: A state characterized by loss of feeling or sensation. This depression of nerve function is usually the result of pharmacologic action and is induced to allow performance of surgery or other painful procedures. [NIH] Angina: Chest pain that originates in the heart. [NIH] Angina Pectoris: The symptom of paroxysmal pain consequent to myocardial ischemia usually of distinctive character, location and radiation, and provoked by a transient stressful situation during which the oxygen requirements of the myocardium exceed the capacity of the coronary circulation to supply it. [NIH] Angiogenesis: Blood vessel formation. Tumor angiogenesis is the growth of blood vessels from surrounding tissue to a solid tumor. This is caused by the release of chemicals by the tumor. [NIH] Angiotensinogen: An alpha-globulin of which a fragment of 14 amino acids is converted by renin to angiotensin I, the inactive precursor of angiotensin II. It is a member of the serpin superfamily. [NIH] Animal model: An animal with a disease either the same as or like a disease in humans. Animal models are used to study the development and progression of diseases and to test new treatments before they are given to humans. Animals with transplanted human cancers or other tissues are called xenograft models. [NIH] Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis. [NIH] Ankle: That part of the lower limb directly above the foot. [NIH] Anode: Electrode held at a positive potential with respect to a cathode. [NIH] Anomalies: Birth defects; abnormalities. [NIH] Anorexia: Lack or loss of appetite for food. Appetite is psychologic, dependent on memory and associations. Anorexia can be brought about by unattractive food, surroundings, or company. [NIH]

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Anorexia Nervosa: The chief symptoms are inability to eat, weight loss, and amenorrhea. [NIH]

Anorexiant: A drug, process, or event that leads to anorexia. [NIH] Anovulation: Suspension or cessation of ovulation in animals and humans. [NIH] Antagonism: Interference with, or inhibition of, the growth of a living organism by another living organism, due either to creation of unfavorable conditions (e. g. exhaustion of food supplies) or to production of a specific antibiotic substance (e. g. penicillin). [NIH] Anthelmintic: An agent that is destructive to worms. [EU] Anthropometric measurements: Measurements of human body height, weight, and size of component parts, including skinfold measurement. Used to study and compare the relative proportions under normal and abnormal conditions. [NIH] Anthropometry: The technique that deals with the measurement of the size, weight, and proportions of the human or other primate body. [NIH] Antibacterial: A substance that destroys bacteria or suppresses their growth or reproduction. [EU] Antibiotic: A drug used to treat infections caused by bacteria and other microorganisms. [NIH]

Antibodies: Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the antigen that induced their synthesis in cells of the lymphoid series (especially plasma cells), or with an antigen closely related to it. [NIH] Antibody: A type of protein made by certain white blood cells in response to a foreign substance (antigen). Each antibody can bind to only a specific antigen. The purpose of this binding is to help destroy the antigen. Antibodies can work in several ways, depending on the nature of the antigen. Some antibodies destroy antigens directly. Others make it easier for white blood cells to destroy the antigen. [NIH] Anticoagulant: A drug that helps prevent blood clots from forming. Also called a blood thinner. [NIH] Anticonvulsant: An agent that prevents or relieves convulsions. [EU] Antidepressant: A drug used to treat depression. [NIH] Antidiabetic: An agent that prevents or alleviates diabetes. [EU] Antiemetic: An agent that prevents or alleviates nausea and vomiting. Also antinauseant. [EU]

Antiepileptic: An agent that combats epilepsy. [EU] Antigen: Any substance which is capable, under appropriate conditions, of inducing a specific immune response and of reacting with the products of that response, that is, with specific antibody or specifically sensitized T-lymphocytes, or both. Antigens may be soluble substances, such as toxins and foreign proteins, or particulate, such as bacteria and tissue cells; however, only the portion of the protein or polysaccharide molecule known as the antigenic determinant (q.v.) combines with antibody or a specific receptor on a lymphocyte. Abbreviated Ag. [EU] Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes immune complex diseases. [NIH] Anti-infective: An agent that so acts. [EU] Anti-Infective Agents: Substances that prevent infectious agents or organisms from spreading or kill infectious agents in order to prevent the spread of infection. [NIH]

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Anti-inflammatory: Having to do with reducing inflammation. [NIH] Anti-Inflammatory Agents: Substances that reduce or suppress inflammation. [NIH] Anti-Obesity Agents: Agents that increase energy expenditure and weight loss by neural and chemical regulation. Beta-adrenergic agents and serotoninergic drugs have been experimentally used in patients with non-insulin dependent diabetes mellitus (NIDDM) to treat obesity. [NIH] Antioxidant: A substance that prevents damage caused by free radicals. Free radicals are highly reactive chemicals that often contain oxygen. They are produced when molecules are split to give products that have unpaired electrons. This process is called oxidation. [NIH] Antipsychotic: Effective in the treatment of psychosis. Antipsychotic drugs (called also neuroleptic drugs and major tranquilizers) are a chemically diverse (including phenothiazines, thioxanthenes, butyrophenones, dibenzoxazepines, dibenzodiazepines, and diphenylbutylpiperidines) but pharmacologically similar class of drugs used to treat schizophrenic, paranoid, schizoaffective, and other psychotic disorders; acute delirium and dementia, and manic episodes (during induction of lithium therapy); to control the movement disorders associated with Huntington's chorea, Gilles de la Tourette's syndrome, and ballismus; and to treat intractable hiccups and severe nausea and vomiting. Antipsychotic agents bind to dopamine, histamine, muscarinic cholinergic, a-adrenergic, and serotonin receptors. Blockade of dopaminergic transmission in various areas is thought to be responsible for their major effects : antipsychotic action by blockade in the mesolimbic and mesocortical areas; extrapyramidal side effects (dystonia, akathisia, parkinsonism, and tardive dyskinesia) by blockade in the basal ganglia; and antiemetic effects by blockade in the chemoreceptor trigger zone of the medulla. Sedation and autonomic side effects (orthostatic hypotension, blurred vision, dry mouth, nasal congestion and constipation) are caused by blockade of histamine, cholinergic, and adrenergic receptors. [EU] Antiseptic: A substance that inhibits the growth and development of microorganisms without necessarily killing them. [EU] Antrectomy: An operation to remove the upper portion of the stomach, called the antrum. This operation helps reduce the amount of stomach acid. It is used when a person has complications from ulcers. [NIH] Anuria: Inability to form or excrete urine. [NIH] Anus: The opening of the rectum to the outside of the body. [NIH] Anxiety: Persistent feeling of dread, apprehension, and impending disaster. [NIH] Aorta: The main trunk of the systemic arteries. [NIH] Aperture: A natural hole of perforation, especially one in a bone. [NIH] Apnea: A transient absence of spontaneous respiration. [NIH] Apnoea: Cessation of breathing. [EU] Apolipoproteins: The protein components of lipoproteins which remain after the lipids to which the proteins are bound have been removed. They play an important role in lipid transport and metabolism. [NIH] Apoptosis: One of the two mechanisms by which cell death occurs (the other being the pathological process of necrosis). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA (DNA fragmentation) at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes

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associated with tumor growth. [NIH] Appetite Regulation: Physiologic mechanisms which regulate or control the appetite and food intake. [NIH] Aqueous: Having to do with water. [NIH] Arachidonate 15-Lipoxygenase: An enzyme that catalyzes the oxidation of arachidonic acid to yield 15-hydroperoxyarachidonate (15-HPETE) which is rapidly converted to 15-hydroxy5,8,11,13-eicosatetraenoate (15-HETE). The 15-hydroperoxides are preferentially formed in neutrophils and lymphocytes. EC 1.13.11.33. [NIH] Arachidonate Lipoxygenases: Enzymes catalyzing the oxidation of arachidonic acid to hydroperoxyarachidonates (HPETES). These products are then rapidly converted by a peroxidase to hydroxyeicosatetraenoic acids (HETES). The positional specificity of the enzyme reaction varies from tissue to tissue. The final lipoxygenase pathway leads to the leukotrienes. EC 1.13.11.- . [NIH] Arachidonic Acid: An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. [NIH] Arcuate Nucleus: A nucleus located in the middle hypothalamus in the most ventral part of the third ventricle near the entrance of the infundibular recess. Its small cells are in close contact with the ependyma. [NIH] Aromatic: Having a spicy odour. [EU] Arterial: Pertaining to an artery or to the arteries. [EU] Arteries: The vessels carrying blood away from the heart. [NIH] Arteriolar: Pertaining to or resembling arterioles. [EU] Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries. [NIH] Arteriolosclerosis: Sclerosis and thickening of the walls of the smaller arteries (arterioles). Hyaline arteriolosclerosis, in which there is homogeneous pink hyaline thickening of the arteriolar walls, is associated with benign nephrosclerosis. Hyperplastic arteriolosclerosis, in which there is a concentric thickening with progressive narrowing of the lumina may be associated with malignant hypertension, nephrosclerosis, and scleroderma. [EU] Arteriosclerosis: Thickening and loss of elasticity of arterial walls. Atherosclerosis is the most common form of arteriosclerosis and involves lipid deposition and thickening of the intimal cell layers within arteries. Additional forms of arteriosclerosis involve calcification of the media of muscular arteries (Monkeberg medial calcific sclerosis) and thickening of the walls of small arteries or arterioles due to cell proliferation or hyaline deposition (arteriolosclerosis). [NIH] Artery: Vessel-carrying blood from the heart to various parts of the body. [NIH] Articular: Of or pertaining to a joint. [EU] Aseptic: Free from infection or septic material; sterile. [EU] Aspartic: The naturally occurring substance is L-aspartic acid. One of the acidic-aminoacids is obtained by the hydrolysis of proteins. [NIH] Aspartic Endopeptidases: A sub-subclass of endopeptidases that depend on an aspartic acid residue for their activity. EC 3.4.23. [NIH] Aspiration: The act of inhaling. [NIH]

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Aspirin: A drug that reduces pain, fever, inflammation, and blood clotting. Aspirin belongs to the family of drugs called nonsteroidal anti-inflammatory agents. It is also being studied in cancer prevention. [NIH] Assay: Determination of the amount of a particular constituent of a mixture, or of the biological or pharmacological potency of a drug. [EU] Astringent: Causing contraction, usually locally after topical application. [EU] Astrocytes: The largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the blood brain barrier. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with microglia) respond to injury. Astrocytes have high- affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitter, but their role in signaling (as in many other functions) is not well understood. [NIH] Asymptomatic: Having no signs or symptoms of disease. [NIH] Ataxia: Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharnyx, larnyx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or peripheral nerve diseases. Motor ataxia may be associated with cerebellar diseases; cerebral cortex diseases; thalamic diseases; basal ganglia diseases; injury to the red nucleus; and other conditions. [NIH] Atelectasis: Incomplete expansion of the lung. [NIH] Atrial: Pertaining to an atrium. [EU] Atrioventricular: Pertaining to an atrium of the heart and to a ventricle. [EU] Atrium: A chamber; used in anatomical nomenclature to designate a chamber affording entrance to another structure or organ. Usually used alone to designate an atrium of the heart. [EU] Atrophy: Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes. [NIH] Atypical: Irregular; not conformable to the type; in microbiology, applied specifically to strains of unusual type. [EU] Audiovisual Aids: Auditory and visual instructional materials. [NIH] Auditory: Pertaining to the sense of hearing. [EU] Autodigestion: Autolysis; a condition found in disease of the stomach: the stomach wall is digested by the gastric juice. [NIH] Autoimmune disease: A condition in which the body recognizes its own tissues as foreign and directs an immune response against them. [NIH] Autonomic: Self-controlling; functionally independent. [EU] Autonomic Nervous System: The enteric, parasympathetic, and sympathetic nervous systems taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the central nervous system, especially the hypothalamus and the solitary nucleus, which receive information relayed from visceral afferents; these and related central and sensory structures are sometimes (but not here) considered to be part of the autonomic nervous system itself. [NIH]

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Autonomic Neuropathy: A disease of the nerves affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Also called visceral neuropathy. [NIH] Aversion therapy: Negative conditioning, consisting of pairing the unwanted symptom or behavior (e. g. alcoholism) with painful or unpleasant stimuli until the undesirable behavior is suppressed. [NIH] Axillary: Pertaining to the armpit area, including the lymph nodes that are located there. [NIH]

Axillary Artery: The continuation of the subclavian artery; it distributes over the upper limb, axilla, chest and shoulder. [NIH] Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body. [NIH] Bacteria: Unicellular prokaryotic microorganisms which generally possess rigid cell walls, multiply by cell division, and exhibit three principal forms: round or coccal, rodlike or bacillary, and spiral or spirochetal. [NIH] Bacterial Infections: Infections by bacteria, general or unspecified. [NIH] Bacterial Physiology: Physiological processes and activities of bacteria. [NIH] Bactericidal: Substance lethal to bacteria; substance capable of killing bacteria. [NIH] Bacteriophage: A virus whose host is a bacterial cell; A virus that exclusively infects bacteria. It generally has a protein coat surrounding the genome (DNA or RNA). One of the coliphages most extensively studied is the lambda phage, which is also one of the most important. [NIH] Bacteriostatic: 1. Inhibiting the growth or multiplication of bacteria. 2. An agent that inhibits the growth or multiplication of bacteria. [EU] Bacterium: Microscopic organism which may have a spherical, rod-like, or spiral unicellular or non-cellular body. Bacteria usually reproduce through asexual processes. [NIH] Balloon dilation: A treatment for benign prostatic hyperplasia or prostate enlargement. A tiny balloon is inflated inside the urethra to make it wider so urine can flow more freely from the bladder. [NIH] Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres. [NIH] Basal Ganglia Diseases: Diseases of the basal ganglia including the putamen; globus pallidus; claustrum; amygdala; and caudate nucleus. Dyskinesias (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include cerebrovascular disease; neurodegenerative diseases; and craniocerebral trauma. [NIH] Base: In chemistry, the nonacid part of a salt; a substance that combines with acids to form salts; a substance that dissociates to give hydroxide ions in aqueous solutions; a substance whose molecule or ion can combine with a proton (hydrogen ion); a substance capable of donating a pair of electrons (to an acid) for the formation of a coordinate covalent bond. [EU] Base Sequence: The sequence of purines and pyrimidines in nucleic acids and polynucleotides. It is also called nucleotide or nucleoside sequence. [NIH] Basement Membrane: Ubiquitous supportive tissue adjacent to epithelium and around smooth and striated muscle cells. This tissue contains intrinsic macromolecular components such as collagen, laminin, and sulfated proteoglycans. As seen by light microscopy one of its

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subdivisions is the basal (basement) lamina. [NIH] Behavior Therapy: The application of modern theories of learning and conditioning in the treatment of behavior disorders. [NIH] Benign: Not cancerous; does not invade nearby tissue or spread to other parts of the body. [NIH]

Benign prostatic hyperplasia: A benign (noncancerous) condition in which an overgrowth of prostate tissue pushes against the urethra and the bladder, blocking the flow of urine. Also called benign prostatic hypertrophy or BPH. [NIH] Beta blocker: A drug used to slow the heart rate and reduce pressure inside blood vessels. It also can regulate heart rhythm. [NIH] Beta-pleated: Particular three-dimensional pattern of amyloidoses. [NIH] Bezoar: A ball of food, mucus, vegetable fiber, hair, or other material that cannot be digested in the stomach. Bezoars can cause blockage, ulcers, and bleeding. [NIH] Bilateral: Affecting both the right and left side of body. [NIH] Bile: An emulsifying agent produced in the liver and secreted into the duodenum. Its composition includes bile acids and salts, cholesterol, and electrolytes. It aids digestion of fats in the duodenum. [NIH] Bile Acids: Acids made by the liver that work with bile to break down fats. [NIH] Bile Acids and Salts: Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones. [NIH] Bile duct: A tube through which bile passes in and out of the liver. [NIH] Biliary: Having to do with the liver, bile ducts, and/or gallbladder. [NIH] Biliary Tract: The gallbladder and its ducts. [NIH] Biliopancreatic Diversion: A surgical procedure which diverts pancreatobiliary secretions via the duodenum and the jejunum into the colon, the remaining small intestine being anastomosed to the stomach after antrectomy. The procedure produces less diarrhea than does jejunoileal bypass. [NIH] Bilirubin: A bile pigment that is a degradation product of heme. [NIH] Bioavailability: The degree to which a drug or other substance becomes available to the target tissue after administration. [EU] Biochemical: Relating to biochemistry; characterized by, produced by, or involving chemical reactions in living organisms. [EU] Biological therapy: Treatment to stimulate or restore the ability of the immune system to fight infection and disease. Also used to lessen side effects that may be caused by some cancer treatments. Also known as immunotherapy, biotherapy, or biological response modifier (BRM) therapy. [NIH] Biopsy: Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body. [NIH] Biotechnology: Body of knowledge related to the use of organisms, cells or cell-derived constituents for the purpose of developing products which are technically, scientifically and clinically useful. Alteration of biologic function at the molecular level (i.e., genetic engineering) is a central focus; laboratory methods used include transfection and cloning

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technologies, sequence and structure analysis algorithms, computer databases, and gene and protein structure function analysis and prediction. [NIH] Biotransformation: The chemical alteration of an exogenous substance by or in a biological system. The alteration may inactivate the compound or it may result in the production of an active metabolite of an inactive parent compound. The alteration may be either nonsynthetic (oxidation-reduction, hydrolysis) or synthetic (glucuronide formation, sulfate conjugation, acetylation, methylation). This also includes metabolic detoxication and clearance. [NIH] Bipolar Disorder: A major affective disorder marked by severe mood swings (manic or major depressive episodes) and a tendency to remission and recurrence. [NIH] Birth Certificates: Official certifications by a physician recording the individual's birth date, place of birth, parentage and other required identifying data which are filed with the local registrar of vital statistics. [NIH] Bivalent: Pertaining to a group of 2 homologous or partly homologous chromosomes during the zygotene stage of prophase to the first metaphase in meiosis. [NIH] Bladder: The organ that stores urine. [NIH] Blood Coagulation: The process of the interaction of blood coagulation factors that results in an insoluble fibrin clot. [NIH] Blood Glucose: Glucose in blood. [NIH] Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation. [NIH] Blood pressure: The pressure of blood against the walls of a blood vessel or heart chamber. Unless there is reference to another location, such as the pulmonary artery or one of the heart chambers, it refers to the pressure in the systemic arteries, as measured, for example, in the forearm. [NIH] Blood vessel: A tube in the body through which blood circulates. Blood vessels include a network of arteries, arterioles, capillaries, venules, and veins. [NIH] Blood Volume: Volume of circulating blood. It is the sum of the plasma volume and erythrocyte volume. [NIH] Blood-Brain Barrier: Specialized non-fenestrated tightly-joined endothelial cells (tight junctions) that form a transport barrier for certain substances between the cerebral capillaries and the brain tissue. [NIH] BMI: Body mass index; the body weight in kilograms divided by the height in meters squared (wt/ht2) used as a practical marker to assess obesity; often referred to as the Quetelet Index. An indicator of optimal weight for health and different from lean mass or percent body fat calculations because it only considers height and weight. [NIH] Body Composition: The relative amounts of various components in the body, such as percent body fat. [NIH] Body Fluids: Liquid components of living organisms. [NIH] Body Image: Individuals' personal concept of their bodies as objects in and bound by space, independently and apart from all other objects. [NIH] Body Mass Index: One of the anthropometric measures of body mass; it has the highest correlation with skinfold thickness or body density. [NIH] Bone Marrow: The soft tissue filling the cavities of bones. Bone marrow exists in two types, yellow and red. Yellow marrow is found in the large cavities of large bones and consists mostly of fat cells and a few primitive blood cells. Red marrow is a hematopoietic tissue and

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is the site of production of erythrocytes and granular leukocytes. Bone marrow is made up of a framework of connective tissue containing branching fibers with the frame being filled with marrow cells. [NIH] Boronic Acids: Inorganic or organic compounds that contain the basic structure RB(OH)2. [NIH]

Bowel: The long tube-shaped organ in the abdomen that completes the process of digestion. There is both a small and a large bowel. Also called the intestine. [NIH] Bowel Movement: Body wastes passed through the rectum and anus. [NIH] Brachial: All the nerves from the arm are ripped from the spinal cord. [NIH] Brachial Artery: The continuation of the axillary artery; it branches into the radial and ulnar arteries. [NIH] Brachytherapy: A collective term for interstitial, intracavity, and surface radiotherapy. It uses small sealed or partly-sealed sources that may be placed on or near the body surface or within a natural body cavity or implanted directly into the tissues. [NIH] Bradykinin: A nonapeptide messenger that is enzymatically produced from kallidin in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from mast cells during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter. [NIH] Brain Stem: The part of the brain that connects the cerebral hemispheres with the spinal cord. It consists of the mesencephalon, pons, and medulla oblongata. [NIH] Branch: Most commonly used for branches of nerves, but applied also to other structures. [NIH]

Breakdown: A physical, metal, or nervous collapse. [NIH] Bromocriptine: A semisynthetic ergot alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion and is used to treat amenorrhea, galactorrhea, and female infertility, and has been proposed for Parkinson disease. [NIH] Bronchial: Pertaining to one or more bronchi. [EU] Bronchioles: The tiny branches of air tubes in the lungs. [NIH] Brown Fat: A thermogenic form of adipose tissue found in newborns of many species, including humans, and in hibernating mammals. The tissue is capable of rapid liberation of energy and seems to be important in the maintenance of body temperature immediately after birth and upon waking from hibernation. [NIH] Bulimia: Episodic binge eating. The episodes may be associated with the fear of not being able to stop eating, depressed mood, or self-deprecating thoughts (binge-eating disorder) and may frequently be terminated by self-induced vomiting (bulimia nervosa). [NIH] Bupropion: A unicyclic, aminoketone antidepressant. The mechanism of its therapeutic actions is not well understood, but it does appear to block dopamine uptake. The hydrochloride is available as an aid to smoking cessation treatment. [NIH] Burns: Injuries to tissues caused by contact with heat, steam, chemicals (burns, chemical), electricity (burns, electric), or the like. [NIH] Burns, Electric: Burns produced by contact with electric current or from a sudden discharge of electricity. [NIH] Bypass: A surgical procedure in which the doctor creates a new pathway for the flow of body fluids. [NIH] Cachexia: General ill health, malnutrition, and weight loss, usually associated with chronic

Dictionary 523

disease. [NIH] Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes smooth muscle, stimulates cardiac muscle, stimulates diuresis, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide phosphodiesterases, antagonism of adenosine receptors, and modulation of intracellular calcium handling. [NIH] Calcification: Deposits of calcium in the tissues of the breast. Calcification in the breast can be seen on a mammogram, but cannot be detected by touch. There are two types of breast calcification, macrocalcification and microcalcification. Macrocalcifications are large deposits and are usually not related to cancer. Microcalcifications are specks of calcium that may be found in an area of rapidly dividing cells. Many microcalcifications clustered together may be a sign of cancer. [NIH] Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. [NIH] Calcium Carbonate: Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement. [NIH] Calcium Oxalate: The calcium salt of oxalic acid, occurring in the urine as crystals and in certain calculi. [NIH] Calculi: An abnormal concretion occurring mostly in the urinary and biliary tracts, usually composed of mineral salts. Also called stones. [NIH] Caloric intake: Refers to the number of calories (energy content) consumed. [NIH] Calorimeter: Measures the amounts of heat absorbed or given off by a solid, a liquid, or a gas. [NIH] Calpain: Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including neuropeptides, cytoskeletal proteins, proteins from smooth muscle, cardiac muscle, liver, platelets and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. [NIH] Capillary: Any one of the minute vessels that connect the arterioles and venules, forming a network in nearly all parts of the body. Their walls act as semipermeable membranes for the interchange of various substances, including fluids, between the blood and tissue fluid; called also vas capillare. [EU] Capillary Fragility: The lack of resistance, or susceptibility, of capillaries to damage or disruption under conditions of increased stress. [NIH] Capsules: Hard or soft soluble containers used for the oral administration of medicine. [NIH] Carbohydrate: An aldehyde or ketone derivative of a polyhydric alcohol, particularly of the pentahydric and hexahydric alcohols. They are so named because the hydrogen and oxygen are usually in the proportion to form water, (CH2O)n. The most important carbohydrates are the starches, sugars, celluloses, and gums. They are classified into mono-, di-, tri-, poly-

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and heterosaccharides. [EU] Carbon Dioxide: A colorless, odorless gas that can be formed by the body and is necessary for the respiration cycle of plants and animals. [NIH] Carcinogen: Any substance that causes cancer. [NIH] Carcinogenic: Producing carcinoma. [EU] Carcinoma: Cancer that begins in the skin or in tissues that line or cover internal organs. [NIH]

Cardia: That part of the stomach surrounded by the esophagogastric junction, characterized by the lack of acid-forming cells. [NIH] Cardiac: Having to do with the heart. [NIH] Cardiac Output: The volume of blood passing through the heart per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with stroke volume (volume per beat). [NIH] Cardiopulmonary: Having to do with the heart and lungs. [NIH] Cardiorespiratory: Relating to the heart and lungs and their function. [EU] Cardioselective: Having greater activity on heart tissue than on other tissue. [EU] Cardiovascular: Having to do with the heart and blood vessels. [NIH] Cardiovascular Abnormalities: Congenital structural abnormalities of the cardiovascular system. [NIH] Cardiovascular disease: Any abnormal condition characterized by dysfunction of the heart and blood vessels. CVD includes atherosclerosis (especially coronary heart disease, which can lead to heart attacks), cerebrovascular disease (e.g., stroke), and hypertension (high blood pressure). [NIH] Cardiovascular System: The heart and the blood vessels by which blood is pumped and circulated through the body. [NIH] Carnitine: Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. [NIH] Carotene: The general name for a group of pigments found in green, yellow, and leafy vegetables, and yellow fruits. The pigments are fat-soluble, unsaturated aliphatic hydrocarbons functioning as provitamins and are converted to vitamin A through enzymatic processes in the intestinal wall. [NIH] Carpal Tunnel Syndrome: A median nerve injury inside the carpal tunnel that results in symptoms of pain, numbness, tingling, clumsiness, and a lack of sweating, which can be caused by work with certain hand and wrist postures. [NIH] Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes. [NIH] Case report: A detailed report of the diagnosis, treatment, and follow-up of an individual patient. Case reports also contain some demographic information about the patient (for example, age, gender, ethnic origin). [NIH] Case series: A group or series of case reports involving patients who were given similar treatment. Reports of case series usually contain detailed information about the individual patients. This includes demographic information (for example, age, gender, ethnic origin) and information on diagnosis, treatment, response to treatment, and follow-up after treatment. [NIH] Catabolism: Any destructive metabolic process by which organisms convert substances into

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excreted compounds. [EU] Catalyse: To speed up a chemical reaction. [EU] Catechin: Extracted from Uncaria gambier, Acacia catechu and other plants; it stabilizes collagen and is therefore used in tanning and dyeing; it prevents capillary fragility and abnormal permeability, but was formerly used as an antidiarrheal. [NIH] Catechol: A chemical originally isolated from a type of mimosa tree. Catechol is used as an astringent, an antiseptic, and in photography, electroplating, and making other chemicals. It can also be man-made. [NIH] Catecholamine: A group of chemical substances manufactured by the adrenal medulla and secreted during physiological stress. [NIH] Catheter: A flexible tube used to deliver fluids into or withdraw fluids from the body. [NIH] Catheterization: Use or insertion of a tubular device into a duct, blood vessel, hollow organ, or body cavity for injecting or withdrawing fluids for diagnostic or therapeutic purposes. It differs from intubation in that the tube here is used to restore or maintain patency in obstructions. [NIH] Cathode: An electrode, usually an incandescent filament of tungsten, which emits electrons in an X-ray tube. [NIH] Caudal: Denoting a position more toward the cauda, or tail, than some specified point of reference; same as inferior, in human anatomy. [EU] Causal: Pertaining to a cause; directed against a cause. [EU] Cause of Death: Factors which produce cessation of all vital bodily functions. They can be analyzed from an epidemiologic viewpoint. [NIH] Cecum: The beginning of the large intestine. The cecum is connected to the lower part of the small intestine, called the ileum. [NIH] Cell: The individual unit that makes up all of the tissues of the body. All living things are made up of one or more cells. [NIH] Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. [NIH] Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function which takes place during the development of the embryo and leads to the formation of specialized cells, tissues, and organs. [NIH] Cell Division: The fission of a cell. [NIH] Cell membrane: Cell membrane = plasma membrane. The structure enveloping a cell, enclosing the cytoplasm, and forming a selective permeability barrier; it consists of lipids, proteins, and some carbohydrates, the lipids thought to form a bilayer in which integral proteins are embedded to varying degrees. [EU] Cell proliferation: An increase in the number of cells as a result of cell growth and cell division. [NIH] Cell Respiration: The metabolic process of all living cells (animal and plant) in which oxygen is used to provide a source of energy for the cell. [NIH] Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. [NIH] Cellobiose: A disaccharide consisting of two glucose units in beta (1-4) glycosidic linkage. Obtained from the partial hydrolysis of cellulose. [NIH]

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Cellulose: A polysaccharide with glucose units linked as in cellobiose. It is the chief constituent of plant fibers, cotton being the purest natural form of the substance. As a raw material, it forms the basis for many derivatives used in chromatography, ion exchange materials, explosives manufacturing, and pharmaceutical preparations. [NIH] Central fat distribution: The waist circumference is an index of body fat distribution. Increasing waist circumference is accompanied by increasing frequencies of overt type 2 diabetes, dyslipidemia, hypertension, coronary heart disease, stroke, and early mortality. In the body fat patterns called android type (apple shaped) fat is deposited around the waist and upper abdominal area and appears most often in men. Abdominal body fat is thought to be associated with a rapid mobilization of fatty acids rather than resulting from other fat depots, although it remains a point of contention. If abdominal fat is indeed more active than other fat depots, it would then provide a mechanism by which we could explain (in part) the increase in blood lipid and glucose levels. The latter have been clearly associated with an increased risk for cardiovascular disease, hypertension, and type 2 diabetes. The gynoid type (pear-shaped) of body fat is usually seen in women. The fat is deposited around the hips, thighs, and buttocks, and presumably is used as energy reserve during pregnancy and lactation. [NIH] Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges. [NIH] Cerebellar: Pertaining to the cerebellum. [EU] Cerebral: Of or pertaining of the cerebrum or the brain. [EU] Cerebral Cortex: The thin layer of gray matter on the surface of the cerebral hemisphere that develops from the telencephalon and folds into gyri. It reaches its highest development in man and is responsible for intellectual faculties and higher mental functions. [NIH] Cerebrovascular: Pertaining to the blood vessels of the cerebrum, or brain. [EU] Cerebrum: The largest part of the brain. It is divided into two hemispheres, or halves, called the cerebral hemispheres. The cerebrum controls muscle functions of the body and also controls speech, emotions, reading, writing, and learning. [NIH] Cervical: Relating to the neck, or to the neck of any organ or structure. Cervical lymph nodes are located in the neck; cervical cancer refers to cancer of the uterine cervix, which is the lower, narrow end (the "neck") of the uterus. [NIH] Cervix: The lower, narrow end of the uterus that forms a canal between the uterus and vagina. [NIH] Character: In current usage, approximately equivalent to personality. The sum of the relatively fixed personality traits and habitual modes of response of an individual. [NIH] Chemoreceptor: A receptor adapted for excitation by chemical substances, e.g., olfactory and gustatory receptors, or a sense organ, as the carotid body or the aortic (supracardial) bodies, which is sensitive to chemical changes in the blood stream, especially reduced oxygen content, and reflexly increases both respiration and blood pressure. [EU] Chemotactic Factors: Chemical substances that attract or repel cells or organisms. The concept denotes especially those factors released as a result of tissue injury, invasion, or immunologic activity, that attract leukocytes, macrophages, or other cells to the site of infection or insult. [NIH] Chin: The anatomical frontal portion of the mandible, also known as the mentum, that contains the line of fusion of the two separate halves of the mandible (symphysis menti). This line of fusion divides inferiorly to enclose a triangular area called the mental protuberance. On each side, inferior to the second premolar tooth, is the mental foramen for

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the passage of blood vessels and a nerve. [NIH] Chlorella: Nonmotile unicellular green algae potentially valuable as a source of high-grade protein and B-complex vitamins. [NIH] Chloroform: A commonly used laboratory solvent. It was previously used as an anesthetic, but was banned from use in the U.S. due to its suspected carcinogenecity. [NIH] Cholecystitis: Inflammation of the gallbladder. [NIH] Cholelithiasis: Presence or formation of gallstones. [NIH] Cholestenones: Cholestenes with one or more double bonds and substituted by any number of keto groups. [NIH] Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils. [NIH] Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis. [NIH] Cholinergic: Resembling acetylcholine in pharmacological action; stimulated by or releasing acetylcholine or a related compound. [EU] Chondrocytes: Polymorphic cells that form cartilage. [NIH] Chorea: Involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement. Hypotonia and pendular reflexes are often associated. Conditions which feature recurrent or persistent episodes of chorea as a primary manifestation of disease are referred to as choreatic disorders. Chorea is also a frequent manifestation of basal ganglia diseases. [NIH] Chromatin: The material of chromosomes. It is a complex of DNA, histones, and nonhistone proteins (chromosomal proteins, non-histone) found within the nucleus of a cell. [NIH] Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens. [NIH] Chromosomal: Pertaining to chromosomes. [EU] Chromosome: Part of a cell that contains genetic information. Except for sperm and eggs, all human cells contain 46 chromosomes. [NIH] Chronic: A disease or condition that persists or progresses over a long period of time. [NIH] Chronic Disease: Disease or ailment of long duration. [NIH] Chronic renal: Slow and progressive loss of kidney function over several years, often resulting in end-stage renal disease. People with end-stage renal disease need dialysis or transplantation to replace the work of the kidneys. [NIH] Chylomicrons: A class of lipoproteins that carry dietary cholesterol and triglycerides from the small intestines to the tissues. [NIH] Ciliary: Inflammation or infection of the glands of the margins of the eyelids. [NIH] Ciliary Neurotrophic Factor: A neurotrophic factor that promotes the survival of various neuronal cell types and may play an important role in the injury response in the nervous system. [NIH] Cirrhosis: A type of chronic, progressive liver disease. [NIH] CIS: Cancer Information Service. The CIS is the National Cancer Institute's link to the public, interpreting and explaining research findings in a clear and understandable manner,

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and providing personalized responses to specific questions about cancer. Access the CIS by calling 1-800-4-CANCER, or by using the Web site at http://cis.nci.nih.gov. [NIH] Clamp: A u-shaped steel rod used with a pin or wire for skeletal traction in the treatment of certain fractures. [NIH] Clarithromycin: A semisynthetic macrolide antibiotic derived from erythromycin that is active against a variety of microorganisms. It can inhibit protein synthesis in bacteria by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation. [NIH] Clear cell carcinoma: A rare type of tumor of the female genital tract in which the inside of the cells looks clear when viewed under a microscope. [NIH] Climacteric: Physiologic period, characterized by endocrine, somatic, and psychic changes with the termination of ovarian function in the female. It may also accompany the normal diminution of sexual activity in the male. [NIH] Clinical Medicine: The study and practice of medicine by direct examination of the patient. [NIH]

Clinical study: A research study in which patients receive treatment in a clinic or other medical facility. Reports of clinical studies can contain results for single patients (case reports) or many patients (case series or clinical trials). [NIH] Clinical trial: A research study that tests how well new medical treatments or other interventions work in people. Each study is designed to test new methods of screening, prevention, diagnosis, or treatment of a disease. [NIH] Clone: The term "clone" has acquired a new meaning. It is applied specifically to the bits of inserted foreign DNA in the hybrid molecules of the population. Each inserted segment originally resided in the DNA of a complex genome amid millions of other DNA segment. [NIH]

Cloning: The production of a number of genetically identical individuals; in genetic engineering, a process for the efficient replication of a great number of identical DNA molecules. [NIH] Coagulation: 1. The process of clot formation. 2. In colloid chemistry, the solidification of a sol into a gelatinous mass; an alteration of a disperse phase or of a dissolved solid which causes the separation of the system into a liquid phase and an insoluble mass called the clot or curd. Coagulation is usually irreversible. 3. In surgery, the disruption of tissue by physical means to form an amorphous residuum, as in electrocoagulation and photocoagulation. [EU] Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis. [NIH] Cochlea: The part of the internal ear that is concerned with hearing. It forms the anterior part of the labyrinth, is conical, and is placed almost horizontally anterior to the vestibule. [NIH]

Cochlear: Of or pertaining to the cochlea. [EU] Codon: A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (codon, terminator). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, transfer) complementary to all codons. These codons are referred to as unassigned codons (codons, nonsense). [NIH] Coenzyme: An organic nonprotein molecule, frequently a phosphorylated derivative of a

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water-soluble vitamin, that binds with the protein molecule (apoenzyme) to form the active enzyme (holoenzyme). [EU] Cofactor: A substance, microorganism or environmental factor that activates or enhances the action of another entity such as a disease-causing agent. [NIH] Colitis: Inflammation of the colon. [NIH] Collagen: A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of skin, connective tissue, and the organic substance of bones and teeth. Different forms of collagen are produced in the body but all consist of three alpha-polypeptide chains arranged in a triple helix. Collagen is differentiated from other fibrous proteins, such as elastin, by the content of proline, hydroxyproline, and hydroxylysine; by the absence of tryptophan; and particularly by the high content of polar groups which are responsible for its swelling properties. [NIH] Collagenases: Enzymes that catalyze the degradation of collagen by acting on the peptide bonds. EC 3.4.24.-. [NIH] Collapse: 1. A state of extreme prostration and depression, with failure of circulation. 2. Abnormal falling in of the walls of any part of organ. [EU] Colloidal: Of the nature of a colloid. [EU] Colon: The long, coiled, tubelike organ that removes water from digested food. The remaining material, solid waste called stool, moves through the colon to the rectum and leaves the body through the anus. [NIH] Colon Polyps: Small, fleshy, mushroom-shaped growths in the colon. [NIH] Colorectal: Having to do with the colon or the rectum. [NIH] Colorectal Cancer: Cancer that occurs in the colon (large intestine) or the rectum (the end of the large intestine). A number of digestive diseases may increase a person's risk of colorectal cancer, including polyposis and Zollinger-Ellison Syndrome. [NIH] Colorectal Surgery: A surgical specialty concerned with the diagnosis and treatment of disorders and abnormalities of the colon, rectum, and anal canal. [NIH] Combination Therapy: Association of 3 drugs to treat AIDS (AZT + DDC or DDI + protease inhibitor). [NIH] Communicable disease: A disease that can be transmitted by contact between persons. [NIH]

Comorbidity: The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival. [NIH] Complement: A term originally used to refer to the heat-labile factor in serum that causes immune cytolysis, the lysis of antibody-coated cells, and now referring to the entire functionally related system comprising at least 20 distinct serum proteins that is the effector not only of immune cytolysis but also of other biologic functions. Complement activation occurs by two different sequences, the classic and alternative pathways. The proteins of the classic pathway are termed 'components of complement' and are designated by the symbols C1 through C9. C1 is a calcium-dependent complex of three distinct proteins C1q, C1r and C1s. The proteins of the alternative pathway (collectively referred to as the properdin system) and complement regulatory proteins are known by semisystematic or trivial names. Fragments resulting from proteolytic cleavage of complement proteins are designated with lower-case letter suffixes, e.g., C3a. Inactivated fragments may be designated with the suffix

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'i', e.g. C3bi. Activated components or complexes with biological activity are designated by a bar over the symbol e.g. C1 or C4b,2a. The classic pathway is activated by the binding of C1 to classic pathway activators, primarily antigen-antibody complexes containing IgM, IgG1, IgG3; C1q binds to a single IgM molecule or two adjacent IgG molecules. The alternative pathway can be activated by IgA immune complexes and also by nonimmunologic materials including bacterial endotoxins, microbial polysaccharides, and cell walls. Activation of the classic pathway triggers an enzymatic cascade involving C1, C4, C2 and C3; activation of the alternative pathway triggers a cascade involving C3 and factors B, D and P. Both result in the cleavage of C5 and the formation of the membrane attack complex. Complement activation also results in the formation of many biologically active complement fragments that act as anaphylatoxins, opsonins, or chemotactic factors. [EU] Complementary and alternative medicine: CAM. Forms of treatment that are used in addition to (complementary) or instead of (alternative) standard treatments. These practices are not considered standard medical approaches. CAM includes dietary supplements, megadose vitamins, herbal preparations, special teas, massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Complementary medicine: Practices not generally recognized by the medical community as standard or conventional medical approaches and used to enhance or complement the standard treatments. Complementary medicine includes the taking of dietary supplements, megadose vitamins, and herbal preparations; the drinking of special teas; and practices such as massage therapy, magnet therapy, spiritual healing, and meditation. [NIH] Compliance: Distensibility measure of a chamber such as the lungs (lung compliance) or bladder. Compliance is expressed as a change in volume per unit change in pressure. [NIH] Compulsion: In psychology, an irresistible urge, sometimes amounting to obsession to perform a particular act which usually is carried out against the performer's will or better judgment. [NIH] Computational Biology: A field of biology concerned with the development of techniques for the collection and manipulation of biological data, and the use of such data to make biological discoveries or predictions. This field encompasses all computational methods and theories applicable to molecular biology and areas of computer-based techniques for solving biological problems including manipulation of models and datasets. [NIH] Computed tomography: CT scan. A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized tomography and computerized axial tomography (CAT) scan. [NIH] Computerized tomography: A series of detailed pictures of areas inside the body, taken from different angles; the pictures are created by a computer linked to an x-ray machine. Also called computerized axial tomography (CAT) scan and computed tomography (CT scan). [NIH] Concentric: Having a common center of curvature or symmetry. [NIH] Conception: The onset of pregnancy, marked by implantation of the blastocyst; the formation of a viable zygote. [EU] Conduction: The transfer of sound waves, heat, nervous impulses, or electricity. [EU] Cone: One of the special retinal receptor elements which are presumed to be primarily concerned with perception of light and color stimuli when the eye is adapted to light. [NIH] Congestion: Excessive or abnormal accumulation of blood in a part. [EU] Congestive heart failure: Weakness of the heart muscle that leads to a buildup of fluid in

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body tissues. [NIH] Conjugated: Acting or operating as if joined; simultaneous. [EU] Conjugation: 1. The act of joining together or the state of being conjugated. 2. A sexual process seen in bacteria, ciliate protozoa, and certain fungi in which nuclear material is exchanged during the temporary fusion of two cells (conjugants). In bacterial genetics a form of sexual reproduction in which a donor bacterium (male) contributes some, or all, of its DNA (in the form of a replicated set) to a recipient (female) which then incorporates differing genetic information into its own chromosome by recombination and passes the recombined set on to its progeny by replication. In ciliate protozoa, two conjugants of separate mating types exchange micronuclear material and then separate, each now being a fertilized cell. In certain fungi, the process involves fusion of two gametes, resulting in union of their nuclei and formation of a zygote. 3. In chemistry, the joining together of two compounds to produce another compound, such as the combination of a toxic product with some substance in the body to form a detoxified product, which is then eliminated. [EU] Conjunctiva: The mucous membrane that lines the inner surface of the eyelids and the anterior part of the sclera. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Connective Tissue: Tissue that supports and binds other tissues. It consists of connective tissue cells embedded in a large amount of extracellular matrix. [NIH] Consciousness: Sense of awareness of self and of the environment. [NIH] Constipation: Infrequent or difficult evacuation of feces. [NIH] Constriction: The act of constricting. [NIH] Constriction, Pathologic: The condition of an anatomical structure's being constricted beyond normal dimensions. [NIH] Consultation: A deliberation between two or more physicians concerning the diagnosis and the proper method of treatment in a case. [NIH] Consummatory Behavior: An act which constitutes the termination of a given instinctive behavior pattern or sequence. [NIH] Consumption: Pulmonary tuberculosis. [NIH] Continuous infusion: The administration of a fluid into a blood vessel, usually over a prolonged period of time. [NIH] Contraindications: Any factor or sign that it is unwise to pursue a certain kind of action or treatment, e. g. giving a general anesthetic to a person with pneumonia. [NIH] Control group: In a clinical trial, the group that does not receive the new treatment being studied. This group is compared to the group that receives the new treatment, to see if the new treatment works. [NIH] Controlled study: An experiment or clinical trial that includes a comparison (control) group. [NIH] Cor: The muscular organ that maintains the circulation of the blood. c. adiposum a heart that has undergone fatty degeneration or that has an accumulation of fat around it; called also fat or fatty, heart. c. arteriosum the left side of the heart, so called because it contains oxygenated (arterial) blood. c. biloculare a congenital anomaly characterized by failure of formation of the atrial and ventricular septums, the heart having only two chambers, a single atrium and a single ventricle, and a common atrioventricular valve. c. bovinum (L. 'ox heart') a greatly enlarged heart due to a hypertrophied left ventricle; called also c. taurinum

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and bucardia. c. dextrum (L. 'right heart') the right atrium and ventricle. c. hirsutum, c. villosum. c. mobile (obs.) an abnormally movable heart. c. pendulum a heart so movable that it seems to be hanging by the great blood vessels. c. pseudotriloculare biatriatum a congenital cardiac anomaly in which the heart functions as a three-chambered heart because of tricuspid atresia, the right ventricle being extremely small or rudimentary and the right atrium greatly dilated. Blood passes from the right to the left atrium and thence disease due to pulmonary hypertension secondary to disease of the lung, or its blood vessels, with hypertrophy of the right ventricle. [EU] Coronary: Encircling in the manner of a crown; a term applied to vessels; nerves, ligaments, etc. The term usually denotes the arteries that supply the heart muscle and, by extension, a pathologic involvement of them. [EU] Coronary heart disease: A type of heart disease caused by narrowing of the coronary arteries that feed the heart, which needs a constant supply of oxygen and nutrients carried by the blood in the coronary arteries. When the coronary arteries become narrowed or clogged by fat and cholesterol deposits and cannot supply enough blood to the heart, CHD results. [NIH] Coronary Thrombosis: Presence of a thrombus in a coronary artery, often causing a myocardial infarction. [NIH] Corpus: The body of the uterus. [NIH] Corpus Luteum: The yellow glandular mass formed in the ovary by an ovarian follicle that has ruptured and discharged its ovum. [NIH] Cortex: The outer layer of an organ or other body structure, as distinguished from the internal substance. [EU] Cortical: Pertaining to or of the nature of a cortex or bark. [EU] Corticosteroids: Hormones that have antitumor activity in lymphomas and lymphoid leukemias; in addition, corticosteroids (steroids) may be used for hormone replacement and for the management of some of the complications of cancer and its treatment. [NIH] Cortisol: A steroid hormone secreted by the adrenal cortex as part of the body's response to stress. [NIH] Cortisone: A natural steroid hormone produced in the adrenal gland. It can also be made in the laboratory. Cortisone reduces swelling and can suppress immune responses. [NIH] Cranial: Pertaining to the cranium, or to the anterior (in animals) or superior (in humans) end of the body. [EU] Creatine: An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. [NIH]

Creatine Kinase: A transferase that catalyzes formation of phosphocreatine from ATP + creatine. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic isoenzymes have been identified in human tissues: MM from skeletal muscle, MB from myocardial tissue, and BB from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins. EC 2.7.3.2. [NIH] Creatinine: A compound that is excreted from the body in urine. Creatinine levels are measured to monitor kidney function. [NIH] Cribriform: Pierced with small holes as in a sieve. Refers to the appearance of a tumor when viewed under a microscope. The tumor appears to have open spaces or small holes inside. [NIH] Cross-Sectional Studies: Studies in which the presence or absence of disease or other

Dictionary 533

health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with longitudinal studies which are followed over a period of time. [NIH] Cues: Signals for an action; that specific portion of a perceptual field or pattern of stimuli to which a subject has learned to respond. [NIH] Culture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as agar or gelatin. [NIH] Curative: Tending to overcome disease and promote recovery. [EU] Cyclic: Pertaining to or occurring in a cycle or cycles; the term is applied to chemical compounds that contain a ring of atoms in the nucleus. [EU] Cyclosporine: A drug used to help reduce the risk of rejection of organ and bone marrow transplants by the body. It is also used in clinical trials to make cancer cells more sensitive to anticancer drugs. [NIH] Cysteine Endopeptidases: Endopeptidases which have a cysteine involved in the catalytic process. This group of enzymes is inactivated by sulfhydryl reagents. EC 3.4.22. [NIH] Cysteinyl: Enzyme released by the cell at a crucial stage in apoptosis in order to shred all cellular proteins. [NIH] Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. [NIH]

Cytochrome: Any electron transfer hemoprotein having a mode of action in which the transfer of a single electron is effected by a reversible valence change of the central iron atom of the heme prosthetic group between the +2 and +3 oxidation states; classified as cytochromes a in which the heme contains a formyl side chain, cytochromes b, which contain protoheme or a closely similar heme that is not covalently bound to the protein, cytochromes c in which protoheme or other heme is covalently bound to the protein, and cytochromes d in which the iron-tetrapyrrole has fewer conjugated double bonds than the hemes have. Well-known cytochromes have been numbered consecutively within groups and are designated by subscripts (beginning with no subscript), e.g. cytochromes c, c1, C2, ... New cytochromes are named according to the wavelength in nanometres of the absorption maximum of the a-band of the iron (II) form in pyridine, e.g., c-555. [EU] Cytokine: Small but highly potent protein that modulates the activity of many cell types, including T and B cells. [NIH] Cytomegalovirus: A genus of the family Herpesviridae, subfamily Betaherpesvirinae, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS. [NIH] Cytoplasm: The protoplasm of a cell exclusive of that of the nucleus; it consists of a continuous aqueous solution (cytosol) and the organelles and inclusions suspended in it (phaneroplasm), and is the site of most of the chemical activities of the cell. [EU] Cytotoxic: Cell-killing. [NIH] Dairy Products: Raw and processed or manufactured milk and milk-derived products. These are usually from cows (bovine) but are also from goats, sheep, reindeer, and water buffalo. [NIH]

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Data Collection: Systematic gathering of data for a particular purpose from various sources, including questionnaires, interviews, observation, existing records, and electronic devices. The process is usually preliminary to statistical analysis of the data. [NIH] De novo: In cancer, the first occurrence of cancer in the body. [NIH] Decarboxylation: The removal of a carboxyl group, usually in the form of carbon dioxide, from a chemical compound. [NIH] Decision Making: The process of making a selective intellectual judgment when presented with several complex alternatives consisting of several variables, and usually defining a course of action or an idea. [NIH] Decubitus: An act of lying down; also the position assumed in lying down. [EU] Defecation: The normal process of elimination of fecal material from the rectum. [NIH] Degenerative: Undergoing degeneration : tending to degenerate; having the character of or involving degeneration; causing or tending to cause degeneration. [EU] Dehydroepiandrosterone: DHEA. A substance that is being studied as a cancer prevention drug. It belongs to the family of drugs called steroids. [NIH] Deletion: A genetic rearrangement through loss of segments of DNA (chromosomes), bringing sequences, which are normally separated, into close proximity. [NIH] Delirium: (DSM III-R) an acute, reversible organic mental disorder characterized by reduced ability to maintain attention to external stimuli and disorganized thinking as manifested by rambling, irrelevant, or incoherent speech; there are also a reduced level of consciousness, sensory misperceptions, disturbance of the sleep-wakefulness cycle and level of psychomotor activity, disorientation to time, place, or person, and memory impairment. Delirium may be caused by a large number of conditions resulting in derangement of cerebral metabolism, including systemic infection, poisoning, drug intoxication or withdrawal, seizures or head trauma, and metabolic disturbances such as hypoxia, hypoglycaemia, fluid, electrolyte, or acid-base imbalances, or hepatic or renal failure. Called also acute confusional state and acute brain syndrome. [EU] Delivery of Health Care: The concept concerned with all aspects of providing and distributing health services to a patient population. [NIH] Dementia: An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness. [NIH] Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other neurons. [NIH] Density: The logarithm to the base 10 of the opacity of an exposed and processed film. [NIH] Depolarization: The process or act of neutralizing polarity. In neurophysiology, the reversal of the resting potential in excitable cell membranes when stimulated, i.e., the tendency of the cell membrane potential to become positive with respect to the potential outside the cell. [EU] Dermal: Pertaining to or coming from the skin. [NIH] Dermatitis: Any inflammation of the skin. [NIH] Dermatologic Agents: Drugs used to treat or prevent skin disorders or for the routine care of skin. [NIH] Desipramine:

A tricyclic dibenzazepine compound that potentiates neurotransmission.

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Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholingeric activity, through its affinity to muscarinic receptors. [NIH] Deuterium: Deuterium. The stable isotope of hydrogen. It has one neutron and one proton in the nucleus. [NIH] Developed Countries: Countries that have reached a level of economic achievement through an increase of production, per capita income and consumption, and utilization of natural and human resources. [NIH] Developing Countries: Countries in the process of change directed toward economic growth, that is, an increase in production, per capita consumption, and income. The process of economic growth involves better utilization of natural and human resources, which results in a change in the social, political, and economic structures. [NIH] Developmental psychology: That branch of psychology which studies the processes of preand post-natal growth and the maturation of behavior. In its broadest sense, developmental psychology includes the periods of infancy, childhood, and adulthood. [NIH] Dexamethasone: (11 beta,16 alpha)-9-Fluoro-11,17,21-trihydroxy-16-methylpregna-1,4diene-3,20-dione. An anti-inflammatory glucocorticoid used either in the free alcohol or esterified form in treatment of conditions that respond generally to cortisone. [NIH] Dexfenfluramine: The S-isomer of fenfluramine. It is a serotonin agonist and is used as an anorectic. Unlike fenfluramine, it does not possess any catecholamine agonist activity. [NIH] Dextroamphetamine: The d-form of amphetamine. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic. [NIH] Dextrorotatory: Turning towards the right hand. [NIH] Diabetes Insipidus: A metabolic disorder due to disorders in the production or release of vasopressin. It is characterized by the chronic excretion of large amounts of low specific gravity urine and great thirst. [NIH] Diabetes Mellitus: A heterogeneous group of disorders that share glucose intolerance in common. [NIH] Diagnostic procedure: A method used to identify a disease. [NIH] Dialyzer: A part of the hemodialysis machine. (See hemodialysis under dialysis.) The dialyzer has two sections separated by a membrane. One section holds dialysate. The other holds the patient's blood. [NIH] Diarrhea: Passage of excessively liquid or excessively frequent stools. [NIH] Diastole: Period of relaxation of the heart, especially the ventricles. [NIH] Diastolic: Of or pertaining to the diastole. [EU] Diencephalon: The paired caudal parts of the prosencephalon from which the thalamus, hypothalamus, epithalamus, and subthalamus are derived. [NIH] Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados. [NIH]

Dietary Fiber: The remnants of plant cell walls that are resistant to digestion by the alimentary enzymes of man. It comprises various polysaccharides and lignins. [NIH]

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Dietetics: The study and regulation of the diet. [NIH] Diethylproprion: An appetite suppressant prescribed in the treatment of obesity. [NIH] Diethylstilbestrol: DES. A synthetic hormone that was prescribed from the early 1940s until 1971 to help women with complications of pregnancy. DES has been linked to an increased risk of clear cell carcinoma of the vagina in daughters of women who used DES. DES may also increase the risk of breast cancer in women who used DES. [NIH] Dietitian: An expert in nutrition who helps people plan what and how much food to eat. [NIH]

Digestion: The process of breakdown of food for metabolism and use by the body. [NIH] Digestive system: The organs that take in food and turn it into products that the body can use to stay healthy. Waste products the body cannot use leave the body through bowel movements. The digestive system includes the salivary glands, mouth, esophagus, stomach, liver, pancreas, gallbladder, small and large intestines, and rectum. [NIH] Digestive tract: The organs through which food passes when food is eaten. These organs are the mouth, esophagus, stomach, small and large intestines, and rectum. [NIH] Dihydrotestosterone: Anabolic agent. [NIH] Dilatation: The act of dilating. [NIH] Dilation: A process by which the pupil is temporarily enlarged with special eye drops (mydriatic); allows the eye care specialist to better view the inside of the eye. [NIH] Dimethyl: A volatile metabolite of the amino acid methionine. [NIH] Diploid: Having two sets of chromosomes. [NIH] Direct: 1. Straight; in a straight line. 2. Performed immediately and without the intervention of subsidiary means. [EU] Disaccharides: Sugars composed of two monosaccharides linked by glycoside bonds. [NIH] Discrete: Made up of separate parts or characterized by lesions which do not become blended; not running together; separate. [NIH] Discrimination: The act of qualitative and/or quantitative differentiation between two or more stimuli. [NIH] Disease Vectors: Invertebrates or non-human vertebrates which transmit infective organisms from one host to another. [NIH] Disinfectant: An agent that disinfects; applied particularly to agents used on inanimate objects. [EU] Disparity: Failure of the two retinal images of an object to fall on corresponding retinal points. [NIH] Disposition: A tendency either physical or mental toward certain diseases. [EU] Dissection: Cutting up of an organism for study. [NIH] Dissociation: 1. The act of separating or state of being separated. 2. The separation of a molecule into two or more fragments (atoms, molecules, ions, or free radicals) produced by the absorption of light or thermal energy or by solvation. 3. In psychology, a defense mechanism in which a group of mental processes are segregated from the rest of a person's mental activity in order to avoid emotional distress, as in the dissociative disorders (q.v.), or in which an idea or object is segregated from its emotional significance; in the first sense it is roughly equivalent to splitting, in the second, to isolation. 4. A defect of mental integration in which one or more groups of mental processes become separated off from normal consciousness and, thus separated, function as a unitary whole. [EU]

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Distal: Remote; farther from any point of reference; opposed to proximal. In dentistry, used to designate a position on the dental arch farther from the median line of the jaw. [EU] Disulphide: A covalent bridge formed by the oxidation of two cysteine residues to a cystine residue. The-S-S-bond is very strong and its presence confers additional stability. [NIH] Diuresis: Increased excretion of urine. [EU] Dopamine: An endogenous catecholamine and prominent neurotransmitter in several systems of the brain. In the synthesis of catecholamines from tyrosine, it is the immediate precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of dopaminergic receptor subtypes mediate its action. Dopamine is used pharmacologically for its direct (beta adrenergic agonist) and indirect (adrenergic releasing) sympathomimetic effects including its actions as an inotropic agent and as a renal vasodilator. [NIH] Dose-dependent: Refers to the effects of treatment with a drug. If the effects change when the dose of the drug is changed, the effects are said to be dose dependent. [NIH] Drive: A state of internal activity of an organism that is a necessary condition before a given stimulus will elicit a class of responses; e.g., a certain level of hunger (drive) must be present before food will elicit an eating response. [NIH] Drug Tolerance: Progressive diminution of the susceptibility of a human or animal to the effects of a drug, resulting from its continued administration. It should be differentiated from drug resistance wherein an organism, disease, or tissue fails to respond to the intended effectiveness of a chemical or drug. It should also be differentiated from maximum tolerated dose and no-observed-adverse-effect level. [NIH] Duodenum: The first part of the small intestine. [NIH] Dyes: Chemical substances that are used to stain and color other materials. The coloring may or may not be permanent. Dyes can also be used as therapeutic agents and test reagents in medicine and scientific research. [NIH] Dyskinesia: Impairment of the power of voluntary movement, resulting in fragmentary or incomplete movements. [EU] Dyslipidemia: Disorders in the lipoprotein metabolism; classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high-density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low-density lipoprotein (LDL) cholesterol and low levels of HDL cholesterol predispose to premature atherosclerosis. [NIH] Dyspepsia: Impaired digestion, especially after eating. [NIH] Dysphagia: Difficulty in swallowing. [EU] Dysplasia: Cells that look abnormal under a microscope but are not cancer. [NIH] Dyspnea: Difficult or labored breathing. [NIH] Dystocia: Difficult childbirth or labor. [NIH] Dystonia: Disordered tonicity of muscle. [EU] Dystrophy: Any disorder arising from defective or faulty nutrition, especially the muscular dystrophies. [EU] Eating Disorders: A group of disorders characterized by physiological and psychological disturbances in appetite or food intake. [NIH] Echocardiography: Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. [NIH]

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Eczema: A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed). [NIH] Edema: Excessive amount of watery fluid accumulated in the intercellular spaces, most commonly present in subcutaneous tissue. [NIH] Effector: It is often an enzyme that converts an inactive precursor molecule into an active second messenger. [NIH] Efficacy: The extent to which a specific intervention, procedure, regimen, or service produces a beneficial result under ideal conditions. Ideally, the determination of efficacy is based on the results of a randomized control trial. [NIH] Elasticity: Resistance and recovery from distortion of shape. [NIH] Elastin: The protein that gives flexibility to tissues. [NIH] Elective: Subject to the choice or decision of the patient or physician; applied to procedures that are advantageous to the patient but not urgent. [EU] Electrocardiogram: Measurement of electrical activity during heartbeats. [NIH] Electrocoagulation: Electrosurgical procedures used to treat hemorrhage (e.g., bleeding ulcers) and to ablate tumors, mucosal lesions, and refractory arrhythmias. [NIH] Electrode: Component of the pacing system which is at the distal end of the lead. It is the interface with living cardiac tissue across which the stimulus is transmitted. [NIH] Electrolyte: A substance that dissociates into ions when fused or in solution, and thus becomes capable of conducting electricity; an ionic solute. [EU] Electroplating: Coating with a metal or alloy by electrolysis. [NIH] Elementary Particles: Individual components of atoms, usually subatomic; subnuclear particles are usually detected only when the atomic nucleus decays and then only transiently, as most of them are unstable, often yielding pure energy without substance, i.e., radiation. [NIH] Embryo: The prenatal stage of mammalian development characterized by rapid morphological changes and the differentiation of basic structures. [NIH] Embryo Transfer: Removal of a mammalian embryo from one environment and replacement in the same or a new environment. The embryo is usually in the pre-nidation phase, i.e., a blastocyst. The process includes embryo or blastocyst transplantation or transfer after in vitro fertilization and transfer of the inner cell mass of the blastocyst. It is not used for transfer of differentiated embryonic tissue, e.g., germ layer cells. [NIH] Emesis: Vomiting; an act of vomiting. Also used as a word termination, as in haematemesis. [EU]

Emollients: Oleagenous substances used topically to soothe, soften or protect skin or mucous membranes. They are used also as vehicles for other dermatologic agents. [NIH] Emphysema: A pathological accumulation of air in tissues or organs. [NIH] Empiric: Empirical; depending upon experience or observation alone, without using scientific method or theory. [EU] Emulsions: Colloids of two immiscible liquids where either phase may be either fatty or aqueous; lipid-in-water emulsions are usually liquid, like milk or lotion and water-in-lipid emulsions tend to be creams. [NIH] Endocrine System: The system of glands that release their secretions (hormones) directly into the circulatory system. In addition to the endocrine glands, included are the chromaffin system and the neurosecretory systems. [NIH]

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Endocrinology: A subspecialty of internal medicine concerned with the metabolism, physiology, and disorders of the endocrine system. [NIH] Endogenous: Produced inside an organism or cell. The opposite is external (exogenous) production. [NIH] Endometrial: Having to do with the endometrium (the layer of tissue that lines the uterus). [NIH]

Endometriosis: A condition in which tissue more or less perfectly resembling the uterine mucous membrane (the endometrium) and containing typical endometrial granular and stromal elements occurs aberrantly in various locations in the pelvic cavity. [NIH] Endometrium: The layer of tissue that lines the uterus. [NIH] Endopeptidases: A subclass of peptide hydrolases. They are classified primarily by their catalytic mechanism. Specificity is used only for identification of individual enzymes. They comprise the serine endopeptidases, EC 3.4.21; cysteine endopeptidases, EC 3.4.22; aspartic endopeptidases, EC 3.4.23, metalloendopeptidases, EC 3.4.24; and a group of enzymes yet to be assigned to any of the above sub-classes, EC 3.4.99. EC 3.4.-. [NIH] Endorphins: One of the three major groups of endogenous opioid peptides. They are large peptides derived from the pro-opiomelanocortin precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; opioid peptides is used for the broader group. [NIH] Endoscope: A thin, lighted tube used to look at tissues inside the body. [NIH] Endoscopic: A technique where a lateral-view endoscope is passed orally to the duodenum for visualization of the ampulla of Vater. [NIH] Endothelial cell: The main type of cell found in the inside lining of blood vessels, lymph vessels, and the heart. [NIH] Endotoxic: Of, relating to, or acting as an endotoxin (= a heat-stable toxin, associated with the outer membranes of certain gram-negative bacteria. Endotoxins are not secreted and are released only when the cells are disrupted). [EU] Endotoxin: Toxin from cell walls of bacteria. [NIH] End-stage renal: Total chronic kidney failure. When the kidneys fail, the body retains fluid and harmful wastes build up. A person with ESRD needs treatment to replace the work of the failed kidneys. [NIH] Energetic: Exhibiting energy : strenuous; operating with force, vigour, or effect. [EU] Energy balance: Energy is the capacity of a body or a physical system for doing work. Energy balance is the state in which the total energy intake equals total energy needs. [NIH] Energy deficit: A state in which total energy intake is less than total energy need. [NIH] Energy Intake: Total number of calories taken in daily whether ingested or by parenteral routes. [NIH] Enkephalin: A natural opiate painkiller, in the hypothalamus. [NIH] Environmental Exposure: The exposure to potentially harmful chemical, physical, or biological agents in the environment or to environmental factors that may include ionizing radiation, pathogenic organisms, or toxic chemicals. [NIH] Environmental Health: The science of controlling or modifying those conditions, influences, or forces surrounding man which relate to promoting, establishing, and maintaining health. [NIH]

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Enzymatic: Phase where enzyme cuts the precursor protein. [NIH] Enzyme: A protein that speeds up chemical reactions in the body. [NIH] Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. [NIH] Ependyma: A thin membrane that lines the ventricles of the brain and the central canal of the spinal cord. [NIH] Ephedrine: An alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used in the treatment of several disorders including asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists. [NIH] Epidemic: Occurring suddenly in numbers clearly in excess of normal expectancy; said especially of infectious diseases but applied also to any disease, injury, or other healthrelated event occurring in such outbreaks. [EU] Epidemiological: Relating to, or involving epidemiology. [EU] Epidermal: Pertaining to or resembling epidermis. Called also epidermic or epidermoid. [EU]

Epidermis: Nonvascular layer of the skin. It is made up, from within outward, of five layers: 1) basal layer (stratum basale epidermidis); 2) spinous layer (stratum spinosum epidermidis); 3) granular layer (stratum granulosum epidermidis); 4) clear layer (stratum lucidum epidermidis); and 5) horny layer (stratum corneum epidermidis). [NIH] Epidermoid carcinoma: A type of cancer in which the cells are flat and look like fish scales. Also called squamous cell carcinoma. [NIH] Epigastric: Having to do with the upper middle area of the abdomen. [NIH] Epinephrine: The active sympathomimetic hormone from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral vessels. It is used in asthma and cardiac failure and to delay absorption of local anesthetics. [NIH] Epithalamus: The dorsal posterior subdivision of the diencephalon. The epithalamus is generally considered to include the habenular nuclei (habenula) and associated fiber bundles, the pineal body, and the epithelial roof of the third ventricle. The anterior and posterior paraventricular nuclei of the thalamus are included with the thalamic nuclei although they develop from the same pronuclear mass as the epithalamic nuclei and are sometimes considered part of the epithalamus. [NIH] Epithelial: Refers to the cells that line the internal and external surfaces of the body. [NIH] Epithelium: One or more layers of epithelial cells, supported by the basal lamina, which covers the inner or outer surfaces of the body. [NIH] Equipment and Supplies: Expendable and nonexpendable equipment, supplies, apparatus, and instruments that are used in diagnostic, surgical, therapeutic, scientific, and experimental procedures. [NIH] Erectile: The inability to get or maintain an erection for satisfactory sexual intercourse. Also called impotence. [NIH] Erection: The condition of being made rigid and elevated; as erectile tissue when filled with blood. [EU] Ergot: Cataract due to ergot poisoning caused by eating of rye cereals contaminated by a

Dictionary 541

fungus. [NIH] Erythrocyte Volume: Volume of circulating erythrocytes. It is usually measured by radioisotope dilution technique. [NIH] Erythrocytes: Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing hemoglobin whose function is to transport oxygen. [NIH] Erythromycin: A bacteriostatic antibiotic substance produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins. [NIH] Esophageal: Having to do with the esophagus, the muscular tube through which food passes from the throat to the stomach. [NIH] Esophageal Varices: Stretched veins in the esophagus that occur when the liver is not working properly. If the veins burst, the bleeding can cause death. [NIH] Esophagus: The muscular tube through which food passes from the throat to the stomach. [NIH]

Essential Tremor: A rhythmic, involuntary, purposeless, oscillating movement resulting from the alternate contraction and relaxation of opposing groups of muscles. [NIH] Estradiol: The most potent mammalian estrogenic hormone. It is produced in the ovary, placenta, testis, and possibly the adrenal cortex. [NIH] Estriol: (16 alpha,17 beta)-Estra-1,3,5(10)-triene-3,16,17-triol. A metabolite of estradiol and usually the predominant estrogenic metabolite in urine. During pregnancy, large amounts of estriol are produced by the placenta. It has also been obtained from plant sources. The 16 beta-isomer has also been isolated from the urine of pregnant women. [NIH] Estrogen: One of the two female sex hormones. [NIH] Estrone: 3-Hydroxyestra-1,3,5(10)-trien-17-one. A metabolite of estradiol but possessing less biological activity. It is found in the urine of pregnant women and mares, in the human placenta, and in the urine of bulls and stallions. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), estrone may reasonably be anticipated to be a carcinogen (Merck, 11th ed). [NIH] Ethanol: A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. [NIH] Ether: One of a class of organic compounds in which any two organic radicals are attached directly to a single oxygen atom. [NIH] Ethinyl Estradiol: A semisynthetic estrogen with high oral estrogenic potency. It is often used as the estrogenic component in oral contraceptives. [NIH] Ethmoid: An unpaired cranial bone which helps form the medial walls of the orbits and contains the themoidal air cells which drain into the nose. [NIH] Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships. [NIH] Etiocholanolone: 3-alpha-Hydroxy-5-beta-androstan-17 one. A ketosteroid of mainly human origin; causes fever, immunostimulation and leukocytosis; used to evaluate adrenal cortex function, bone marrow performance and in neoplastic disease for immunostimulation. Synonym: 5-isoandrosterone. [NIH]

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Evacuation: An emptying, as of the bowels. [EU] Evoke: The electric response recorded from the cerebral cortex after stimulation of a peripheral sense organ. [NIH] Excipients: Usually inert substances added to a prescription in order to provide suitable consistency to the dosage form; a binder, matrix, base or diluent in pills, tablets, creams, salves, etc. [NIH] Excitation: An act of irritation or stimulation or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons. [EU] Excrete: To get rid of waste from the body. [NIH] Exercise Therapy: Motion of the body or its parts to relieve symptoms or to improve function, leading to physical fitness, but not physical education and training. [NIH] Exhaustion: The feeling of weariness of mind and body. [NIH] Exocrine: Secreting outwardly, via a duct. [EU] Exocytosis: Cellular release of material within membrane-limited vesicles by fusion of the vesicles with the cell membrane. [NIH] Exogenous: Developed or originating outside the organism, as exogenous disease. [EU] Exon: The part of the DNA that encodes the information for the actual amino acid sequence of the protein. In many eucaryotic genes, the coding sequences consist of a series of exons alternating with intron sequences. [NIH] Expiration: The act of breathing out, or expelling air from the lungs. [EU] Expiratory: The volume of air which leaves the breathing organs in each expiration. [NIH] Extracellular: Outside a cell or cells. [EU] Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere. [NIH] Extracellular Matrix Proteins: Macromolecular organic compounds that contain carbon, hydrogen, oxygen, nitrogen, and usually, sulfur. These macromolecules (proteins) form an intricate meshwork in which cells are embedded to construct tissues. Variations in the relative types of macromolecules and their organization determine the type of extracellular matrix, each adapted to the functional requirements of the tissue. The two main classes of macromolecules that form the extracellular matrix are: glycosaminoglycans, usually linked to proteins (proteoglycans), and fibrous proteins (e.g., collagen, elastin, fibronectins and laminin). [NIH] Extracellular Space: Interstitial space between cells, occupied by fluid as well as amorphous and fibrous substances. [NIH] Extracorporeal: Situated or occurring outside the body. [EU] Extrapyramidal: Outside of the pyramidal tracts. [EU] Extreme obesity: A body mass index [NIH] Eye Infections: Infection, moderate to severe, caused by bacteria, fungi, or viruses, which occurs either on the external surface of the eye or intraocularly with probable inflammation, visual impairment, or blindness. [NIH] Factor V: Heat- and storage-labile plasma glycoprotein which accelerates the conversion of prothrombin to thrombin in blood coagulation. Factor V accomplishes this by forming a complex with factor Xa, phospholipid, and calcium (prothrombinase complex). Deficiency of

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factor V leads to Owren's disease. [NIH] Failure to Thrive: A condition in which an infant or child's weight gain and growth are far below usual levels for age. [NIH] Fallopian tube: The oviduct, a muscular tube about 10 cm long, lying in the upper border of the broad ligament. [NIH] Family Planning: Programs or services designed to assist the family in controlling reproduction by either improving or diminishing fertility. [NIH] Fasciculation: A small local contraction of muscles, visible through the skin, representing a spontaneous discharge of a number of fibres innervated by a single motor nerve filament. [EU]

Fat: Total lipids including phospholipids. [NIH] Fatigue: The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli. [NIH]

Fatty acids: A major component of fats that are used by the body for energy and tissue development. [NIH] Fatty Liver: The buildup of fat in liver cells. The most common cause is alcoholism. Other causes include obesity, diabetes, and pregnancy. Also called steatosis. [NIH] Feces: The excrement discharged from the intestines, consisting of bacteria, cells exfoliated from the intestines, secretions, chiefly of the liver, and a small amount of food residue. [EU] Feeding Behavior: Behavioral responses or sequences associated with eating including modes of feeding, rhythmic patterns of eating, and time intervals. [NIH] Femoral: Pertaining to the femur, or to the thigh. [EU] Femur: The longest and largest bone of the skeleton, it is situated between the hip and the knee. [NIH] Fenfluramine: A centrally active drug that apparently both blocks serotonin uptake and provokes transport-mediated serotonin release. [NIH] Fertilization in Vitro: Fertilization of an egg outside the body when the egg is normally fertilized in the body. [NIH] Fetal Blood: Blood of the fetus. Exchange of nutrients and waste between the fetal and maternal blood occurs via the placenta. The cord blood is blood contained in the umbilical vessels at the time of delivery. [NIH] Fetal Death: Death of the young developing in utero. [NIH] Fetal Macrosomia: A complication of several conditions including diabetes mellitus and prolonged pregnancy. A macrosomic fetus is defined as weighing more than 4000 grams. [NIH]

Fetus: The developing offspring from 7 to 8 weeks after conception until birth. [NIH] Fibrin: A protein derived from fibrinogen in the presence of thrombin, which forms part of the blood clot. [NIH] Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three nonidentical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products. [NIH] Fibrinolysis: The natural enzymatic dissolution of fibrin. [NIH]

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Fibroblast Growth Factor: Peptide isolated from the pituitary gland and from the brain. It is a potent mitogen which stimulates growth of a variety of mesodermal cells including chondrocytes, granulosa, and endothelial cells. The peptide may be active in wound healing and animal limb regeneration. [NIH] Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury. [NIH] Flatulence: Production or presence of gas in the gastrointestinal tract which may be expelled through the anus. [NIH] Flatus: Gas passed through the rectum. [NIH] Flavoring Agents: Substances added to foods and medicine to improve the quality of taste. [NIH]

Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants. [NIH] Fluvoxamine: A selective serotonin reuptake inhibitor. It is effective in the treatment of depression, obsessive-compulsive disorders, anxiety, panic disorders, and alcohol amnestic disorders. [NIH] Focus Groups: A method of data collection and a qualitative research tool in which a small group of individuals are brought together and allowed to interact in a discussion of their opinions about topics, issues, or questions. [NIH] Foetoplacental: Pertaining to the fetus and placenta. [EU] Fold: A plication or doubling of various parts of the body. [NIH] Follicles: Shafts through which hair grows. [NIH] Food Additives: Substances which are of little or no nutritive value, but are used in the processing or storage of foods or animal feed, especially in the developed countries; includes antioxidants, food preservatives, food coloring agents, flavoring agents, anti-infective agents (both plain and local), vehicles, excipients and other similarly used substances. Many of the same substances are pharmaceutic aids when added to pharmaceuticals rather than to foods. [NIH]

Food Preferences: The selection of one food over another. [NIH] Food Preservatives: Substances capable of inhibiting, retarding or arresting the process of fermentation, acidification or other deterioration of foods. [NIH] Forearm: The part between the elbow and the wrist. [NIH] Frameshift: A type of mutation which causes out-of-phase transcription of the base sequence; such mutations arise from the addition or delection of nucleotide(s) in numbers other than 3 or multiples of 3. [NIH] Frameshift Mutation: A type of mutation in which a number of nucleotides not divisible by three is deleted from or inserted into a coding sequence, thereby causing an alteration in the reading frame of the entire sequence downstream of the mutation. These mutations may be induced by certain types of mutagens or may occur spontaneously. [NIH] Fructose: A type of sugar found in many fruits and vegetables and in honey. Fructose is used to sweeten some diet foods. It is considered a nutritive sweetener because it has calories. [NIH] Fundus: The larger part of a hollow organ that is farthest away from the organ's opening. The bladder, gallbladder, stomach, uterus, eye, and cavity of the middle ear all have a fundus. [NIH]

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Fungi: A kingdom of eukaryotic, heterotrophic organisms that live as saprobes or parasites, including mushrooms, yeasts, smuts, molds, etc. They reproduce either sexually or asexually, and have life cycles that range from simple to complex. Filamentous fungi refer to those that grow as multicelluar colonies (mushrooms and molds). [NIH] Galanin: A neurotransmitter. [NIH] Gallate: Antioxidant present in tea. [NIH] Gallbladder: The pear-shaped organ that sits below the liver. Bile is concentrated and stored in the gallbladder. [NIH] Gallstones: The solid masses or stones made of cholesterol or bilirubin that form in the gallbladder or bile ducts. [NIH] Gamma-interferon: Interferon produced by T-lymphocytes in response to various mitogens and antigens. Gamma interferon appears to have potent antineoplastic, immunoregulatory and antiviral activity. [NIH] Ganglia: Clusters of multipolar neurons surrounded by a capsule of loosely organized connective tissue located outside the central nervous system. [NIH] Ganglion: 1. A knot, or knotlike mass. 2. A general term for a group of nerve cell bodies located outside the central nervous system; occasionally applied to certain nuclear groups within the brain or spinal cord, e.g. basal ganglia. 3. A benign cystic tumour occurring on a aponeurosis or tendon, as in the wrist or dorsum of the foot; it consists of a thin fibrous capsule enclosing a clear mucinous fluid. [EU] Gas: Air that comes from normal breakdown of food. The gases are passed out of the body through the rectum (flatus) or the mouth (burp). [NIH] Gastric: Having to do with the stomach. [NIH] Gastric Balloon: An inflatable device implanted in the stomach as an adjunct to therapy of morbid obesity. Specific types include the silicone Garren-Edwards Gastric Bubble (GEGB), approved by the FDA in 1985, and the Ballobes Balloon. [NIH] Gastric banding: Surgery to limit the amount of food the stomach can hold by closing part of it off. A band made of special material is placed around the stomach near its upper end, creating a small pouch and a narrow passage into the larger remainder of the stomach. The small outlet delays the emptying of food from the pouch and causes a feeling of fullness. [NIH]

Gastric Bypass: Surgical procedure in which the stomach is transected high on the body. The resulting proximal remnant is joined to a loop of the jejunum in an end-to-side anastomosis. This procedure is used frequently in the treatment of morbid obesity. [NIH] Gastric Emptying: The evacuation of food from the stomach into the duodenum. [NIH] Gastric Fundus: The superior portion of the body of the stomach above the level of the cardiac notch. [NIH] Gastric Inhibitory Polypeptide: A gastrointestinal hormone consisting of a 43-amino acid polypeptide (molecular weight 5105). It inhibits gastric secretion and motility and stimulates release of insulin. [NIH] Gastrin: A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]

Gastroenterologist: A doctor who specializes in diagnosing and treating disorders of the digestive system. [NIH] Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver,

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gallbladder, and pancreas). [NIH] Gastroesophageal Reflux: Reflux of gastric juice and/or duodenal contents (bile acids, pancreatic juice) into the distal esophagus, commonly due to incompetence of the lower esophageal sphincter. Gastric regurgitation is an extension of this process with entry of fluid into the pharynx or mouth. [NIH] Gastrointestinal: Refers to the stomach and intestines. [NIH] Gastrointestinal Hormones: Hormones secreted by the gastrointestinal mucosa that affect the timing or the quality of secretion of digestive enzymes, and regulate the motor activity of the digestive system organs. [NIH] Gastrointestinal tract: The stomach and intestines. [NIH] Gastroplasty: Surgical treatment of the stomach or lower esophagus used to decrease the size of the stomach. The procedure is used mainly in the treatment of morbid obesity and to correct defects in the lower esophagus or the stomach. Different procedures employed include vertical (mesh) banded gastroplasty, silicone elastomer ring vertical gastroplasty and horizontal banded gastroplasty. [NIH] Gastrostomy: Creation of an artificial external opening into the stomach for nutritional support or gastrointestinal compression. [NIH] Gelatin: A product formed from skin, white connective tissue, or bone collagen. It is used as a protein food adjuvant, plasma substitute, hemostatic, suspending agent in pharmaceutical preparations, and in the manufacturing of capsules and suppositories. [NIH] Gelatinases: A class of enzymes that catalyzes the degradation of gelatin by acting on the peptide bonds. EC 3.4.24.-. [NIH] Gene: The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes contain the information for making a specific protein. [NIH]

Gene Expression: The phenotypic manifestation of a gene or genes by the processes of gene action. [NIH] Gene Rearrangement: The ordered rearrangement of gene regions by DNA recombination such as that which occurs normally during development. [NIH] Gene Therapy: The introduction of new genes into cells for the purpose of treating disease by restoring or adding gene expression. Techniques include insertion of retroviral vectors, transfection, homologous recombination, and injection of new genes into the nuclei of single cell embryos. The entire gene therapy process may consist of multiple steps. The new genes may be introduced into proliferating cells in vivo (e.g., bone marrow) or in vitro (e.g., fibroblast cultures) and the modified cells transferred to the site where the gene expression is required. Gene therapy may be particularly useful for treating enzyme deficiency diseases, hemoglobinopathies, and leukemias and may also prove useful in restoring drug sensitivity, particularly for leukemia. [NIH] General practitioner: A medical practitioner who does not specialize in a particular branch of medicine or limit his practice to a specific class of diseases. [NIH] Genetic Code: The specifications for how information, stored in nucleic acid sequence (base sequence), is translated into protein sequence (amino acid sequence). The start, stop, and order of amino acids of a protein is specified by consecutive triplets of nucleotides called codons (codon). [NIH] Genetic Counseling: Advising families of the risks involved pertaining to birth defects, in order that they may make an informed decision on current or future pregnancies. [NIH] Genetic Engineering: Directed modification of the gene complement of a living organism

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by such techniques as altering the DNA, substituting genetic material by means of a virus, transplanting whole nuclei, transplanting cell hybrids, etc. [NIH] Genetic testing: Analyzing DNA to look for a genetic alteration that may indicate an increased risk for developing a specific disease or disorder. [NIH] Genetics: The biological science that deals with the phenomena and mechanisms of heredity. [NIH] Genital: Pertaining to the genitalia. [EU] Genitourinary: Pertaining to the genital and urinary organs; urogenital; urinosexual. [EU] Genotype: The genetic constitution of the individual; the characterization of the genes. [NIH] Germ Cells: The reproductive cells in multicellular organisms. [NIH] Gestation: The period of development of the young in viviparous animals, from the time of fertilization of the ovum until birth. [EU] Gestational: Psychosis attributable to or occurring during pregnancy. [NIH] Ginseng: An araliaceous genus of plants that contains a number of pharmacologically active agents used as stimulants, sedatives, and tonics, especially in traditional medicine. [NIH]

Gland: An organ that produces and releases one or more substances for use in the body. Some glands produce fluids that affect tissues or organs. Others produce hormones or participate in blood production. [NIH] Glomerular: Pertaining to or of the nature of a glomerulus, especially a renal glomerulus. [EU]

Glomeruli: Plural of glomerulus. [NIH] Glucocorticoid: A compound that belongs to the family of compounds called corticosteroids (steroids). Glucocorticoids affect metabolism and have anti-inflammatory and immunosuppressive effects. They may be naturally produced (hormones) or synthetic (drugs). [NIH] Glucose: D-Glucose. A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement. [NIH] Glucose Intolerance: A pathological state in which the fasting plasma glucose level is less than 140 mg per deciliter and the 30-, 60-, or 90-minute plasma glucose concentration following a glucose tolerance test exceeds 200 mg per deciliter. This condition is seen frequently in diabetes mellitus but also occurs with other diseases. [NIH] Glucose tolerance: The power of the normal liver to absorb and store large quantities of glucose and the effectiveness of intestinal absorption of glucose. The glucose tolerance test is a metabolic test of carbohydrate tolerance that measures active insulin, a hepatic function based on the ability of the liver to absorb glucose. The test consists of ingesting 100 grams of glucose into a fasting stomach; blood sugar should return to normal in 2 to 21 hours after ingestion. [NIH] Glucose Tolerance Test: Determination of whole blood or plasma sugar in a fasting state before and at prescribed intervals (usually 1/2 hr, 1 hr, 3 hr, 4 hr) after taking a specified amount (usually 100 gm orally) of glucose. [NIH] Glucuronic Acid: Derivatives of uronic acid found throughout the plant and animal kingdoms. They detoxify drugs and toxins by conjugating with them to form glucuronides in the liver which are more water-soluble metabolites that can be easily eliminated from the body. [NIH]

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Glucuronides: Glycosides of glucuronic acid formed by the reaction of uridine diphosphate glucuronic acid with certain endogenous and exogenous substances. Their formation is important for the detoxification of drugs, steroid excretion and bilirubin metabolism to a more water-soluble compound that can be eliminated in the urine and bile. [NIH] Glutamate: Excitatory neurotransmitter of the brain. [NIH] Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid (glutamate) is the most common excitatory neurotransmitter in the central nervous system. [NIH] Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide. [NIH] Glycerol: A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. [NIH]

Glycerophospholipids: Derivatives of phosphatidic acid in which the hydrophobic regions are composed of two fatty acids and a polar alcohol is joined to the C-3 position of glycerol through a phosphodiester bond. They are named according to their polar head groups, such as phosphatidylcholine and phosphatidylethanolamine. [NIH] Glycine: A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. [NIH] Glycogen: A sugar stored in the liver and muscles. It releases glucose into the blood when cells need it for energy. Glycogen is the chief source of stored fuel in the body. [NIH] Glycoprotein: A protein that has sugar molecules attached to it. [NIH] Glycosaminoglycans: Heteropolysaccharides which contain an N-acetylated hexosamine in a characteristic repeating disaccharide unit. The repeating structure of each disaccharide involves alternate 1,4- and 1,3-linkages consisting of either N-acetylglucosamine or Nacetylgalactosamine. [NIH] Glycoside: Any compound that contains a carbohydrate molecule (sugar), particularly any such natural product in plants, convertible, by hydrolytic cleavage, into sugar and a nonsugar component (aglycone), and named specifically for the sugar contained, as glucoside (glucose), pentoside (pentose), fructoside (fructose) etc. [EU] Gonad: A sex organ, such as an ovary or a testicle, which produces the gametes in most multicellular animals. [NIH] Gonadal: Pertaining to a gonad. [EU] Gout: Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi. [NIH] Governing Board: The group in which legal authority is vested for the control of healthrelated institutions and organizations. [NIH] Government Agencies: Administrative units of government responsible for policy making and management of governmental activities in the U.S. and abroad. [NIH] Grade: The grade of a tumor depends on how abnormal the cancer cells look under a microscope and how quickly the tumor is likely to grow and spread. Grading systems are different for each type of cancer. [NIH] Graft: Healthy skin, bone, or other tissue taken from one part of the body and used to replace diseased or injured tissue removed from another part of the body. [NIH] Grafting: The operation of transfer of tissue from one site to another. [NIH]

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Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups: neutrophils, eosinophils, and basophils. [NIH] Granulosa Cells: Cells of the membrana granulosa lining the vesicular ovarian follicle which become luteal cells after ovulation. [NIH] Grasses: A large family, Gramineae, of narrow-leaved herbaceous monocots. Many grasses produce highly allergenic pollens and are hosts to cattle parasites and toxic fungi. [NIH] Gravidity: Pregnancy; the condition of being pregnant, without regard to the outcome. [EU] Group dynamics: Is concerned with examining the complex relations which exist between members of a group and the effect of these relationships on the operational effectiveness of the group as a whole. [NIH] Growth: The progressive development of a living being or part of an organism from its earliest stage to maturity. [NIH] Growth factors: Substances made by the body that function to regulate cell division and cell survival. Some growth factors are also produced in the laboratory and used in biological therapy. [NIH] Gynaecomastia: Excessive development of the male mammary glands, even to the functional state. [EU] Gyrus Cinguli: One of the convolutions on the medial surface of the cerebral hemisphere. It surrounds the rostral part of the brain and interhemispheric commissure and forms part of the limbic system. [NIH] Habitual: Of the nature of a habit; according to habit; established by or repeated by force of habit, customary. [EU] Haematemesis: The vomiting of blood. [EU] Haemorrhage: The escape of blood from the vessels; bleeding. Small haemorrhages are classified according to size as petechiae (very small), purpura (up to 1 cm), and ecchymoses (larger). The massive accumulation of blood within a tissue is called a haematoma. [EU] Handicap: A handicap occurs as a result of disability, but disability does not always constitute a handicap. A handicap may be said to exist when a disability causes a substantial and continuing reduction in a person's capacity to function socially and vocationally. [NIH] Haploid: An organism with one basic chromosome set, symbolized by n; the normal condition of gametes in diploids. [NIH] Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the major histocompatibility complex. [NIH] Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response. [NIH] Headache: Pain in the cranial region that may occur as an isolated and benign symptom or as a manifestation of a wide variety of conditions including subarachnoid hemorrhage; craniocerebral trauma; central nervous system infections; intracranial hypertension; and other disorders. In general, recurrent headaches that are not associated with a primary disease process are referred to as headache disorders (e.g., migraine). [NIH] Health Behavior: Behaviors expressed by individuals to protect, maintain or promote their health status. For example, proper diet, and appropriate exercise are activities perceived to influence health status. Life style is closely associated with health behavior and factors influencing life style are socioeconomic, educational, and cultural. [NIH]

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Health Care Costs: The actual costs of providing services related to the delivery of health care, including the costs of procedures, therapies, and medications. It is differentiated from health expenditures, which refers to the amount of money paid for the services, and from fees, which refers to the amount charged, regardless of cost. [NIH] Health Education: Education that increases the awareness and favorably influences the attitudes and knowledge relating to the improvement of health on a personal or community basis. [NIH] Health Expenditures: The amounts spent by individuals, groups, nations, or private or public organizations for total health care and/or its various components. These amounts may or may not be equivalent to the actual costs (health care costs) and may or may not be shared among the patient, insurers, and/or employers. [NIH] Health Policy: Decisions, usually developed by government policymakers, for determining present and future objectives pertaining to the health care system. [NIH] Health Promotion: Encouraging consumer behaviors most likely to optimize health potentials (physical and psychosocial) through health information, preventive programs, and access to medical care. [NIH] Health Services: Services for the diagnosis and treatment of disease and the maintenance of health. [NIH] Health Status: The level of health of the individual, group, or population as subjectively assessed by the individual or by more objective measures. [NIH] Health Surveys: A systematic collection of factual data pertaining to health and disease in a human population within a given geographic area. [NIH] Heart attack: A seizure of weak or abnormal functioning of the heart. [NIH] Heart failure: Loss of pumping ability by the heart, often accompanied by fatigue, breathlessness, and excess fluid accumulation in body tissues. [NIH] Hematopoiesis: The development and formation of various types of blood cells. [NIH] Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins. [NIH] Hemodialysis: The use of a machine to clean wastes from the blood after the kidneys have failed. The blood travels through tubes to a dialyzer, which removes wastes and extra fluid. The cleaned blood then flows through another set of tubes back into the body. [NIH] Hemodynamics: The movements of the blood and the forces involved in systemic or regional blood circulation. [NIH] Hemoglobin: One of the fractions of glycosylated hemoglobin A1c. Glycosylated hemoglobin is formed when linkages of glucose and related monosaccharides bind to hemoglobin A and its concentration represents the average blood glucose level over the previous several weeks. HbA1c levels are used as a measure of long-term control of plasma glucose (normal, 4 to 6 percent). In controlled diabetes mellitus, the concentration of glycosylated hemoglobin A is within the normal range, but in uncontrolled cases the level may be 3 to 4 times the normal conentration. Generally, complications are substantially lower among patients with Hb levels of 7 percent or less than in patients with HbA1c levels of 9 percent or more. [NIH] Hemoglobin A: Normal adult human hemoglobin. The globin moiety consists of two alpha and two beta chains. [NIH] Hemoglobinopathies: A group of inherited disorders characterized by structural alterations within the hemoglobin molecule. [NIH]

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Hemoglobinuria: The presence of free hemoglobin in the urine. [NIH] Hemorrhage: Bleeding or escape of blood from a vessel. [NIH] Hemostasis: The process which spontaneously arrests the flow of blood from vessels carrying blood under pressure. It is accomplished by contraction of the vessels, adhesion and aggregation of formed blood elements, and the process of blood or plasma coagulation. [NIH]

Hepatic: Refers to the liver. [NIH] Hepatitis: Inflammation of the liver and liver disease involving degenerative or necrotic alterations of hepatocytes. [NIH] Hepatocellular: Pertaining to or affecting liver cells. [EU] Hepatocellular carcinoma: A type of adenocarcinoma, the most common type of liver tumor. [NIH] Hepatocytes: The main structural component of the liver. They are specialized epithelial cells that are organized into interconnected plates called lobules. [NIH] Herbicides: Pesticides used to destroy unwanted vegetation, especially various types of weeds, grasses, and woody plants. [NIH] Hereditary: Of, relating to, or denoting factors that can be transmitted genetically from one generation to another. [NIH] Heredity: 1. The genetic transmission of a particular quality or trait from parent to offspring. 2. The genetic constitution of an individual. [EU] Hernia: Protrusion of a loop or knuckle of an organ or tissue through an abnormal opening. [NIH]

Heterodimer: Zippered pair of nonidentical proteins. [NIH] Heterogeneity: The property of one or more samples or populations which implies that they are not identical in respect of some or all of their parameters, e. g. heterogeneity of variance. [NIH] Heterogenic: Derived from a different source or species. Also called heterogenous. [NIH] Heterogenous: Derived from a different source or species. Also called heterogenic. [NIH] Heterozygote: An individual having different alleles at one or more loci in homologous chromosome segments. [NIH] Hibernation: The dormant state in which some animal species pass the winter. It is characterized by narcosis and by sharp reduction in body temperature and metabolic activity and by a depression of vital signs. It is a natural physiological process in many warm-blooded animals. [NIH] High blood cholesterol: Cholesterol is the most abundant steroid in animal tissues, especially in bile and gallstones. The relationship between the intake of cholesterol and its manufacture by the body to its utilization, sequestration, or excretion from the body is called the cholesterol balance. When cholesterol accumulates, the balance is positive; when it declines, the balance is negative. In 1993, the NHLBI National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults issued an updated set of recommendations for monitoring and treatment of blood cholesterol levels. The NCEP guidelines recommended that total cholesterol levels and subfractions of high-density lipoprotein (HDL) cholesterol be measured beginning at age 20 in all adults, with subsequent periodic screenings as needed. Even in the group of patients at lowest risk for coronary heart disease (total cholesterol 200 mg/dL and HDL 35 mg/dL), the NCEP recommended that rescreening take place at least

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once every 5 years or upon physical examination. [NIH] High-density lipoproteins: Lipoproteins that contain a small amount of cholesterol and carry cholesterol away from body cells and tissues to the liver for excretion from the body. Low-level HDL increases the risk of heart disease, so the higher the HDL level, the better. The HDL component normally contains 20 to 30 percent of total cholesterol, and HDL levels are inversely correlated with coronary heart disease risk. [NIH] Hippocampus: A curved elevation of gray matter extending the entire length of the floor of the temporal horn of the lateral ventricle (Dorland, 28th ed). The hippocampus, subiculum, and dentate gyrus constitute the hippocampal formation. Sometimes authors include the entorhinal cortex in the hippocampal formation. [NIH] Histamine: 1H-Imidazole-4-ethanamine. A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. [NIH] Histidine: An essential amino acid important in a number of metabolic processes. It is required for the production of histamine. [NIH] Histocompatibility: The degree of antigenic similarity between the tissues of different individuals, which determines the acceptance or rejection of allografts. [NIH] Holidays: Days commemorating events. Holidays also include vacation periods. [NIH] Homeostasis: The processes whereby the internal environment of an organism tends to remain balanced and stable. [NIH] Homologous: Corresponding in structure, position, origin, etc., as (a) the feathers of a bird and the scales of a fish, (b) antigen and its specific antibody, (c) allelic chromosomes. [EU] Homosexuality: Sexual attraction or relationship between members of the same sex. [NIH] Hormonal: Pertaining to or of the nature of a hormone. [EU] Hormone: A substance in the body that regulates certain organs. Hormones such as gastrin help in breaking down food. Some hormones come from cells in the stomach and small intestine. [NIH] Hormone Replacement Therapy: Therapeutic use of hormones to alleviate the effects of hormone deficiency. [NIH] Host: Any animal that receives a transplanted graft. [NIH] Human growth hormone: A protein hormone, secreted by the anterior lobe of the pituitary, which promotes growth of the whole body by stimulating protein synthesis. The human gene has already been cloned and successfully expressed in bacteria. [NIH] Humoral: Of, relating to, proceeding from, or involving a bodily humour - now often used of endocrine factors as opposed to neural or somatic. [EU] Hybrid: Cross fertilization between two varieties or, more usually, two species of vines, see also crossing. [NIH] Hydrogen: The first chemical element in the periodic table. It has the atomic symbol H, atomic number 1, and atomic weight 1. It exists, under normal conditions, as a colorless, odorless, tasteless, diatomic gas. Hydrogen ions are protons. Besides the common H1 isotope, hydrogen exists as the stable isotope deuterium and the unstable, radioactive isotope tritium. [NIH] Hydrogen Peroxide: A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials. [NIH] Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of

Dictionary 553

water. [NIH] Hydrophobic: Not readily absorbing water, or being adversely affected by water, as a hydrophobic colloid. [EU] Hydroxylysine: A hydroxylated derivative of the amino acid lysine that is present in certain collagens. [NIH] Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ascorbic acid can result in impaired hydroxyproline formation. [NIH] Hygienic: Pertaining to hygiene, or conducive to health. [EU] Hypercapnia: A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood. [NIH] Hypercholesterolemia: Abnormally high levels of cholesterol in the blood. [NIH] Hyperglycemia: Abnormally high blood sugar. [NIH] Hyperlipidaemia: A general term for elevated concentrations of any or all of the lipids in the plasma, including hyperlipoproteinaemia, hypercholesterolaemia, etc. [EU] Hyperlipidemia: An excess of lipids in the blood. [NIH] Hyperphagia: Ingestion of a greater than optimal quantity of food. [NIH] Hypersecretion: Excessive secretion. [EU] Hypersensitivity: Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen. [NIH] Hypertension: Persistently high arterial blood pressure. Currently accepted threshold levels are 140 mm Hg systolic and 90 mm Hg diastolic pressure. [NIH] Hyperthyroidism: Excessive functional activity of the thyroid gland. [NIH] Hypertriglyceridemia: Condition of elevated triglyceride concentration in the blood; an inherited form occurs in familial hyperlipoproteinemia IIb and hyperlipoproteinemia type IV. It has been linked to higher risk of heart disease and arteriosclerosis. [NIH] Hypertrophy: General increase in bulk of a part or organ, not due to tumor formation, nor to an increase in the number of cells. [NIH] Hyperuricemia: A buildup of uric acid (a byproduct of metabolism) in the blood; a side effect of some anticancer drugs. [NIH] Hypoglycemia: Abnormally low blood sugar [NIH] Hypoglycemic: An orally active drug that produces a fall in blood glucose concentration. [NIH]

Hypoglycemic Agents: Agents which lower the blood glucose level. [NIH] Hypogonadism: Condition resulting from or characterized by abnormally decreased functional activity of the gonads, with retardation of growth and sexual development. [NIH] Hypoplasia: Incomplete development or underdevelopment of an organ or tissue. [EU] Hypotension: Abnormally low blood pressure. [NIH] Hypothalamic: Of or involving the hypothalamus. [EU] Hypothalamus: Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle. [NIH] Hypothyroidism: Deficiency of thyroid activity. In adults, it is most common in women and is characterized by decrease in basal metabolic rate, tiredness and lethargy, sensitivity to

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cold, and menstrual disturbances. If untreated, it progresses to full-blown myxoedema. In infants, severe hypothyroidism leads to cretinism. In juveniles, the manifestations are intermediate, with less severe mental and developmental retardation and only mild symptoms of the adult form. When due to pituitary deficiency of thyrotropin secretion it is called secondary hypothyroidism. [EU] Hypotonia: A condition of diminished tone of the skeletal muscles; diminished resistance of muscles to passive stretching. [EU] Hypoventilation: A reduction in the amount of air entering the pulmonary alveoli. [NIH] Hysterectomy: Excision of the uterus. [NIH] Id: The part of the personality structure which harbors the unconscious instinctive desires and strivings of the individual. [NIH] Ileal: Related to the ileum, the lowest end of the small intestine. [NIH] Ileum: The lower end of the small intestine. [NIH] Illusion: A false interpretation of a genuine percept. [NIH] Imidazole: C3H4N2. The ring is present in polybenzimidazoles. [NIH] Immune function: Production and action of cells that fight disease or infection. [NIH] Immune response: (antigens). [NIH]

The activity of the immune system against foreign substances

Immune system: The organs, cells, and molecules responsible for the recognition and disposal of foreign ("non-self") material which enters the body. [NIH] Immunity: Nonsusceptibility to the invasive or pathogenic effects of foreign microorganisms or to the toxic effect of antigenic substances. [NIH] Immunization: Deliberate stimulation of the host's immune response. Active immunization involves administration of antigens or immunologic adjuvants. Passive immunization involves administration of immune sera or lymphocytes or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow). [NIH] Immunocompetence: The ability of lymphoid cells to mount a humoral or cellular immune response when challenged by antigen. [NIH] Immunodeficiency: The decreased ability of the body to fight infection and disease. [NIH] Immunodiffusion: Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction. [NIH]

Immunoelectrophoresis: A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera. [NIH] Immunogenic: Producing immunity; evoking an immune response. [EU] Immunoglobulins: Glycoproteins present in the blood (antibodies) and in other tissue. They are classified by structure and activity into five classes (IgA, IgD, IgE, IgG, IgM). [NIH] Immunology: The study of the body's immune system. [NIH] Immunosuppressive: Describes the ability to lower immune system responses. [NIH] Impairment: In the context of health experience, an impairment is any loss or abnormality of psychological, physiological, or anatomical structure or function. [NIH]

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Implantation: The insertion or grafting into the body of biological, living, inert, or radioactive material. [EU] Impotence: The inability to perform sexual intercourse. [NIH] In vitro: In the laboratory (outside the body). The opposite of in vivo (in the body). [NIH] In vivo: In the body. The opposite of in vitro (outside the body or in the laboratory). [NIH] Incision: A cut made in the body during surgery. [NIH] Incompetence: Physical or mental inadequacy or insufficiency. [EU] Incontinence: Inability to control the flow of urine from the bladder (urinary incontinence) or the escape of stool from the rectum (fecal incontinence). [NIH] Indicative: That indicates; that points out more or less exactly; that reveals fairly clearly. [EU]

Induction: The act or process of inducing or causing to occur, especially the production of a specific morphogenetic effect in the developing embryo through the influence of evocators or organizers, or the production of anaesthesia or unconsciousness by use of appropriate agents. [EU] Infancy: The period of complete dependency prior to the acquisition of competence in walking, talking, and self-feeding. [NIH] Infant, Newborn: An infant during the first month after birth. [NIH] Infarction: A pathological process consisting of a sudden insufficient blood supply to an area, which results in necrosis of that area. It is usually caused by a thrombus, an embolus, or a vascular torsion. [NIH] Infection: 1. Invasion and multiplication of microorganisms in body tissues, which may be clinically unapparent or result in local cellular injury due to competitive metabolism, toxins, intracellular replication, or antigen-antibody response. The infection may remain localized, subclinical, and temporary if the body's defensive mechanisms are effective. A local infection may persist and spread by extension to become an acute, subacute, or chronic clinical infection or disease state. A local infection may also become systemic when the microorganisms gain access to the lymphatic or vascular system. 2. An infectious disease. [EU]

Infertility: The diminished or absent ability to conceive or produce an offspring while sterility is the complete inability to conceive or produce an offspring. [NIH] Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function. [NIH] Inflammatory bowel disease: A general term that refers to the inflammation of the colon and rectum. Inflammatory bowel disease includes ulcerative colitis and Crohn's disease. [NIH]

Infusion: A method of putting fluids, including drugs, into the bloodstream. Also called intravenous infusion. [NIH] Ingestion: Taking into the body by mouth [NIH] Inhibin: Glyceroprotein hormone produced in the seminiferous tubules by the Sertoli cells in the male and by the granulosa cells in the female follicles. The hormone inhibits FSH and LH synthesis and secretion by the pituitary cells thereby affecting sexual maturation and fertility. [NIH] Initiation: Mutation induced by a chemical reactive substance causing cell changes; being a step in a carcinogenic process. [NIH]

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Inorganic: Pertaining to substances not of organic origin. [EU] Inotropic: Affecting the force or energy of muscular contractions. [EU] Inpatients: Persons admitted to health facilities which provide board and room, for the purpose of observation, care, diagnosis or treatment. [NIH] Insecticides: Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. [NIH] Insight: The capacity to understand one's own motives, to be aware of one's own psychodynamics, to appreciate the meaning of symbolic behavior. [NIH] Insomnia: Difficulty in going to sleep or getting enough sleep. [NIH] Insufflation: The act of blowing a powder, vapor, or gas into any body cavity for experimental, diagnostic, or therapeutic purposes. [NIH] Insulin: A protein hormone secreted by beta cells of the pancreas. Insulin plays a major role in the regulation of glucose metabolism, generally promoting the cellular utilization of glucose. It is also an important regulator of protein and lipid metabolism. Insulin is used as a drug to control insulin-dependent diabetes mellitus. [NIH] Insulin-dependent diabetes mellitus: A disease characterized by high levels of blood glucose resulting from defects in insulin secretion, insulin action, or both. Autoimmune, genetic, and environmental factors are involved in the development of type I diabetes. [NIH] Insulin-like: Muscular growth factor. [NIH] Intercellular Adhesion Molecule-1: A cell-surface ligand with a role in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue. [NIH] Interleukin-1: A soluble factor produced by monocytes, macrophages, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. IL-1 consists of two distinct forms, IL-1 alpha and IL-1 beta which perform the same functions but are distinct proteins. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation. The factor is distinct from interleukin-2. [NIH] Interleukin-2: Chemical mediator produced by activated T lymphocytes and which regulates the proliferation of T cells, as well as playing a role in the regulation of NK cell activity. [NIH] Intermittent: Occurring at separated intervals; having periods of cessation of activity. [EU] Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults. [NIH] Interpersonal Relations: The reciprocal interaction of two or more persons. [NIH] Interstitial: Pertaining to or situated between parts or in the interspaces of a tissue. [EU] Intervertebral: Situated between two contiguous vertebrae. [EU] Intestinal: Having to do with the intestines. [NIH] Intestinal Obstruction: Any impairment, arrest, or reversal of the normal flow of intestinal contents toward the anus. [NIH] Intestine: A long, tube-shaped organ in the abdomen that completes the process of digestion. There is both a large intestine and a small intestine. Also called the bowel. [NIH] Intoxication: Poisoning, the state of being poisoned. [EU] Intracellular: Inside a cell. [NIH]

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Intracranial Pressure: Pressure within the cranial cavity. It is influenced by brain mass, the circulatory system, CSF dynamics, and skull rigidity. [NIH] Intramuscular: IM. Within or into muscle. [NIH] Intramuscular injection: IM. Injection into a muscle. [NIH] Intraperitoneal: IP. Within the peritoneal cavity (the area that contains the abdominal organs). [NIH] Intravenous: IV. Into a vein. [NIH] Intrinsic: Situated entirely within or pertaining exclusively to a part. [EU] Intubation: Introduction of a tube into a hollow organ to restore or maintain patency if obstructed. It is differentiated from catheterization in that the insertion of a catheter is usually performed for the introducing or withdrawing of fluids from the body. [NIH] Invasive: 1. Having the quality of invasiveness. 2. Involving puncture or incision of the skin or insertion of an instrument or foreign material into the body; said of diagnostic techniques. [EU]

Involuntary: Reaction occurring without intention or volition. [NIH] Ionizing: Radiation comprising charged particles, e. g. electrons, protons, alpha-particles, etc., having sufficient kinetic energy to produce ionization by collision. [NIH] Ions: An atom or group of atoms that have a positive or negative electric charge due to a gain (negative charge) or loss (positive charge) of one or more electrons. Atoms with a positive charge are known as cations; those with a negative charge are anions. [NIH] Ischemia: Deficiency of blood in a part, due to functional constriction or actual obstruction of a blood vessel. [EU] Ischemic stroke: A condition in which the blood supply to part of the brain is cut off. Also called "plug-type" strokes. Blocked arteries starve areas of the brain controlling sight, speech, sensation, and movement so that these functions are partially or completely lost. Ischemic stroke is the most common type of stroke, accounting for 80 percent of all strokes. Most ischemic strokes are caused by a blood clot called a thrombus, which blocks blood flow in the arteries feeding the brain, usually the carotid artery in the neck, the major vessel bringing blood to the brain. When it becomes blocked, the risk of stroke is very high. [NIH] Islet: Cell producing insulin in pancreas. [NIH] Isoenzyme: Different forms of an enzyme, usually occurring in different tissues. The isoenzymes of a particular enzyme catalyze the same reaction but they differ in some of their properties. [NIH] Jejunoileal Bypass: A surgical procedure consisting of the anastomosis of the proximal part of the jejunum to the distal portion of the ileum, so as to bypass the nutrient-absorptive segment of the small intestine, to treat morbid obesity. [NIH] Jejunum: That portion of the small intestine which extends from the duodenum to the ileum; called also intestinum jejunum. [EU] Joint: The point of contact between elements of an animal skeleton with the parts that surround and support it. [NIH] Kainate: Glutamate receptor. [NIH] Karyotype: The characteristic chromosome complement of an individual, race, or species as defined by their number, size, shape, etc. [NIH] Kb: A measure of the length of DNA fragments, 1 Kb = 1000 base pairs. The largest DNA fragments are up to 50 kilobases long. [NIH]

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Keto: It consists of 8 carbon atoms and within the endotoxins, it connects poysaccharide and lipid A. [NIH] Ketoacidosis: Acidosis accompanied by the accumulation of ketone bodies (ketosis) in the body tissues and fluids, as in diabetic acidosis. [EU] Ketone Bodies: Chemicals that the body makes when there is not enough insulin in the blood and it must break down fat for its energy. Ketone bodies can poison and even kill body cells. When the body does not have the help of insulin, the ketones build up in the blood and then "spill" over into the urine so that the body can get rid of them. The body can also rid itself of one type of ketone, called acetone, through the lungs. This gives the breath a fruity odor. Ketones that build up in the body for a long time lead to serious illness and coma. [NIH] Ketosis: A condition of having ketone bodies build up in body tissues and fluids. The signs of ketosis are nausea, vomiting, and stomach pain. Ketosis can lead to ketoacidosis. [NIH] Ketosteroids: Steroid derivatives formed by oxidation of a methyl group on the side chain or a methylene group in the ring skeleton to form a ketone. [NIH] Kidney Cortex: The outer zone of the kidney, beneath the capsule, consisting of kidney glomerulus; kidney tubules, distal; and kidney tubules, proximal. [NIH] Kidney Disease: Any one of several chronic conditions that are caused by damage to the cells of the kidney. People who have had diabetes for a long time may have kidney damage. Also called nephropathy. [NIH] Kidney Failure: The inability of a kidney to excrete metabolites at normal plasma levels under conditions of normal loading, or the inability to retain electrolytes under conditions of normal intake. In the acute form (kidney failure, acute), it is marked by uremia and usually by oliguria or anuria, with hyperkalemia and pulmonary edema. The chronic form (kidney failure, chronic) is irreversible and requires hemodialysis. [NIH] Kidney Failure, Acute: A clinical syndrome characterized by a sudden decrease in glomerular filtration rate, often to values of less than 1 to 2 ml per minute. It is usually associated with oliguria (urine volumes of less than 400 ml per day) and is always associated with biochemical consequences of the reduction in glomerular filtration rate such as a rise in blood urea nitrogen (BUN) and serum creatinine concentrations. [NIH] Kidney Failure, Chronic: An irreversible and usually progressive reduction in renal function in which both kidneys have been damaged by a variety of diseases to the extent that they are unable to adequately remove the metabolic products from the blood and regulate the body's electrolyte composition and acid-base balance. Chronic kidney failure requires hemodialysis or surgery, usually kidney transplantation. [NIH] Kidney Transplantation: another. [NIH]

The transference of a kidney from one human or animal to

Kinetic: Pertaining to or producing motion. [EU] Labile: 1. Gliding; moving from point to point over the surface; unstable; fluctuating. 2. Chemically unstable. [EU] Lactation: The period of the secretion of milk. [EU] Laparoscopy: Examination, therapy or surgery of the abdomen's interior by means of a laparoscope. [NIH] Large Intestine: The part of the intestine that goes from the cecum to the rectum. The large intestine absorbs water from stool and changes it from a liquid to a solid form. The large intestine is 5 feet long and includes the appendix, cecum, colon, and rectum. Also called colon. [NIH]

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Larynx: An irregularly shaped, musculocartilaginous tubular structure, lined with mucous membrane, located at the top of the trachea and below the root of the tongue and the hyoid bone. It is the essential sphincter guarding the entrance into the trachea and functioning secondarily as the organ of voice. [NIH] Latent: Phoria which occurs at one distance or another and which usually has no troublesome effect. [NIH] Laxative: An agent that acts to promote evacuation of the bowel; a cathartic or purgative. [EU]

Least-Squares Analysis: A principle of estimation in which the estimates of a set of parameters in a statistical model are those quantities minimizing the sum of squared differences between the observed values of a dependent variable and the values predicted by the model. [NIH] Lens: The transparent, double convex (outward curve on both sides) structure suspended between the aqueous and vitreous; helps to focus light on the retina. [NIH] Leptin: A 16-kD peptide hormone secreted from white adipocytes and implicated in the regulation of food intake and energy balance. Leptin provides the key afferent signal from fat cells in the feedback system that controls body fat stores. [NIH] Lethal: Deadly, fatal. [EU] Lethargy: Abnormal drowsiness or stupor; a condition of indifference. [EU] Leukemia: Cancer of blood-forming tissue. [NIH] Leukocytes: White blood cells. These include granular leukocytes (basophils, eosinophils, and neutrophils) as well as non-granular leukocytes (lymphocytes and monocytes). [NIH] Leukocytosis: A transient increase in the number of leukocytes in a body fluid. [NIH] Leukotrienes: A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. [NIH] Libido: The psychic drive or energy associated with sexual instinct in the broad sense (pleasure and love-object seeking). It may also connote the psychic energy associated with instincts in general that motivate behavior. [NIH] Library Services: circulation. [NIH]

Services offered to the library user. They include reference and

Life Expectancy: A figure representing the number of years, based on known statistics, to which any person of a given age may reasonably expect to live. [NIH] Ligament: A band of fibrous tissue that connects bones or cartilages, serving to support and strengthen joints. [EU] Likelihood Functions: Functions constructed from a statistical model and a set of observed data which give the probability of that data for various values of the unknown model parameters. Those parameter values that maximize the probability are the maximum likelihood estimates of the parameters. [NIH] Limbic: Pertaining to a limbus, or margin; forming a border around. [EU] Limbic System: A set of forebrain structures common to all mammals that is defined functionally and anatomically. It is implicated in the higher integration of visceral, olfactory, and somatic information as well as homeostatic responses including fundamental survival

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behaviors (feeding, mating, emotion). For most authors, it includes the amygdala, epithalamus, gyrus cinguli, hippocampal formation (see hippocampus), hypothalamus, parahippocampal gyrus, septal nuclei, anterior nuclear group of thalamus, and portions of the basal ganglia. (Parent, Carpenter's Human Neuroanatomy, 9th ed, p744; NeuroNames, http://rprcsgi.rprc.washington.edu/neuronames/index.html (September 2, 1998)). [NIH] Linear Models: Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression. [NIH] Linkage: The tendency of two or more genes in the same chromosome to remain together from one generation to the next more frequently than expected according to the law of independent assortment. [NIH] Linkage Disequilibrium: Nonrandom association of linked genes. This is the tendency of the alleles of two separate but already linked loci to be found together more frequently than would be expected by chance alone. [NIH] Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3. [NIH] Lipid: Fat. [NIH] Lipid A: Lipid A is the biologically active component of lipopolysaccharides. It shows strong endotoxic activity and exhibits immunogenic properties. [NIH] Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor. [NIH] Lipodystrophy: A collection of rare conditions resulting from defective fat metabolism and characterized by atrophy of the subcutaneous fat. They include total, congenital or acquired, partial, abdominal infantile, and localized lipodystrophy. [NIH] Lipolysis: The hydrolysis of lipids. [NIH] Lipoma: A benign tumor composed of fat cells. [NIH] Lipopolysaccharides: Substance consisting of polysaccaride and lipid. [NIH] Lipoprotein: Any of the lipid-protein complexes in which lipids are transported in the blood; lipoprotein particles consist of a spherical hydrophobic core of triglycerides or cholesterol esters surrounded by an amphipathic monolayer of phospholipids, cholesterol, and apolipoproteins; the four principal classes are high-density, low-density, and very-lowdensity lipoproteins and chylomicrons. [EU] Lipoprotein Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34. [NIH] Lipoprotein(a): A family of lipoprotein particles varying in density and size depending on the protein-lipid ratio and the protein composition. These particles consist of apolipoprotein B-100 covalently linked to apolipoprotein-a by one or two disulfide bonds. There is a correlation between high plasma levels of this lipoprotein and increased risk for atherosclerotic cardiovascular disease. [NIH] Liposome: A spherical particle in an aqueous medium, formed by a lipid bilayer enclosing an aqueous compartment. [EU]

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Lipoxygenase: An enzyme of the oxidoreductase class that catalyzes reactions between linoleate and other fatty acids and oxygen to form hydroperoxy-fatty acid derivatives. Related enzymes in this class include the arachidonate lipoxygenases, arachidonate 5lipoxygenase, arachidonate 12-lipoxygenase, and arachidonate 15-lipoxygenase. EC 1.13.11.12. [NIH] Lithium: An element in the alkali metals family. It has the atomic symbol Li, atomic number 3, and atomic weight 6.94. Salts of lithium are used in treating manic-depressive disorders. [NIH]

Liver: A large, glandular organ located in the upper abdomen. The liver cleanses the blood and aids in digestion by secreting bile. [NIH] Liver Transplantation: The transference of a part of or an entire liver from one human or animal to another. [NIH] Lobe: A portion of an organ such as the liver, lung, breast, or brain. [NIH] Loc: A brain region associated with object recognition. [NIH] Localization: The process of determining or marking the location or site of a lesion or disease. May also refer to the process of keeping a lesion or disease in a specific location or site. [NIH] Localized: Cancer which has not metastasized yet. [NIH] Locomotion: Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms. [NIH] Logistic Models: Statistical models which describe the relationship between a qualitative dependent variable (that is, one which can take only certain discrete values, such as the presence or absence of a disease) and an independent variable. A common application is in epidemiology for estimating an individual's risk (probability of a disease) as a function of a given risk factor. [NIH] Longitudinal Studies: Studies in which variables relating to an individual or group of individuals are assessed over a period of time. [NIH] Longitudinal study: Also referred to as a "cohort study" or "prospective study"; the analytic method of epidemiologic study in which subsets of a defined population can be identified who are, have been, or in the future may be exposed or not exposed, or exposed in different degrees, to a factor or factors hypothesized to influence the probability of occurrence of a given disease or other outcome. The main feature of this type of study is to observe large numbers of subjects over an extended time, with comparisons of incidence rates in groups that differ in exposure levels. [NIH] Loop: A wire usually of platinum bent at one end into a small loop (usually 4 mm inside diameter) and used in transferring microorganisms. [NIH] Low-calorie diet: Caloric restriction of about 800 to 1,500 calories (approximately 12 to 15 kcal/kg of body weight) per day. [NIH] Low-density lipoprotein: Lipoprotein that contains most of the cholesterol in the blood. LDL carries cholesterol to the tissues of the body, including the arteries. A high level of LDL increases the risk of heart disease. LDL typically contains 60 to 70 percent of the total serum cholesterol and both are directly correlated with CHD risk. [NIH] Lower Esophageal Sphincter: The muscle between the esophagus and stomach. When a person swallows, this muscle relaxes to let food pass from the esophagus to the stomach. It stays closed at other times to keep stomach contents from flowing back into the esophagus. [NIH]

Lubricants: Oily or slippery substances. [NIH]

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Lumbar: Pertaining to the loins, the part of the back between the thorax and the pelvis. [EU] Lumen: The cavity or channel within a tube or tubular organ. [EU] Lung volume: The amount of air the lungs hold. [NIH] Lutein Cells: The cells of the corpus luteum which are derived from the granulosa cells and the theca cells of the Graafian follicle. [NIH] Lymph: The almost colorless fluid that travels through the lymphatic system and carries cells that help fight infection and disease. [NIH] Lymph node: A rounded mass of lymphatic tissue that is surrounded by a capsule of connective tissue. Also known as a lymph gland. Lymph nodes are spread out along lymphatic vessels and contain many lymphocytes, which filter the lymphatic fluid (lymph). [NIH]

Lymphatic: The tissues and organs, including the bone marrow, spleen, thymus, and lymph nodes, that produce and store cells that fight infection and disease. [NIH] Lymphoblastic: One of the most aggressive types of non-Hodgkin lymphoma. [NIH] Lymphoblasts: Interferon produced predominantly by leucocyte cells. [NIH] Lymphocytes: White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each); those with characteristics of neither major class are called null cells. [NIH] Lymphoid: Referring to lymphocytes, a type of white blood cell. Also refers to tissue in which lymphocytes develop. [NIH] Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue. [NIH] Macrolides: A group of organic compounds that contain a macrocyclic lactone ring linked glycosidically to one or more sugar moieties. [NIH] Macrophage: A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells. [NIH] Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques. [NIH] Major Histocompatibility Complex: The genetic region which contains the loci of genes which determine the structure of the serologically defined (SD) and lymphocyte-defined (LD) transplantation antigens, genes which control the structure of the immune responseassociated (Ia) antigens, the immune response (Ir) genes which control the ability of an animal to respond immunologically to antigenic stimuli, and genes which determine the structure and/or level of the first four components of complement. [NIH] Malabsorption: Impaired intestinal absorption of nutrients. [EU] Malignancy: A cancerous tumor that can invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malignant: Cancerous; a growth with a tendency to invade and destroy nearby tissue and spread to other parts of the body. [NIH] Malnutrition: A condition caused by not eating enough food or not eating a balanced diet. [NIH]

Mammary: Pertaining to the mamma, or breast. [EU]

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Mammography: Radiographic examination of the breast. [NIH] Mania: Excitement of psychotic proportions manifested by mental and physical hyperactivity, disorganization of behaviour, and elevation of mood. [EU] Manic: Affected with mania. [EU] Manifest: Being the part or aspect of a phenomenon that is directly observable : concretely expressed in behaviour. [EU] Man-made: Ionizing radiation emitted by artificial or concentrated natural, radioactive material or resulting from the operation of high voltage apparatus, such as X-ray apparatus or particle accelerators, of nuclear reactors, or from nuclear explosions. [NIH] Marital Status: A demographic parameter indicating a person's status with respect to marriage, divorce, widowhood, singleness, etc. [NIH] Mastication: The act and process of chewing and grinding food in the mouth. [NIH] Maternal Behavior: The behavior patterns associated with or characteristic of a mother. [NIH]

Matrilysin: The smallest member of the matrix metalloproteinases. It plays a role in tumor progression. EC 3.4.24.23. [NIH] Matrix metalloproteinase: A member of a group of enzymes that can break down proteins, such as collagen, that are normally found in the spaces between cells in tissues (i.e., extracellular matrix proteins). Because these enzymes need zinc or calcium atoms to work properly, they are called metalloproteinases. Matrix metalloproteinases are involved in wound healing, angiogenesis, and tumor cell metastasis. [NIH] Maxillary: Pertaining to the maxilla : the irregularly shaped bone that with its fellow forms the upper jaw. [EU] Maxillary Nerve: The intermediate sensory division of the trigeminal (5th cranial) nerve. The maxillary nerve carries general afferents from the intermediate region of the face including the lower eyelid, nose and upper lip, the maxillary teeth, and parts of the dura. [NIH]

Meat: The edible portions of any animal used for food including domestic mammals (the major ones being cattle, swine, and sheep) along with poultry, fish, shellfish, and game. [NIH]

Meatus: A canal running from the internal auditory foramen through the petrous portion of the temporal bone. It gives passage to the facial and auditory nerves together with the auditory branch of the basilar artery and the internal auditory veins. [NIH] Medial: Lying near the midsaggital plane of the body; opposed to lateral. [NIH] Median Nerve: A major nerve of the upper extremity. In humans, the fibers of the median nerve originate in the lower cervical and upper thoracic spinal cord (usually C6 to T1), travel via the brachial plexus, and supply sensory and motor innervation to parts of the forearm and hand. [NIH] Mediate: Indirect; accomplished by the aid of an intervening medium. [EU] Mediator: An object or substance by which something is mediated, such as (1) a structure of the nervous system that transmits impulses eliciting a specific response; (2) a chemical substance (transmitter substance) that induces activity in an excitable tissue, such as nerve or muscle; or (3) a substance released from cells as the result of the interaction of antigen with antibody or by the action of antigen with a sensitized lymphocyte. [EU] Medical Records: illnesses. [NIH]

Recording of pertinent information concerning patient's illness or

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Medical Staff: Professional medical personnel who provide care to patients in an organized facility, institution or agency. [NIH] Medicament: A medicinal substance or agent. [EU] MEDLINE: An online database of MEDLARS, the computerized bibliographic Medical Literature Analysis and Retrieval System of the National Library of Medicine. [NIH] Medullary: Pertaining to the marrow or to any medulla; resembling marrow. [EU] Meiosis: A special method of cell division, occurring in maturation of the germ cells, by means of which each daughter nucleus receives half the number of chromosomes characteristic of the somatic cells of the species. [NIH] Melanin: The substance that gives the skin its color. [NIH] Melanocytes: Epidermal dendritic pigment cells which control long-term morphological color changes by alteration in their number or in the amount of pigment they produce and store in the pigment containing organelles called melanosomes. Melanophores are larger cells which do not exist in mammals. [NIH] Melanoma: A form of skin cancer that arises in melanocytes, the cells that produce pigment. Melanoma usually begins in a mole. [NIH] Melanosis: Disorders of increased melanin pigmentation that develop without preceding inflammatory disease. [NIH] Membrane: A very thin layer of tissue that covers a surface. [NIH] Membrane Lipids: Lipids, predominantly phospholipids, cholesterol and small amounts of glycolipids found in membranes including cellular and intracellular membranes. These lipids may be arranged in bilayers in the membranes with integral proteins between the layers and peripheral proteins attached to the outside. Membrane lipids are required for active transport, several enzymatic activities and membrane formation. [NIH] Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory. [NIH] Menarche: The establishment or beginning of the menstrual function. [EU] Meninges: The three membranes that cover and protect the brain and spinal cord. [NIH] Menopause: Permanent cessation of menstruation. [NIH] Menstrual Cycle: The period of the regularly recurring physiologic changes in the endometrium occurring during the reproductive period in human females and some primates and culminating in partial sloughing of the endometrium (menstruation). [NIH] Menstruation: The normal physiologic discharge through the vagina of blood and mucosal tissues from the nonpregnant uterus. [NIH] Mental: Pertaining to the mind; psychic. 2. (L. mentum chin) pertaining to the chin. [EU] Mental Disorders: Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function. [NIH] Mental Health: The state wherein the person is well adjusted. [NIH] Mental Processes: Conceptual functions or thinking in all its forms. [NIH] Mental Retardation: Refers to sub-average general intellectual functioning which originated during the developmental period and is associated with impairment in adaptive behavior. [NIH] Mesolimbic: Inner brain region governing emotion and drives. [NIH]

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Meta-Analysis: A quantitative method of combining the results of independent studies (usually drawn from the published literature) and synthesizing summaries and conclusions which may be used to evaluate therapeutic effectiveness, plan new studies, etc., with application chiefly in the areas of research and medicine. [NIH] Metabolic disorder: A condition in which normal metabolic processes are disrupted, usually because of a missing enzyme. [NIH] Metabolite: Any substance produced by metabolism or by a metabolic process. [EU] Metalloendopeptidases: Endopeptidases which use a metal, normally zinc, in the catalytic mechanism. This group of enzymes is inactivated by metal chelators. EC 3.4.24. [NIH] Metallothionein: A low-molecular-weight (approx. 10 kD) protein occurring in the cytoplasm of kidney cortex and liver. It is rich in cysteinyl residues and contains no aromatic amino acids. Metallothionein shows high affinity for bivalent heavy metals. [NIH] Metastasis: The spread of cancer from one part of the body to another. Tumors formed from cells that have spread are called "secondary tumors" and contain cells that are like those in the original (primary) tumor. The plural is metastases. [NIH] Methionine: A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. [NIH] MI: Myocardial infarction. Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Microbe: An organism which cannot be observed with the naked eye; e. g. unicellular animals, lower algae, lower fungi, bacteria. [NIH] Microbiology: The study of microorganisms such as fungi, bacteria, algae, archaea, and viruses. [NIH] Microglia: The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling. [NIH] Microorganism: An organism that can be seen only through a microscope. Microorganisms include bacteria, protozoa, algae, and fungi. Although viruses are not considered living organisms, they are sometimes classified as microorganisms. [NIH] Microspheres: Small uniformly-sized spherical particles frequently labeled with radioisotopes or various reagents acting as tags or markers. [NIH] Midaxillary line: An imaginary vertical line that passes midway between the anterior and posterior axillary (armpit) folds. [NIH] Migration: The systematic movement of genes between populations of the same species, geographic race, or variety. [NIH] Millimeter: A measure of length. A millimeter is approximately 26-times smaller than an inch. [NIH] Minority Groups: A subgroup having special characteristics within a larger group, often bound together by special ties which distinguish it from the larger group. [NIH] Mitosis: A method of indirect cell division by means of which the two daughter nuclei

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normally receive identical complements of the number of chromosomes of the somatic cells of the species. [NIH] Mobilization: The process of making a fixed part or stored substance mobile, as by separating a part from surrounding structures to make it accessible for an operative procedure or by causing release into the circulation for body use of a substance stored in the body. [EU] Modification: A change in an organism, or in a process in an organism, that is acquired from its own activity or environment. [NIH] Molecular: Of, pertaining to, or composed of molecules : a very small mass of matter. [EU] Molecule: A chemical made up of two or more atoms. The atoms in a molecule can be the same (an oxygen molecule has two oxygen atoms) or different (a water molecule has two hydrogen atoms and one oxygen atom). Biological molecules, such as proteins and DNA, can be made up of many thousands of atoms. [NIH] Monitor: An apparatus which automatically records such physiological signs as respiration, pulse, and blood pressure in an anesthetized patient or one undergoing surgical or other procedures. [NIH] Monoamine: Enzyme that breaks down dopamine in the astrocytes and microglia. [NIH] Monoamine Oxidase: An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4. [NIH] Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate bone marrow and released into the blood; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles. [NIH] Monogenic: A human disease caused by a mutation in a single gene. [NIH] Mononuclear: A cell with one nucleus. [NIH] Monotherapy: A therapy which uses only one drug. [EU] Monounsaturated fat: An unsaturated fat that is found primarily in plant foods, including olive and canola oils. [NIH] Morphological: Relating to the configuration or the structure of live organs. [NIH] Morphology: The science of the form and structure of organisms (plants, animals, and other forms of life). [NIH] Motilin: A 22-amino acid polypeptide (molecular weight 2700) isolated from the duodenum. At low pH it inhibits gastric motor activity, whereas at high pH it has a stimulating effect. [NIH] Motility: The ability to move spontaneously. [EU] Motion Sickness: Sickness caused by motion, as sea sickness, train sickness, car sickness, and air sickness. [NIH] Motor Activity: The physical activity of an organism as a behavioral phenomenon. [NIH] Motor Skills: Performance of complex motor acts. [NIH] Movement Disorders: Syndromes which feature dyskinesias as a cardinal manifestation of

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the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions. [NIH] Mucosa: A mucous membrane, or tunica mucosa. [EU] Mucus: The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells. [NIH] Multicenter study: A clinical trial that is carried out at more than one medical institution. [NIH]

Muscle Fibers: Large single cells, either cylindrical or prismatic in shape, that form the basic unit of muscle tissue. They consist of a soft contractile substance enclosed in a tubular sheath. [NIH] Muscle Hypertonia: Abnormal increase in skeletal or smooth muscle tone. Skeletal muscle hypertonicity may be associated with pyramidal tract lesions or basal ganglia diseases. [NIH] Muscular Atrophy: Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation. [NIH] Muscular Dystrophies: A general term for a group of inherited disorders which are characterized by progressive degeneration of skeletal muscles. [NIH] Musculoskeletal System: Themuscles, bones, and cartilage of the body. [NIH] Mutagens: Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes. [NIH] Mydriatic: 1. Dilating the pupil. 2. Any drug that dilates the pupil. [EU] Myocardial infarction: Gross necrosis of the myocardium as a result of interruption of the blood supply to the area; it is almost always caused by atherosclerosis of the coronary arteries, upon which coronary thrombosis is usually superimposed. [NIH] Myocardial Ischemia: A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (coronary arteriosclerosis), to obstruction by a thrombus (coronary thrombosis), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (myocardial infarction). [NIH] Myocardium: The muscle tissue of the heart composed of striated, involuntary muscle known as cardiac muscle. [NIH] Myofibrils: Highly organized bundles of actin, myosin, and other proteins in the cytoplasm of skeletal and cardiac muscle cells that contract by a sliding filament mechanism. [NIH] Myoglobin: A conjugated protein which is the oxygen-transporting pigment of muscle. It is made up of one globin polypeptide chain and one heme group. [NIH] Myotonic Dystrophy: A condition presenting muscle weakness and wasting which may be progressive. [NIH] Naive: Used to describe an individual who has never taken a certain drug or class of drugs (e. g., AZT-naive, antiretroviral-naive), or to refer to an undifferentiated immune system cell. [NIH] Narcolepsy: A condition of unknown cause characterized by a periodic uncontrollable tendency to fall asleep. [NIH] Nasal Cavity: The proximal portion of the respiratory passages on either side of the nasal septum, lined with ciliated mucosa, extending from the nares to the pharynx. [NIH]

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Nasal Septum: The partition separating the two nasal cavities in the midplane, composed of cartilaginous, membranous and bony parts. [NIH] Natriuresis: The excretion of abnormal amounts of sodium in the urine. [EU] Nausea: An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses. [NIH] NCI: National Cancer Institute. NCI, part of the National Institutes of Health of the United States Department of Health and Human Services, is the federal government's principal agency for cancer research. NCI conducts, coordinates, and funds cancer research, training, health information dissemination, and other programs with respect to the cause, diagnosis, prevention, and treatment of cancer. Access the NCI Web site at http://cancer.gov. [NIH] Need: A state of tension or dissatisfaction felt by an individual that impels him to action toward a goal he believes will satisfy the impulse. [NIH] Neonatal: Pertaining to the first four weeks after birth. [EU] Neoplasia: Abnormal and uncontrolled cell growth. [NIH] Neoplasm: A new growth of benign or malignant tissue. [NIH] Neoplastic: Pertaining to or like a neoplasm (= any new and abnormal growth); pertaining to neoplasia (= the formation of a neoplasm). [EU] Nephropathy: Disease of the kidneys. [EU] Nerve: A cordlike structure of nervous tissue that connects parts of the nervous system with other tissues of the body and conveys nervous impulses to, or away from, these tissues. [NIH] Nerve Endings: Specialized terminations of peripheral neurons. Nerve endings include neuroeffector junction(s) by which neurons activate target organs and sensory receptors which transduce information from the various sensory modalities and send it centrally in the nervous system. Presynaptic nerve endings are presynaptic terminals. [NIH] Nervous System: The entire nerve apparatus composed of the brain, spinal cord, nerves and ganglia. [NIH] Networks: Pertaining to a nerve or to the nerves, a meshlike structure of interlocking fibers or strands. [NIH] Neural: 1. Pertaining to a nerve or to the nerves. 2. Situated in the region of the spinal axis, as the neutral arch. [EU] Neuroeffector Junction: The synapse between a neuron (presynaptic) and an effector cell other than another neuron (postsynaptic). Neuroeffector junctions include synapses onto muscles and onto secretory cells. [NIH] Neuroendocrine: Having to do with the interactions between the nervous system and the endocrine system. Describes certain cells that release hormones into the blood in response to stimulation of the nervous system. [NIH] Neurogenic: Loss of bladder control caused by damage to the nerves controlling the bladder. [NIH] Neurogenic Inflammation: Inflammation caused by an injurious stimulus of peripheral neurons and resulting in release of neuropeptides which affect vascular permeability and help initiate proinflammatory and immune reactions at the site of injury. [NIH] Neuroleptic: A term coined to refer to the effects on cognition and behaviour of antipsychotic drugs, which produce a state of apathy, lack of initiative, and limited range of emotion and in psychotic patients cause a reduction in confusion and agitation and normalization of psychomotor activity. [EU]

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Neurologic: Having to do with nerves or the nervous system. [NIH] Neuromuscular: Pertaining to muscles and nerves. [EU] Neuromuscular Diseases: A general term encompassing lower motor neuron disease; peripheral nervous system diseases; and certain muscular diseases. Manifestations include muscle weakness; fasciculation; muscle atrophy; spasm; myokymia; muscle hypertonia, myalgias, and musclehypotonia. [NIH] Neuromuscular Junction: The synapse between a neuron and a muscle. [NIH] Neuronal: Pertaining to a neuron or neurons (= conducting cells of the nervous system). [EU]

Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the nervous system. [NIH] Neuropathy: A problem in any part of the nervous system except the brain and spinal cord. Neuropathies can be caused by infection, toxic substances, or disease. [NIH] Neuropeptide: A member of a class of protein-like molecules made in the brain. Neuropeptides consist of short chains of amino acids, with some functioning as neurotransmitters and some functioning as hormones. [NIH] Neurosurgery: A surgical specialty concerned with the treatment of diseases and disorders of the brain, spinal cord, and peripheral and sympathetic nervous system. [NIH] Neurotensin: A biologically active tridecapeptide isolated from the hypothalamus. It has been shown to induce hypotension in the rat, to stimulate contraction of guinea pig ileum and rat uterus, and to cause relaxation of rat duodenum. There is also evidence that it acts as both a peripheral and a central nervous system neurotransmitter. [NIH] Neurotransmitter: Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic cleft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic acid, substance P, enkephalins, endorphins, and serotonin. [EU] Neutrophil: A type of white blood cell. [NIH] NHANES: National Health and Nutrition Examination Survey; conducted every 10 years by the National Center for Health Statistics to survey the dietary habits and health of U.S. residents. [NIH] Nicotine: Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. [NIH] Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight 14. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells. [NIH] Nonverbal Communication: Transmission of emotions, ideas, and attitudes between individuals in ways other than the spoken language. [NIH] Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. [NIH]

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Normal Distribution: Continuous frequency distribution of infinite range. Its properties are as follows: 1) continuous, symmetrical distribution with both tails extending to infinity; 2) arithmetic mean, mode, and median identical; and 3) shape completely determined by the mean and standard deviation. [NIH] Nuclear: A test of the structure, blood flow, and function of the kidneys. The doctor injects a mildly radioactive solution into an arm vein and uses x-rays to monitor its progress through the kidneys. [NIH] Nuclei: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nucleic acid: Either of two types of macromolecule (DNA or RNA) formed by polymerization of nucleotides. Nucleic acids are found in all living cells and contain the information (genetic code) for the transfer of genetic information from one generation to the next. [NIH] Nucleus: A body of specialized protoplasm found in nearly all cells and containing the chromosomes. [NIH] Nurse Practitioners: Nurses who are specially trained to assume an expanded role in providing medical care under the supervision of a physician. [NIH] Nursing Care: Care given to patients by nursing service personnel. [NIH] Nutritional Support: The administration of nutrients for assimilation and utilization by a patient by means other than normal eating. It does not include fluid therapy which normalizes body fluids to restore water-electrolyte balance. [NIH] Nutritive Value: An indication of the contribution of a food to the nutrient content of the diet. This value depends on the quantity of a food which is digested and absorbed and the amounts of the essential nutrients (protein, fat, carbohydrate, minerals, vitamins) which it contains. This value can be affected by soil and growing conditions, handling and storage, and processing. [NIH] Obsessive-Compulsive Disorder: An anxiety disorder characterized by recurrent, persistent obsessions or compulsions. Obsessions are the intrusive ideas, thoughts, or images that are experienced as senseless or repugnant. Compulsions are repetitive and seemingly purposeful behavior which the individual generally recognizes as senseless and from which the individual does not derive pleasure although it may provide a release from tension. [NIH] Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases. [NIH] Odour: A volatile emanation that is perceived by the sense of smell. [EU] Oestrogen: A generic term for oestrus-producing steroid compounds; the female sex hormones. In humans, oestrogen is formed in the ovary, possibly the adrenal cortex, the testis, and the foetoplacental unit; it has various functions in both sexes. It is responsible for the development of the female secondary sex characteristics, and during the menstrual cycle it acts on the female genitalia to produce an environment suitable for the fertilization, implantation, and nutrition of the early embryo. Oestrogen is used in oral contraceptives and as a palliative in cancer of the breast after menopause and cancer of the prostate; other uses include the relief of the discomforts of menopause, inhibition of lactation, and treatment of osteoporosis, threatened abortion, and various functional ovarian disorders.

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[EU]

Office Visits: Visits made by patients to health service providers' offices for diagnosis, treatment, and follow-up. [NIH] Olfaction: Function of the olfactory apparatus to perceive and discriminate between the molecules that reach it, in gas form from an external environment, directly or indirectly via the nose. [NIH] Olfactory Bulb: Ovoid body resting on the cribriform plate of the ethmoid bone where the olfactory nerve terminates. The olfactory bulb contains several types of nerve cells including the mitral cells, on whose dendrites the olfactory nerve synapses, forming the olfactory glomeruli. The accessory olfactory bulb, which receives the projection from the vomeronasal organ via the vomeronasal nerve, is also included here. [NIH] Olfactory Nerve: The 1st cranial nerve. The olfactory nerve conveys the sense of smell. It is formed by the axons of olfactory receptor neurons which project from the olfactory epithelium (in the nasal epithelium) to the olfactory bulb. [NIH] Oligomenorrhea: Abnormally infrequent menstruation. [NIH] Oliguria: Clinical manifestation of the urinary system consisting of a decrease in the amount of urine secreted. [NIH] Omega-3 fatty acid: A type of fat obtained in the diet and involved in immunity. [NIH] Omega-6 Fatty Acids: Unsaturated fatty acids required for the growth of mammals. They are constituents of phospholipids and glycerides in cell membranes. [NIH] Oncogene: A gene that normally directs cell growth. If altered, an oncogene can promote or allow the uncontrolled growth of cancer. Alterations can be inherited or caused by an environmental exposure to carcinogens. [NIH] Opacity: Degree of density (area most dense taken for reading). [NIH] Ophthalmic: Pertaining to the eye. [EU] Opsin: A protein formed, together with retinene, by the chemical breakdown of metarhodopsin. [NIH] Optic Chiasm: The X-shaped structure formed by the meeting of the two optic nerves. At the optic chiasm the fibers from the medial part of each retina cross to project to the other side of the brain while the lateral retinal fibers continue on the same side. As a result each half of the brain receives information about the contralateral visual field from both eyes. [NIH]

Optic Nerve: The 2nd cranial nerve. The optic nerve conveys visual information from the retina to the brain. The nerve carries the axons of the retinal ganglion cells which sort at the optic chiasm and continue via the optic tracts to the brain. The largest projection is to the lateral geniculate nuclei; other important targets include the superior colliculi and the suprachiasmatic nuclei. Though known as the second cranial nerve, it is considered part of the central nervous system. [NIH] Optic Nerve Diseases: Conditions which produce injury or dysfunction of the second cranial or optic nerve, which is generally considered a component of the central nervous system. Damage to optic nerve fibers may occur at or near their origin in the retina, at the optic disk, or in the nerve, optic chiasm, optic tract, or lateral geniculate nuclei. Clinical manifestations may include decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect. [NIH] Organelles: Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the mitochondria; the golgi apparatus; endoplasmic reticulum; lysomomes; plastids; and vacuoles. [NIH]

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Orlistat: A lipase inhibitor used for weight loss. Lipase is an enzyme found in the bowel that assists in lipid absorption by the body. Orlistat blocks this enzyme, reducing the amount of fat the body absorbs by about 30 percent. It is known colloquially as a "fat blocker." Because more oily fat is left in the bowel to be excreted, Orlistat can cause an oily anal leakage and fecal incontinence. Orlistat may not be suitable for people with bowel conditions such as irritable bowel syndrome or Crohn's disease. [NIH] Orthostatic: Pertaining to or caused by standing erect. [EU] Osmosis: Tendency of fluids (e.g., water) to move from the less concentrated to the more concentrated side of a semipermeable membrane. [NIH] Osmotic: Pertaining to or of the nature of osmosis (= the passage of pure solvent from a solution of lesser to one of greater solute concentration when the two solutions are separated by a membrane which selectively prevents the passage of solute molecules, but is permeable to the solvent). [EU] Osteoarthritis: A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans. [NIH] Osteoporosis: Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis and age-related (or senile) osteoporosis. [NIH] Outpatient: A patient who is not an inmate of a hospital but receives diagnosis or treatment in a clinic or dispensary connected with the hospital. [NIH] Ovaries: The pair of female reproductive glands in which the ova, or eggs, are formed. The ovaries are located in the pelvis, one on each side of the uterus. [NIH] Ovary: Either of the paired glands in the female that produce the female germ cells and secrete some of the female sex hormones. [NIH] Overweight: An excess of body weight but not necessarily body fat; a body mass index of 25 to 29.9 kg/m2. [NIH] Ovum: A female germ cell extruded from the ovary at ovulation. [NIH] Oxalate: A chemical that combines with calcium in urine to form the most common type of kidney stone (calcium oxalate stone). [NIH] Oxalic Acid: A strong dicarboxylic acid occurring in many plants and vegetables. It is produced in the body by metabolism of glyoxylic acid or ascorbic acid. It is not metabolized but excreted in the urine. It is used as an analytical reagent and general reducing agent. [NIH] Oxidants: Oxidizing agents or electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (oxidation-reduction). In vivo, it appears that phagocyte-generated oxidants function as tumor promoters or cocarcinogens rather than as complete carcinogens perhaps because of the high levels of endogenous antioxidant defenses. It is also thought that oxidative damage in joints may trigger the autoimmune response that characterizes the persistence of the rheumatoid disease process. [NIH]

Oxidation: The act of oxidizing or state of being oxidized. Chemically it consists in the increase of positive charges on an atom or the loss of negative charges. Most biological oxidations are accomplished by the removal of a pair of hydrogen atoms (dehydrogenation) from a molecule. Such oxidations must be accompanied by reduction of an acceptor molecule. Univalent o. indicates loss of one electron; divalent o., the loss of two electrons. [EU]

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Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471). [NIH] Oxidative Phosphorylation: Electron transfer through the cytochrome system liberating free energy which is transformed into high-energy phosphate bonds. [NIH] Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi). [NIH] Oxygen Consumption: The oxygen consumption is determined by calculating the difference between the amount of oxygen inhaled and exhaled. [NIH] Palliative: 1. Affording relief, but not cure. 2. An alleviating medicine. [EU] Pancreas: A mixed exocrine and endocrine gland situated transversely across the posterior abdominal wall in the epigastric and hypochondriac regions. The endocrine portion is comprised of the Islets of Langerhans, while the exocrine portion is a compound acinar gland that secretes digestive enzymes. [NIH] Pancreatic: Having to do with the pancreas. [NIH] Pancreatic cancer: Cancer of the pancreas, a salivary gland of the abdomen. [NIH] Pancreatic Juice: The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum. [NIH] Pancreatic Polypeptide: A 36-amino acid polypeptide with physiological regulatory functions. It is secreted by pancreatic tissue. Plasma pancreatic polypeptide increases after ingestion of food, with age, and in disease states. A lack of pancreatic polypeptide in the islets of Langerhans has been associated with the obese syndrome in rats and mice. [NIH] Pancreatitis: Acute or chronic inflammation of the pancreas, which may be asymptomatic or symptomatic, and which is due to autodigestion of a pancreatic tissue by its own enzymes. It is caused most often by alcoholism or biliary tract disease; less commonly it may be associated with hyperlipaemia, hyperparathyroidism, abdominal trauma (accidental or operative injury), vasculitis, or uraemia. [EU] Panic: A state of extreme acute, intense anxiety and unreasoning fear accompanied by disorganization of personality function. [NIH] Panic Disorder: A type of anxiety disorder characterized by unexpected panic attacks that last minutes or, rarely, hours. Panic attacks begin with intense apprehension, fear or terror and, often, a feeling of impending doom. Symptoms experienced during a panic attack include dyspnea or sensations of being smothered; dizziness, loss of balance or faintness; choking sensations; palpitations or accelerated heart rate; shakiness; sweating; nausea or other form of abdominal distress; depersonalization or derealization; paresthesias; hot flashes or chills; chest discomfort or pain; fear of dying and fear of not being in control of oneself or going crazy. Agoraphobia may also develop. Similar to other anxiety disorders, it may be inherited as an autosomal dominant trait. [NIH] Papilledema: Swelling around the optic disk. [NIH] Paradoxical: Occurring at variance with the normal rule. [EU] Parenteral: Not through the alimentary canal but rather by injection through some other route, as subcutaneous, intramuscular, intraorbital, intracapsular, intraspinal, intrasternal, intravenous, etc. [EU]

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Parity: The number of offspring a female has borne. It is contrasted with gravidity, which refers to the number of pregnancies, regardless of outcome. [NIH] Parkinsonism: A group of neurological disorders characterized by hypokinesia, tremor, and muscular rigidity. [EU] Paroxetine: A serotonin uptake inhibitor that is effective in the treatment of depression. [NIH]

Paroxysmal: Recurring in paroxysms (= spasms or seizures). [EU] Parturition: The act or process of given birth to a child. [EU] Pathogen: Any disease-producing microorganism. [EU] Pathogenesis: The cellular events and reactions that occur in the development of disease. [NIH]

Pathologic: 1. Indicative of or caused by a morbid condition. 2. Pertaining to pathology (= branch of medicine that treats the essential nature of the disease, especially the structural and functional changes in tissues and organs of the body caused by the disease). [EU] Pathologic Processes: The abnormal mechanisms and forms involved in the dysfunctions of tissues and organs. [NIH] Pathologies: The study of abnormality, especially the study of diseases. [NIH] Pathophysiology: Altered functions in an individual or an organ due to disease. [NIH] Patient Compliance: regimen. [NIH]

Voluntary cooperation of the patient in following a prescribed

Patient Education: The teaching or training of patients concerning their own health needs. [NIH]

Patient Selection: Criteria and standards used for the determination of the appropriateness of the inclusion of patients with specific conditions in proposed treatment plans and the criteria used for the inclusion of subjects in various clinical trials and other research protocols. [NIH] Pediatrics: A medical specialty concerned with maintaining health and providing medical care to children from birth to adolescence. [NIH] Pelvic: Pertaining to the pelvis. [EU] Pelvis: The lower part of the abdomen, located between the hip bones. [NIH] Penicillin: An antibiotic drug used to treat infection. [NIH] Penis: The external reproductive organ of males. It is composed of a mass of erectile tissue enclosed in three cylindrical fibrous compartments. Two of the three compartments, the corpus cavernosa, are placed side-by-side along the upper part of the organ. The third compartment below, the corpus spongiosum, houses the urethra. [NIH] Pepsin: An enzyme made in the stomach that breaks down proteins. [NIH] Peptide: Any compound consisting of two or more amino acids, the building blocks of proteins. Peptides are combined to make proteins. [NIH] Peptide Chain Elongation: The process whereby an amino acid is joined through a substituted amide linkage to a chain of peptides. [NIH] Peptide Hydrolases: A subclass of enzymes from the hydrolase class that catalyze the hydrolysis of peptide bonds. Exopeptidases and endopeptidases make up the sub-subclasses for this group. EC 3.4. [NIH] Perception: The ability quickly and accurately to recognize similarities and differences among presented objects, whether these be pairs of words, pairs of number series, or

Dictionary 575

multiple sets of these or other symbols such as geometric figures. [NIH] Percutaneous: Performed through the skin, as injection of radiopacque material in radiological examination, or the removal of tissue for biopsy accomplished by a needle. [EU] Perforation: 1. The act of boring or piercing through a part. 2. A hole made through a part or substance. [EU] Perfusion: Bathing an organ or tissue with a fluid. In regional perfusion, a specific area of the body (usually an arm or a leg) receives high doses of anticancer drugs through a blood vessel. Such a procedure is performed to treat cancer that has not spread. [NIH] Perinatal: Pertaining to or occurring in the period shortly before and after birth; variously defined as beginning with completion of the twentieth to twenty-eighth week of gestation and ending 7 to 28 days after birth. [EU] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Periodontal disease: Disease involving the supporting structures of the teeth (as the gums and periodontal membranes). [NIH] Peripheral blood: Blood circulating throughout the body. [NIH] Peripheral Nervous System: The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors. [NIH] Peripheral Nervous System Diseases: Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves. [NIH] Peripheral Vascular Disease: Disease in the large blood vessels of the arms, legs, and feet. People who have had diabetes for a long time may get this because major blood vessels in their arms, legs, and feet are blocked and these limbs do not receive enough blood. The signs of PVD are aching pains in the arms, legs, and feet (especially when walking) and foot sores that heal slowly. Although people with diabetes cannot always avoid PVD, doctors say they have a better chance of avoiding it if they take good care of their feet, do not smoke, and keep both their blood pressure and diabetes under good control. [NIH] Peritoneal: Having to do with the peritoneum (the tissue that lines the abdominal wall and covers most of the organs in the abdomen). [NIH] Peritoneal Cavity: The space enclosed by the peritoneum. It is divided into two portions, the greater sac and the lesser sac or omental bursa, which lies behind the stomach. The two sacs are connected by the foramen of Winslow, or epiploic foramen. [NIH] Peritoneal Dialysis: Dialysis fluid being introduced into and removed from the peritoneal cavity as either a continuous or an intermittent procedure. [NIH] Peritoneum: Endothelial lining of the abdominal cavity, the parietal peritoneum covering the inside of the abdominal wall and the visceral peritoneum covering the bowel, the mesentery, and certain of the organs. The portion that covers the bowel becomes the serosal layer of the bowel wall. [NIH] Peroral: Performed through or administered through the mouth. [EU] Pesticides: Chemicals used to destroy pests of any sort. The concept includes fungicides (industrial fungicides), insecticides, rodenticides, etc. [NIH] Petroleum: Naturally occurring complex liquid hydrocarbons which, after distillation, yield

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combustible fuels, petrochemicals, and lubricants. [NIH] PH: The symbol relating the hydrogen ion (H+) concentration or activity of a solution to that of a given standard solution. Numerically the pH is approximately equal to the negative logarithm of H+ concentration expressed in molarity. pH 7 is neutral; above it alkalinity increases and below it acidity increases. [EU] Phagocyte: An immune system cell that can surround and kill microorganisms and remove dead cells. Phagocytes include macrophages. [NIH] Pharmaceutic Aids: Substances which are of little or no therapeutic value, but are necessary in the manufacture, compounding, storage, etc., of pharmaceutical preparations or drug dosage forms. They include solvents, diluting agents, and suspending agents, and emulsifying agents. Also, antioxidants; preservatives, pharmaceutical; dyes (coloring agents); flavoring agents; vehicles; excipients; ointment bases. [NIH] Pharmaceutical Preparations: Drugs intended for human or veterinary use, presented in their finished dosage form. Included here are materials used in the preparation and/or formulation of the finished dosage form. [NIH] Pharmacodynamics: The study of the biochemical and physiological effects of drugs and the mechanisms of their actions, including the correlation of actions and effects of drugs with their chemical structure; also, such effects on the actions of a particular drug or drugs. [EU]

Pharmacokinetic: The mathematical analysis of the time courses of absorption, distribution, and elimination of drugs. [NIH] Pharmacologic: Pertaining to pharmacology or to the properties and reactions of drugs. [EU] Pharmacotherapy: A regimen of using appetite suppressant medications to manage obesity by decreasing appetite or increasing the feeling of satiety. These medications decrease appetite by increasing serotonin or catecholamine—two brain chemicals that affect mood and appetite. [NIH] Pharynx: The hollow tube about 5 inches long that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). [NIH] Phenotype: The outward appearance of the individual. It is the product of interactions between genes and between the genotype and the environment. This includes the killer phenotype, characteristic of yeasts. [NIH] Phentermine: A central nervous system stimulant and sympathomimetic with actions and uses similar to those of dextroamphetamine. It has been used most frequently in the treatment of obesity. [NIH] Phenyl: Ingredient used in cold and flu remedies. [NIH] Phenylalanine: An aromatic amino acid that is essential in the animal diet. It is a precursor of melanin, dopamine, noradrenalin, and thyroxine. [NIH] Phenylpropanolamine: A sympathomimetic that acts mainly by causing release of norepinephrine but also has direct agonist activity at some adrenergic receptors. It is most commonly used as a nasal vasoconstrictor and an appetite depressant. [NIH] Phospholipases: A class of enzymes that catalyze the hydrolysis of phosphoglycerides or glycerophosphatidates. EC 3.1.-. [NIH] Phospholipids: Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides; glycerophospholipids) or sphingosine (sphingolipids). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system. [NIH]

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Phosphorus: A non-metallic element that is found in the blood, muscles, nevers, bones, and teeth, and is a component of adenosine triphosphate (ATP; the primary energy source for the body's cells.) [NIH] Phosphorylase: An enzyme of the transferase class that catalyzes the phosphorylysis of a terminal alpha-1,4-glycosidic bond at the non-reducing end of a glycogen molecule, releasing a glucose 1-phosphate residue. Phosphorylase should be qualified by the natural substance acted upon. EC 2.4.1.1. [NIH] Phosphorylated: Attached to a phosphate group. [NIH] Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. [NIH] Photocoagulation: Using a special strong beam of light (laser) to seal off bleeding blood vessels such as in the eye. The laser can also burn away blood vessels that should not have grown in the eye. This is the main treatment for diabetic retinopathy. [NIH] Photoperiod: The time period of daily exposure that an organism receives from daylight or artificial light. It is believed that photoperiodic responses may affect the control of energy balance and thermoregulation. [NIH] Physical Examination: Systematic and thorough inspection of the patient for physical signs of disease or abnormality. [NIH] Physical Fitness: A state of well-being in which performance is optimal, often as a result of physical conditioning which may be prescribed for disease therapy. [NIH] Physical Therapy: The restoration of function and the prevention of disability following disease or injury with the use of light, heat, cold, water, electricity, ultrasound, and exercise. [NIH]

Physiologic: Having to do with the functions of the body. When used in the phrase "physiologic age," it refers to an age assigned by general health, as opposed to calendar age. [NIH]

Physiology: The science that deals with the life processes and functions of organismus, their cells, tissues, and organs. [NIH] Pigmentation: Coloration or discoloration of a part by a pigment. [NIH] Pigments: Any normal or abnormal coloring matter in plants, animals, or micro-organisms. [NIH]

Pilot Projects: Small-scale tests of methods and procedures to be used on a larger scale if the pilot study demonstrates that these methods and procedures can work. [NIH] Pilot study: The initial study examining a new method or treatment. [NIH] Pituitary Gland: A small, unpaired gland situated in the sella turcica tissue. It is connected to the hypothalamus by a short stalk. [NIH] Placenta: A highly vascular fetal organ through which the fetus absorbs oxygen and other nutrients and excretes carbon dioxide and other wastes. It begins to form about the eighth day of gestation when the blastocyst adheres to the decidua. [NIH] Placental tissue: The tissue intervening between fetal blood and maternal blood in the placenta; it acts as a selective membrane regulating the passage of substances from the maternal to the fetal blood. [NIH] Plants: Multicellular, eukaryotic life forms of the kingdom Plantae. They are characterized by a mainly photosynthetic mode of nutrition; essentially unlimited growth at localized regions of cell divisions (meristems); cellulose within cells providing rigidity; the absence of organs of locomotion; absense of nervous and sensory systems; and an alteration of haploid

578 Obesity

and diploid generations. [NIH] Plaque: A clear zone in a bacterial culture grown on an agar plate caused by localized destruction of bacterial cells by a bacteriophage. The concentration of infective virus in a fluid can be estimated by applying the fluid to a culture and counting the number of. [NIH] Plasma: The clear, yellowish, fluid part of the blood that carries the blood cells. The proteins that form blood clots are in plasma. [NIH] Plasma cells: A type of white blood cell that produces antibodies. [NIH] Plasma protein: One of the hundreds of different proteins present in blood plasma, including carrier proteins ( such albumin, transferrin, and haptoglobin), fibrinogen and other coagulation factors, complement components, immunoglobulins, enzyme inhibitors, precursors of substances such as angiotension and bradykinin, and many other types of proteins. [EU] Plasmin: A product of the lysis of plasminogen (profibrinolysin) by plasminogen activators. It is composed of two polypeptide chains, light (B) and heavy (A), with a molecular weight of 75,000. It is the major proteolytic enzyme involved in blood clot retraction or the lysis of fibrin and quickly inactivated by antiplasmins. EC 3.4.21.7. [NIH] Plasminogen: Precursor of fibrinolysin (plasmin). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent. [NIH] Plasminogen Activator Inhibitor 1: A member of the serpin family of proteins. It inhibits both the tissue-type and urokinase-type plasminogen activators. [NIH] Plasminogen Activators: A heterogeneous group of proteolytic enzymes that convert plasminogen to plasmin. They are concentrated in the lysosomes of most cells and in the vascular endothelium, particularly in the vessels of the microcirculation. EC 3.4.21.-. [NIH] Plastic surgeon: A surgeon who specializes in reducing scarring or disfigurement that may occur as a result of accidents, birth defects, or treatment for diseases. [NIH] Platelet Activation: A series of progressive, overlapping events triggered by exposure of the platelets to subendothelial tissue. These events include shape change, adhesiveness, aggregation, and release reactions. When carried through to completion, these events lead to the formation of a stable hemostatic plug. [NIH] Platelets: A type of blood cell that helps prevent bleeding by causing blood clots to form. Also called thrombocytes. [NIH] Platinum: Platinum. A heavy, soft, whitish metal, resembling tin, atomic number 78, atomic weight 195.09, symbol Pt. (From Dorland, 28th ed) It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as "alutiae". [NIH]

Pneumonia: Inflammation of the lungs. [NIH] Poisoning: A condition or physical state produced by the ingestion, injection or inhalation of, or exposure to a deleterious agent. [NIH] Policy Making: The decision process by which individuals, groups or institutions establish policies pertaining to plans, programs or procedures. [NIH] Pollen: The male fertilizing element of flowering plants analogous to sperm in animals. It is released from the anthers as yellow dust, to be carried by insect or other vectors, including wind, to the ovary (stigma) of other flowers to produce the embryo enclosed by the seed. The pollens of many plants are allergenic. [NIH]

Dictionary 579

Polycystic: An inherited disorder characterized by many grape-like clusters of fluid-filled cysts that make both kidneys larger over time. These cysts take over and destroy working kidney tissue. PKD may cause chronic renal failure and end-stage renal disease. [NIH] Polycystic Ovary Syndrome: Clinical symptom complex characterized by oligomenorrhea or amenorrhea, anovulation, and regularly associated with bilateral polycystic ovaries. [NIH] Polymers: Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., polypeptides, proteins, plastics). [NIH] Polymorphic: Occurring in several or many forms; appearing in different forms at different stages of development. [EU] Polymorphism: The occurrence together of two or more distinct forms in the same population. [NIH] Polyposis: The development of numerous polyps (growths that protrude from a mucous membrane). [NIH] Polysaccharide: A type of carbohydrate. It contains sugar molecules that are linked together chemically. [NIH] Polyunsaturated fat: An unsaturated fat found in greatest amounts in foods derived from plants, including safflower, sunflower, corn, and soybean oils. [NIH] Porphyrins: A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin. [NIH] Posterior: Situated in back of, or in the back part of, or affecting the back or dorsal surface of the body. In lower animals, it refers to the caudal end of the body. [EU] Postmenopausal: Refers to the time after menopause. Menopause is the time in a woman's life when menstrual periods stop permanently; also called "change of life." [NIH] Postnatal: Occurring after birth, with reference to the newborn. [EU] Postoperative: After surgery. [NIH] Postoperative Complications: Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery. [NIH] Postprandial: Occurring after dinner, or after a meal; postcibal. [EU] Postsynaptic: Nerve potential generated by an inhibitory hyperpolarizing stimulation. [NIH] Post-translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Potassium: An element that is in the alkali group of metals. It has an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte and it plays a significant role in the regulation of fluid volume and maintenance of the water-electrolyte balance. [NIH] Potentiates: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiating: A degree of synergism which causes the exposure of the organism to a harmful substance to worsen a disease already contracted. [NIH] Potentiation: An overall effect of two drugs taken together which is greater than the sum of

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the effects of each drug taken alone. [NIH] Practicability: A non-standard characteristic of an analytical procedure. It is dependent on the scope of the method and is determined by requirements such as sample throughout and costs. [NIH] Practice Guidelines: Directions or principles presenting current or future rules of policy for the health care practitioner to assist him in patient care decisions regarding diagnosis, therapy, or related clinical circumstances. The guidelines may be developed by government agencies at any level, institutions, professional societies, governing boards, or by the convening of expert panels. The guidelines form a basis for the evaluation of all aspects of health care and delivery. [NIH] Precursor: Something that precedes. In biological processes, a substance from which another, usually more active or mature substance is formed. In clinical medicine, a sign or symptom that heralds another. [EU] Predisposition: A latent susceptibility to disease which may be activated under certain conditions, as by stress. [EU] Pre-Eclampsia: Development of hypertension with proteinuria, edema, or both, due to pregnancy or the influence of a recent pregnancy. It occurs after the 20th week of gestation, but it may develop before this time in the presence of trophoblastic disease. [NIH] Pregnancy Complications: The co-occurrence of pregnancy and a disease. The disease may precede or follow conception and it may or may not have a deleterious effect on the pregnant woman or fetus. [NIH] Pregnancy Outcome: Results of conception and ensuing pregnancy, including live birth, stillbirth, spontaneous abortion, induced abortion. The outcome may follow natural or artificial insemination or any of the various reproduction techniques, such as embryo transfer or fertilization in vitro. [NIH] Prejudice: A preconceived judgment made without adequate evidence and not easily alterable by presentation of contrary evidence. [NIH] Preload: The tension in the heart muscle at the end of diastole (before the contraction). [EU] Premenopausal: Refers to the time before menopause. Menopause is the time of life when a women's menstrual periods stop permanently; also called "change of life." [NIH] Preoptic Area: Region of hypothalamus between the anterior commissure and optic chiasm. [NIH]

Presynaptic: Situated proximal to a synapse, or occurring before the synapse is crossed. [EU] Presynaptic Terminals: The distal terminations of axons which are specialized for the release of neurotransmitters. Also included are varicosities along the course of axons which have similar specializations and also release transmitters. Presynaptic terminals in both the central and peripheral nervous systems are included. [NIH] Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from incidence, which refers to the number of new cases in the population at a given time. [NIH] Primary Prevention: Prevention of disease or mental disorders in susceptible individuals or populations through promotion of health, including mental health, and specific protection, as in immunization, as distinguished from the prevention of complications or after-effects of existing disease. [NIH] Probe: An instrument used in exploring cavities, or in the detection and dilatation of strictures, or in demonstrating the potency of channels; an elongated instrument for exploring or sounding body cavities. [NIH]

Dictionary 581

Prodrug: A substance that gives rise to a pharmacologically active metabolite, although not itself active (i. e. an inactive precursor). [NIH] Progeny: The offspring produced in any generation. [NIH] Progesterone: Pregn-4-ene-3,20-dione. The principal progestational hormone of the body, secreted by the corpus luteum, adrenal cortex, and placenta. Its chief function is to prepare the uterus for the reception and development of the fertilized ovum. It acts as an antiovulatory agent when administered on days 5-25 of the menstrual cycle. [NIH] Progression: Increase in the size of a tumor or spread of cancer in the body. [NIH] Progressive: Advancing; going forward; going from bad to worse; increasing in scope or severity. [EU] Progressive disease: Cancer that is increasing in scope or severity. [NIH] Projection: A defense mechanism, operating unconsciously, whereby that which is emotionally unacceptable in the self is rejected and attributed (projected) to others. [NIH] Prolactin: Pituitary lactogenic hormone. A polypeptide hormone with a molecular weight of about 23,000. It is essential in the induction of lactation in mammals at parturition and is synergistic with estrogen. The hormone also brings about the release of progesterone from lutein cells, which renders the uterine mucosa suited for the embedding of the ovum should fertilization occur. [NIH] Proline: A non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. [NIH] Promoter: A chemical substance that increases the activity of a carcinogenic process. [NIH] Prone: Having the front portion of the body downwards. [NIH] Pro-Opiomelanocortin: A precursor protein, MW 30,000, synthesized mainly in the anterior pituitary gland but also found in the hypothalamus, brain, and several peripheral tissues. It incorporates the amino acid sequences of ACTH and beta-lipotropin. These two hormones, in turn, contain the biologically active peptides MSH, corticotropin-like intermediate lobe peptide, alpha-lipotropin, endorphins, and methionine enkephalin. [NIH] Prophase: The first phase of cell division, in which the chromosomes become visible, the nucleus starts to lose its identity, the spindle appears, and the centrioles migrate toward opposite poles. [NIH] Prophylaxis: An attempt to prevent disease. [NIH] Proportional: Being in proportion : corresponding in size, degree, or intensity, having the same or a constant ratio; of, relating to, or used in determining proportions. [EU] Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol is used in the treatment or prevention of many disorders including acute myocardial infarction, arrhythmias, angina pectoris, hypertension, hypertensive emergencies, hyperthyroidism, migraine, pheochromocytoma, menopause, and anxiety. [NIH] Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group. [NIH] Prospective study: An epidemiologic study in which a group of individuals (a cohort), all free of a particular disease and varying in their exposure to a possible risk factor, is followed over a specific amount of time to determine the incidence rates of the disease in the exposed and unexposed groups. [NIH] Prostaglandin: Any of a group of components derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway that are extremely potent

582 Obesity

mediators of a diverse group of physiologic processes. The abbreviation for prostaglandin is PG; specific compounds are designated by adding one of the letters A through I to indicate the type of substituents found on the hydrocarbon skeleton and a subscript (1, 2 or 3) to indicate the number of double bonds in the hydrocarbon skeleton e.g., PGE2. The predominant naturally occurring prostaglandins all have two double bonds and are synthesized from arachidonic acid (5,8,11,14-eicosatetraenoic acid) by the pathway shown in the illustration. The 1 series and 3 series are produced by the same pathway with fatty acids having one fewer double bond (8,11,14-eicosatrienoic acid or one more double bond (5,8,11,14,17-eicosapentaenoic acid) than arachidonic acid. The subscript a or ß indicates the configuration at C-9 (a denotes a substituent below the plane of the ring, ß, above the plane). The naturally occurring PGF's have the a configuration, e.g., PGF2a. All of the prostaglandins act by binding to specific cell-surface receptors causing an increase in the level of the intracellular second messenger cyclic AMP (and in some cases cyclic GMP also). The effect produced by the cyclic AMP increase depends on the specific cell type. In some cases there is also a positive feedback effect. Increased cyclic AMP increases prostaglandin synthesis leading to further increases in cyclic AMP. [EU] Prostaglandins A: (13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE. PGA(1) and PGA(2) as well as their 19hydroxy derivatives are found in many organs and tissues. [NIH] Prostate: A gland in males that surrounds the neck of the bladder and the urethra. It secretes a substance that liquifies coagulated semen. It is situated in the pelvic cavity behind the lower part of the pubic symphysis, above the deep layer of the triangular ligament, and rests upon the rectum. [NIH] Prostatic Hyperplasia: Enlargement or overgrowth of the prostate gland as a result of an increase in the number of its constituent cells. [NIH] Protease: Proteinase (= any enzyme that catalyses the splitting of interior peptide bonds in a protein). [EU] Protein C: A vitamin-K dependent zymogen present in the blood, which, upon activation by thrombin and thrombomodulin exerts anticoagulant properties by inactivating factors Va and VIIIa at the rate-limiting steps of thrombin formation. [NIH] Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. Quaternary protein structure describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain). [NIH] Protein S: The vitamin K-dependent cofactor of activated protein C. Together with protein C, it inhibits the action of factors VIIIa and Va. A deficiency in protein S can lead to recurrent venous and arterial thrombosis. [NIH] Proteins: Polymers of amino acids linked by peptide bonds. The specific sequence of amino acids determines the shape and function of the protein. [NIH] Proteinuria: The presence of protein in the urine, indicating that the kidneys are not working properly. [NIH] Proteoglycan: A molecule that contains both protein and glycosaminoglycans, which are a type of polysaccharide. Proteoglycans are found in cartilage and other connective tissues. [NIH]

Proteolytic: 1. Pertaining to, characterized by, or promoting proteolysis. 2. An enzyme that promotes proteolysis (= the splitting of proteins by hydrolysis of the peptide bonds with

Dictionary 583

formation of smaller polypeptides). [EU] Prothrombin: A plasma protein that is the inactive precursor of thrombin. It is converted to thrombin by a prothrombin activator complex consisting of factor Xa, factor V, phospholipid, and calcium ions. Deficiency of prothrombin leads to hypoprothrombinemia. [NIH]

Protocol: The detailed plan for a clinical trial that states the trial's rationale, purpose, drug or vaccine dosages, length of study, routes of administration, who may participate, and other aspects of trial design. [NIH] Protons: Stable elementary particles having the smallest known positive charge, found in the nuclei of all elements. The proton mass is less than that of a neutron. A proton is the nucleus of the light hydrogen atom, i.e., the hydrogen ion. [NIH] Protozoa: A subkingdom consisting of unicellular organisms that are the simplest in the animal kingdom. Most are free living. They range in size from submicroscopic to macroscopic. Protozoa are divided into seven phyla: Sarcomastigophora, Labyrinthomorpha, Apicomplexa, Microspora, Ascetospora, Myxozoa, and Ciliophora. [NIH] Proximal: Nearest; closer to any point of reference; opposed to distal. [EU] Pruritic: Pertaining to or characterized by pruritus. [EU] Pseudotumor Cerebri: A condition marked by raised intracranial pressure and characterized clinically by headaches; nausea; papilledema, peripheral constriction of the visual fields, transient visual obscurations, and pulsatile tinnitus. Obesity is frequently associated with this condition, which primarily affects women between 20 and 44 years of age. Chronic papilledema may lead to optic nerve injury (optic nerve diseases) and visual loss (blindness). [NIH] Psychiatric: Pertaining to or within the purview of psychiatry. [EU] Psychiatry: The medical science that deals with the origin, diagnosis, prevention, and treatment of mental disorders. [NIH] Psychic: Pertaining to the psyche or to the mind; mental. [EU] Psychoactive: Those drugs which alter sensation, mood, consciousness or other psychological or behavioral functions. [NIH] Psychogenic: Produced or caused by psychic or mental factors rather than organic factors. [EU]

Psychology: The science dealing with the study of mental processes and behavior in man and animals. [NIH] Psychosis: A mental disorder characterized by gross impairment in reality testing as evidenced by delusions, hallucinations, markedly incoherent speech, or disorganized and agitated behaviour without apparent awareness on the part of the patient of the incomprehensibility of his behaviour; the term is also used in a more general sense to refer to mental disorders in which mental functioning is sufficiently impaired as to interfere grossly with the patient's capacity to meet the ordinary demands of life. Historically, the term has been applied to many conditions, e.g. manic-depressive psychosis, that were first described in psychotic patients, although many patients with the disorder are not judged psychotic. [EU] Psychotherapy: A generic term for the treatment of mental illness or emotional disturbances primarily by verbal or nonverbal communication. [NIH] Psychotomimetic: Psychosis miming. [NIH] Psyllium: Dried, ripe seeds of Plantago psyllium, P. indica, and P. ovata (Plantaginaceae). Plantain seeds swell in water and are used as demulcents and bulk laxatives. [NIH]

584 Obesity

Puberty: The period during which the secondary sex characteristics begin to develop and the capability of sexual reproduction is attained. [EU] Public Health: Branch of medicine concerned with the prevention and control of disease and disability, and the promotion of physical and mental health of the population on the international, national, state, or municipal level. [NIH] Public Policy: A course or method of action selected, usually by a government, from among alternatives to guide and determine present and future decisions. [NIH] Pulmonary: Relating to the lungs. [NIH] Pulmonary Alveoli: Small polyhedral outpouchings along the walls of the alveolar sacs, alveolar ducts and terminal bronchioles through the walls of which gas exchange between alveolar air and pulmonary capillary blood takes place. [NIH] Pulmonary Artery: The short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs. [NIH] Pulmonary Edema: An accumulation of an excessive amount of watery fluid in the lungs, may be caused by acute exposure to dangerous concentrations of irritant gasses. [NIH] Pulmonary Embolism: Embolism in the pulmonary artery or one of its branches. [NIH] Pulmonary Emphysema: Condition of the lungs characterized by increase beyond normal in the size of air spaces distal to the terminal bronchioles, either from dilatation of the alveoli or from destruction of their walls. [NIH] Pulmonary hypertension: Abnormally high blood pressure in the arteries of the lungs. [NIH] Pulse: The rhythmical expansion and contraction of an artery produced by waves of pressure caused by the ejection of blood from the left ventricle of the heart as it contracts. [NIH]

Punishment: The application of an unpleasant stimulus or penalty for the purpose of eliminating or correcting undesirable behavior. [NIH] Pupil: The aperture in the iris through which light passes. [NIH] Purulent: Consisting of or containing pus; associated with the formation of or caused by pus. [EU] Pyloric Sphincter: The muscle between the stomach and the small intestine. [NIH] Pyloroplasty: An operation to widen the opening between the stomach and the small intestine. This allows stomach contents to pass more freely from the stomach. [NIH] Pylorus: The opening in a vertebrate from the stomach into the intestine. [EU] Pyridoxal: 3-Hydroxy-5-(hydroxymethyl)-2-methyl-4- pyridinecarboxaldehyde. [NIH] Pyridoxal Phosphate: 3-Hydroxy-2-methyl-5-((phosphonooxy)methyl)-4pyridinecarboxaldehyde. An enzyme co-factor vitamin. [NIH] Quality of Life: A generic concept reflecting concern with the modification and enhancement of life attributes, e.g., physical, political, moral and social environment. [NIH] Quercetin: Aglucon of quercetrin, rutin, and other glycosides. It is widely distributed in the plant kingdom, especially in rinds and barks, clover blossoms, and ragweed pollen. [NIH] Race: A population within a species which exhibits general similarities within itself, but is both discontinuous and distinct from other populations of that species, though not sufficiently so as to achieve the status of a taxon. [NIH] Racemic: Optically inactive but resolvable in the way of all racemic compounds. [NIH] Radiation:

Emission or propagation of electromagnetic energy (waves/rays), or the

Dictionary 585

waves/rays themselves; a stream of electromagnetic particles (electrons, neutrons, protons, alpha particles) or a mixture of these. The most common source is the sun. [NIH] Radioactive: Giving off radiation. [NIH] Radiological: Pertaining to radiodiagnostic and radiotherapeutic procedures, and interventional radiology or other planning and guiding medical radiology. [NIH] Radiology: A specialty concerned with the use of x-ray and other forms of radiant energy in the diagnosis and treatment of disease. [NIH] Radiotherapy: The use of ionizing radiation to treat malignant neoplasms and other benign conditions. The most common forms of ionizing radiation used as therapy are x-rays, gamma rays, and electrons. A special form of radiotherapy, targeted radiotherapy, links a cytotoxic radionuclide to a molecule that targets the tumor. When this molecule is an antibody or other immunologic molecule, the technique is called radioimmunotherapy. [NIH] Raloxifene: A second generation selective estrogen receptor modulator (SERM) used to prevent osteoporosis in postmenopausal women. It has estrogen agonist effects on bone and cholesterol metabolism but behaves as a complete estrogen antagonist on mammary gland and uterine tissue. [NIH] Randomized: Describes an experiment or clinical trial in which animal or human subjects are assigned by chance to separate groups that compare different treatments. [NIH] Randomized clinical trial: A study in which the participants are assigned by chance to separate groups that compare different treatments; neither the researchers nor the participants can choose which group. Using chance to assign people to groups means that the groups will be similar and that the treatments they receive can be compared objectively. At the time of the trial, it is not known which treatment is best. It is the patient's choice to be in a randomized trial. [NIH] Receptor: A molecule inside or on the surface of a cell that binds to a specific substance and causes a specific physiologic effect in the cell. [NIH] Receptors, Serotonin: Cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. [NIH] Recombinant: A cell or an individual with a new combination of genes not found together in either parent; usually applied to linked genes. [EU] Recombination: The formation of new combinations of genes as a result of segregation in crosses between genetically different parents; also the rearrangement of linked genes due to crossing-over. [NIH] Rectum: The last 8 to 10 inches of the large intestine. [NIH] Recurrence: The return of a sign, symptom, or disease after a remission. [NIH] Red blood cells: RBCs. Cells that carry oxygen to all parts of the body. Also called erythrocytes. [NIH] Red Nucleus: A pinkish-yellow portion of the midbrain situated in the rostral mesencephalic tegmentum. It receives a large projection from the contralateral half of the cerebellum via the superior cerebellar peduncle and a projection from the ipsilateral motor cortex. [NIH] Reductase: Enzyme converting testosterone to dihydrotestosterone. [NIH] Refer: To send or direct for treatment, aid, information, de decision. [NIH] Reflux: The term used when liquid backs up into the esophagus from the stomach. [NIH] Refraction: A test to determine the best eyeglasses or contact lenses to correct a refractive

586 Obesity

error (myopia, hyperopia, or astigmatism). [NIH] Regeneration: The natural renewal of a structure, as of a lost tissue or part. [EU] Regimen: A treatment plan that specifies the dosage, the schedule, and the duration of treatment. [NIH] Regression Analysis: Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see linear models) the relationship is constrained to be a straight line and least-squares analysis is used to determine the best fit. In logistic regression (see logistic models) the dependent variable is qualitative rather than continuously variable and likelihood functions are used to find the best relationship. In multiple regression the dependent variable is considered to depend on more than a single independent variable. [NIH]

Regurgitation: A backward flowing, as the casting up of undigested food, or the backward flowing of blood into the heart, or between the chambers of the heart when a valve is incompetent. [EU] Relapse: The return of signs and symptoms of cancer after a period of improvement. [NIH] Relative risk: The ratio of the incidence rate of a disease among individuals exposed to a specific risk factor to the incidence rate among unexposed individuals; synonymous with risk ratio. Alternatively, the ratio of the cumulative incidence rate in the exposed to the cumulative incidence rate in the unexposed (cumulative incidence ratio). The term relative risk has also been used synonymously with odds ratio. This is because the odds ratio and relative risk approach each other if the disease is rare ( 5 percent of population) and the number of subjects is large. [NIH] Remission: A decrease in or disappearance of signs and symptoms of cancer. In partial remission, some, but not all, signs and symptoms of cancer have disappeared. In complete remission, all signs and symptoms of cancer have disappeared, although there still may be cancer in the body. [NIH] Renal failure: Progressive renal insufficiency and uremia, due to irreversible and progressive renal glomerular tubular or interstitial disease. [NIH] Renin: An enzyme which is secreted by the kidney and is formed from prorenin in plasma and kidney. The enzyme cleaves the Leu-Leu bond in angiotensinogen to generate angiotensin I. EC 3.4.23.15. (Formerly EC 3.4.99.19). [NIH] Renin-Angiotensin System: A system consisting of renin, angiotensin-converting enzyme, and angiotensin II. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming angiotensin I. The converting enzyme contained in the lung acts on angiotensin I in the plasma converting it to angiotensin II, the most powerful directly pressor substance known. It causes contraction of the arteriolar smooth muscle and has other indirect actions mediated through the adrenal cortex. [NIH] Reproduction Techniques: Methods pertaining to the generation of new individuals. [NIH] Reproductive cells: Egg and sperm cells. Each mature reproductive cell carries a single set of 23 chromosomes. [NIH] Resection: Removal of tissue or part or all of an organ by surgery. [NIH] Resolving: The ability of the eye or of a lens to make small objects that are close together, separately visible; thus revealing the structure of an object. [NIH] Respiration: The act of breathing with the lungs, consisting of inspiration, or the taking into the lungs of the ambient air, and of expiration, or the expelling of the modified air which contains more carbon dioxide than the air taken in (Blakiston's Gould Medical Dictionary,

Dictionary 587

4th ed.). This does not include tissue respiration (= oxygen consumption) or cell respiration (= cell respiration). [NIH] Resting metabolic rate: RMR accounts for 65 to 75 percent of daily energy expenditure and represents the minimum energy needed to maintain all physiological cell functions in the resting state. The principal determinant of RMR is lean body mass (LBM). Obese subjects have a higher RMR in absolute terms than lean individuals, an equivalent RMR when corrected for LBM and per unit surface area, and a lower RMR when expressed per kilogram of body weight. Obese persons require more energy for any given activity because of a larger mass, but they tend to be more sedentary than lean subjects. [NIH] Restoration: Broad term applied to any inlay, crown, bridge or complete denture which restores or replaces loss of teeth or oral tissues. [NIH] Reticulata: Part of substantia nigra. [NIH] Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the optic nerve and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the choroid and the inner surface with the vitreous body. The outer-most layer is pigmented, whereas the inner nine layers are transparent. [NIH] Retinal: 1. Pertaining to the retina. 2. The aldehyde of retinol, derived by the oxidative enzymatic splitting of absorbed dietary carotene, and having vitamin A activity. In the retina, retinal combines with opsins to form visual pigments. One isomer, 11-cis retinal combines with opsin in the rods (scotopsin) to form rhodopsin, or visual purple. Another, all-trans retinal (trans-r.); visual yellow; xanthopsin) results from the bleaching of rhodopsin by light, in which the 11-cis form is converted to the all-trans form. Retinal also combines with opsins in the cones (photopsins) to form the three pigments responsible for colour vision. Called also retinal, and retinene1. [EU] Retinoblastoma: An eye cancer that most often occurs in children younger than 5 years. It occurs in hereditary and nonhereditary (sporadic) forms. [NIH] Retinol: Vitamin A. It is essential for proper vision and healthy skin and mucous membranes. Retinol is being studied for cancer prevention; it belongs to the family of drugs called retinoids. [NIH] Retinopathy: 1. Retinitis (= inflammation of the retina). 2. Retinosis (= degenerative, noninflammatory condition of the retina). [EU] Retrospective: Looking back at events that have already taken place. [NIH] Retroviral vector: RNA from a virus that is used to insert genetic material into cells. [NIH] Rheumatism: A group of disorders marked by inflammation or pain in the connective tissue structures of the body. These structures include bone, cartilage, and fat. [NIH] Rheumatoid: Resembling rheumatism. [EU] Rheumatoid arthritis: A form of arthritis, the cause of which is unknown, although infection, hypersensitivity, hormone imbalance and psychologic stress have been suggested as possible causes. [NIH] Rhinitis: Inflammation of the mucous membrane of the nose. [NIH] Rhodopsin: A photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinal, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. [NIH] Ribose: A pentose active in biological systems usually in its D-form. [NIH] Rigidity: Stiffness or inflexibility, chiefly that which is abnormal or morbid; rigor. [EU]

588 Obesity

Risk factor: A habit, trait, condition, or genetic alteration that increases a person's chance of developing a disease. [NIH] Rod: A reception for vision, located in the retina. [NIH] Rodenticides: rodents. [NIH]

Substances used to destroy or inhibit the action of rats, mice, or other

Rosiglitazone: A drug taken to help reduce the amount of sugar in the blood. Rosiglitazone helps make insulin more effective and improves regulation of blood sugar. It belongs to the family of drugs called thiazolidinediones. [NIH] Rural Population: The inhabitants of rural areas or of small towns classified as rural. [NIH] Rutin: 3-((6-O-(6-Deoxy-alpha-L-mannopyranosyl)-beta-D-glucopyranosyl)oxy)-2-(3,4dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one. Found in many plants, including buckwheat, tobacco, forsythia, hydrangea, pansies, etc. It has been used therapeutically to decrease capillary fragility. [NIH] Sagittal: The line of direction passing through the body from back to front, or any vertical plane parallel to the medial plane of the body and inclusive of that plane; often restricted to the medial plane, the plane of the sagittal suture. [NIH] Salicylic: A tuberculosis drug. [NIH] Salivary: The duct that convey saliva to the mouth. [NIH] Salivary glands: Glands in the mouth that produce saliva. [NIH] Sapogenins: The aglucon moiety of a saponin molecule. It may be triterpenoid or steroid, usually spirostan, in nature. [NIH] Saponin: A substance found in soybeans and many other plants. Saponins may help lower cholesterol and may have anticancer effects. [NIH] Satiation: Full gratification of a need or desire followed by a state of relative insensitivity to that particular need or desire. [NIH] Saturated fat: A type of fat found in greatest amounts in foods from animals, such as fatty cuts of meat, poultry with the skin, whole-milk dairy products, lard, and in some vegetable oils, including coconut, palm kernel, and palm oils. Saturated fat raises blood cholesterol more than anything else eaten. On a Step I Diet, no more than 8 to 10 percent of total calories should come from saturated fat, and in the Step II Diet, less than 7 percent of the day's total calories should come from saturated fat. [NIH] Schizoid: Having qualities resembling those found in greater degree in schizophrenics; a person of schizoid personality. [NIH] Schizophrenia: A mental disorder characterized by a special type of disintegration of the personality. [NIH] Schizotypal Personality Disorder: A personality disorder in which there are oddities of thought (magical thinking, paranoid ideation, suspiciousness), perception (illusions, depersonalization), speech (digressive, vague, overelaborate), and behavior (inappropriate affect in social interactions, frequently social isolation) that are not severe enough to characterize schizophrenia. [NIH] Schwannoma: A tumor of the peripheral nervous system that begins in the nerve sheath (protective covering). It is almost always benign, but rare malignant schwannomas have been reported. [NIH] Sclerosis: A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve. [NIH] Screening: Checking for disease when there are no symptoms. [NIH]

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Secondary tumor: Cancer that has spread from the organ in which it first appeared to another organ. For example, breast cancer cells may spread (metastasize) to the lungs and cause the growth of a new tumor. When this happens, the disease is called metastatic breast cancer, and the tumor in the lungs is called a secondary tumor. Also called secondary cancer. [NIH] Secretin: A hormone made in the duodenum. Causes the stomach to make pepsin, the liver to make bile, and the pancreas to make a digestive juice. [NIH] Secretion: 1. The process of elaborating a specific product as a result of the activity of a gland; this activity may range from separating a specific substance of the blood to the elaboration of a new chemical substance. 2. Any substance produced by secretion. [EU] Secretory: Secreting; relating to or influencing secretion or the secretions. [NIH] Sedentary: 1. Sitting habitually; of inactive habits. 2. Pertaining to a sitting posture. [EU] Seizures: Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as epilepsy or "seizure disorder." [NIH] Selective estrogen receptor modulator: SERM. A drug that acts like estrogen on some tissues, but blocks the effect of estrogen on other tissues. Tamoxifen and raloxifene are SERMs. [NIH] Self Care: Performance of activities or tasks traditionally performed by professional health care providers. The concept includes care of oneself or one's family and friends. [NIH] Self-Help Groups: Organizations which provide an environment encouraging social interactions through group activities or individual relationships especially for the purpose of rehabilitating or supporting patients, individuals with common health problems, or the elderly. They include therapeutic social clubs. [NIH] Semen: The thick, yellowish-white, viscid fluid secretion of male reproductive organs discharged upon ejaculation. In addition to reproductive organ secretions, it contains spermatozoa and their nutrient plasma. [NIH] Seminal vesicles: Glands that help produce semen. [NIH] Seminiferous tubule: Tube used to transport sperm made in the testes. [NIH] Semisynthetic: Produced by chemical manipulation of naturally occurring substances. [EU] Senile: Relating or belonging to old age; characteristic of old age; resulting from infirmity of old age. [NIH] Sepsis: The presence of bacteria in the bloodstream. [NIH] Septal: An abscess occurring at the root of the tooth on the proximal surface. [NIH] Septal Nuclei: Neural nuclei situated in the septal region. They have afferent and cholinergic efferent connections with a variety of forebrain and brainstem areas including the hippocampus, the lateral hypothalamus, the tegmentum, and the amygdala. Included are the dorsal, lateral, medial, and triangular septal nuclei, septofimbrial nucleus, nucleus of diagonal band, nucleus of anterior commissure, and the nucleus of stria terminalis. [NIH] Sequence Homology: The degree of similarity between sequences. Studies of amino acid and nucleotide sequences provide useful information about the genetic relatedness of certain species. [NIH] Sequential treatment: One treatment after the other. [NIH] Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines,

590 Obesity

pyrimidines, and other amino acids. [NIH] Serine Endopeptidases: Any member of the group of endopeptidases containing at the active site a serine residue involved in catalysis. EC 3.4.21. [NIH] Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-tryptophan. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (receptors, serotonin) explain the broad physiological actions and distribution of this biochemical mediator. [NIH] Sertraline: A selective serotonin uptake inhibitor that is used in the treatment of depression. [NIH]

Serum: The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed. [NIH] Sex Characteristics: Those characteristics that distinguish one sex from the other. The primary sex characteristics are the ovaries and testes and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction. [NIH] Sex Determination: female or male. [NIH]

The biological characteristics which distinguish human beings as

Shivering: Involuntary contraction or twitching of the muscles. It is a physiologic method of heat production in man and other mammals. [NIH] Shock: The general bodily disturbance following a severe injury; an emotional or moral upset occasioned by some disturbing or unexpected experience; disruption of the circulation, which can upset all body functions: sometimes referred to as circulatory shock. [NIH]

Sibutramine: A drug used for the management of obesity that helps reduce food intake and is indicated for weight loss and maintenance of weight loss when used in conjunction with a reduced-calorie diet. It works to suppress the appetite primarily by inhibiting the reuptake of the neurotransmitters norepinephrine and serotonin. Side effects include dry mouth, headache, constipation, insomnia, and a slight increase in average blood pressure. In some patients it causes a higher blood pressure increase. [NIH] Side effect: A consequence other than the one(s) for which an agent or measure is used, as the adverse effects produced by a drug, especially on a tissue or organ system other than the one sought to be benefited by its administration. [EU] Signal Transduction: The intercellular or intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GABA-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptormediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway. [NIH] Signs and Symptoms: Clinical manifestations that can be either objective when observed by

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a physician, or subjective when perceived by the patient. [NIH] Skeletal: Having to do with the skeleton (boney part of the body). [NIH] Skeleton: The framework that supports the soft tissues of vertebrate animals and protects many of their internal organs. The skeletons of vertebrates are made of bone and/or cartilage. [NIH] Skull: The skeleton of the head including the bones of the face and the bones enclosing the brain. [NIH] Sleep apnea: A serious, potentially life-threatening breathing disorder characterized by repeated cessation of breathing due to either collapse of the upper airway during sleep or absence of respiratory effort. [NIH] Small intestine: The part of the digestive tract that is located between the stomach and the large intestine. [NIH] Smoking Cessation: Discontinuation of the habit of smoking, the inhaling and exhaling of tobacco smoke. [NIH] Smooth muscle: Muscle that performs automatic tasks, such as constricting blood vessels. [NIH]

Social Class: A stratum of people with similar position and prestige; includes social stratification. Social class is measured by criteria such as education, occupation, and income. [NIH]

Social Environment: The aggregate of social and cultural institutions, forms, patterns, and processes that influence the life of an individual or community. [NIH] Social pressure: A strategy used in behavior therapy in which individuals are told that they possess the basic self-control ability to lose weight, but that coming to group meetings will strengthen their abilities. The group is asked to listen and give advice, similar to the way many self-help groups, based on social support, operate. [NIH] Social Problems: Situations affecting a significant number of people, that are believed to be sources of difficulty or threaten the stability of the community, and that require programs of amelioration. [NIH] Social Support: Support systems that provide assistance and encouragement to individuals with physical or emotional disabilities in order that they may better cope. Informal social support is usually provided by friends, relatives, or peers, while formal assistance is provided by churches, groups, etc. [NIH] Sodium: An element that is a member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. With a valence of 1, it has a strong affinity for oxygen and other nonmetallic elements. Sodium provides the chief cation of the extracellular body fluids. Its salts are the most widely used in medicine. (From Dorland, 27th ed) Physiologically the sodium ion plays a major role in blood pressure regulation, maintenance of fluid volume, and electrolyte balance. [NIH] Sodium Channels: Cell membrane glycoproteins selective for sodium ions. Fast sodium current is associated with the action potential in neural membranes. [NIH] Soft tissue: Refers to muscle, fat, fibrous tissue, blood vessels, or other supporting tissue of the body. [NIH] Solvent: 1. Dissolving; effecting a solution. 2. A liquid that dissolves or that is capable of dissolving; the component of a solution that is present in greater amount. [EU] Soma: The body as distinct from the mind; all the body tissue except the germ cells; all the axial body. [NIH]

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Somatic: 1. Pertaining to or characteristic of the soma or body. 2. Pertaining to the body wall in contrast to the viscera. [EU] Somatic cells: All the body cells except the reproductive (germ) cells. [NIH] Somatostatin: A polypeptide hormone produced in the hypothalamus, and other tissues and organs. It inhibits the release of human growth hormone, and also modulates important physiological functions of the kidney, pancreas, and gastrointestinal tract. Somatostatin receptors are widely expressed throughout the body. Somatostatin also acts as a neurotransmitter in the central and peripheral nervous systems. [NIH] Somites: Paired, segmented masses of mesodermal tissue that form along the length of the neural tube during the early stage of embryonic development. They give rise to the vertebral column and other tissues including voluntary muscle, bone, connective tissue, and the dermal layers of the skin. [NIH] Sorbitol: A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. It is also used in many manufacturing processes, as a pharmaceutical aid, and in several research applications. [NIH] Sound wave: An alteration of properties of an elastic medium, such as pressure, particle displacement, or density, that propagates through the medium, or a superposition of such alterations. [NIH] Soybean Oil: Oil from soybean or soybean plant. [NIH] Spasm: An involuntary contraction of a muscle or group of muscles. Spasms may involve skeletal muscle or smooth muscle. [NIH] Specialist: In medicine, one who concentrates on 1 special branch of medical science. [NIH] Species: A taxonomic category subordinate to a genus (or subgenus) and superior to a subspecies or variety, composed of individuals possessing common characters distinguishing them from other categories of individuals of the same taxonomic level. In taxonomic nomenclature, species are designated by the genus name followed by a Latin or Latinized adjective or noun. [EU] Specificity: Degree of selectivity shown by an antibody with respect to the number and types of antigens with which the antibody combines, as well as with respect to the rates and the extents of these reactions. [NIH] Spectrum: A charted band of wavelengths of electromagnetic vibrations obtained by refraction and diffraction. By extension, a measurable range of activity, such as the range of bacteria affected by an antibiotic (antibacterial s.) or the complete range of manifestations of a disease. [EU] Sperm: The fecundating fluid of the male. [NIH] Sphincter: A ringlike band of muscle fibres that constricts a passage or closes a natural orifice; called also musculus sphincter. [EU] Spinal cord: The main trunk or bundle of nerves running down the spine through holes in the spinal bone (the vertebrae) from the brain to the level of the lower back. [NIH] Spleen: An organ that is part of the lymphatic system. The spleen produces lymphocytes, filters the blood, stores blood cells, and destroys old blood cells. It is located on the left side of the abdomen near the stomach. [NIH] Spontaneous Abortion: The non-induced birth of an embryo or of fetus prior to the stage of viability at about 20 weeks of gestation. [NIH]

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Sporadic: Neither endemic nor epidemic; occurring occasionally in a random or isolated manner. [EU] Squamous: Scaly, or platelike. [EU] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells resembling fish scales. Squamous cells are found in the tissue that forms the surface of the skin, the lining of the hollow organs of the body, and the passages of the respiratory and digestive tracts. Also called epidermoid carcinoma. [NIH] Squamous cells: Flat cells that look like fish scales under a microscope. These cells cover internal and external surfaces of the body. [NIH] Stabilization: The creation of a stable state. [EU] Statistically significant: Describes a mathematical measure of difference between groups. The difference is said to be statistically significant if it is greater than what might be expected to happen by chance alone. [NIH] Steatosis: Fatty degeneration. [EU] Steel: A tough, malleable, iron-based alloy containing up to, but no more than, two percent carbon and often other metals. It is used in medicine and dentistry in implants and instrumentation. [NIH] Sterility: 1. The inability to produce offspring, i.e., the inability to conceive (female s.) or to induce conception (male s.). 2. The state of being aseptic, or free from microorganisms. [EU] Steroid: A group name for lipids that contain a hydrogenated cyclopentanoperhydrophenanthrene ring system. Some of the substances included in this group are progesterone, adrenocortical hormones, the gonadal hormones, cardiac aglycones, bile acids, sterols (such as cholesterol), toad poisons, saponins, and some of the carcinogenic hydrocarbons. [EU] Stillbirth: The birth of a dead fetus or baby. [NIH] Stimulant: 1. Producing stimulation; especially producing stimulation by causing tension on muscle fibre through the nervous tissue. 2. An agent or remedy that produces stimulation. [EU] Stimulus: That which can elicit or evoke action (response) in a muscle, nerve, gland or other excitable issue, or cause an augmenting action upon any function or metabolic process. [NIH] Stomach: An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the esophagus and the beginning of the duodenum. [NIH] Stool: The waste matter discharged in a bowel movement; feces. [NIH] Stress: Forcibly exerted influence; pressure. Any condition or situation that causes strain or tension. Stress may be either physical or psychologic, or both. [NIH] Stroke: Sudden loss of function of part of the brain because of loss of blood flow. Stroke may be caused by a clot (thrombosis) or rupture (hemorrhage) of a blood vessel to the brain. [NIH]

Stromal: Large, veil-like cell in the bone marrow. [NIH] Struvite: A type of kidney stone caused by infection. [NIH] Subacute: Somewhat acute; between acute and chronic. [EU]

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Subclinical: Without clinical manifestations; said of the early stage(s) of an infection or other disease or abnormality before symptoms and signs become apparent or detectable by clinical examination or laboratory tests, or of a very mild form of an infection or other disease or abnormality. [EU] Subcutaneous: Beneath the skin. [NIH] Subspecies: A category intermediate in rank between species and variety, based on a smaller number of correlated characters than are used to differentiate species and generally conditioned by geographical and/or ecological occurrence. [NIH] Substance P: An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of pain, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses. [NIH]

Substrate: A substance upon which an enzyme acts. [EU] Supplementation: Adding nutrients to the diet. [NIH] Support group: A group of people with similar disease who meet to discuss how better to cope with their cancer and treatment. [NIH] Suppositories: A small cone-shaped medicament having cocoa butter or gelatin at its basis and usually intended for the treatment of local conditions in the rectum. [NIH] Suppression: A conscious exclusion of disapproved desire contrary with repression, in which the process of exclusion is not conscious. [NIH] Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system. [NIH] Sympathomimetic: 1. Mimicking the effects of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. 2. An agent that produces effects similar to those of impulses conveyed by adrenergic postganglionic fibres of the sympathetic nervous system. Called also adrenergic. [EU] Symphysis: A secondary cartilaginous joint. [NIH] Symptomatic: Having to do with symptoms, which are signs of a condition or disease. [NIH] Synapse: The region where the processes of two neurons come into close contiguity, and the nervous impulse passes from one to the other; the fibers of the two are intermeshed, but, according to the general view, there is no direct contiguity. [NIH] Synapsis: The pairing between homologous chromosomes of maternal and paternal origin during the prophase of meiosis, leading to the formation of gametes. [NIH] Synaptic: Pertaining to or affecting a synapse (= site of functional apposition between neurons, at which an impulse is transmitted from one neuron to another by electrical or chemical means); pertaining to synapsis (= pairing off in point-for-point association of homologous chromosomes from the male and female pronuclei during the early prophase of meiosis). [EU] Synaptic Transmission: The communication from a neuron to a target (neuron, muscle, or secretory cell) across a synapse. In chemical synaptic transmission, the presynaptic neuron releases a neurotransmitter that diffuses across the synaptic cleft and binds to specific synaptic receptors. These activated receptors modulate ion channels and/or secondmessenger systems to influence the postsynaptic cell. Electrical transmission is less common

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in the nervous system, and, as in other tissues, is mediated by gap junctions. [NIH] Synergistic: Acting together; enhancing the effect of another force or agent. [EU] Systemic: Affecting the entire body. [NIH] Systems Theory: Principles, models, and laws that apply to complex interrelationships and interdependencies of sets of linked components which form a functioning whole, a system. Any system may be composed of components which are systems in their own right (subsystems), such as several organs within an individual organism. [NIH] Systolic: Indicating the maximum arterial pressure during contraction of the left ventricle of the heart. [EU] Systolic blood pressure: The maximum pressure in the artery produced as the heart contracts and blood begins to flow. [NIH] Systolic heart failure: Inability of the heart to contract with enough force to pump adequate amounts of blood through the body. [NIH] Tamoxifen: A first generation selective estrogen receptor modulator (SERM). It acts as an agonist for bone tissue and cholesterol metabolism but is an estrogen antagonist in mammary and uterine. [NIH] Tardive: Marked by lateness, late; said of a disease in which the characteristic lesion is late in appearing. [EU] Telangiectasia: The permanent enlargement of blood vessels, causing redness in the skin or mucous membranes. [NIH] Telecommunications: Transmission of information over distances via electronic means. [NIH]

Temporal: One of the two irregular bones forming part of the lateral surfaces and base of the skull, and containing the organs of hearing. [NIH] Temporal Lobe: Lower lateral part of the cerebral hemisphere. [NIH] Teratogenesis: Production of monstrous growths or fetuses. [NIH] Terminator: A DNA sequence sited at the end of a transcriptional unit that signals the end of transcription. [NIH] Testis: Either of the paired male reproductive glands that produce the male germ cells and the male hormones. [NIH] Testosterone: A hormone that promotes the development and maintenance of male sex characteristics. [NIH] Thalamic: Cell that reaches the lateral nucleus of amygdala. [NIH] Thalamic Diseases: Disorders of the centrally located thalamus, which integrates a wide range of cortical and subcortical information. Manifestations include sensory loss, movement disorders; ataxia, pain syndromes, visual disorders, a variety of neuropsychological conditions, and coma. Relatively common etiologies include cerebrovascular disorders; craniocerebral trauma; brain neoplasms; brain hypoxia; intracranial hemorrhages; and infectious processes. [NIH] Thalamus: Paired bodies containing mostly gray substance and forming part of the lateral wall of the third ventricle of the brain. The thalamus represents the major portion of the diencephalon and is commonly divided into cellular aggregates known as nuclear groups. [NIH]

Therapeutics: The branch of medicine which is concerned with the treatment of diseases, palliative or curative. [NIH]

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Thermogenesis: The generation of heat in order to maintain body temperature. The uncoupled oxidation of fatty acids contained within brown adipose tissue and shivering are examples of thermogenesis in mammals. [NIH] Thermoregulation: Heat regulation. [EU] Thigh: A leg; in anatomy, any elongated process or part of a structure more or less comparable to a leg. [NIH] Thinness: A state of insufficient flesh on the body usually defined as having a body weight less than skeletal and physical standards. [NIH] Third Ventricle: A narrow cleft inferior to the corpus callosum, within the diencephalon, between the paired thalami. Its floor is formed by the hypothalamus, its anterior wall by the lamina terminalis, and its roof by ependyma. It communicates with the fourth ventricle by the cerebral aqueduct, and with the lateral ventricles by the interventricular foramina. [NIH] Thorax: A part of the trunk between the neck and the abdomen; the chest. [NIH] Threshold: For a specified sensory modality (e. g. light, sound, vibration), the lowest level (absolute threshold) or smallest difference (difference threshold, difference limen) or intensity of the stimulus discernible in prescribed conditions of stimulation. [NIH] Thrombin: An enzyme formed from prothrombin that converts fibrinogen to fibrin. (Dorland, 27th ed) EC 3.4.21.5. [NIH] Thrombocytes: Blood cells that help prevent bleeding by causing blood clots to form. Also called platelets. [NIH] Thromboembolism: Obstruction of a vessel by a blood clot that has been transported from a distant site by the blood stream. [NIH] Thrombolytic: 1. Dissolving or splitting up a thrombus. 2. A thrombolytic agent. [EU] Thrombomodulin: A cell surface glycoprotein of endothelial cells that binds thrombin and serves as a cofactor in the activation of protein C and its regulation of blood coagulation. [NIH]

Thrombosis: The formation or presence of a blood clot inside a blood vessel. [NIH] Thromboxanes: Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase. [NIH] Thrombus: An aggregation of blood factors, primarily platelets and fibrin with entrapment of cellular elements, frequently causing vascular obstruction at the point of its formation. Some authorities thus differentiate thrombus formation from simple coagulation or clot formation. [EU] Thyroid: A gland located near the windpipe (trachea) that produces thyroid hormone, which helps regulate growth and metabolism. [NIH] Thyrotropin: A peptide hormone secreted by the anterior pituitary. It promotes the growth of the thyroid gland and stimulates the synthesis of thyroid hormones and the release of thyroxine by the thyroid gland. [NIH] Thyroxine: An amino acid of the thyroid gland which exerts a stimulating effect on thyroid metabolism. [NIH] Tin: A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71. [NIH] Tinnitus: Sounds that are perceived in the absence of any external noise source which may take the form of buzzing, ringing, clicking, pulsations, and other noises. Objective tinnitus

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refers to noises generated from within the ear or adjacent structures that can be heard by other individuals. The term subjective tinnitus is used when the sound is audible only to the affected individual. Tinnitus may occur as a manifestation of cochlear diseases; vestibulocochlear nerve diseases; intracranial hypertension; craniocerebral trauma; and other conditions. [NIH] Tissue: A group or layer of cells that are alike in type and work together to perform a specific function. [NIH] Tissue Plasminogen Activator: A proteolytic enzyme in the serine protease family found in many tissues which converts plasminogen to plasmin. It has fibrin-binding activity and is immunologically different from urinary plasminogen activator. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases. EC 3.4.21.68. [NIH] Tolerance: 1. The ability to endure unusually large doses of a drug or toxin. 2. Acquired drug tolerance; a decreasing response to repeated constant doses of a drug or the need for increasing doses to maintain a constant response. [EU] Tomography: Imaging methods that result in sharp images of objects located on a chosen plane and blurred images located above or below the plane. [NIH] Tone: 1. The normal degree of vigour and tension; in muscle, the resistance to passive elongation or stretch; tonus. 2. A particular quality of sound or of voice. 3. To make permanent, or to change, the colour of silver stain by chemical treatment, usually with a heavy metal. [EU] Tonus: A state of slight tension usually present in muscles even when they are not undergoing active contraction. [NIH] Tooth Preparation: Procedures carried out with regard to the teeth or tooth structures preparatory to specified dental therapeutic and surgical measures. [NIH] Topical: On the surface of the body. [NIH] Toxic: Having to do with poison or something harmful to the body. Toxic substances usually cause unwanted side effects. [NIH] Toxicity: The quality of being poisonous, especially the degree of virulence of a toxic microbe or of a poison. [EU] Toxicokinetics: Study of the absorption, distribution, metabolism, and excretion of test substances. [NIH] Toxicology: The science concerned with the detection, chemical composition, and pharmacologic action of toxic substances or poisons and the treatment and prevention of toxic manifestations. [NIH] Toxin: A poison; frequently used to refer specifically to a protein produced by some higher plants, certain animals, and pathogenic bacteria, which is highly toxic for other living organisms. Such substances are differentiated from the simple chemical poisons and the vegetable alkaloids by their high molecular weight and antigenicity. [EU] Trace element: Substance or element essential to plant or animal life, but present in extremely small amounts. [NIH] Trachea: The cartilaginous and membranous tube descending from the larynx and branching into the right and left main bronchi. [NIH] Traction: The act of pulling. [NIH] Transduction: The transfer of genes from one cell to another by means of a viral (in the case of bacteria, a bacteriophage) vector or a vector which is similar to a virus particle

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(pseudovirion). [NIH] Transfection: The uptake of naked or purified DNA into cells, usually eukaryotic. It is analogous to bacterial transformation. [NIH] Transfusion: The infusion of components of blood or whole blood into the bloodstream. The blood may be donated from another person, or it may have been taken from the person earlier and stored until needed. [NIH] Translation: The process whereby the genetic information present in the linear sequence of ribonucleotides in mRNA is converted into a corresponding sequence of amino acids in a protein. It occurs on the ribosome and is unidirectional. [NIH] Translational: The cleavage of signal sequence that directs the passage of the protein through a cell or organelle membrane. [NIH] Translocation: The movement of material in solution inside the body of the plant. [NIH] Transmitter: A chemical substance which effects the passage of nerve impulses from one cell to the other at the synapse. [NIH] Transplantation: Transference of a tissue or organ, alive or dead, within an individual, between individuals of the same species, or between individuals of different species. [NIH] Transversion: A base-pair substitution mutation in which a purine-pyrimidine pair is replaced by the equivalent pyrimidine-purine pair, i. e. A-T becomes T-A. [NIH] Trauma: Any injury, wound, or shock, must frequently physical or structural shock, producing a disturbance. [NIH] Treatment Failure: A measure of the quality of health care by assessment of unsuccessful results of management and procedures used in combating disease, in individual cases or series. [NIH] Treatment Outcome: Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, practicability, etc., of these interventions in individual cases or series. [NIH]

Triad: Trivalent. [NIH] Tricuspid Atresia: Absence of the orifice between the right atrium and ventricle, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy because the right ventricle is absent or not functional. [NIH] Tricyclic: Containing three fused rings or closed chains in the molecular structure. [EU] Trigeminal: Cranial nerve V. It is sensory for the eyeball, the conjunctiva, the eyebrow, the skin of face and scalp, the teeth, the mucous membranes in the mouth and nose, and is motor to the muscles of mastication. [NIH] Trigeminal Nerve: The 5th and largest cranial nerve. The trigeminal nerve is a mixed motor and sensory nerve. The larger sensory part forms the ophthalmic, mandibular, and maxillary nerves which carry afferents sensitive to external or internal stimuli from the skin, muscles, and joints of the face and mouth and from the teeth. Most of these fibers originate from cells of the trigeminal ganglion and project to the trigeminal nucleus of the brain stem. The smaller motor part arises from the brain stem trigeminal motor nucleus and innervates the muscles of mastication. [NIH] Trigger zone: Dolorogenic zone (= producing or causing pain). [EU] Triglyceride: A lipid carried through the blood stream to tissues. Most of the body's fat tissue is in the form of triglycerides, stored for use as energy. Triglycerides are obtained

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primarily from fat in foods. [NIH] Trophic: Of or pertaining to nutrition. [EU] Truncal: The bilateral dissection of the abdominal branches of the vagus nerve. [NIH] Trypsin: A serine endopeptidase that is formed from trypsinogen in the pancreas. It is converted into its active form by enteropeptidase in the small intestine. It catalyzes hydrolysis of the carboxyl group of either arginine or lysine. EC 3.4.21.4. [NIH] Tryptophan: An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor serotonin and niacin. [NIH] Tuberous Sclerosis: A rare congenital disease in which the essential pathology is the appearance of multiple tumors in the cerebrum and in other organs, such as the heart or kidneys. [NIH] Tumor Necrosis Factor: Serum glycoprotein produced by activated macrophages and other mammalian mononuclear leukocytes which has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. It mimics the action of endotoxin but differs from it. It has a molecular weight of less than 70,000 kDa. [NIH] Tumour: 1. Swelling, one of the cardinal signs of inflammations; morbid enlargement. 2. A new growth of tissue in which the multiplication of cells is uncontrolled and progressive; called also neoplasm. [EU] Tunica: A rather vague term to denote the lining coat of hollow organs, tubes, or cavities. [NIH]

Type 2 diabetes: Usually characterized by a gradual onset with minimal or no symptoms of metabolic disturbance and no requirement for exogenous insulin. The peak age of onset is 50 to 60 years. Obesity and possibly a genetic factor are usually present. [NIH] Tyrosine: A non-essential amino acid. In animals it is synthesized from phenylalanine. It is also the precursor of epinephrine, thyroid hormones, and melanin. [NIH] Ulcer: A localized necrotic lesion of the skin or a mucous surface. [NIH] Unconscious: Experience which was once conscious, but was subsequently rejected, as the "personal unconscious". [NIH] Unsaturated Fats: A type of fat. [NIH] Uraemia: 1. An excess in the blood of urea, creatinine, and other nitrogenous end products of protein and amino acids metabolism; more correctly referred to as azotemia. 2. In current usage the entire constellation of signs and symptoms of chronic renal failure, including nausea, vomiting anorexia, a metallic taste in the mouth, a uraemic odour of the breath, pruritus, uraemic frost on the skin, neuromuscular disorders, pain and twitching in the muscles, hypertension, edema, mental confusion, and acid-base and electrolyte imbalances. [EU]

Urbanization: The process whereby a society changes from a rural to an urban way of life. It refers also to the gradual increase in the proportion of people living in urban areas. [NIH] Uremia: The illness associated with the buildup of urea in the blood because the kidneys are not working effectively. Symptoms include nausea, vomiting, loss of appetite, weakness, and mental confusion. [NIH] Ureters: Tubes that carry urine from the kidneys to the bladder. [NIH] Urethra: The tube through which urine leaves the body. It empties urine from the bladder. [NIH]

Uric: A kidney stone that may result from a diet high in animal protein. When the body breaks down this protein, uric acid levels rise and can form stones. [NIH]

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Urinary: Having to do with urine or the organs of the body that produce and get rid of urine. [NIH] Urinary Calculi: Calculi in any part of the urinary tract. According to their composition or pattern of chemical composition distribution, urinary calculi types may include alternating or combination, cystine, decubitus, encysted, fibrin, hemp seed, matrix, mulberry, oxalate, struvite, urostealith, and xanthic calculi. [NIH] Urinary Plasminogen Activator: A proteolytic enzyme that converts plasminogen to plasmin where the preferential cleavage is between arginine and valine. It was isolated originally from human urine, but is found in most tissues of most vertebrates. EC 3.4.21.73. [NIH]

Urinary tract: The organs of the body that produce and discharge urine. These include the kidneys, ureters, bladder, and urethra. [NIH] Urine: Fluid containing water and waste products. Urine is made by the kidneys, stored in the bladder, and leaves the body through the urethra. [NIH] Urogenital: Pertaining to the urinary and genital apparatus; genitourinary. [EU] Urogenital System: All the organs involved in reproduction and the formation and release of urine. It includes the kidneys, ureters, bladder, urethra, and the organs of reproduction ovaries, uterus, fallopian tubes, vagina, and clitoris in women and the testes, seminal vesicles, prostate, seminal ducts, and penis in men. [NIH] Urokinase: A drug that dissolves blood clots or prevents them from forming. [NIH] Uterine Contraction: Contraction of the uterine muscle. [NIH] Uterus: The small, hollow, pear-shaped organ in a woman's pelvis. This is the organ in which a fetus develops. Also called the womb. [NIH] Vaccine: A substance or group of substances meant to cause the immune system to respond to a tumor or to microorganisms, such as bacteria or viruses. [NIH] Vagal: Pertaining to the vagus nerve. [EU] Vagina: The muscular canal extending from the uterus to the exterior of the body. Also called the birth canal. [NIH] Vaginitis: Inflammation of the vagina characterized by pain and a purulent discharge. [NIH] Vagotomy: The interruption or removal of any part of the vagus (10th cranial) nerve. Vagotomy may be performed for research or for therapeutic purposes. [NIH] Vagus Nerve: The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx). [NIH] Valproic Acid: A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GABA levels in the brain or by altering the properties of voltage dependent sodium channels. [NIH] Varicose: The common ulcer in the lower third of the leg or near the ankle. [NIH] Varicose vein: An abnormal swelling and tortuosity especially of the superficial veins of the legs. [EU] Vascular: Pertaining to blood vessels or indicative of a copious blood supply. [EU] Vasculitis: Inflammation of a blood vessel. [NIH] Vasoconstriction: Narrowing of the blood vessels without anatomic change, for which

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constriction, pathologic is used. [NIH] Vasodilator: An agent that widens blood vessels. [NIH] VE: The total volume of gas either inspired or expired in one minute. [NIH] Vein: Vessel-carrying blood from various parts of the body to the heart. [NIH] Venous: Of or pertaining to the veins. [EU] Venous Thrombosis: The formation or presence of a thrombus within a vein. [NIH] Venter: Belly. [NIH] Ventral: 1. Pertaining to the belly or to any venter. 2. Denoting a position more toward the belly surface than some other object of reference; same as anterior in human anatomy. [EU] Ventricle: One of the two pumping chambers of the heart. The right ventricle receives oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary artery. The left ventricle receives oxygen-rich blood from the left atrium and pumps it to the body through the aorta. [NIH] Ventricular: Pertaining to a ventricle. [EU] Ventricular Dysfunction: A condition in which the ventricles of the heart exhibit a decreased functionality. [NIH] Venules: The minute vessels that collect blood from the capillary plexuses and join together to form veins. [NIH] Vertebrae: A bony unit of the segmented spinal column. [NIH] Vertebral: Of or pertaining to a vertebra. [EU] Vertical banded gastroplasty: A surgical treatment for extreme obesity; an operation on the stomach that involves constructing a small pouch in the stomach that empties through a narrow opening into the distal stomach and duodenum. [NIH] Veterinary Medicine: The medical science concerned with the prevention, diagnosis, and treatment of diseases in animals. [NIH] Video Recording: The storing or preserving of video signals for television to be played back later via a transmitter or receiver. Recordings may be made on magnetic tape or discs (videodisc recording). [NIH] Videodisc Recording: The storing of visual and usually sound signals on discs for later reproduction on a television screen or monitor. [NIH] Viral: Pertaining to, caused by, or of the nature of virus. [EU] Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. [NIH] Virus: Submicroscopic organism that causes infectious disease. In cancer therapy, some viruses may be made into vaccines that help the body build an immune response to, and kill, tumor cells. [NIH] Viscera: Any of the large interior organs in any one of the three great cavities of the body, especially in the abdomen. [NIH] Visceral: , from viscus a viscus) pertaining to a viscus. [EU] Visceral Afferents: The sensory fibers innervating the viscera. [NIH] Visceral fat: One of the three compartments of abdominal fat. Retroperitoneal and subcutaneous are the other two compartments. [NIH] Visual field: The entire area that can be seen when the eye is forward, including peripheral

602 Obesity

vision. [NIH] Vital Statistics: Used for general articles concerning statistics of births, deaths, marriages, etc. [NIH] Vitro: Descriptive of an event or enzyme reaction under experimental investigation occurring outside a living organism. Parts of an organism or microorganism are used together with artificial substrates and/or conditions. [NIH] Vivo: Outside of or removed from the body of a living organism. [NIH] VLCD: The VLCD of 800 (approximately 6-10 kcal/kg body weight) or fewer calories per day is conducted under physician supervision and monitoring and is restricted to severely obese persons. [NIH] Vocal cord: The vocal folds of the larynx. [NIH] Volition: Voluntary activity without external compulsion. [NIH] Vomeronasal Organ: A specialized part of the olfactory system located anteriorly in the nasal cavity within the nasal septum. Chemosensitive cells of the vomeronasal organ project via the vomeronasal nerve to the accessory olfactory bulb. The primary function of this organ appears to be in sensing pheromones which regulate reproductive and other social behaviors. While the structure has been thought absent in higher primate adults, data now suggests it may be present in adult humans. [NIH] Waist circumference: To define the level at which the waist circumference is measured, a bony landmark is first located and marked. The subject stands, and the technician, positioned to the right of the subject, palpates the upper hip bone to locate the right ileum. Just above the uppermost lateral border of the right ileum, a horizontal mark is drawn and then crossed with a vertical mark on the midaxillary line. The measuring tape is then placed around the trunk, at the level of the mark on the right side, making sure that it is on a level horizontal plane on all sides. The tape is then tightened slightly without compressing the skin and underlying subcutaneous tissues. The measure is recorded in centimeters to the nearest millimeter. [NIH] War: Hostile conflict between organized groups of people. [NIH] Weight Gain: Increase in body weight over existing weight. [NIH] Weight Perception: Recognition and discrimination of the heaviness of a lifted object. [NIH] Wheezing: Breathing with a rasp or whistling sound; a sign of airway constriction or obstruction. [NIH] White blood cell: A type of cell in the immune system that helps the body fight infection and disease. White blood cells include lymphocytes, granulocytes, macrophages, and others. [NIH]

Windpipe: A rigid tube, 10 cm long, extending from the cricoid cartilage to the upper border of the fifth thoracic vertebra. [NIH] Withdrawal: 1. A pathological retreat from interpersonal contact and social involvement, as may occur in schizophrenia, depression, or schizoid avoidant and schizotypal personality disorders. 2. (DSM III-R) A substance-specific organic brain syndrome that follows the cessation of use or reduction in intake of a psychoactive substance that had been regularly used to induce a state of intoxication. [EU] Wound Healing: Restoration of integrity to traumatized tissue. [NIH] Wound Infection: Invasion of the site of trauma by pathogenic microorganisms. [NIH] Xamoterol: A selective beta-1-adrenergic partial agonist. Because it is a partial agonist it acts like an agonist when sympathetic activity is low and as an antagonist when sympathetic

Dictionary 603

activity is high. It reduces myocardial ischemia and improves ventricular function in patients with mild to moderate heart failure. In patients with severe heart failure it has been shown to produce benefits in systolic and diastolic function. [NIH] Xenograft: The cells of one species transplanted to another species. [NIH] X-ray: High-energy radiation used in low doses to diagnose diseases and in high doses to treat cancer. [NIH] Yeasts: A general term for single-celled rounded fungi that reproduce by budding. Brewers' and bakers' yeasts are Saccharomyces cerevisiae; therapeutic dried yeast is dried yeast. [NIH] Zygote: The fertilized ovum. [NIH] Zymogen: Inactive form of an enzyme which can then be converted to the active form, usually by excision of a polypeptide, e. g. trypsinogen is the zymogen of trypsin. [NIH]

605

INDEX 5 5-Hydroxytryptophan, 198, 272, 273, 348, 349, 350, 382, 509 A Abdomen, 234, 282, 509, 522, 540, 556, 558, 561, 573, 574, 575, 592, 593, 596, 600, 601 Abdominal fat, 9, 12, 227, 275, 419, 449, 460, 509, 526, 601 Aberrant, 77, 274, 366, 367, 389, 392, 431, 509 Ablation, 77, 509 Abortion, 509, 570, 580 Acanthosis Nigricans, 225, 509 Acceptor, 509, 560, 572 Acculturation, 207, 509 ACE, 490, 509 Acetone, 294, 509, 558 Acetylcholine, 291, 376, 509, 527, 569 Acidity, 509, 576 Acidosis, 509, 558 Activities of Daily Living, 219, 509 Acute lymphoblastic leukemia, 510 Acute lymphocytic leukemia, 510 Acyl, 510 Adaptability, 510, 525 Adaptation, 224, 434, 510 Adenine, 510 Adenocarcinoma, 8, 510, 551 Adenoma, 8, 510 Adenosine, 306, 383, 510, 523, 577 Adenovirus, 510 Adipose Tissue, 73, 76, 77, 79, 172, 190, 206, 264, 270, 271, 277, 279, 280, 295, 302, 305, 315, 324, 326, 327, 336, 337, 340, 343, 356, 366, 371, 375, 377, 388, 397, 428, 429, 431, 509, 510, 522, 560, 596 Adjustment, 4, 5, 9, 11, 210, 213, 276, 400, 465, 510 Adjuvant, 300, 510, 546 Adolescence, 226, 230, 404, 409, 430, 434, 453, 510, 574 Adrenal Cortex, 510, 512, 532, 541, 570, 581, 586 Adrenal Medulla, 286, 510, 525, 540, 569 Adrenergic Agents, 510, 516 Adsorption, 294, 511 Adsorptive, 511 Adult-Onset Diabetes, 228, 285, 420, 511

Adverse Effect, 417, 511, 590 Aerobic, 9, 15, 213, 219, 417, 490, 511 Aerobic Exercise, 15, 213, 511 Aetiology, 169, 511 Afferent, 264, 511, 559, 571, 589 Affinity, 355, 511, 518, 535, 565, 591 Afterload, 418, 511 Agar, 351, 511, 533, 554, 578 Age Groups, 74, 511 Age of Onset, 182, 511, 599 Aged, 80 and Over, 511 Airway, 511, 591, 602 Akathisia, 511, 516 Albumin, 307, 512, 578 Aldosterone, 418, 512 Alertness, 512, 523 Algorithms, 512, 521 Alimentary, 363, 512, 535, 573 Alkaline, 509, 512, 513, 523 Alkaloid, 512, 522, 569 Alleles, 512, 551, 560 Allografts, 512, 552 Alloys, 512, 528 Allylamine, 512, 513 Alpha 1-Antitrypsin, 496, 512 Alpha 1-Antitrypsin Deficiency, 496, 512 Alpha-Linolenic Acid, 198, 296, 512 Alternative medicine, 440, 512 Alveoli, 512, 584 Ameliorating, 339, 364, 380, 512 Amenorrhea, 193, 513, 515, 522, 579 Amine, 246, 328, 329, 341, 384, 513, 552 Amino Acid Sequence, 298, 299, 334, 347, 388, 513, 515, 542, 546, 581 Aminoethyl, 298, 513 Ammonia, 513 Amnestic, 513, 544 Amphetamine, 292, 318, 319, 383, 513, 535 Amplification, 170, 513 Ampulla, 513, 539 Amygdala, 393, 513, 519, 560, 589, 595 Amyloid, 368, 513 Anabolic, 243, 330, 331, 513, 536 Anaerobic, 513 Anaesthesia, 513, 555 Anal, 513, 529, 561, 572 Analgesics, 351, 514 Analog, 310, 318, 514

606 Obesity

Analogous, 242, 277, 307, 514, 578, 598 Anaphylatoxins, 514, 530 Anastomosis, 514, 545, 557 Anatomical, 317, 514, 518, 526, 531, 554, 565, 588 Androgens, 168, 281, 330, 510, 514 Anemia, 424, 432, 469, 514, 528 Anesthesia, 511, 514 Angina, 193, 514, 581 Angina Pectoris, 514, 581 Angiogenesis, 514, 563 Angiotensinogen, 514, 586 Animal model, 299, 310, 312, 314, 321, 322, 323, 324, 325, 362, 397, 431, 514 Anions, 512, 514, 557 Ankle, 514, 600 Anode, 7, 514 Anomalies, 468, 514 Anorexiant, 266, 300, 515 Anovulation, 515, 579 Antagonism, 174, 304, 305, 515, 523 Anthelmintic, 382, 515 Anthropometric measurements, 399, 515 Anthropometry, 401, 515 Antibacterial, 515, 592 Antibiotic, 296, 432, 515, 528, 541, 574, 592 Antibodies, 298, 299, 308, 347, 352, 354, 355, 371, 372, 515, 549, 554, 578 Antibody, 280, 511, 515, 529, 549, 552, 554, 555, 563, 585, 592 Anticoagulant, 515, 582 Anticonvulsant, 515, 600 Antidepressant, 312, 314, 321, 322, 323, 325, 509, 515, 522, 544 Antidiabetic, 515, 548 Antiemetic, 515, 516 Antiepileptic, 509, 515 Antigen, 511, 515, 530, 552, 553, 554, 555, 563, 565 Antigen-Antibody Complex, 515, 530 Anti-infective, 515, 544, 552 Anti-Infective Agents, 515, 544 Anti-inflammatory, 320, 392, 516, 518, 535, 547 Anti-Inflammatory Agents, 320, 516, 518 Anti-Obesity Agents, 242, 244, 245, 289, 306, 307, 320, 321, 339, 345, 353, 408, 516 Antioxidant, 516, 545, 572, 573 Antipsychotic, 516, 568 Antiseptic, 509, 516, 525 Antrectomy, 516, 520 Anuria, 516, 558

Anus, 513, 516, 522, 529, 544, 556 Anxiety, 179, 483, 511, 516, 544, 570, 573, 581 Aorta, 391, 516, 601 Aperture, 313, 359, 516, 584 Apnea, 197, 226, 278, 289, 304, 340, 343, 356, 390, 488, 505, 516, 591 Apnoea, 332, 516 Apolipoproteins, 516, 560 Apoptosis, 74, 79, 366, 392, 516, 533 Appetite Regulation, 320, 517 Aqueous, 294, 517, 519, 533, 538, 552, 559, 560 Arachidonate 15-Lipoxygenase, 517, 561 Arachidonate Lipoxygenases, 517, 561 Arachidonic Acid, 277, 517, 559, 581 Arcuate Nucleus, 301, 517 Aromatic, 335, 336, 517, 565, 576 Arterial, 281, 295, 359, 512, 517, 527, 531, 553, 582, 595 Arteries, 516, 517, 521, 522, 532, 557, 561, 565, 567, 584, 596 Arteriolar, 517, 522, 586 Arterioles, 517, 521, 523, 567 Arteriolosclerosis, 517 Arteriosclerosis, 233, 267, 286, 517, 553, 567 Articular, 517, 572 Aseptic, 517, 593 Aspartic, 517, 539 Aspartic Endopeptidases, 517, 539 Aspiration, 360, 517 Aspirin, 221, 518 Assay, 376, 518 Astringent, 518, 525 Astrocytes, 518, 565, 566 Asymptomatic, 442, 518, 573 Ataxia, 469, 518, 595 Atelectasis, 518 Atrial, 267, 312, 321, 322, 323, 325, 518, 531, 598 Atrioventricular, 518, 531 Atrium, 518, 531, 598, 601 Atrophy, 469, 518, 560, 569 Atypical, 312, 321, 322, 323, 325, 518 Audiovisual Aids, 495, 518 Auditory, 287, 518, 563, 600 Autodigestion, 518, 573 Autoimmune disease, 366, 518 Autonomic, 509, 516, 518, 519, 569, 575, 594 Autonomic Nervous System, 518, 575, 594

Index 607

Autonomic Neuropathy, 519 Aversion therapy, 414, 519 Axillary, 519, 522, 565 Axillary Artery, 519, 522 Axons, 519, 571, 580 B Bacteria, 510, 511, 515, 519, 520, 528, 531, 539, 542, 543, 552, 565, 589, 592, 597, 600 Bacterial Infections, 296, 519 Bacterial Physiology, 510, 519 Bactericidal, 519, 541 Bacteriophage, 519, 578, 597 Bacteriostatic, 519, 541 Bacterium, 519, 531 Balloon dilation, 519 Basal Ganglia, 516, 518, 519, 527, 545, 560, 567 Basal Ganglia Diseases, 518, 519, 527, 567 Base, 276, 447, 510, 519, 534, 542, 544, 546, 557, 558, 595, 598, 599 Base Sequence, 519, 544, 546 Basement Membrane, 519, 542 Behavior Therapy, 12, 190, 357, 402, 452, 460, 488, 520, 591 Benign, 334, 510, 517, 519, 520, 545, 549, 560, 568, 585, 588 Benign prostatic hyperplasia, 519, 520 Beta blocker, 343, 520 Beta-pleated, 513, 520 Bezoar, 356, 520 Bilateral, 520, 579, 599 Bile, 11, 354, 378, 379, 520, 545, 546, 548, 551, 561, 589, 593 Bile Acids, 520, 546, 593 Bile Acids and Salts, 520 Bile duct, 520, 545 Biliary, 391, 520, 523, 573 Biliary Tract, 520, 523, 573 Biliopancreatic Diversion, 481, 520 Bilirubin, 512, 520, 545, 548 Bioavailability, 265, 520 Biochemical, 305, 423, 512, 520, 558, 572, 576, 590 Biological therapy, 520, 549 Biopsy, 6, 520, 575 Biotechnology, 71, 317, 415, 440, 459, 467, 468, 469, 470, 520 Biotransformation, 521 Bipolar Disorder, 231, 521 Birth Certificates, 465, 521 Bivalent, 521, 565

Bladder, 299, 340, 519, 520, 521, 530, 544, 555, 568, 582, 599, 600 Blood Coagulation, 521, 523, 542, 596 Blood Glucose, 11, 13, 190, 218, 234, 353, 361, 427, 433, 442, 460, 464, 521, 550, 553, 556 Blood Platelets, 521, 590 Blood vessel, 218, 235, 509, 514, 520, 521, 524, 525, 526, 527, 531, 532, 539, 557, 575, 577, 591, 593, 595, 596, 600, 601 Blood Volume, 418, 521 Blood-Brain Barrier, 521 Body Fluids, 265, 335, 521, 522, 570, 591 Body Image, 211, 215, 287, 399, 400, 402, 521 Bone Marrow, 510, 521, 533, 541, 546, 554, 562, 566, 593 Boronic Acids, 341, 522 Bowel, 279, 306, 311, 373, 374, 513, 522, 536, 555, 556, 559, 572, 575, 593 Bowel Movement, 522, 536, 593 Brachial, 218, 522, 563 Brachial Artery, 218, 522 Brachytherapy, 173, 522 Bradykinin, 522, 578 Brain Stem, 522, 598 Branch, 462, 503, 522, 535, 546, 563, 574, 584, 592, 595 Breakdown, 279, 312, 321, 322, 323, 325, 522, 536, 545, 571 Bromocriptine, 522 Bronchial, 522, 552 Bronchioles, 495, 512, 522, 584 Brown Fat, 366, 522 Bupropion, 304, 522 Burns, 191, 265, 366, 416, 522 Burns, Electric, 522 Bypass, 8, 211, 226, 279, 283, 284, 290, 310, 311, 357, 362, 373, 374, 427, 429, 433, 443, 480, 481, 522, 545, 557 C Caffeine, 185, 213, 382, 383, 523 Calcification, 517, 523 Calcium, 227, 272, 273, 279, 348, 349, 350, 424, 453, 523, 529, 542, 563, 572, 583, 590 Calcium Carbonate, 228, 523 Calcium Oxalate, 279, 523, 572 Calculi, 523, 548, 600 Calorimeter, 429, 523 Calpain, 523 Capillary, 522, 523, 525, 560, 584, 588, 601 Capillary Fragility, 523, 525, 588

608 Obesity

Capsules, 228, 319, 360, 523, 546 Carbon Dioxide, 524, 534, 553, 577, 586 Carcinogen, 524, 541 Carcinogenic, 524, 555, 581, 593 Carcinoma, 334, 524 Cardia, 524 Cardiac Output, 418, 524 Cardiopulmonary, 418, 524 Cardiorespiratory, 208, 511, 524 Cardioselective, 524, 581 Cardiovascular Abnormalities, 524 Cardiovascular disease, 11, 77, 173, 175, 221, 230, 232, 233, 246, 247, 248, 249, 250, 251, 252, 253, 254, 255, 256, 257, 258, 259, 260, 261, 262, 263, 274, 275, 291, 297, 304, 310, 311, 318, 338, 340, 343, 363, 374, 381, 383, 389, 396, 397, 424, 428, 443, 445, 463, 484, 524, 526, 560 Cardiovascular System, 233, 373, 519, 524 Carnitine, 380, 524 Carotene, 524, 587 Carpal Tunnel Syndrome, 524 Carrier Proteins, 524, 578 Case report, 189, 524, 528 Case series, 524, 528 Catabolism, 181, 352, 524 Catalyse, 335, 336, 525 Catechin, 186, 525 Catechol, 346, 525 Catecholamine, 525, 535, 537, 576 Catheter, 223, 235, 245, 312, 319, 375, 525, 557 Catheterization, 525, 557 Cathode, 514, 525 Caudal, 525, 535, 553, 579 Causal, 419, 489, 525 Cause of Death, 311, 374, 462, 525 Cecum, 525, 558 Cell Death, 75, 366, 516, 525 Cell Differentiation, 525, 590 Cell Division, 469, 519, 525, 549, 564, 565, 577, 581 Cell membrane, 265, 524, 525, 534, 542, 571, 576, 591 Cell proliferation, 517, 525, 590 Cell Respiration, 525, 587 Cell Survival, 392, 525, 549 Cellobiose, 525, 526 Cellulose, 283, 284, 525, 526, 577 Central fat distribution, 526 Cerebellar, 518, 526, 585

Cerebral, 320, 518, 519, 521, 522, 526, 534, 540, 542, 549, 595, 596 Cerebral Cortex, 518, 526, 542 Cerebrovascular, 519, 524, 526, 595 Cerebrum, 526, 599 Cervical, 5, 6, 526, 563 Cervix, 509, 526 Character, 297, 514, 526, 534 Chemoreceptor, 516, 526 Chemotactic Factors, 526, 530 Chin, 173, 188, 526, 564 Chlorella, 351, 527 Chloroform, 294, 527 Cholecystitis, 304, 527 Cholelithiasis, 293, 333, 352, 527 Cholestenones, 281, 527 Cholesterol Esters, 527, 560 Cholinergic, 516, 527, 569, 589 Chondrocytes, 527, 544 Chorea, 516, 527 Chromatin, 366, 516, 527, 562 Chromium, 176, 177, 230, 403, 527 Chromosomal, 386, 393, 513, 527 Chromosome, 77, 274, 275, 393, 468, 527, 531, 549, 551, 557, 560 Chronic renal, 425, 527, 579, 599 Chylomicrons, 527, 560 Ciliary, 72, 73, 333, 388, 527 Ciliary Neurotrophic Factor, 333, 388, 527 Cirrhosis, 194, 527 CIS, 475, 527, 587 Clamp, 218, 223, 528 Clarithromycin, 296, 528 Clear cell carcinoma, 528, 536 Climacteric, 373, 528 Clinical Medicine, 528, 580 Clinical study, 218, 528 Clone, 432, 528 Cloning, 274, 300, 309, 367, 389, 520, 528 Coagulation, 183, 288, 521, 528, 551, 578, 596 Cobalt, 345, 528 Cochlea, 528 Cochlear, 309, 528, 597 Codon, 368, 528, 546 Coenzyme, 199, 528 Cofactor, 382, 529, 582, 596 Colitis, 529, 555 Collagen, 513, 519, 525, 529, 542, 546, 563, 581 Collagenases, 367, 529 Collapse, 522, 529, 591

Index 609

Colloidal, 512, 529 Colon, 7, 194, 432, 437, 445, 469, 483, 485, 520, 529, 555, 558 Colon Polyps, 432, 529 Colorectal, 8, 73, 194, 529 Colorectal Cancer, 73, 194, 529 Colorectal Surgery, 529 Combination Therapy, 233, 304, 357, 358, 529 Communicable disease, 529 Comorbidity, 186, 485, 529 Complement, 363, 514, 529, 530, 546, 557, 562, 578 Complementary and alternative medicine, 179, 180, 202, 530 Complementary medicine, 180, 530 Compliance, 180, 316, 317, 530 Compulsion, 530, 602 Computational Biology, 459, 467, 530 Computed tomography, 421, 530 Computerized tomography, 235, 530 Concentric, 418, 517, 530 Conception, 509, 530, 543, 580, 593 Conduction, 235, 530 Cone, 530, 594 Congestion, 516, 530 Congestive heart failure, 283, 284, 418, 462, 530 Conjugated, 170, 199, 296, 520, 531, 533, 567 Conjugation, 307, 521, 531 Conjunctiva, 531, 598 Connective Tissue, 522, 529, 531, 544, 545, 546, 562, 582, 587, 592 Consciousness, 514, 531, 534, 536, 583 Constipation, 169, 377, 516, 531, 590 Constriction, 531, 557, 583, 601, 602 Constriction, Pathologic, 531, 601 Consultation, 223, 411, 531 Consummatory Behavior, 272, 531 Continuous infusion, 293, 531 Contraindications, ii, 531 Control group, 11, 490, 531 Controlled study, 74, 221, 531 Cor, 73, 306, 531, 581 Coronary heart disease, 11, 234, 277, 293, 332, 333, 340, 352, 360, 365, 381, 390, 418, 419, 424, 483, 485, 524, 526, 532, 551, 552 Coronary Thrombosis, 532, 565, 567 Corpus, 532, 562, 574, 581, 596 Corpus Luteum, 532, 562, 581

Cortex, 532, 552, 585 Cortical, 532, 589, 595 Corticosteroids, 532, 547 Cortisol, 79, 171, 187, 243, 331, 512, 532 Cortisone, 532, 535 Cranial, 532, 541, 549, 557, 563, 571, 575, 598, 600 Creatine, 273, 274, 389, 532 Creatine Kinase, 274, 389, 532 Creatinine, 532, 558, 599 Cribriform, 532, 571 Cross-Sectional Studies, 485, 532 Cues, 533 Culture Media, 511, 533 Curative, 346, 360, 533, 595 Cyclic, 357, 358, 523, 533, 579, 582 Cyclosporine, 533 Cysteine Endopeptidases, 533, 539 Cysteinyl, 533, 565 Cystine, 533, 537, 600 Cytochrome, 533, 573 Cytokine, 8, 533 Cytomegalovirus, 299, 533 Cytoplasm, 516, 525, 533, 549, 562, 565, 566, 567 Cytotoxic, 533, 585, 590 D Dairy Products, 533, 588 Data Collection, 534, 544 De novo, 363, 534 Decarboxylation, 534, 552 Decision Making, 10, 421, 534 Decubitus, 534, 600 Defecation, 380, 534 Degenerative, 312, 365, 376, 421, 496, 534, 551, 567, 572, 587 Dehydroepiandrosterone, 168, 199, 281, 284, 285, 308, 330, 534 Deletion, 78, 516, 534 Delirium, 516, 534 Delivery of Health Care, 534, 550 Dementia, 516, 534 Dendrites, 534, 569, 571 Depolarization, 534, 590 Dermal, 534, 592 Dermatitis, 534, 538 Dermatologic Agents, 534, 538 Desipramine, 285, 286, 534 Deuterium, 535, 552 Developed Countries, 309, 338, 363, 365, 482, 485, 535, 544 Developing Countries, 535

610 Obesity

Developmental psychology, 287, 535 Dexamethasone, 535 Dexfenfluramine, 423, 535 Dextroamphetamine, 318, 319, 513, 535, 576 Dextrorotatory, 304, 535 Diabetes Insipidus, 340, 343, 535 Diagnostic procedure, 241, 440, 535 Dialyzer, 535, 550 Diarrhea, 279, 288, 377, 520, 535 Diastole, 535, 580 Diastolic, 535, 553, 603 Diencephalon, 535, 540, 553, 595, 596 Dietary Fats, 535, 560 Dietary Fiber, 346, 423, 480, 535 Dietetics, 173, 184, 287, 407, 536 Diethylproprion, 286, 536 Diethylstilbestrol, 277, 536 Dietitian, 7, 228, 398, 536 Digestion, 283, 284, 287, 288, 361, 512, 520, 522, 535, 536, 537, 556, 560, 561, 593 Digestive system, 238, 341, 342, 373, 536, 545, 546 Digestive tract, 8, 519, 536, 591, 593 Dihydrotestosterone, 536, 585 Dilatation, 509, 536, 580, 584 Dilation, 522, 536 Dimethyl, 307, 346, 536 Diploid, 536, 578 Disaccharides, 288, 536 Discrete, 204, 328, 329, 536, 561 Discrimination, 332, 390, 477, 536, 602 Disease Vectors, 536, 556 Disinfectant, 536, 541 Disparity, 536 Disposition, 275, 536 Dissection, 204, 536, 599 Dissociation, 511, 536 Distal, 3, 245, 276, 317, 537, 538, 546, 557, 558, 580, 583, 584, 601 Disulphide, 328, 329, 537 Diuresis, 523, 537 Dopamine, 286, 307, 481, 513, 516, 522, 535, 537, 566, 569, 576 Dose-dependent, 345, 537 Drive, ii, vii, 8, 167, 242, 337, 395, 396, 398, 400, 419, 432, 477, 480, 489, 537, 559 Drug Tolerance, 537, 597 Duodenum, 520, 537, 539, 545, 557, 566, 569, 573, 589, 593, 601 Dyes, 513, 537, 576 Dyskinesia, 516, 537

Dyspepsia, 432, 537 Dysphagia, 432, 537 Dysplasia, 469, 537 Dyspnea, 505, 537, 573 Dystocia, 380, 537 Dystonia, 516, 537 Dystrophy, 206, 469, 537 E Echocardiography, 235, 537 Eczema, 293, 333, 352, 538 Edema, 538, 580, 599 Effector, 509, 529, 538, 568 Elasticity, 517, 538 Elastin, 367, 529, 538, 542 Elective, 538 Electrocardiogram, 220, 235, 538 Electrocoagulation, 528, 538 Electrode, 7, 242, 319, 337, 514, 525, 538 Electrolyte, 512, 534, 538, 558, 570, 579, 591, 599 Electroplating, 525, 538 Elementary Particles, 538, 583 Embryo, 509, 525, 538, 555, 570, 578, 580, 592 Embryo Transfer, 538, 580 Emesis, 377, 538 Emollients, 392, 538 Emphysema, 495, 538 Empiric, 268, 303, 316, 538 Emulsions, 511, 538 Endocrine System, 538, 539, 568 Endogenous, 237, 396, 523, 537, 538, 539, 548, 572 Endometrial, 539 Endometriosis, 334, 539 Endometrium, 445, 485, 539, 564 Endopeptidases, 367, 517, 533, 539, 565, 574, 590 Endorphins, 539, 569, 581 Endoscope, 539 Endoscopic, 276, 312, 359, 376, 480, 539 Endothelial cell, 368, 369, 521, 539, 544, 596 Endotoxic, 539, 560 Endotoxin, 76, 539, 599 End-stage renal, 425, 527, 539, 579 Energetic, 224, 269, 539 Energy deficit, 399, 539 Enkephalin, 539, 581 Environmental Exposure, 539, 571 Environmental Health, 458, 460, 539

Index 611

Enzymatic, 286, 386, 513, 523, 524, 530, 540, 543, 552, 564, 587 Enzyme Inhibitors, 540, 578 Ependyma, 517, 540, 596 Ephedrine, 185, 189, 540 Epidemiological, 221, 372, 396, 418, 419, 424, 428, 480, 540 Epidermal, 280, 540, 564 Epidermis, 540 Epidermoid carcinoma, 540, 593 Epigastric, 540, 573 Epinephrine, 510, 537, 540, 569, 599 Epithalamus, 535, 540, 560 Epithelial, 510, 540, 551 Epithelium, 519, 540, 571 Equipment and Supplies, 454, 540 Erectile, 331, 369, 384, 385, 540, 574 Erection, 540 Ergot, 522, 540 Erythrocyte Volume, 521, 541 Erythrocytes, 514, 522, 523, 541, 585 Erythromycin, 432, 528, 541 Esophageal, 7, 287, 432, 541 Esophageal Varices, 432, 541 Esophagus, 8, 276, 282, 291, 313, 359, 445, 536, 541, 545, 546, 561, 576, 585, 593 Essential Tremor, 469, 541 Estradiol, 9, 277, 338, 541 Estriol, 277, 541 Estrogen, 9, 14, 277, 334, 373, 449, 541, 581, 585, 589, 595 Estrone, 277, 541 Ethanol, 294, 541 Ether, 294, 295, 341, 541 Ethinyl Estradiol, 277, 541 Ethmoid, 541, 571 Ethnic Groups, 447, 541 Etiocholanolone, 330, 541 Evacuation, 531, 542, 545, 559 Evoke, 542, 593 Excipients, 542, 544, 576 Excitation, 526, 542, 569 Excrete, 516, 542, 558 Exercise Therapy, 542 Exhaustion, 195, 515, 542 Exocrine, 542, 573 Exocytosis, 286, 542 Exogenous, 266, 319, 511, 521, 538, 539, 542, 548, 599 Exon, 79, 274, 542 Expiration, 542, 586 Expiratory, 542

Extracellular, 367, 513, 518, 531, 542, 563, 591 Extracellular Matrix, 367, 531, 542, 563 Extracellular Matrix Proteins, 542, 563 Extracellular Space, 542 Extracorporeal, 386, 542 Extrapyramidal, 511, 516, 537, 542 Extreme obesity, 279, 283, 284, 391, 542, 601 Eye Infections, 510, 542 F Factor V, 542, 584 Failure to Thrive, 543 Fallopian tube, 543, 600 Family Planning, 459, 543 Fasciculation, 543, 569 Fatigue, 413, 543, 550 Fatty Liver, 277, 378, 543 Feces, 531, 543, 593 Feeding Behavior, 267, 357, 358, 543 Femoral, 295, 543 Femur, 543 Fenfluramine, 233, 266, 338, 382, 423, 535, 543 Fertilization in Vitro, 543, 580 Fetal Blood, 543, 577 Fetal Death, 465, 543 Fetal Macrosomia, 543 Fetus, 431, 509, 543, 544, 577, 580, 592, 593, 600 Fibrin, 521, 543, 578, 596, 597, 600 Fibrinogen, 543, 578, 596 Fibrinolysis, 183, 543 Fibroblast Growth Factor, 352, 544 Fibrosis, 268, 299, 303, 308, 315, 347, 372, 469, 512, 544, 588 Flatulence, 361, 377, 544 Flatus, 544, 545 Flavoring Agents, 544, 576 Fluoxetine, 266, 273, 333, 349, 544 Fluvoxamine, 266, 544 Focus Groups, 452, 544 Foetoplacental, 544, 570 Fold, 228, 234, 294, 391, 544 Follicles, 544, 555 Food Additives, 175, 544 Food Preferences, 10, 208, 544 Food Preservatives, 544 Forearm, 218, 521, 544, 563 Frameshift, 544 Frameshift Mutation, 544 Fructose, 288, 544, 548

612 Obesity

Fundus, 291, 544 Fungi, 531, 542, 545, 549, 565, 603 G Galanin, 305, 545 Gallate, 346, 382, 545 Gallbladder, 289, 432, 445, 485, 488, 509, 520, 527, 536, 544, 545, 546 Gallstones, 7, 8, 9, 195, 312, 376, 432, 520, 527, 545, 551 Gamma-interferon, 545, 556 Ganglia, 509, 519, 545, 568, 575, 594 Ganglion, 545, 571, 598 Gas, 218, 513, 523, 524, 544, 545, 552, 556, 569, 571, 584, 601 Gastric Balloon, 287, 545 Gastric banding, 290, 359, 362, 481, 545 Gastric Emptying, 287, 545 Gastric Fundus, 313, 545 Gastric Inhibitory Polypeptide, 339, 545 Gastrin, 545, 552 Gastroenterologist, 7, 545 Gastroenterology, 7, 8, 183, 432, 545 Gastroesophageal Reflux, 7, 8, 195, 432, 546 Gastrointestinal Hormones, 339, 546 Gastrointestinal tract, 276, 279, 282, 287, 290, 362, 453, 541, 544, 546, 559, 590, 592 Gastroplasty, 208, 311, 357, 359, 373, 374, 546 Gastrostomy, 282, 312, 359, 376, 546 Gelatin, 297, 533, 546, 548, 594 Gelatinases, 367, 546 Gene Expression, 75, 79, 172, 268, 303, 308, 316, 345, 347, 355, 371, 372, 381, 470, 546 Gene Rearrangement, 75, 546 Gene Therapy, 73, 386, 510, 546 General practitioner, 546 Genetic Code, 546, 570 Genetic Counseling, 495, 546 Genetic Engineering, 278, 520, 528, 546 Genetic testing, 547 Genital, 519, 528, 547, 600 Genitourinary, 547, 600 Genotype, 168, 332, 390, 512, 547, 576 Germ Cells, 354, 355, 547, 564, 572, 591, 595 Gestation, 547, 575, 577, 580, 592 Gestational, 195, 424, 465, 547 Ginseng, 353, 547 Gland, 243, 329, 330, 393, 510, 532, 547, 553, 562, 573, 577, 582, 585, 589, 593, 596 Glomerular, 547, 558, 586

Glomeruli, 547, 571 Glucocorticoid, 71, 74, 79, 243, 305, 331, 535, 547 Glucose Intolerance, 225, 234, 292, 414, 419, 535, 547 Glucose tolerance, 14, 77, 192, 221, 223, 225, 226, 234, 275, 288, 295, 369, 396, 547 Glucose Tolerance Test, 14, 221, 223, 547 Glucuronic Acid, 379, 547, 548 Glucuronides, 547, 548 Glutamate, 171, 548, 557 Glutamic Acid, 548, 569, 581 Glyburide, 548 Glycerol, 548, 576 Glycerophospholipids, 548, 576 Glycine, 305, 513, 520, 548, 569, 589 Glycogen, 243, 331, 548, 577 Glycoprotein, 512, 542, 543, 548, 596, 599 Glycosaminoglycans, 542, 548, 582 Glycoside, 372, 536, 548 Gonad, 548 Gonadal, 548, 593 Gout, 195, 286, 332, 390, 391, 488, 548 Governing Board, 548, 580 Government Agencies, 492, 548, 580 Grade, 173, 212, 228, 426, 444, 485, 527, 548 Graft, 512, 548, 552 Grafting, 548, 555 Granulocytes, 549, 590, 602 Granulosa Cells, 549, 555, 562 Grasses, 549, 551 Gravidity, 549, 574 Group dynamics, 490, 549 Growth, 72, 74, 75, 171, 195, 204, 206, 234, 243, 280, 288, 293, 299, 328, 329, 330, 331, 352, 367, 369, 384, 401, 405, 410, 422, 423, 430, 431, 442, 452, 469, 484, 510, 514, 515, 516, 517, 519, 525, 533, 535, 543, 544, 549, 552, 553, 556, 562, 565, 568, 571, 577, 589, 596, 599 Growth factors, 243, 280, 330, 331, 549, 565 Gynaecomastia, 549 Gyrus Cinguli, 549, 560 H Habitual, 211, 281, 358, 526, 549 Haematemesis, 538, 549 Haemorrhage, 509, 549 Haploid, 549, 577 Haplotypes, 549 Haptens, 511, 549 Headache, 523, 549, 590

Index 613

Health Behavior, 549 Health Care Costs, 203, 462, 485, 550 Health Education, 224, 397, 420, 495, 550 Health Expenditures, 550 Health Policy, 397, 550 Health Promotion, 179, 180, 186, 187, 449, 462, 474, 475, 478, 479, 483, 484, 550 Health Services, 534, 550 Health Status, 5, 191, 205, 549, 550 Health Surveys, 430, 550 Heart attack, 391, 524, 550 Heart failure, 540, 550, 603 Hematopoiesis, 369, 550 Heme, 520, 533, 550, 567, 579 Hemodialysis, 425, 523, 535, 550, 558 Hemodynamics, 418, 550 Hemoglobin, 13, 514, 541, 550, 551, 579 Hemoglobin A, 550, 579 Hemoglobinopathies, 546, 550 Hemoglobinuria, 469, 551 Hemorrhage, 538, 549, 551, 593 Hemostasis, 551, 590 Hepatic, 7, 8, 226, 265, 512, 534, 547, 551, 566 Hepatitis, 432, 551 Hepatocellular, 551 Hepatocellular carcinoma, 551 Hepatocytes, 551 Herbicides, 351, 551 Hereditary, 496, 512, 548, 551, 567, 587 Heredity, 314, 324, 418, 427, 453, 546, 547, 551 Hernia, 279, 551 Heterodimer, 75, 551 Heterogeneity, 511, 551 Heterogenic, 551 Heterogenous, 314, 324, 551 Heterozygote, 299, 551 Hibernation, 522, 551 High blood cholesterol, 425, 551 High-density lipoproteins, 289, 552 Hippocampus, 552, 560, 589 Histamine, 78, 390, 514, 516, 552 Histidine, 292, 552 Histocompatibility, 75, 552 Holidays, 448, 552 Homeostasis, 270, 271, 302, 552 Homologous, 309, 512, 521, 546, 551, 552, 594 Homosexuality, 414, 552 Hormonal, 305, 518, 552 Hormone Replacement Therapy, 9, 552

Host, 298, 308, 311, 347, 352, 371, 372, 374, 391, 512, 519, 536, 552, 554, 559, 601 Human growth hormone, 328, 329, 384, 552, 592 Humoral, 552, 554 Hybrid, 528, 552 Hydrogen, 223, 320, 321, 509, 513, 519, 523, 535, 542, 552, 560, 566, 572, 576, 583 Hydrogen Peroxide, 552, 560 Hydrolysis, 294, 335, 336, 517, 521, 525, 552, 560, 574, 576, 582, 599 Hydrophobic, 548, 553, 560 Hydroxylysine, 529, 553 Hydroxyproline, 513, 529, 553 Hygienic, 245, 359, 553 Hypercapnia, 553 Hypercholesterolemia, 191, 195, 237, 292, 293, 331, 333, 352, 369, 379, 384, 385, 537, 553 Hyperglycemia, 71, 184, 191, 221, 288, 292, 295, 320, 333, 353, 377, 388, 442, 553 Hyperlipidaemia, 274, 389, 553 Hyperphagia, 268, 281, 303, 309, 316, 347, 357, 358, 553 Hypersecretion, 293, 364, 553 Hypersensitivity, 553, 559, 587 Hyperthyroidism, 553, 581 Hypertriglyceridemia, 229, 331, 384, 385, 537, 553 Hypertrophy, 78, 334, 418, 520, 532, 553, 598 Hyperuricemia, 419, 548, 553 Hypoglycemia, 218, 553 Hypoglycemic, 221, 320, 553 Hypoglycemic Agents, 221, 553 Hypogonadism, 468, 553 Hypoplasia, 553 Hypotension, 516, 553, 569 Hypothalamic, 8, 72, 74, 172, 192, 204, 293, 305, 319, 423, 507, 553 Hypothyroidism, 553 Hypotonia, 527, 554 Hypoventilation, 289, 468, 505, 554 Hysterectomy, 5, 554 I Id, 176, 192, 475, 476, 478, 490, 491, 494, 502, 504, 554 Ileal, 311, 554 Ileum, 279, 525, 554, 557, 569, 602 Illusion, 314, 324, 554 Imidazole, 390, 552, 554 Immune function, 372, 554

614 Obesity

Immune response, 510, 515, 518, 532, 549, 554, 562, 594, 601 Immune system, 266, 372, 520, 554, 559, 562, 567, 576, 600, 602 Immunity, 554, 571 Immunization, 401, 554, 580 Immunocompetence, 554 Immunodeficiency, 189, 266, 366, 369, 469, 554 Immunodiffusion, 511, 554 Immunoelectrophoresis, 511, 554 Immunogenic, 554, 560 Immunoglobulins, 554, 578 Immunology, 510, 511, 554 Immunosuppressive, 547, 554 Impairment, 295, 518, 534, 537, 542, 554, 556, 564, 583 Implantation, 242, 337, 530, 555, 570 Impotence, 540, 555 In vitro, 221, 280, 289, 326, 327, 369, 538, 546, 555 In vivo, 75, 221, 280, 327, 328, 336, 360, 361, 369, 372, 396, 546, 555, 572, 596 Incision, 555, 557 Incompetence, 546, 555 Incontinence, 540, 555, 572 Indicative, 365, 400, 555, 574, 600 Induction, 326, 327, 396, 514, 516, 555, 581 Infancy, 535, 555 Infant, Newborn, 511, 555 Infarction, 230, 555 Infertility, 195, 214, 481, 522, 555 Inflammatory bowel disease, 432, 555 Infusion, 73, 77, 223, 555, 598 Ingestion, 213, 264, 287, 288, 297, 311, 351, 372, 373, 374, 547, 553, 555, 573, 578 Inhibin, 555 Initiation, 555 Inorganic, 244, 290, 345, 522, 556, 567 Inotropic, 537, 556 Inpatients, 556 Insecticides, 292, 556, 575 Insight, 219, 220, 224, 556 Insomnia, 383, 401, 556, 590 Insufflation, 284, 556 Insulin-dependent diabetes mellitus, 275, 312, 321, 322, 323, 325, 353, 556 Insulin-like, 328, 329, 556 Intercellular Adhesion Molecule-1, 556 Interleukin-1, 556 Interleukin-2, 556 Intermittent, 243, 329, 330, 556, 575

Interpersonal Relations, 399, 556 Interstitial, 522, 542, 556, 586 Intervertebral, 556 Intestinal, 211, 221, 245, 276, 279, 339, 363, 427, 524, 547, 556, 562 Intestinal Obstruction, 276, 279, 556 Intestine, 283, 284, 339, 341, 342, 379, 391, 443, 520, 522, 525, 529, 537, 552, 554, 556, 557, 558, 584, 591, 599 Intoxication, 534, 556, 602 Intracellular, 523, 555, 556, 564, 579, 582, 585, 590 Intracranial Pressure, 557, 583 Intramuscular, 9, 75, 281, 557, 573 Intramuscular injection, 75, 557 Intraperitoneal, 274, 389, 557 Intravenous, 219, 223, 277, 386, 555, 557, 573 Intrinsic, 511, 519, 557 Intubation, 525, 557 Invasive, 242, 290, 300, 317, 337, 357, 362, 443, 450, 554, 557, 562 Involuntary, 519, 527, 541, 557, 567, 590, 592 Ionizing, 539, 557, 563, 585 Ions, 509, 519, 536, 538, 552, 557, 583, 591 Ischemia, 518, 557 Ischemic stroke, 557 Islet, 170, 557 Isoenzyme, 532, 557 J Jejunoileal Bypass, 279, 300, 520, 557 Jejunum, 279, 520, 545, 557 Joint, 4, 416, 506, 517, 557, 572, 594 K Kainate, 304, 557 Karyotype, 557 Kb, 392, 458, 557 Keto, 281, 527, 558 Ketoacidosis, 509, 558 Ketone Bodies, 509, 558 Ketosis, 558 Ketosteroids, 281, 558 Kidney Cortex, 558, 565 Kidney Failure, 286, 353, 539, 558 Kidney Failure, Acute, 558 Kidney Failure, Chronic, 558 Kidney Transplantation, 425, 558 Kinetic, 557, 558 L Labile, 529, 542, 558 Lactation, 439, 526, 558, 570, 581

Index 615

Laparoscopy, 443, 558 Large Intestine, 449, 525, 529, 536, 556, 558, 585, 591 Larynx, 559, 597, 600, 602 Latent, 559, 580 Laxative, 511, 559, 592 Least-Squares Analysis, 559, 586 Lens, 559, 586 Lethal, 519, 559 Lethargy, 553, 559 Leukemia, 469, 546, 559 Leukocytes, 522, 526, 549, 559, 566, 599 Leukocytosis, 541, 559 Leukotrienes, 517, 559 Libido, 514, 559 Library Services, 502, 559 Life Expectancy, 283, 284, 559 Ligament, 543, 559, 582 Likelihood Functions, 559, 586 Limbic, 305, 513, 549, 559 Limbic System, 305, 513, 549, 559 Linear Models, 560, 586 Linkage, 301, 309, 525, 560, 574 Linkage Disequilibrium, 560 Lipase, 13, 78, 190, 201, 341, 342, 363, 382, 560, 572 Lipid A, 275, 281, 328, 329, 330, 344, 384, 485, 526, 560, 572 Lipid Peroxidation, 560, 573 Lipodystrophy, 189, 560 Lipolysis, 77, 265, 267, 311, 312, 321, 322, 323, 325, 360, 363, 366, 367, 560 Lipoma, 560 Lipopolysaccharides, 560 Lipoprotein Lipase, 186, 219, 431, 560 Lipoprotein(a), 560 Liposome, 277, 560 Lipoxygenase, 392, 517, 559, 561 Lithium, 516, 561 Liver Transplantation, 561 Lobe, 552, 561, 581 Loc, 561 Localization, 320, 561 Localized, 281, 320, 555, 560, 561, 566, 577, 578, 599 Locomotion, 380, 561, 577 Logistic Models, 561, 586 Longitudinal Studies, 396, 533, 561 Longitudinal study, 233, 485, 561 Loop, 328, 329, 334, 368, 388, 545, 551, 561 Low-calorie diet, 186, 269, 453, 561

Low-density lipoprotein, 289, 537, 560, 561 Lower Esophageal Sphincter, 311, 546, 561 Lubricants, 561, 576 Lumbar, 562 Lumen, 276, 356, 359, 562 Lung volume, 562 Lutein Cells, 562, 581 Lymph, 519, 526, 539, 562 Lymph node, 519, 526, 562 Lymphatic, 555, 562, 592 Lymphoblastic, 562 Lymphoblasts, 510, 562 Lymphocytes, 515, 517, 545, 554, 556, 559, 562, 592, 602 Lymphoid, 515, 532, 554, 562 Lymphoma, 469, 562 M Macrolides, 432, 562 Macrophage, 556, 562 Magnetic Resonance Imaging, 15, 223, 421, 562 Major Histocompatibility Complex, 549, 562 Malabsorption, 279, 469, 481, 562 Malignancy, 369, 509, 562 Malignant, 469, 510, 517, 562, 568, 585, 588 Malnutrition, 266, 512, 518, 522, 562, 567 Mammary, 549, 560, 562, 585, 595 Mammography, 5, 6, 563 Mania, 563 Manic, 231, 516, 521, 561, 563, 583 Manifest, 266, 563 Man-made, 525, 563 Marital Status, 4, 5, 563 Mastication, 563, 598 Maternal Behavior, 392, 563 Matrilysin, 367, 563 Matrix metalloproteinase, 367, 563 Maxillary, 563, 598 Maxillary Nerve, 563, 598 Meat, 168, 277, 296, 328, 329, 384, 535, 563, 588 Meatus, 563, 600 Medial, 393, 517, 541, 549, 563, 571, 588, 589 Median Nerve, 524, 563 Mediate, 537, 563 Mediator, 556, 563, 590 Medical Records, 4, 563 Medical Staff, 454, 564

616 Obesity

Medicament, 278, 281, 289, 290, 298, 332, 336, 337, 341, 342, 358, 379, 564, 594 MEDLINE, 459, 463, 467, 469, 564 Medullary, 564 Meiosis, 521, 564, 594 Melanin, 305, 357, 358, 564, 576, 599 Melanocytes, 564 Melanoma, 469, 564 Melanosis, 509, 564 Membrane Lipids, 564, 576 Memory, 514, 534, 564 Menarche, 207, 564 Meninges, 526, 564 Menopause, 186, 205, 230, 325, 334, 564, 570, 579, 580, 581 Menstrual Cycle, 564, 570, 581 Menstruation, 6, 196, 513, 564, 571 Mental Disorders, 239, 564, 580, 583 Mental Health, v, 207, 239, 332, 369, 452, 458, 466, 477, 564, 580, 584 Mental Processes, 536, 564, 583 Mental Retardation, 468, 470, 564 Mesolimbic, 516, 564 Meta-Analysis, 565 Metabolite, 243, 329, 330, 338, 521, 536, 541, 565, 581 Metalloendopeptidases, 539, 565 Metallothionein, 76, 172, 565 Metastasis, 367, 563, 565 Methionine, 536, 565, 581 MI, 171, 275, 375, 480, 508, 565 Microbe, 565, 597 Microbiology, 510, 518, 565 Microglia, 518, 565, 566 Microorganism, 529, 565, 574, 602 Microspheres, 360, 565 Midaxillary line, 565, 602 Migration, 556, 565 Millimeter, 565, 602 Minority Groups, 450, 482, 487, 565 Mitosis, 516, 565 Mobilization, 213, 326, 327, 526, 566 Monitor, 218, 532, 566, 570, 601 Monoamine, 307, 513, 535, 566 Monoamine Oxidase, 513, 535, 566 Monocytes, 367, 556, 559, 566 Monogenic, 314, 324, 566 Mononuclear, 566, 599 Monotherapy, 13, 304, 566 Monounsaturated fat, 296, 566 Morphological, 366, 538, 564, 566 Morphology, 566

Motilin, 432, 566 Motility, 312, 316, 321, 322, 323, 325, 432, 545, 566, 590 Motion Sickness, 566, 568 Motor Activity, 316, 339, 546, 566 Motor Skills, 462, 566 Movement Disorders, 516, 566, 595 Mucosa, 313, 546, 567, 581 Mucus, 520, 567 Multicenter study, 567 Muscle Fibers, 567 Muscle Hypertonia, 567, 569 Muscular Atrophy, 469, 567 Muscular Dystrophies, 537, 567 Musculoskeletal System, 391, 567 Mutagens, 544, 567 Mydriatic, 536, 567 Myocardial infarction, 11, 365, 532, 565, 567, 581 Myocardial Ischemia, 514, 567, 603 Myocardium, 514, 565, 567 Myofibrils, 523, 567 Myoglobin, 567, 579 Myotonic Dystrophy, 393, 469, 567 N Naive, 430, 567 Narcolepsy, 285, 286, 535, 540, 567 Nasal Cavity, 282, 567, 602 Nasal Septum, 567, 568, 602 Natriuresis, 568 Nausea, 377, 383, 515, 516, 558, 568, 573, 583, 599 NCI, 1, 238, 457, 475, 528, 568 Neonatal, 172, 568 Neoplasia, 469, 568 Neoplasm, 568, 599 Neoplastic, 541, 562, 568 Nephropathy, 338, 558, 568 Nerve Endings, 286, 308, 568 Networks, 214, 568 Neural, 8, 511, 513, 516, 535, 552, 565, 566, 568, 589, 591, 592 Neuroeffector Junction, 568 Neuroendocrine, 72, 306, 568 Neurogenic, 264, 312, 321, 322, 323, 325, 568 Neurogenic Inflammation, 312, 321, 322, 323, 325, 568 Neuroleptic, 511, 516, 568 Neurologic, 268, 303, 309, 316, 347, 569 Neuromuscular, 180, 509, 569, 599 Neuromuscular Diseases, 180, 569

Index 617

Neuromuscular Junction, 509, 569 Neuronal, 307, 376, 527, 569 Neurons, 534, 545, 568, 569, 571, 594 Neuropathy, 519, 569 Neuropeptide, 76, 272, 292, 299, 301, 305, 345, 348, 445, 569 Neurosurgery, 320, 569 Neurotensin, 369, 569 Neutrophil, 512, 556, 569 NHANES, 451, 478, 489, 569 Nicotine, 73, 376, 569 Nitrogen, 244, 352, 512, 513, 514, 542, 558, 569, 599 Nonverbal Communication, 569, 583 Norepinephrine, 285, 286, 307, 510, 535, 537, 540, 569, 576, 590 Normal Distribution, 299, 570 Nuclear, 295, 519, 528, 531, 545, 560, 563, 570, 595 Nuclei, 513, 531, 540, 546, 547, 562, 565, 570, 571, 583, 589 Nucleic acid, 343, 352, 365, 366, 367, 370, 519, 546, 567, 569, 570 Nurse Practitioners, 192, 570 Nursing Care, 570 Nutritional Support, 546, 570 Nutritive Value, 544, 570 O Obsessive-Compulsive Disorder, 544, 570 Odds Ratio, 7, 570, 586 Odour, 517, 570, 599 Oestrogen, 74, 570 Office Visits, 424, 571 Olfaction, 392, 571 Olfactory Bulb, 393, 571, 602 Olfactory Nerve, 7, 571 Oligomenorrhea, 571, 579 Oliguria, 558, 571 Omega-3 fatty acid, 296, 571 Omega-6 Fatty Acids, 296, 571 Oncogene, 469, 571 Opacity, 534, 571 Ophthalmic, 571, 598 Opsin, 571, 587 Optic Chiasm, 553, 571, 580 Optic Nerve, 571, 583, 587 Optic Nerve Diseases, 571, 583 Organelles, 533, 564, 566, 571 Orlistat, 13, 174, 191, 202, 226, 423, 572 Orthostatic, 516, 572 Osmosis, 572 Osmotic, 288, 512, 572

Osteoporosis, 172, 243, 299, 324, 325, 331, 570, 572, 585 Outpatient, 218, 220, 572 Ovaries, 334, 572, 579, 590, 600 Ovary, 532, 541, 548, 570, 572, 578 Ovum, 532, 547, 572, 581, 603 Oxalate, 572, 600 Oxalic Acid, 523, 572 Oxidants, 292, 572 Oxidation, 72, 419, 509, 516, 517, 521, 533, 537, 558, 560, 572, 573, 596 Oxidation-Reduction, 521, 572, 573 Oxidative Phosphorylation, 270, 271, 302, 371, 375, 573 Oxidative Stress, 345, 444, 573 Oxygen Consumption, 213, 573, 587 P Palliative, 570, 573, 595 Pancreas, 339, 427, 509, 536, 546, 556, 557, 560, 573, 589, 592, 599 Pancreatic, 172, 272, 311, 348, 364, 382, 469, 524, 546, 573 Pancreatic cancer, 469, 573 Pancreatic Juice, 546, 573 Pancreatic Polypeptide, 272, 348, 573 Pancreatitis, 8, 432, 573 Panic, 544, 573 Panic Disorder, 544, 573 Papilledema, 573, 583 Paradoxical, 77, 573 Parenteral, 539, 573 Parity, 204, 465, 574 Parkinsonism, 516, 574 Paroxetine, 291, 292, 574 Paroxysmal, 469, 514, 574 Parturition, 574, 581 Pathogen, 574 Pathogenesis, 7, 72, 76, 168, 191, 366, 408, 432, 574 Pathologic, 509, 516, 520, 532, 553, 574, 579 Pathologic Processes, 516, 574 Pathologies, 286, 574 Pathophysiology, 300, 411, 574 Patient Compliance, 269, 341, 574 Patient Education, 479, 481, 500, 502, 508, 574 Patient Selection, 10, 480, 574 Pelvic, 539, 574, 582 Pelvis, 509, 562, 572, 574, 600 Penicillin, 515, 574 Penis, 574, 600 Pepsin, 574, 589

618 Obesity

Peptide Chain Elongation, 528, 574 Peptide Hydrolases, 539, 574 Perception, 206, 360, 530, 574, 588 Percutaneous, 312, 359, 375, 376, 575 Perforation, 516, 575 Perfusion, 575 Perinatal, 464, 575 Periodontal disease, 575 Peripheral blood, 281, 367, 575 Peripheral Nervous System, 569, 575, 580, 588, 592, 594 Peripheral Nervous System Diseases, 569, 575 Peripheral Vascular Disease, 285, 353, 575 Peritoneal, 425, 557, 575 Peritoneal Cavity, 557, 575 Peritoneal Dialysis, 425, 575 Peritoneum, 575 Peroral, 313, 575 Pesticides, 292, 551, 556, 575 Petroleum, 294, 575 PH, 189, 321, 371, 462, 576 Phagocyte, 572, 576 Pharmaceutic Aids, 544, 576 Pharmaceutical Preparations, 340, 526, 541, 546, 576 Pharmacodynamics, 576 Pharmacokinetic, 576 Pharmacologic, 8, 272, 273, 348, 349, 350, 352, 397, 423, 461, 514, 576, 597 Pharmacotherapy, 300, 352, 398, 460, 487, 488, 576 Pharynx, 546, 567, 576, 600 Phenotype, 72, 78, 309, 314, 324, 345, 432, 576 Phentermine, 233, 266, 272, 273, 338, 348, 349, 350, 423, 576 Phenyl, 244, 292, 306, 321, 340, 341, 382, 576 Phenylalanine, 285, 286, 576, 599 Phenylpropanolamine, 286, 338, 474, 576 Phospholipases, 576, 590 Phospholipids, 168, 277, 543, 560, 564, 571, 576 Phosphorus, 523, 577 Phosphorylase, 523, 577 Phosphorylated, 528, 577 Phosphorylation, 577 Photocoagulation, 528, 577 Photoperiod, 577 Physical Examination, 218, 222, 227, 480, 552, 577

Physical Fitness, 207, 209, 212, 219, 431, 451, 463, 542, 577 Physical Therapy, 400, 460, 496, 577 Physiologic, 219, 264, 279, 311, 511, 517, 528, 564, 577, 582, 585, 590 Physiology, 12, 170, 171, 172, 264, 280, 326, 327, 345, 353, 383, 402, 405, 539, 545, 577 Pigmentation, 72, 564, 577 Pigments, 524, 528, 577, 587 Pilot Projects, 577 Pilot study, 221, 224, 227, 230, 577 Pituitary Gland, 544, 577, 581 Placenta, 541, 543, 544, 577, 581 Placental tissue, 577 Plaque, 425, 578 Plasma cells, 515, 578 Plasma protein, 388, 512, 578, 583 Plasmin, 578, 597, 600 Plasminogen, 79, 578, 597, 600 Plasminogen Activator Inhibitor 1, 79, 578 Plasminogen Activators, 578 Plastic surgeon, 234, 578 Platelet Activation, 578, 590 Platelets, 523, 578, 596 Platinum, 561, 578 Pneumonia, 531, 578 Poisoning, 534, 540, 556, 568, 578 Policy Making, 548, 578 Pollen, 578, 584 Polycystic, 214, 293, 333, 352, 424, 469, 579 Polycystic Ovary Syndrome, 214, 579 Polymers, 288, 340, 341, 342, 579, 582 Polymorphic, 365, 527, 579 Polyposis, 529, 579 Polysaccharide, 515, 526, 579, 582 Polyunsaturated fat, 168, 579, 596 Porphyrins, 345, 579 Posterior, 513, 518, 540, 565, 573, 579 Postmenopausal, 9, 14, 74, 373, 572, 579, 585 Postnatal, 72, 328, 329, 384, 431, 579 Postoperative, 283, 284, 480, 579 Postoperative Complications, 283, 284, 579 Postprandial, 221, 579 Postsynaptic, 568, 579, 590, 594 Post-translational, 368, 579 Potassium, 177, 218, 512, 579 Potentiates, 534, 556, 579 Potentiating, 299, 579 Potentiation, 579, 590

Index 619

Practicability, 580, 598 Practice Guidelines, 466, 490, 491, 580 Pre-Eclampsia, 580 Pregnancy Complications, 436, 580 Pregnancy Outcome, 580 Prejudice, 332, 580 Preload, 418, 580 Premenopausal, 15, 203, 219, 227, 580 Preoptic Area, 393, 580 Presynaptic, 333, 568, 569, 580, 594 Presynaptic Terminals, 568, 580 Primary Prevention, 210, 228, 230, 379, 422, 485, 580 Probe, 305, 319, 354, 355, 580 Prodrug, 291, 335, 336, 581 Progeny, 531, 581 Progesterone, 9, 581, 593 Progression, 180, 419, 514, 563, 581 Progressive disease, 311, 373, 374, 581 Projection, 569, 571, 581, 585 Prolactin, 292, 468, 522, 581 Proline, 529, 553, 581 Promoter, 74, 299, 355, 376, 403, 581 Prone, 73, 219, 247, 248, 249, 250, 251, 252, 253, 254, 255, 256, 257, 258, 259, 260, 261, 262, 263, 264, 318, 453, 581 Pro-Opiomelanocortin, 539, 581 Prophase, 521, 581, 594 Prophylaxis, 306, 344, 351, 363, 378, 382, 386, 387, 581 Proportional, 275, 581 Propranolol, 304, 581 Prospective Studies, 314, 324, 581 Prospective study, 446, 561, 581 Prostaglandin, 326, 581, 596 Prostaglandins A, 582 Prostate, 173, 334, 445, 469, 519, 520, 570, 582, 600 Prostatic Hyperplasia, 582 Protease, 512, 513, 529, 582, 597 Protein C, 295, 297, 345, 375, 444, 512, 513, 516, 519, 528, 560, 582 Protein Conformation, 513, 582 Protein S, 226, 243, 279, 331, 352, 415, 469, 470, 521, 528, 541, 546, 552, 582 Proteinuria, 338, 580, 582 Proteoglycan, 265, 582 Proteolytic, 368, 512, 529, 543, 578, 582, 597, 600 Prothrombin, 542, 583, 596 Protocol, 583

Protons, 270, 271, 302, 371, 375, 552, 557, 583, 585 Protozoa, 531, 565, 583 Proximal, 4, 245, 537, 545, 557, 558, 567, 580, 583, 589 Pruritic, 538, 583 Pseudotumor Cerebri, 304, 583 Psychiatric, 292, 564, 583 Psychiatry, 583 Psychic, 528, 559, 564, 583, 589 Psychoactive, 583, 602 Psychogenic, 264, 583 Psychology, 207, 216, 400, 405, 411, 414, 530, 535, 536, 583 Psychosis, 516, 547, 583 Psychotherapy, 283, 284, 583 Psychotomimetic, 513, 535, 583 Psyllium, 202, 583 Puberty, 207, 220, 237, 330, 396, 398, 584 Public Policy, 420, 459, 584 Pulmonary Alveoli, 554, 584 Pulmonary Artery, 521, 584, 601 Pulmonary Edema, 196, 558, 584 Pulmonary Embolism, 299, 584 Pulmonary Emphysema, 367, 512, 584 Pulmonary hypertension, 266, 304, 532, 584 Pulse, 317, 447, 566, 584 Punishment, 414, 488, 584 Pupil, 536, 567, 584 Purulent, 584, 600 Pyloric Sphincter, 290, 310, 362, 373, 374, 584 Pyloroplasty, 310, 373, 374, 584 Pylorus, 356, 584 Pyridoxal, 382, 584 Pyridoxal Phosphate, 382, 584 Q Quality of Life, 172, 266, 440, 446, 482, 483, 495, 496, 584 Quercetin, 221, 584 R Race, 4, 5, 182, 222, 298, 304, 307, 465, 557, 565, 584 Racemic, 298, 304, 307, 584 Radiation, 514, 538, 539, 557, 563, 584, 585, 603 Radioactive, 552, 555, 563, 570, 585 Radiological, 575, 585 Radiology, 6, 585 Radiotherapy, 522, 585 Raloxifene, 334, 585, 589

620 Obesity

Randomized, 13, 174, 181, 189, 219, 224, 227, 233, 236, 400, 460, 538, 585 Randomized clinical trial, 233, 585 Receptors, Serotonin, 585, 590 Recombinant, 75, 274, 308, 352, 370, 371, 372, 388, 389, 585 Recombination, 531, 546, 585 Rectum, 516, 522, 529, 534, 536, 544, 545, 555, 558, 582, 585, 594 Recurrence, 311, 373, 374, 521, 585 Red blood cells, 218, 541, 585 Red Nucleus, 518, 585 Reductase, 585 Refer, 1, 392, 529, 539, 545, 561, 567, 568, 583, 585, 597 Reflux, 8, 437, 546, 585 Refraction, 585, 592 Regeneration, 544, 586 Regimen, 242, 300, 337, 352, 430, 480, 538, 574, 576, 586 Regression Analysis, 465, 586 Regurgitation, 546, 586 Relapse, 214, 215, 397, 586 Relative risk, 465, 586 Remission, 521, 585, 586 Renal failure, 265, 338, 534, 586 Renin, 418, 514, 586 Renin-Angiotensin System, 586 Reproduction Techniques, 580, 586 Reproductive cells, 547, 586 Resection, 264, 586 Resolving, 276, 586 Respiration, 269, 516, 524, 526, 566, 586 Resting metabolic rate, 223, 314, 324, 587 Restoration, 577, 587, 602 Reticulata, 190, 587 Retina, 559, 571, 587, 588 Retinal, 309, 530, 536, 571, 587 Retinoblastoma, 469, 587 Retinol, 587 Retinopathy, 577, 587 Retrospective, 6, 464, 587 Retroviral vector, 546, 587 Rheumatism, 587 Rheumatoid, 367, 572, 587 Rheumatoid arthritis, 367, 587 Rhinitis, 540, 587 Rhodopsin, 571, 587 Ribose, 510, 587 Rigidity, 557, 574, 577, 587 Rod, 313, 519, 528, 588 Rodenticides, 575, 588

Rosiglitazone, 377, 588 Rural Population, 588 Rutin, 584, 588 S Sagittal, 9, 588 Salicylic, 290, 588 Salivary, 533, 536, 573, 588 Salivary glands, 533, 536, 588 Sapogenins, 329, 588 Saponin, 588 Satiation, 588 Saturated fat, 275, 296, 336, 337, 422, 423, 588 Schizoid, 588, 602 Schizophrenia, 231, 588, 602 Schizotypal Personality Disorder, 588, 602 Schwannoma, 588 Sclerosis, 281, 295, 359, 469, 517, 588 Secondary tumor, 565, 589 Secretin, 339, 589 Secretory, 10, 568, 589, 594 Seizures, 468, 534, 574, 589 Selective estrogen receptor modulator, 585, 589, 595 Self Care, 509, 589 Self-Help Groups, 589, 591 Semen, 582, 589 Seminal vesicles, 589, 600 Seminiferous tubule, 555, 589 Semisynthetic, 522, 528, 541, 589 Senile, 572, 589 Sepsis, 265, 589 Septal, 560, 589 Septal Nuclei, 560, 589 Sequence Homology, 367, 589 Sequential treatment, 589 Serine, 539, 589, 590, 597, 599 Serine Endopeptidases, 539, 590 Serotonin, 266, 285, 307, 333, 382, 509, 516, 535, 543, 544, 566, 569, 574, 576, 585, 590, 599 Sertraline, 266, 590 Sex Characteristics, 510, 514, 570, 584, 590, 595 Sex Determination, 469, 590 Shivering, 270, 271, 302, 371, 375, 590, 596 Shock, 590, 598 Sibutramine, 76, 202, 307, 346, 423, 440, 590 Signal Transduction, 171, 590 Signs and Symptoms, 586, 590, 599 Skeleton, 291, 543, 557, 558, 582, 591

Index 621

Skull, 557, 591, 595 Smoking Cessation, 230, 232, 460, 486, 522, 591 Smooth muscle, 312, 321, 322, 323, 325, 391, 512, 514, 523, 552, 567, 586, 591, 592, 594 Social Class, 591 Social Environment, 225, 584, 591 Social pressure, 450, 591 Social Problems, 289, 332, 591 Social Support, 180, 215, 591 Sodium, 418, 422, 424, 512, 548, 568, 591, 600 Sodium Channels, 591, 600 Soft tissue, 521, 591 Solvent, 509, 527, 541, 548, 572, 591 Soma, 591, 592 Somatic, 354, 355, 386, 510, 528, 552, 559, 564, 566, 575, 592, 600 Somatic cells, 354, 355, 386, 564, 566, 592 Somatostatin, 293, 364, 592 Somites, 392, 592 Sorbitol, 288, 592 Sound wave, 530, 592 Soybean Oil, 579, 592 Spasm, 569, 592 Specialist, 416, 497, 536, 592 Specificity, 511, 517, 539, 592 Spectrum, 265, 565, 592 Sperm, 514, 527, 578, 586, 589, 592 Sphincter, 290, 362, 559, 592 Spinal cord, 518, 522, 526, 527, 540, 545, 563, 564, 568, 569, 575, 592, 594 Spleen, 533, 562, 592 Spontaneous Abortion, 580, 592 Sporadic, 587, 593 Squamous, 540, 593 Squamous cell carcinoma, 540, 593 Squamous cells, 593 Stabilization, 224, 593 Statistically significant, 5, 13, 14, 593 Steatosis, 8, 226, 543, 593 Steel, 528, 593 Sterility, 78, 555, 593 Steroid, 237, 243, 307, 330, 415, 520, 532, 548, 551, 558, 570, 588, 593 Stillbirth, 580, 593 Stimulant, 292, 513, 523, 535, 552, 576, 593 Stimulus, 537, 538, 542, 568, 584, 593, 596 Stool, 341, 342, 380, 529, 555, 558, 593 Stromal, 539, 593 Struvite, 593, 600

Subacute, 555, 593 Subclinical, 214, 555, 589, 594 Subcutaneous, 9, 14, 15, 295, 345, 366, 510, 538, 560, 573, 594, 601, 602 Subspecies, 592, 594 Substance P, 541, 565, 589, 594 Substrate, 268, 274, 303, 316, 389, 540, 594 Supplementation, 189, 192, 272, 273, 288, 290, 348, 349, 350, 362, 594 Support group, 495, 496, 507, 594 Suppositories, 360, 546, 594 Suppression, 273, 286, 296, 350, 382, 393, 594 Sympathetic Nervous System, 315, 324, 518, 569, 594 Sympathomimetic, 292, 513, 535, 537, 540, 569, 576, 594 Symphysis, 526, 582, 594 Symptomatic, 9, 573, 594 Synapse, 291, 510, 535, 568, 569, 580, 594, 598 Synapsis, 594 Synaptic, 333, 569, 590, 594 Synaptic Transmission, 569, 594 Synergistic, 318, 382, 581, 595 Systemic, 342, 388, 418, 516, 521, 534, 540, 550, 555, 595, 598 Systems Theory, 287, 595 Systolic, 13, 553, 595, 603 Systolic blood pressure, 13, 595 Systolic heart failure, 595 T Tamoxifen, 334, 589, 595 Tardive, 516, 595 Telangiectasia, 469, 595 Telecommunications, 264, 595 Temporal, 288, 513, 552, 563, 595 Temporal Lobe, 513, 595 Teratogenesis, 595 Terminator, 528, 595 Testis, 541, 570, 595 Testosterone, 585, 595 Thalamic, 518, 540, 595 Thalamic Diseases, 518, 595 Thalamus, 535, 540, 560, 595 Therapeutics, 209, 309, 396, 566, 595 Thermogenesis, 189, 224, 269, 271, 301, 315, 324, 366, 371, 375, 406, 596 Thermoregulation, 269, 392, 577, 596 Thigh, 9, 543, 596 Thinness, 400, 596 Third Ventricle, 517, 540, 553, 595, 596

622 Obesity

Thorax, 509, 562, 596, 600 Threshold, 428, 553, 596 Thrombin, 542, 543, 582, 583, 596 Thrombocytes, 578, 596 Thromboembolism, 312, 376, 596 Thrombolytic, 578, 596 Thrombomodulin, 582, 596 Thrombosis, 354, 582, 593, 596 Thromboxanes, 517, 596 Thrombus, 532, 555, 557, 567, 596, 601 Thyroid, 171, 202, 380, 506, 553, 596, 599 Thyrotropin, 554, 596 Thyroxine, 512, 576, 596 Tin, 357, 524, 578, 596 Tinnitus, 583, 596 Tissue Plasminogen Activator, 597 Tomography, 428, 530, 597 Tone, 78, 554, 567, 572, 597 Tonus, 597 Tooth Preparation, 510, 597 Topical, 518, 541, 552, 597 Toxic, v, 169, 186, 291, 292, 531, 539, 549, 554, 569, 597 Toxicity, 244, 277, 296, 345, 597 Toxicokinetics, 597 Toxicology, 170, 460, 597 Toxin, 539, 597 Trace element, 527, 528, 596, 597 Trachea, 559, 576, 596, 597 Traction, 528, 597 Transduction, 590, 597 Transfection, 520, 546, 598 Transfusion, 288, 598 Translation, 513, 541, 598 Translational, 598 Translocation, 528, 541, 598 Transmitter, 509, 518, 537, 563, 569, 598, 601 Transplantation, 527, 538, 554, 562, 598 Transversion, 309, 598 Trauma, 289, 519, 534, 549, 573, 595, 597, 598, 602 Treatment Failure, 598 Treatment Outcome, 398, 598 Triad, 598 Tricuspid Atresia, 532, 598 Tricyclic, 534, 598 Trigeminal, 7, 563, 598 Trigeminal Nerve, 7, 598 Trigger zone, 516, 598 Triglyceride, 220, 222, 289, 311, 321, 322, 323, 325, 419, 553, 598

Trophic, 243, 331, 599 Truncal, 14, 599 Trypsin, 512, 599 Tryptophan, 529, 590, 599 Tuberous Sclerosis, 469, 599 Tumor Necrosis Factor, 78, 326, 327, 599 Tumour, 393, 545, 599 Tunica, 567, 599 Tyrosine, 74, 272, 273, 285, 286, 292, 348, 349, 350, 537, 599 U Ulcer, 599, 600 Unconscious, 554, 599 Unsaturated Fats, 296, 599 Uraemia, 573, 599 Urbanization, 482, 599 Uremia, 558, 586, 599 Ureters, 599, 600 Urethra, 519, 520, 574, 582, 599, 600 Uric, 548, 553, 599 Urinary, 279, 523, 540, 547, 555, 571, 597, 600 Urinary Calculi, 279, 600 Urinary Plasminogen Activator, 597, 600 Urinary tract, 600 Urogenital, 373, 547, 600 Urogenital System, 373, 600 Urokinase, 578, 600 Uterine Contraction, 509, 600 Uterus, 509, 526, 532, 539, 544, 554, 564, 569, 572, 581, 600 V Vaccine, 335, 510, 583, 600 Vagal, 264, 600 Vagina, 526, 536, 564, 600 Vaginitis, 6, 197, 600 Vagotomy, 300, 600 Vagus Nerve, 264, 599, 600 Valproic Acid, 304, 600 Varicose, 197, 293, 312, 333, 352, 376, 600 Varicose vein, 293, 312, 333, 352, 376, 600 Vasculitis, 573, 600 Vasoconstriction, 272, 540, 600 Vasodilator, 522, 537, 552, 601 VE, 219, 601 Vein, 218, 223, 235, 557, 570, 601 Venous, 283, 284, 418, 582, 598, 601 Venous Thrombosis, 601 Venter, 601 Ventral, 204, 334, 517, 553, 601 Ventricle, 513, 518, 531, 552, 584, 595, 596, 598, 601

Index 623

Ventricular, 418, 531, 598, 601, 603 Ventricular Dysfunction, 601 Venules, 521, 523, 601 Vertebrae, 556, 592, 601 Vertebral, 592, 601 Vertical banded gastroplasty, 481, 601 Veterinary Medicine, 459, 601 Video Recording, 427, 601 Videodisc Recording, 601 Viral, 334, 335, 597, 601 Virulence, 597, 601 Virus, 72, 75, 189, 266, 334, 335, 519, 547, 578, 587, 597, 601 Viscera, 592, 601 Visceral Afferents, 518, 600, 601 Visceral fat, 9, 15, 232, 419, 601 Visual field, 571, 583, 601 Vital Statistics, 521, 602 Vitro, 602 Vivo, 360, 361, 372, 602 VLCD, 475, 602 Vocal cord, 417, 602 Volition, 359, 557, 602

Vomeronasal Organ, 571, 602 W Waist circumference, 14, 72, 428, 450, 526, 602 War, 175, 602 Weight Perception, 602 Wheezing, 495, 602 White blood cell, 510, 515, 559, 562, 567, 569, 578, 602 Windpipe, 576, 596, 602 Withdrawal, 73, 245, 534, 602 Wound Healing, 243, 331, 544, 563, 602 Wound Infection, 279, 602 X Xamoterol, 290, 602 Xenograft, 514, 603 X-ray, 223, 228, 235, 506, 525, 530, 563, 570, 585, 603 Y Yeasts, 545, 576, 603 Z Zygote, 530, 531, 603 Zymogen, 582, 603

624 Obesity

Index 625

626 Obesity