Eating Disorders

Psychological Disorders

Eating Disorders

Psychological Disorders

Addiction Anxiety Disorders Eating Disorders Depression and Manic Depression

Psychological Disorders

Eating Disorders

Pamela K. Keel Foreword by

Pat Levitt, Ph.D. Vanderbilt Kennedy Center for Research on Human Development Vanderbilt University

Eating Disorders Copyright © 2006 by Infobase Publishing All rights reserved. No part of this book may be reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage or retrieval systems, without permission in writing from the publisher. For information contact: Chelsea House An imprint of Infobase Publishing 132 West 31st Street New York NY 10001 ISBN-10: 0-7910-8540-6 ISBN-13: 978-0-7910-8540-0 Library of Congress Cataloging-in-Publication Data Keel, Pamela K., 1970– Eating disorders / Pamela K. Keel. p. cm. — (Psychological disorders) Includes bibliographical references and index. ISBN 0-7910-8540-6 1. Eating disorders I. Title. II. Psychological disorders (Chelsea House Publishers) RC552.E18K44 2005b 616.85'26—dc22 2005021406 Chelsea House books are available at special discounts when purchased in bulk quantities for businesses, associations, institutions, or sales promotions. Please call our Special Sales Department in New York at (212) 967-8800 or (800) 322-8755. You can find Chelsea House on the World Wide Web at http://www.chelseahouse.com Text and cover design by Keith Trego Printed in the United States of America Bang EJB 10 9 8 7 6 5 4 3 2 This book is printed on acid-free paper.

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Table of Contents

Foreword

1 Introduction 2 Anorexia Nervosa 3 Bulimia Nervosa 4 Binge Eating Disorder and Eating Disorders Not Otherwise Specified 5 Causes of Eating Disorders 6 Treatment 7 Future Directions

vi 1 10 29

48 58 74 84

Notes

94

Glossary

97

Further Reading

102

Websites

103

Index

105

Foreword

Pat Levitt, Ph.D. Kennedy Center for Research on Human Development Vanderbilt University

Think of the most complicated aspect of our universe, and then multiply that by infinity! Even the most enthusiastic of mathematicians and physicists acknowledge that the brain is by far the most challenging entity to understand. By design, the human brain is made up of billions of cells called neurons, which use chemical neurotransmitters to communicate with each other through connections called synapses. Each brain cell has about 2000 synapses. Connections between neurons are not formed in a random fashion, but rather, are organized into a type of architecture that is far more complex than any of today’s supercomputers. And, not only is the brain’s connective architecture more complex than any computer, but its connections are capable of changing to improve the way a circuit functions. For example, the way we learn new information involves changes in circuits that actually improve performance. Yet some change can also result in a disruption of connections, like changes that occur in disorders such as drug addiction, depression, schizophrenia, epilepsy, or even changes that can increase a person’s risk of suicide. Genes and the environment are powerful forces in building the brain during development, and ensuring normal brain functioning, but can also be the root causes of psychological and neurological disorders when things go awry. The way in which brain architecture is built before birth and in childhood will determine how well the brain functions when we are adults, and even how susceptible we are to such diseases as depression, anxiety or attention disorders, which can severely

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FOREWORD

disturb brain function. In a sense, then, understanding how the brain is built can lead us to a clearer picture of the ways in which our brain works, how we can improve its functioning, and what we can do to repair it when diseases strike. Brain architecture reflects the highly specialized jobs that are performed by human beings, such as seeing, hearing, feeling, smelling and moving. Different brain areas are specialized to control specific functions. Each specialized area must communicate well with other areas for the brain to accomplish even more complex tasks, like controlling body physiology—our patterns of sleep, for example, or even our eating habits, both of which can become disrupted if brain development or function is disturbed in some way. The brain controls our feelings, fears and emotions, our ability to learn and store new information, and how well we recall old information. The brain does all this, and more, by building, during development, the circuits that control these functions, much like a hard-wired computer. Even small abnormalities that occur during early brain development through gene mutations, viral infection or fetal exposure to alcohol can increase the risk of developing a wide range of psychological disorders later in life. Those who study the relationship between brain architecture and function, and the diseases that affect this bond, are neuroscientists. Those who study and treat the disorders that are caused by changes in brain architecture and chemistry are psychiatrists and psychologists. Over the last 50 years, we have learned quite a lot about how brain architecture and chemistry work and how genetics contribute to brain structure and function. Genes are very important in controlling the initial phases of building the brain. In fact, almost every gene in the human genome is needed to build the brain. This process of brain development actually starts prior to birth, with almost all the

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neurons we will ever have in our brain produced by mid-gestation. The assembly of the architecture, in the form of intricate circuits, begins by this time, and by birth, we have the basic organization laid out. But the work is not yet complete, because billions of connections form over a remarkably long period of time, extending through puberty. The brain of a child is being built and modified on a daily basis, even during sleep. While there are thousands of chemical building blocks, such as proteins, lipids and carbohydrates, that are used, much like bricks and mortar, to put the architecture together, the highly detailed connectivity that emerges during childhood depends greatly upon experiences and our environment. In building a house, we use specific blueprints to assemble the basic structures, like a foundation, walls, floors, and ceilings. The brain is assembled similarly. Plumbing and electricity, like the basic circuitry of the brain, are put in place early in the building process. But for all of this early work, there is another very important phase of development, which is termed ‘experience-dependent’ development. During the first three years of life, our brains actually form far more connections than we will ever need, almost forty percent more! Why would this occur? Well, in fact, the early circuits form in this way so that we can use experience to mold our brain architecture to best suit the functions that we are likely to need for the rest of our lives. Experience is not just important for the circuits that control our senses. A young child who experiences toxic stress, like physical abuse, will have their brain architecture changed in regions that will result in poorer control of emotions and feelings as an adult. Experience is powerful. When we repeatedly practice on the piano, or shoot a basketball hundreds of times daily, we are using experience to model our brain connections to function at

FOREWORD

their finest. Some will achieve better results than others, perhaps because the initial phases of circuit-building provided a better base, just like the architecture of houses may differ in terms of their functionality. We are working to understand the brain structure and function that results from the powerful combination of genes building the initial architecture and a child’s experience adding the all-important detailed touches. We also know that, like an old home, the architecture can break down. The aging process can be particularly hard on the ability of brain circuits to function at their best, because positive change comes less readily as we get older. Synapses may be lost and brain chemistry can change over time. The difficulties in understanding how architecture gets built are paralleled by the complexities of what happens to that architecture as we grow older. Dementia associated with brain deterioration as a complication of Alzheimer’s disease or memory loss associated with aging or alcoholism are active avenues of research in the neuroscience community. There is truth, for both development and in aging, in the old adage ‘use it or lose it.’ Neuroscientists are pursuing the idea that brain architecture and chemistry can be modified well beyond childhood. If we understand the mechanisms that make it easy for a young, healthy brain to learn or repair itself following an accident, perhaps we can use those same tools to optimize the functioning of aging brains. We already know many ways in which we can improve the functioning of the aging or injured brain. For example, for an individual who has suffered a stroke that has caused structural damage to brain architecture, physical exercise can be quite powerful in helping to reorganize circuits so that they function better, even in an elderly individual. And you know that when you exercise and sleep regularly, you just feel better. Your brain chemistry and

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architecture are functioning at their best. Another example of ways we can improve nervous system function are the drugs that are used to treat mental illnesses. These drugs are designed to change brain chemistry so that the neurotransmitters used for communication between brain cells can function more normally. These same types of drugs, however, when taken in excess or abused, can actually damage brain chemistry and change brain architecture so that it functions more poorly. As you read the series Psychological Disorders, the images of altered brain organization and chemistry will come to mind in thinking about complex diseases such as schizophrenia or drug addiction. There is nothing more fascinating and important to understand for the well-being of humans. But also keep in mind that as neuroscientists, we are on a mission to comprehend human nature, the way we perceive the world, how we recognize color, why we smile when thinking about the Thanksgiving turkey, the emotion of experiencing our first kiss, or how we can remember the winner of the 1953 World Series. If you are interested in people, and the world in which we leave live, you are a neuroscientist, too. Pat Levitt, Ph.D. Director, Vanderbilt Kennedy Center for Research on Human Development Vanderbilt University Nashville, Tennessee

Introduction

1

Milaena was brought into treatment for an eating disorder shortly after her 12th birthday. She weighed 78 pounds (35.5 kg) and was 4 feet, 11inches (1.5 meters) tall. She had started losing weight about two months before her 12th birthday, losing 17 pounds (7.7 kg) over the course of nine weeks. At first, her parents blamed her loss of appetite on the flu that had been going around. However, Milaena continued to complain that she wasn’t hungry at meals even after she felt well enough to go to school. After two weeks of this, her parents took her to the doctor. An extensive physical exam and tests showed no cause for Milaena’s weight loss. The doctor asked whether Milaena might have an eating disorder, but her parents insisted that there must be something physically wrong with their daughter. They felt certain that she wasn’t eating because she was sick. As they continued to search for the cause of her weight loss, Milaena continued to lose weight, all along saying that she just wasn’t hungry. Her parents did not know what to do to help their daughter. Desperate for a clue about what was going on, Milaena’s mother read Milaena’s diary, looking back to when the problem first began. In the diary, Milaena described her terror that she would be the fattest girl at her birthday party and detailed her plan to lose weight. Milaena’s diary provided a daily log of 1

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Eating Disorders

Figure 1.1 A preoccupation with one’s weight is a result of eating disorders. People with disorders such as anorexia nervosa, bulimia nervosa, and binge eating jeopardize their health to maintain or achieve a weight that is less than average for their particular height.

Introduction

the exact number of calories she was eating, the exact number of calories she was burning, and the estimated number of calories she was getting rid of by vomiting intentionally. Her parents took her for medical treatment immediately after reading the diary, but they feared that they had already lost their daughter. They felt that they could no longer trust her, and they worried that Milaena would never forgive them for invading her privacy.

Like thousands of girls, Milaena suffers from an eating disorder. Eating disorders include problems with eating too little and problems with eating too much. Although eating disorders often involve weight problems (weighing too little as a result of not eating or weighing too much because of overeating), many people who suffer from eating disorders do not look particularly underweight or overweight. In addition, not all people who are underweight or overweight have an eating disorder. Almost everyone overeats at one time or another, and most girls have gone on a diet, eating far less than would be considered normal or healthy. Overeating and dieting are not, in themselves, eating disorders. However, they may be related to the risk for developing an eating disorder (Figure 1.1). ANOREXIA NERVOSA

Anorexia nervosa is a condition in which a person starves him-

or herself. The key feature of this eating disorder is the refusal to eat enough food, resulting in a body weight that is far below a healthy level. Sometimes, individuals with anorexia nervosa are described as looking “painfully thin.” This is a good description because many people with anorexia nervosa experience a lot of physical discomfort because of their low body weight. In addition to having a low weight, people with

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Eating Disorders

St. Catherine of Siena Understanding the history of eating disorders is difficult because few historical texts deal with the emotional experiences of girls or women. One exception to this is St. Catherine of Siena (1347–1380). Born into a wealthy home before becoming a Roman Catholic nun, Catherine was a prolific writer who left behind many accounts of her own experiences with fasting. Catherine’s difficulties with eating first appeared during her childhood. As a child, she refused to eat meat, would engage in religious fasts, and had a fierce independent streak. After her older sister died in childbirth, Catherine developed a deep antipathy toward marriage and motherhood. She cut off her hair and took measures to make herself unattractive. At about age 16, Catherine developed a pattern of self-starvation. She started by consuming only bread, water, and vegetables. At around 23, she eliminated bread and vegetables and lived on communion wafers, water, and bitter herbs. She would suck and chew on bitter herbs and spit out the juice and saliva. In addition to extreme fasting, Catherine engaged in strenuous physical activities, including cleaning, service to the poor,

Introduction

and long, vigorous walks. Catherine also engaged in selfinduced vomiting. Catherine viewed her self-starvation as a form of illness that she was forced to bear, in her own words (translated from the original) Catherine wrote, “I prayed continually and I pray to God and will pray that he will grace me in this matter of eating so that I may live like other creatures.” Despite her prayers, it is clear that Catherine’s behaviors were intentional. Church superiors were concerned that Catherine’s extreme fasting would result in death by her own hand—or suicide, which is a sin within the Catholic Church. According to writer Rudolph Bell, in response to these concerns, “Catherine shot back that eating would kill her anyway so she might as well die of starvation, and do as she wished in the meantime.” Catherine died from the effects of starvation on April 29, 1380, at the age of 33. Whether Catherine suffered from anorexia nervosa has long been debated. It is certain that a fear of becoming fat did not motivate her food refusal. Thus, she does not meet the diagnostic criteria for anorexia nervosa. Cases of “spiritual starvation” have been found in women in the 20th century in the United States. These cases resemble anorexia nervosa in all respects with one exception: They do not appear to be motivated by a desire to lose weight. Perhaps in modern-day patients, fear of becoming fat is an interpretation of self-starvation rather than its cause. A challenge in understanding any eating disorder is distinguishing between the causes and effects of the disorder. Sources: Bell, Rudolph M. Holy Anorexia. Chicago: University of Chicago Press, 1985; Bynum, Caroline W. Holy Feast and Holy Fast: The Religious Significance of Food to Medieval Women. Berkeley: University of California Press, 1987.

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anorexia nervosa have an intense fear of gaining weight or becoming fat. These individuals may believe they are fat even when they are extremely thin, they may deny the dangers associated with their low weight, or they may feel that controlling their weight is more important than anything else. In girls and women, anorexia nervosa also involves the loss of menstrual periods. Anorexia nervosa occurs most often in adolescent and young adult women and has been estimated to affect 0.5% to 1.0% of all females. That means that between 1 in 200 and 1 in 100 females suffer from anorexia nervosa at some point in their lives. Anorexia nervosa is far less common in males, affecting 0.05% to 0.1% of men (or 1 in 2,000 to 1 in 1,000 men) at some point in their lives. Anorexia nervosa has become more common over the last 100 years; however, the disorder is not a “modern” condition. In 1874, British physician Sir William Gull first used the term anorexia nervosa to describe several adolescent female patients who engaged in self-starvation that led to severe weight loss. Just prior to Gull’s description of the disorder, a French physician, Charles Lasegue,1 described l’anorexie hysterique, a persistent pattern of self-starvation among adolescent girls. In the experience of both physicians, some patients recovered after refeeding, while others died from starvation despite intense efforts on the part of relatives and doctors to help them. Examining historical texts suggests that anorexia nervosa may have existed long before it was officially recognized at the end of the 1800s.2 Historical documents describe fasting girls in the 1800s, miraculous maids in the 1700s, and saints of the Roman Catholic Church from the 1200s to 1700s who all appear to have suffered from self-starvation conditions. There is also evidence that anorexia nervosa exists in many different cultures.2 Cases of anorexia nervosa have been described

Introduction

in patients who have had no prior exposure to Western ideals of beauty, such as an 18-year-old nomadic girl from the Middle East who had lived her entire life in the desert with no exposure to modern media. BULIMIA NERVOSA

Bulimia nervosa is characterized by episodes of binge eating in

which an individual feels a loss of control over food consumption and eats very large amounts of food in single sittings. The person then uses extreme measures to avoid weight gain, such as self-induced vomiting, laxative abuse, diuretic abuse, fasting, or excessive exercise. Like people with anorexia nervosa, individuals with bulimia nervosa base their self-worth on their weight and shape. Bulimia nervosa most often occurs in adolescent and young adult females, affecting 0.5% to 3.0% of women (1 in 200 to 1 in 33) at some point in their lives. Bulimia nervosa is more common than anorexia nervosa. However, like anorexia nervosa, bulimia nervosa is far less common in males. Estimates suggest that 0.05% to 0.3% of men (or 1 in 2,000 to 1 in 300) suffer from bulimia nervosa at some point in their lives. Bulimia nervosa appears to be a modern problem. British physician Gerald Russell first used the term bulimia nervosa in 1979 to describe normal-weight female patients who binged and vomited. Many of these patients had suffered from anorexia nervosa prior to developing bulimia nervosa, which suggested a link between the two eating disorders. Rates of bulimia nervosa increased dramatically over a very short period of time in the second half of the 20th century. Recent data suggest that rates of bulimia nervosa may have peaked in the 1980s, with the disorder affecting as many as 1 in 5 college women.3 In addition to being a modern problem, bulimia nervosa appears to be a problem restricted to Western cultures such as the United

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States and England or to individuals who have been exposed to Western ideals. BINGE EATING DISORDER AND OTHER EATING DISORDERS NOT OTHERWISE SPECIFIED (EDNOS)

Binge eating disorder (BED) is characterized by binge eating in

the absence of extreme weight control behaviors. As a result of frequent binge eating episodes, individuals with binge eating disorder tend to be significantly overweight, or obese. However, a person does not have to be overweight to be diagnosed with binge eating disorder. Binge eating disorder is considered an eating disorder not otherwise specified (EDNOS) because individuals with the disorder have a clinically significant problem controlling their eating but they do not fulfill the requirements to be diagnosed with either anorexia nervosa or bulimia nervosa. People who have other EDNOS include those who purge after eating normal amounts of food, individuals who chew food and then spit it out, and people who do not meet the full criteria for a diagnosis of either anorexia nervosa or bulimia nervosa. Of the various EDNOS, the most research has been completed on binge eating disorder. Binge eating disorder affects 0.7% to 4% of the general population (1 in 100 to 1 in 25 people). The disorder affects approximately 30% of people (1 in 3) who are trying to lose weight through a weight control program. It is more common among women than men; however, the difference between women and men is smaller than for anorexia or bulimia nervosa. Specifically, for every three women with binge eating disorder, there are two men with binge eating disorder. It is not possible to determine whether rates of binge eating disorder have risen or fallen over time. Historical references to gluttony suggest that problems with overeating are not new. However, the disorder is

Introduction

of little concern in times and cultures where food is too scarce to allow for binge eating episodes. EATING DISORDERS AND RACE/ETHNICITY

Eating disorders have been closely tied to cultural ideals of feminine beauty. This association has led some individuals to assume that mainstream ideals would only place members of racial/ethnic majority groups at risk. This assumption has been supported for some eating disorders in some comparisons of ethnic/racial groups. Specifically, anorexia nervosa and bulimia nervosa appear to be less common in African-American women than in white women.4 Binge eating disorder is also more common in white women than African-American women, but the difference in frequency was less dramatic. Aside from lower rates of eating disorders in African-American women, there is no evidence that eating disorders are less common in women of other ethnic/racial minority groups. Moreover, adolescents from many ethnic/racial backgrounds have similar rates of disordered eating attitudes and behaviors. It does not seem that white girls are at a particularly increased risk for developing eating disorders. Instead, it seems that African-American girls may be protected from developing anorexia nervosa and bulimia nervosa. Differences among groups in risk for developing eating disorders provide important leads for understanding the causes of eating disorders (see Chapter 5).

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Anorexia Nervosa

I have heard girls and women say that they wish they could have

anorexia, “at least for a little while.” This wish seems to come from two aspects of anorexia nervosa that are appealing. First, individuals with anorexia nervosa are able to lose a lot of weight. Given the increasing rates of overweight individuals and obesity and the multibillion-dollar diet industry, it is clear that most individuals find it very difficult to lose weight. So, the idea of having anorexia nervosa is appealing to some people because it seems to be a way to lose weight easily. Having anorexia may be viewed as a means to a makeover. Second, people who have anorexia nervosa seem to have incredible willpower. Most individuals who fail to lose weight or fail to maintain weight loss feel they have failed because of some personal weakness. People who have anorexia nervosa never seem to fall prey to the same weaknesses of appetite. Strangely, these two views are contradictory. If it really were easy for people with anorexia nervosa to lose weight, then they would not be demonstrating great willpower. However, if it takes great willpower to resist urges to eat, then it must not be easy for individuals with anorexia nervosa to lose weight. Not only is it impossible for both of these things to be true, but it turns out that both are false. There is nothing easy about what individuals with anorexia nervosa go through in their pursuit of 10

Anorexia Nervosa

weight loss. In addition, although the refusal to eat is intentional, the person’s intense fear of food and eating is not. People with anorexia nervosa may choose not to eat, but they do not choose to have anorexia nervosa. It chooses them. Individuals with great willpower are those who fight against anorexia nervosa despite the intense fear and feelings of loss of control it causes. People who say that they wish they could have anorexia nervosa might as well wish that they could contract a deadly parasite that would eat away at their bodies. CASE STUDY

Ashley developed anorexia nervosa during her senior year of high school. She had always been an athlete and played on all the team sports through junior high and high school. She was also a star student. At then end of the 8th grade, she had been voted top female student in front of the school assembly, and her boyfriend, Todd, had been chosen top male student. Each year of high school, Ashley was elected to the homecoming court until her senior year, when she should have been voted homecoming queen. Ashley’s problems began during the spring of her junior year, when she was caught cheating on an exam in precalculus. Ashley had been part of a popular and competitive group of female friends who had been together since junior high. Most members of her clique were straight-A students and active in extracurricular activities. They had always been supportive of each other, but had also always been very aware of who was doing the best. Each girl in the group wanted to become valedictorian for the graduating class, but Ashley had remained in the lead throughout high school, with her perfect 4.0 grade point average. This, combined with her annual title of homecoming princess, placed Ashley at the top. After her cheating was revealed, other stories came out as

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well. Some girls said Ashley had not been helpful on group projects, but had taken credit for their work. Other girls said that if they called Ashley to find out what they had missed at school after a sick day, they were told she was too busy to talk on the phone. Several of Ashley’s friends felt that Ashley had betrayed them. Even those girls who felt sorry for Ashley were worried about their own reputations in school and were careful to express their support only in private and to express their disapproval in public. While the girls whispered behind Ashley’s back, the boys started to confront her directly, making suggestive jokes at her expense. Without her group of friends to support her, Ashley did not know how to respond. By the end of her junior year, Ashley’s cheating resulted in a failing grade in precalculus. She was placed on academic probation, was expelled from the honor society, and was suspended from the softball team. To make up for lost practices, Ashley started to watch what she was eating and began to work out on her own. Her new workout regimen helped fill the time she used to spend at practice and hanging out with her friends. Although Ashley had never been fat, she became fascinated by the increasing muscle definition she achieved with her new workout. She found that exercising and weight loss gave her a sense of order and control that she was lacking since losing her academic reputation and her circle of friends. She started to buy magazines that promised physical perfection. Each article offered different explanations of how the body used food for energy and different advice on how to use diet and exercise to achieve the perfect body. Ashley followed each diet religiously, adding the requirements of one diet to the rules she was already following from previous diets. Soon, Ashley had just a small list of foods that she would eat. When fall nominations for homecoming queen were

Anorexia Nervosa

announced, Ashley was confronted by the far-reaching effects of her fall from grace—she was not nominated. Instead, her best friend from junior high school and one of her former friends, Sarah, became homecoming queen. Sarah was short and round and a bundle of energy. Of Ashley’s friends, Sarah was one of the few who would still talk to Ashley. Sarah knew that Ashley did all of the assigned reading and homework and studied many hours for every exam. Sarah believed that Ashley would have received As even without cheating and thought that Ashley’s cheating was related to her fears of failure. Ashley was grateful for Sarah’s friendship. At the same time, however, Ashley felt that she needed to be better than Sarah at something. Ashley chose weight. At 5 feet, 7 inches (1.7 meters) tall, Ashley was more than 8 inches (20 cm) taller than Sarah, who was not quite 4 feet, 11 inches (1.5 meters). Because Sarah was so short, she had always weighed less than Ashley. Ashley decided that she would change that. Sarah became concerned about Ashley’s weight loss. Ashley misunderstood Sarah’s dismay when Ashley could fit into Sarah’s clothes. Ashley thought that Sarah felt inferior. Instead, Sarah was horrified to see Ashley’s rib cage when she was changing clothes. Sarah wasn’t sure what to do. She talked with some of her closest friends to get advice. However, this made the situation worse. Rumors started circulating around school that Ashley had an eating disorder. All of the criticism that had been leveled at Ashley after her cheating came back in a new form, as judgment against her for having an eating disorder. Ashley denied the accusations and felt more alone than ever. Ashley stopped talking to Sarah and blamed Sarah for all her problems. Sarah decided to talk to Ashley’s parents about Ashley’s eating habits and weight loss. Ashley’s parents did not know what to think about Sarah’s concerns, but agreed to take

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Ashley to a doctor who could discuss healthy ways to manage her weight. Because Ashley was not yet 18 years old, the doctor shared her medical findings with Ashley’s parents. Ashley’s height was measured at 5 feet, 6 inches (1.67 meters), and her weight was measured at 93.5 pounds (42.5 kg), making her weight 72% of what would be expected for her height. Ashley challenged the accuracy of the measurements because she knew that she was 5 feet, 7 inches. However, the doctor explained that Ashley’s extreme dieting may have caused some bone loss and shrinking, similar to what is often seen in elderly people. Ashley had also stopped menstruating. Because her periods had always been irregular during sports seasons, she had not been concerned when her periods stopped altogether. However, she had not menstruated for over seven months. When the doctor explained the number of calories adolescent girls should eat to stay healthy, Ashley was horrified by the amount of food she was being asked to eat. Ashley insisted that eating so much food would make her fat. She was already unpopular at school. She could not tolerate the idea of being fat, too.

Ashley’s case demonstrates many of the symptoms and features of anorexia nervosa. She deliberately maintains a weight that is well below normal for her height. She expresses an intense fear of becoming fat and does not recognize the dangers of maintaining her current low weight. She has also stopped her menstrual cycles. Like many patients with anorexia nervosa, Ashley is perfectionistic (although not actually perfect), competitive, and is motivated by an intense fear of failure. EFFECTS OF ANOREXIA NERVOSA

Anorexia nervosa affects how a person feels, thinks, and

Anorexia Nervosa

15

Figure 2.1 Anorexia nervosa results in a loss not only of body fat, but also muscle, bone, and even organ tissue. The loss of such vital components causes the body to age prematurely, “shrinking” as an elderly person’s frame might and increasing the risk for bone fractures.

behaves, and it also affects physical health and how the individual gets along with other people. Many of the condition’s effects on feelings, thoughts, and behaviors actually occur because of what anorexia nervosa does to the body. Physical Effects of Anorexia Nervosa

By definition, anorexia nervosa involves significant weight loss. Most individuals think of weight loss as a loss of fat. However, weight loss in people with anorexia nervosa is due to a loss of not only fat, but also muscle, organ tissue, and bone (Figure 2.1). When the body lacks food to use for fuel, it begins to break down body tissue for energy. Although the body uses fat tissue first, it switches to other bodily tissues when it is starving. The lack of food also prevents the body from building new tissue, which can lead to significant delays in growth during adolescence

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as well as major delays in healing after an injury. In addition to losing weight, Ashley’s height was reduced because of bone loss. Loss of bone mass increases the risk of serious bone fractures. Without enough food, many systems of the body cannot function normally. In addition to the loss of menstrual function Ashley showed, patients with anorexia nervosa have problems with regulating body temperature, sleeping properly, bowel function, heart rate, and blood pressure. People with anorexia nervosa suffer from insomnia, constipation, slow heart rate, low blood pressure, and hair loss. They also constantly feel cold because their bodies cannot control their temperature, and they often have a difficult time finding a comfortable position. This is both a result of general restlessness and a lack of fat to cushion bones from surfaces. Although anorexia nervosa causes hair loss in most patients, some people with anorexia nervosa develop a fine, downy hair all over their body called lanugo. Lanugo is a kind of hair that develops as the fetus grows in the womb to help regulate the fetus’s body temperature. In patients with anorexia nervosa, lanugo appears to serve the same purpose. The loss of organ tissue includes the loss of brain tissue. The brain contains gray matter and white matter with a core of ventricles that contain cerebrospinal fluid in the center. The gray matter is where brain cells (neurons) are located. These neurons enable the brain to receive information about the outside environment and about what is happening inside the body and to send information to the muscles about how to react to these cues. Patients with anorexia nervosa have increased ventricle size and decreased brain mass. Finally, anorexia nervosa can lead to death. Approximately 1 in 20 patients die. Compared to other mental disorders, anorexia nervosa has the highest risk of death.

Anorexia Nervosa

Emotional Effects of Anorexia Nervosa

For many individuals with anorexia nervosa, weight loss is accompanied by emotional numbing. For Ashley, this emotional numbing may have helped her cope with the losses she experienced after she was caught cheating. Although they may feel less sad and angry, people with anorexia nervosa also feel less happy and engaged. They stop laughing. They stop crying. All of their emotions are reserved for one specific thing—fear of losing control over eating and weight. Anxiety becomes increasingly intense and paralyzing. The person sees further weight loss as a way to relieve the overwhelming fear. People with anorexia nervosa believe that if they can just lose more weight, they will no longer feel frightened. Instead, increased weight loss only makes the anxiety and fear worse. Some patients reach a point at which they literally want to weigh nothing at all—they want to lose weight until they don’t exist anymore. The desire to live and thrive decreases so much that nonsuicidal patients with anorexia nervosa are similar to suicidal patients in that they are more repelled by life and less repelled by death, compared to nonsuicidal psychiatric patients and healthy people.5 In addition to starvation, suicide is a leading cause of death in anorexia nervosa. Cognitive Effects of Anorexia Nervosa

The word cognitive refers to thoughts and thought processes. Cognitive abilities include attention, memory, recall, decisionmaking, planning, and problem-solving. Attention is the ability to keep your mind focused on this sentence. Memory is the ability to remember what this sentence said as you read the next sentence. Recall is the ability to tell someone else what cognitive means without looking it up. Decision-making is the ability to decide whether to continue reading this chapter, grab a different book, or stop reading altogether. Planning is the ability to decide

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on a course of action that will lead to some desired future outcome, such as planning to read one chapter of a book each day so that you will finish it by the end of a week. Problem-solving is the ability to resolve conflicts, such as when you realize that there are eight chapters in your book and only seven days in the week and decide to read two, shorter chapters in a single day so you can finish the book in one week. Given the effects of anorexia nervosa on brain tissue, it is not surprising that the disorder impairs the ability to think. Specifically, people with anorexia nervosa have problems with attention, concentration, memory, and the ability to solve prob-

Minnesota Starvation Study In the 1940s, Ancel Keys, a researcher at the University of Minnesota, conducted a study to understand the effects of starvation and the best ways to restore weight. The purpose of the study was to understand how to help World War II soldiers who had been held prisoner in Nazi concentration camps. Subjects in the study were conscientious objectors to World War II. Although conscientious objectors could not be asked to serve their country in ways that would lead to another person’s death, they could be drafted to take part in research that would help rehabilitate World War II soldiers. In addition, conscientious objectors were ideal subjects because they did not differ physically or psychologically from the men who went to war. Men who had been disqualified for military service for physical or psychological reasons might not respond to starvation or refeeding the way that soldiers would. After completing medical and psychological evaluations to confirm their health, the research subjects were placed on a

Anorexia Nervosa

lems. Intelligence test scores have been shown to decrease during the illness and return to pre-illness levels after the weight returns to a healthy level. Although individuals who undertake fasts claim to experience increased clarity of thought and may seem very rational and unemotional, individuals with anorexia nervosa often make irrational statements and draw irrational conclusions. For example, Ashley is unable to understand that her dramatic weight loss upsets Sarah because Sarah is worried about Ashley’s health. Instead, she expects that Sarah would feel envious of Ashley’s figure. People with anorexia nervosa may claim that they follow a healthy diet that reduces the risks of

diet to produce extreme weight loss. This study provided valuable information about the effects of starvation. During the course of weight loss, the men in the study became withdrawn and depressed. Although none of these men sought weight loss for personal reasons, the conscientious objectors showed many of the same food obsessions seen in patients with Conscientious objectors to World War II were subjects in a study to anorexia nervosa. In fact, understand the effect of starvation. after successfully returning to their normal weight, several of the study’s participants went into food-related careers, such as becoming chefs.

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obesity. In fact, they are ignoring the health risks associated with their starvation, which may be even more dangerous than being overweight. They ignore evidence that they were less obsessed with their eating and weight before they developed anorexia nervosa. They claim that their fears will be resolved if they carefully follow a specific regimen and reach a specific target weight. People who have anorexia nervosa may claim that the physical discomfort they feel while eating poses a more serious threat to their health than not eating. Anorexia nervosa is often accompanied by preoccupations with food, eating, and weight. For example, Ashley spends a great deal of time poring over magazine articles about diets and exercise. Some of this behavior may be explained by the effort required for the patient to maintain a diet strict enough to cause significant weight loss or to maintain a very low weight. However, a famous study conducted in the 1940s in Minnesota suggests that much of this is a consequence of starvation rather than its cause (see “Minnesota Starvation Study, pages 18–19). Behavioral Effects of Anorexia Nervosa

In addition to preoccupations with food, eating, and weight, people who suffer from anorexia nervosa develop rituals. These rituals may include keeping detailed records of the calories they consume and burn, and how much they weigh. In addition, individuals may engage in elaborate rituals at mealtimes. These serve to increase the amount of contact they have with food while limiting the amount of food they actually eat. Common rituals include eating foods that are normally eaten with utensils with the fingers, cutting food into very small pieces, putting strange combinations of foods together, adding unusual seasonings and condiments to foods (for example, adding mustard to oatmeal), or eating food from a single small dish. Individuals may also engage in specific rituals for weighing themselves, weigh themselves

Anorexia Nervosa

repeatedly throughout the day, or check specific body parts (for example, they may check to see if they can wrap their fingers around their wrist or count a specific number of ribs). Exercise regimens can also become highly ritualized. A person may intend to do 45 sit-ups. If he or she gets interrupted at number 43, the person will start over again from the beginning, in order to complete exactly 45 sit-ups. The preoccupations and rituals seen in people with anorexia nervosa resemble the behaviors of people who have obsessivecompulsive disorder. This anxiety disorder leads sufferers to do things like repeatedly wash their hands or turn light switches on and off a specific number of times before leaving a room. Interestingly, anorexia nervosa and obsessive-compulsive disorder frequently occur at the same time in the same individual. Interpersonal Effects of Anorexia Nervosa

Individuals with anorexia nervosa often become increasingly socially isolated. Their refusal to eat cuts off participation in many social activities, and they may even avoid attending events if food will be present. Avoiding these events may be motivated by a fear that they will lose control and eat, or by a fear of having people notice that they do not eat. The effects of starvation may make it difficult for individuals with anorexia nervosa to follow normal, everyday conversations. In addition, the effects of starvation on emotions may reduce a person’s motivation to interact with others. A person with anorexia nervosa may choose to engage in extensive exercise regimens instead of spending time with friends and family. In Ashley’s case, her social isolation appeared to serve as a trigger for her anorexia nervosa. In addition, her peers’ reactions to her problems isolated her further. However, the decision to focus all of her attention and energy on eating was made by Ashley. For Ashley, this was her way to avoid

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directly dealing with the effects her cheating had on her friendships and reputation in school. Rather than pursuing the perfect body, Ashley might have tried to repair her friendships, focused on the few friendships that survived the incident, or developed new friendships. RECOGNIZING ANOREXIA NERVOSA

Why didn’t Ashley’s parents see that their daughter was in trouble before Sarah approached them? Why didn’t Ashley’s teachers notice that something was wrong? If Ashley was so emaciated from starvation, why did it take so long for anyone to notice? Although it seems hard to believe that a condition that is so physically obvious would go unnoticed, it often does (Figure 2.2). Being underweight is not the same thing as having anorexia nervosa. There is a wide range of body types that are normal and healthy for different people. Thus, there are individuals who weigh considerably less than what is considered average for their height, age, and gender, but they do not have a problem. They are simply naturally thin. These people often have thin parents and thin relatives. Being underweight may be a normal part of adolescent development for many people. Even people who are not thin in their natural constitution may go through a period in adolescence when their height shoots up but their weight does not keep up. This process can be especially distressing for adolescent boys who feel that they are too skinny and not as muscular as they would like to be. These periods of uneven growth are usually time-limited, and weight eventually catches up to height. Losing significant amounts of weight does not happen overnight. For people who have daily interactions with a person who is suffering from anorexia nervosa, the person’s weight on one may not be markedly different from his or her weight on the next. As a result, people may gradually get used to seeing the

Anorexia Nervosa

Figure 2.2 This table shows some of the demographics on eating disorders, most specifically, anorexia nervosa.

person weigh less without noticing the weight loss. Dramatic weight changes may be noticed only when looking at pictures taken several months earlier or by someone who has not seen the person for a longer period of time (such as a grandparent or other extended family member). Most people view weight loss as a positive change. Because many people are overweight and actively diet to try to lose weight, there is a tendency to applaud weight loss rather than worry about it. Indeed, many individuals who develop anorexia nervosa at first receive praise for losing weight and for seeming to demonstrate willpower around food.

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Current ideals of beauty in Western societies like the United States are significantly underweight. Portraying extremely thin actresses and models as beauty icons makes it harder for people to recognize that these states are unhealthy. People with anorexia nervosa often wear clothes that hide their weight and shape. Sometimes they wear large, baggy clothes because they feel that they weigh too much and are embarrassed by the size of certain body parts. At other times, the person may wear baggy clothes to keep others from noticing that he or she has lost an alarming amount of weight. Sometimes, people with anorexia nervosa wear large clothes because they feel cold and need several layers of clothing to keep warm because of the effects starvation has on the body’s ability to regulate temperature. Regardless of the actual motivation that underlies wearing oversized clothes, it may be difficult for others to notice significant weight loss, because it is not possible to see the person’s body clearly. Given that low weight may be normal for some individuals and may be hidden from view, how does one tell if a person may be suffering from anorexia nervosa? The first sign, of course, is weight loss. Although individuals who are constitutionally thin or are going through a growth spurt during adolescence may appear to be very thin, he or she will not have actually lost any weight. That means the clothes that he or she wore before should still fit (although they might be a little too short after the growth spurt). Thus, if a person seems to be swimming in his or her regular clothes, it might be worth trying to figure out whether the person is wearing clothes that once fit or clothes that were bought larger than he or she needs. A second sign would be cessation of growth and developmental processes. In addition to loss of menstrual cycles in females, an individual with anorexia nervosa may also fail to grow in height during adolescence. So, an individual whose

Anorexia Nervosa

development seems to have halted or even reversed may be showing the effects of self-starvation. A third sign would be if the person displays odd behaviors around food, eating, and exercise. Although dieting is extremely common among teenage girls, ineffective dieting is the norm. That is, many girls are on diets that they do not stick to very well. If a person does not need to lose weight and yet seems to be very dedicated to avoiding specific foods or eating very small portions, this may be a sign of anorexia nervosa. Such behaviors may be masked by claims that the person is too busy to eat or has already eaten. If a person is never seen eating and is underweight, then it is reasonable to conclude that he or she may have anorexia nervosa. Similarly, if an underweight person engages in strange rituals around eating that prolong the amount of time required to eat and reduce the actual amount of food eaten, then he or she may have anorexia nervosa. A fourth sign would be if a very thin person makes self-deprecating comments that suggest that he or she believes him- or herself to be overweight. Again, although self-deprecating comments are normal among teenage girls, for girls who are underweight, comments about being fat are simply inappropriate. If they are insincere, such comments may be an attempt to make heavier girls feel inferior. If they are sincere, such comments may represent significant disturbances in the way the person perceives his or her body, as is the case with anorexia nervosa. A fifth sign would be extensive, time-consuming exercise workouts that seem to go beyond what would be required for health or athletic performance. People should be willing not to exercise when they are sick or injured, since exercising under these conditions could cause serious health problems. Similarly, people should not sacrifice important academic and social activities or sleep in favor of self-imposed exercise plans.

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HOW TO RESPOND TO SUSPICIONS OF AN EATING DISORDER

This section will start with what you should not do in response to suspicions that a person has an eating disorder. Doing nothing is unacceptable. Eating disorders are dangerous conditions that can ultimately lead to death. Pretending that nothing is wrong may seem like silent approval to a person who has an eating disorder. Talking to your friends to get their opinion on whether or not someone has an eating disorder is also not a good idea. Your friends won’t know any more than you do whether or not someone has an eating disorder. The person who may have an eating disorder may feel like you are gossiping and trying to hurt him or her by discussing private problems with others. Both responses are probably the most common responses to suspicions, because doing nothing may reduce anxiety and avoid conflict, and talking to friends provides reassurance. Unfortunately, both responses make the person who suspects there is a problem feel better without necessarily offering any benefit for the person who may have an eating disorder. So, what should you do if you suspect that someone you know may have an eating disorder? First, remember that suspicion is not the same as fact. Even if the person seems to show all the signs of anorexia nervosa, there may be other reasons for weight loss, food refusal, and social withdrawal. For example, a person who is undergoing chemotherapy for cancer may experience hair and weight loss, may be unable to eat certain foods due to nausea, and may withdraw from friends. Although it is highly unlikely that the person would be engaging in strenuous exercise, his or her condition may well mimic much of what was described for anorexia nervosa, since the physical effects of significant weight loss are the same, regardless of the underlying reason. To find out what’s going on, use an information-seeking approach. Do not assume that you already know what is happening.

Anorexia Nervosa

Second, talk to someone who is in a position to help the person about whom you are concerned. For example, a school guidance counselor will maintain the confidentiality of what you discuss, will be able to try to help the student in question, and can help reduce your concerns. Do not attempt to be the person’s therapist. Although peer counseling can be helpful, peer counselors undergo a great deal of training and receive supervision before they help others. If you have concerns about the ability of school counselors to respond to this issue, you may wish to speak with a school nurse. Both school counselors and school nurses have received education and training to allow them to help students with mental health concerns like eating disorders. In contrast, a teacher does not necessarily have this kind of background. In addition, the person about whom you are concerned may feel betrayed if you speak with someone he or she has as a teacher. For these reasons, it is better to talk to a school counselor or nurse than to a teacher. Seek out information on eating disorders and be willing to listen in a way that will be supportive of the person but not of the eating disorder. This sounds much easier than it is. For most individuals with anorexia nervosa, their disorder is ego-syntonic. Ego-syntonic means that the disorder does not feel like something that is happening to them; instead, it feels like something they are choosing to do. It feels like something that they want to do. Indeed, the first criterion for anorexia nervosa is a refusal to maintain a minimum healthy weight. Thus, to be diagnosed with anorexia nervosa, a person must demonstrate deliberate attempts to reduce weight or to maintain a very low weight. Because anorexia nervosa is ego-syntonic, this makes it seem like part of the person. As a result, efforts to help stop the eating disorder may feel like an attempt to change the person, or a rejection of who and what the person is, cares about, and believes in. Because an individual with anorexia nervosa views

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him- or herself as merged with the disorder, it becomes hard for others to see the person differently. However, it’s important to remember that this is an illusion created by the illness. Although people with anorexia nervosa choose not to eat, they never chose to develop anorexia nervosa. It is important to remember that the person existed as a unique individual before anorexia nervosa developed. •

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SUMMARY

A useful way to think about anorexia nervosa when supporting a friend or relative is to view anorexia nervosa as a parasite. Parasites are biological organisms that cannot exist without a host. Anorexia nervosa does not exist without the person it afflicts. Parasites thrive by feeding off of the host, often by depleting resources intended to further the host’s survival. Anorexia nervosa, too, feeds off of its host. Parasites are capable of changing the behavior of the host to allow the parasite to survive, even at the expense of the host’s survival. Anorexia nervosa promotes a series of behaviors that increase the strength of the eating disorder at the expense of the person. Finally, if not treated and removed, parasites can kill their hosts. Anorexia nervosa can kill that person if not treated.

Bulimia Nervosa

3

Bulimia nervosa is far more common than anorexia nervosa in

the United States. In fact, the relative frequency of bulimic symptom patterns (bingeing and vomiting), far outstrips the frequency of the purely restricting eating patterns. This is because many people who suffer from anorexia nervosa also have bulimic symptoms. These individuals are considered to have the binge-purge subtype of anorexia nervosa (as opposed to the restricting subtype, which involves the use of fasting and exercise to produce and sustain weight loss). When followed over time, most people who have anorexia nervosa and do not recover eventually develop binge eating and/or purging behaviors. If many individuals with anorexia nervosa also binge and purge, then what exactly distinguishes bulimia nervosa from anorexia nervosa? The simple answer is weight. Although people with bulimia nervosa and people with anorexia nervosa may display very similar behaviors—binge eating and purging— those who have bulimia nervosa do not reach a weight that is much lower than what would be expected for their age and height. Maintaining a relatively normal weight appears to protect individuals with bulimia nervosa from many of the negative consequences described in Chapter 2 for people with anorexia nervosa. Most importantly, there is a far lower risk of death with bulimia nervosa than with anorexia nervosa. Death is over 10 29

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times more likely for a patient with anorexia nervosa than one with bulimia nervosa. Does the lower death rate mean that bulimia nervosa is a less severe disorder? Not necessarily. Bulimia nervosa still has medical risks, and the potential for these risks to contribute to death over a prolonged period of time is not known. However, in an overall comparison, it would seem that health is less severely compromised in bulimia nervosa than in anorexia nervosa. Unlike with anorexia nervosa, individuals with bulimia nervosa are more likely to view themselves as suffering from their eating disorder. Bulimic symptoms tend to be highly ego-dystonic. That is, binge eating and purging are experienced as distressing problems that the person is unable to control. I have never heard people say that they wish they had bulimia nervosa. Even from the outside, people seem to understand that patients with bulimia nervosa do not enjoy their symptoms, and there is little admiration for individuals who suffer from binge/purge patterns. Whereas people with anorexia nervosa may be viewed as having a lot of self-control, those who have bulimia nervosa are viewed as having little self-control. In addition, they are often perceived as being secretive and deceitful. However, like stereotypes concerning people with anorexia nervosa, generalizations about people with bulimia nervosa are neither logical nor accurate. For binge eating and purging to be secretive and deceitful, the behaviors would have to be a hidden problem in a person who seemed to be functioning reasonably well in other aspects of life. Many individuals with bulimia nervosa are reasonably high functioning in terms of grades in school, participation in extracurricular activities, and their ability to form friendships. In addition, there are people with bulimia nervosa who have difficulties in many parts of their lives. Their eating problems appear to be one more expression of underlying difficulties in coping with emotional stress, interpersonal problems,

Bulimia Nervosa

and urges to find immediate gratification or escape. Bulimia nervosa is a heterogeneous disorder. That is, it affects a broad range of people, some of whom are very similar to individuals who develop anorexia nervosa, some of whom are very different from people with anorexia nervosa, and many of whom are similar to people who never develop an eating disorder at all. CASE STUDY 1

Beth was slightly overweight as a child. She was never so heavy that she was called “fat” or teased about her weight. However, as she approached adolescence, she felt that she wasn’t attracting the attention of boys like her friends were. Because of her size, she couldn’t wear the same kinds of clothes that her friends wore. Instead, Beth often shared clothes with her mother and would opt to wear sweaters and skirts to school instead of midriff-baring tops and hip-hugging pants. She looked nice, and all of her friends told her she was pretty, but she also looked “old.” When she went to the mall, Beth was more likely to get attention from older men than from boys her own age. This made her feel uncomfortable about her appearance and about her weight. So, she decided to go on a diet that she read about in a magazine. The diet seemed fairly straightforward, and so was her goal. She wanted to lose enough weight so that she would not be able to share clothes with her mother and so that she would need to get new (preferably more fashionable) clothes for the upcoming school year. Beth started her diet during the summer before 8th grade. At first, she did very well with her diet. She lost 12 pounds (5.4 kg) and dropped from a size 12 to a size 6. Just as Beth had planned, her mother had to take Beth shopping before the school year started because none of Beth’s clothes from the previous year fit her anymore. Beth’s new clothes were very similar to the styles her friends wore.

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Beth was pleased by the attention she received on the first day of school and by the similarity between her outfit and that of one of her most popular friends. One of the boys in Beth’s homeroom even asked what other classes she was in that year. The school year was off to a great start—with one exception. When Beth got home from school that afternoon, she had two hours to herself before her parents got home from work. Beth didn’t have any homework. She didn’t play on a sports team and she wasn’t a cheerleader, so she didn’t have any kind of practice after school. Instead, she would go home and watch television. This made her want to snack. However, according to her diet, she wasn’t supposed to eat anything between lunch and dinner. This had been easy to do during the summer. But it was very hard after school began. Beth was hungry and bored, and the commercials kept showing food. Eventually, Beth broke down and ate an entire package of cookies and two big bowls of ice cream. Then she panicked. She had never eaten so much food at one time. She felt bloated, and her clothes felt too tight. Beth felt desperate to undo what she had done. She felt like she was going to be sick. She went to the bathroom and vomited. There, in the toilet, was everything she had just eaten. As she flushed the toilet, she felt like she had escaped from a horrible mistake she had made (and would never make again). She brushed her teeth and cleaned the bathroom to remove any evidence of what had happened. She waited for her parents to comment on the missing cookies or ice cream, but no one noticed. Beth thought she would never let it happen again, but she was wrong. The next week, she binged again. This time, though, Beth knew that her parents would notice another package of cookies missing and another gallon of ice cream nearly empty. So, she went out and replaced the

Bulimia Nervosa

foods she had eaten. Unfortunately, going out to replace the food she had eaten reminded her of all the foods she had been avoiding on her diet. The convenience store on the corner became the supplier for her binge episodes. Beth found that she could not keep herself down to a size 6, and she was soon wearing her mother’s clothes again. Her mother didn’t care; her friends didn’t care; but Beth cared. She tried to go back on her diet, but she could not stop binge eating. Both her eating and her weight made her feel like a failure. To other people, Beth seemed smart, funny, and nice. She told herself that if her weight went beyond a size 12, then she would tell someone about her problem. Otherwise, she would try to stop on her own.

CASE STUDY 2

Nina was a walking “after-school special.” She did everything that teenage girls were warned not to do. She took drugs; she slept with boys and did not practice safe sex. She did not drive safely. She cut school. She even cut herself. And she had an eating disorder. Nina would go out with a group of guys at 2:00 A.M. to the local fast-food fried chicken and biscuit chain. The group would order a 12-piece dinner for each person, and the guys would pay for Nina’s if she ate the whole thing. Sometimes, Nina would show off her appetite by finishing her dinner as well as any food that the guys didn’t finish from their own meals. The guys often joked that they didn’t know how one person could eat and drink so much and stay so skinny. To stay thin, Nina didn’t eat before 8:00 P.M. at night, she vomited almost everything she ate, and she took large amounts of diet pills, diuretics, and laxatives. The only things that Nina did to maintain her health were drinking sports

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drinks to keep her electrolytes balanced and taking a multivitamin to replace what she didn’t get from food. However, at the age of 19, Nina looked like she was 42. Her skin was tinged with yellow and was sunken around her eyes and cheeks. Her eyes were bloodshot. The back of her hand was callused from scraping up against her teeth when she would gag herself to vomit. Her breath often stank from a combination of cigarettes, coffee, vomit, and cavities. Her teeth were stained brown where they weren’t black from decay. Although Nina always said that she was just trying to have a good time, she looked and felt miserable.

The stories of Beth and Nina present very different pictures of bulimia nervosa. Both young women suffer from binge eating episodes, and both purge in response to these episodes to control their weight. Both place undue emphasis on the importance of weight and shape. However, for Beth, bulimia nervosa represents a relatively narrow problem within her life. The disorder has not impacted her grades or her relationships with other people. In addition, the factors that appear to have contributed to the onset of bulimia nervosa appear to be relatively clear. In contrast, many of Nina’s behaviors are so dangerous that it might be more urgent to address some of her other patterns (such as cutting, unsafe sex, and drug use) before worrying about her eating disorder. It would be difficult to attribute Nina’s problems to her binge eating and purging because the eating disorder seems to be part of a larger problem that is endangering Nina. And it is not clear why things have gone so far out of control in Nina’s life. The rest of this chapter will use the cases of Beth and Nina to describe the effects of bulimia nervosa and to show how to recognize when bulimia nervosa is occurring in others.

Bulimia Nervosa

EFFECTS OF BULIMIA NERVOSA

Like anorexia nervosa, bulimia nervosa affects how an individual feels, thinks, and behaves, and it impacts physical health and how the person gets along with others. In most cases, people who have bulimia nervosa are aware of the effects that their disorder has on their physical health. However, they are more afraid of gaining weight or becoming fat than of damaging their bodies. Unlike anorexia nervosa, bulimia nervosa does not result in low body weight (if the person had low body weight, then he or she would be diagnosed with the binge/purge subtype of anorexia nervosa). Physical Effects of Bulimia Nervosa

Many of the physical effects of bulimia nervosa are caused by the use of inappropriate compensatory behaviors—particularly purging. Some of the physical effects of bulimia nervosa are evident in Nina’s case. For example, tooth decay is a common problem among people who use self-induced vomiting to counteract the effects of binge eating. Vomit brings stomach acid into the mouth. This stomach acid eats through tooth enamel and leaves teeth vulnerable to the effects of harmful bacteria. Over time, this can cause a loss of teeth, and some people with bulimia nervosa eventually need dentures. The stomach acid in vomit can also eat through the lining of the esophagus (Figure 3.1) and lead to esophageal tears. Repeated vomiting can cause the salivary glands (parotid glands) to swell (Figure 3.2). The parotid glands are located on both sides of the face, near the jaw line. Because of this swelling, people who frequently self-induce vomiting often have unusually round-looking faces and “chipmunk-cheeks.” The loss of stomach acid (which is high in potassium, K+) through vomit causes electrolyte imbalances that can cause problems with kidney, intestinal, and heart function. Patients with bulimia nervosa are at particular risk for very low

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Figure 3.1 The physical effects of bulimia nervosa are mainly caused by purging. The stomach acid in vomit can eat through the lining of the esophagus and lead to esophageal tears. Stomach acid also eats through tooth enamel and leaves teeth vulnerable to harmful bacteria.

blood levels of potassium, called hypokalemia. This is a very dangerous condition that requires immediate medical attention to prevent sudden death from heart failure.

Bulimia Nervosa

Parotid gland

Normal Parotid Glands

Swollen gland

Enlarged Parotid Glands

Swollen gland

Figure 3.2 Enlarged parotid glands are often caused by repeated vomiting.

The abuse of laxatives and diuretics also causes electrolyte imbalances. In addition, laxative abuse causes a loss of intestine motility. This means that the intestines lose their ability to contract and move the bowels to produce bowel movements. As a consequence, people who use laxatives often find that they have to take more and more to produce the desired effect. In addition, if they try to suddenly stop using the laxatives, they often

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experience constipation. Both laxatives and diuretics contribute to dehydration, and water retention is a common side effect after stopping laxative and diuretic use. A particularly dangerous form of purging occurs among individuals with bulimia nervosa who also have insulin-dependent diabetes mellitus. These people may try to avoid weight gain by reducing or eliminating their insulin doses. This causes hyperglycemia. When a lack of insulin is combined with bingeeating episodes on high sugar foods, coma or death can occur. Over the long term, sustained hyperglycemia leads to blindness, loss of kidney function, congestive heart disease, inability to heal, increased risk of infections, and loss of limbs through amputation. Binge eating causes the stomach to stretch, resulting in increased stomach capacity. One result of a larger stomach capacity is decreased satiety function. That is, people who engage in repeated binge episodes are less likely to feel full when they eat a normal amount of food. This probably increases the risk for binge eating episodes. In very rare cases, binge episodes have caused death by gastric rupture—the stomach literally splits open due to overeating and then the person bleeds to death internally. Another physical effect of bulimia nervosa is skin problems. Nina has calluses on her hand because she uses her fingers to gag herself. The repeated rubbing of the back of the hand against the upper teeth to induce vomiting causes these calluses. In addition to the obvious damage to the skin, the use of fingers or any other instrument to force a gag reflex may lead to tears in the esophagus (Figure 3.3). Emotional Effects of Bulimia Nervosa

Emotions certainly contribute to the development of bulimia nervosa. However, bulimia nervosa also appears to increase

Bulimia Nervosa

39

How Bulimia Affects the Body Brain Depression, fear of gaining weight, anxiety, dizziness, shame, low self esteem. Throat & Esophagus Sore, irritated, can tear and rupture, blood in vomit.

Anemia

Heart Irregular heart beat, heart muscle weakened, heart failure, low pulse and blood pressure.

Body fluids Dehydration, low potassium, magnesium, and sodium.

Mouth cavities, tooth enamel erosion, gum disease, teeth sensitive to hot and cold foods. Cheek Swelling, soreness.

Muscle fatigue

Stomach Ulcers, pain, can rupture, delayed emptying. Hormones Irregular or absent period.

Intestines Constipation, irregular bowel movements, bloating, diarrhea, abdominal cramping.

Skin Abrasion of knuckles, dry skin.

Figure 3.3 Bulimia affects the body in many ways. In addition to skin damage, the use of fingers or an instrument to force a gag reflex may cause tears in the esophagus.

emotional distress. Because of the negative way other people react to the symptoms of bulimia nervosa, those who have the disorder often feel a great deal of shame. This shame results

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from different aspects of the disorder. For one, there is the sense of gluttony. Then, there is the waste of huge amounts of food. Bulimic patients often say that they feel like they might as well throw the food into the garbage, since it ultimately gets flushed down the toilet. People with bulimia nervosa also feel acutely aware of their inability to stop themselves from bingeing. For some, like Beth, this loss of control is very inconsistent with how they normally feel, and that is frightening. Binge episodes also contribute to fears of gaining weight or becoming fat.

Princess Diana Among the many famous people who have suffered from bulimia nervosa, Diana, Princes of Wales was perhaps the bestknown. According to interviews she gave, Diana developed bulimic symptoms shortly after her engagement to Prince Charles, when she was only 19 years old. At 19, Diana was at the peak age for the onset of bulimia nervosa. Her engagement brought a great deal of media attention. This, combined with the pressure of joining one of the most famous families in the world, caused enormous stress and limited options for coping with that stress. According to Diana, her symptoms grew worse after her wedding. In an interview with the British Broadcasting Corporation (BBC) given in 1995, Diana described her illness: I had bulimia for a number of years. And that’s like a secret disease. You inflict it upon yourself because your self-esteem is at a low ebb, and you don’t think you’re worthy or valuable. You fill your stomach up four or five times a day—some do it more—and it gives you a feeling of comfort. It’s like having a pair of arms around you, but it’s temporarily, temporary. Then you’re disgusted

Bulimia Nervosa

After a binge, people with bulimia nervosa express feelings of intense anxiety that are only eased once they have “undone” the damage of their binge episode by purging what they have eaten. However, purging eliminates only a small portion of food consumed and is not an effective means of weight control. The emotional effects of vomiting increase the likelihood that the person will intentionally vomit again the next time he or she engages in a binge. In addition, the knowledge that they have a way to “get rid” of the food eaten during a binge episode

at the bloatedness of your stomach, and then you bring it all up again. And it’s a repetitive pattern which is very destructive to yourself. [ . . .] You, you have to know that when you have bulimia you’re very ashamed of yourself and you hate yourself, so—and people think you’re wasting food—so you don’t discuss it with people. And the thing about bulimia is your weight always stays the same, whereas with anorexia you visibly shrink. So you can pretend the whole way through. There’s no proof.

This excerpt reveals the vicious cycle in which many people with bulimia find themselves trapped. Binge eating and purging serve as a way to cope with distress, but then cause additional distress and a further loss of self-worth. Although medical treatment can be very effective in helping people recover from bulimia nervosa, many people delay getting help because, at first, they believe they will be able to stop on their own and, later, because they feel ashamed of their illness. Source: Bashir, Martin. “Interview with Princess Diana.” 1995. Available online at http://www.pbs.org/wgbh/pages/frontline/shows/royals/interviews/bbc.html.

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makes it harder for people with bulimia nervosa to avoid binge eating. Unlike patients with anorexia nervosa, patients with bulimia nervosa rarely express disgust toward food. However, they do express disgust toward themselves and toward their bodies. During particularly severe binge eating episodes, patients may become so caught up in the process of bingeing that they will consume unusual foods (such as condiments or orange or banana peels) after they run out of regular food. Cognitive Effects of Bulimia Nervosa

One interesting aspect of bulimia nervosa is its ability to leave cognitive functioning largely intact. That is, people with bulimia nervosa appear to maintain their ability to remember, concentrate, think, plan, and execute their plans. Moreover, bulimia nervosa is not associated with any impairment in school or work function. As we saw, Beth appears to be able to balance her lifestyle perfectly, showing no outward sign of her inner turmoil. Although Nina has clear problems with her school performance because of her truancy, this is not directly related to her eating disorder. Instead, her academic problems appear to be part of a larger pattern of issues with impulse control that likely caused her eating disorder (rather than being caused by her eating disorder). Bulimia nervosa does impact thoughts surrounding food and weight. Specifically, people with bulimia nervosa are likely to engage in cognitive distortions that help them maintain their illness. For example, a person with bulimia nervosa may categorize all foods as either “good” or “bad” ( “safe” or “dangerous”). These labels are often related to the nutritional properties of food; for example, high-fat or high-sugar/high-carbohydrate foods are considered “bad” and are avoided. However, a person with bulimia nervosa is not able to avoid these foods entirely.

Bulimia Nervosa

When he or she eats a single bad food (for example, a piece of cake at a friend’s birthday party), that one “mistake” is enough to deem the whole day a failure. This kind of black-and-white thinking (called dichotomous thinking) increases the likelihood of binge eating. If eating one piece of cake is as bad as eating an entire cake, then why not eat the whole cake? For many people, the answer is that they would not want a whole cake. For people with bulimia nervosa, however, the whole cake may serve as just the beginning for a binge episode in which they let themselves go completely. This appears to be triggered, to some extent, by the constant use of dietary restrictions. Imagine that you were told that, starting tomorrow, you could never eat another potato chip or cookie for the rest of your life. You might decide that it would be worth it to try to have your fill tonight so that you would never want another cookie. In a sense, this is the thought process for a person who has bulimia nervosa. Because people with bulimia nervosa are almost constantly trying to follow strict diets, they convince themselves that they will never eat another chip or cookie (or whatever their favorite, most fattening food may be). Once they declare that they will never eat a certain food again, that food becomes even more tempting and desirable, because, in addition to tasting good, it is also forbidden. Behavioral Effects of Bulimia Nervosa

For people who are trying to hide their eating disorder, the greatest behavioral impact of bulimia nervosa is its impact on honesty. People who are attempting to hide the fact that they are engaging in large binge episodes and purging are forced into awkward situations, given the social nature of food. They may make up reasons to avoid attending dinners or parties, for fear of having a binge episode. People with bulimia nervosa will also sometimes feel compelled to “get rid of ” normal-sized meals.

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The constant pattern of dieting and the attempts to make up for failures to stick to the diet leads the person to see even normal meals as excessive. A meal may not necessarily be excessive, but it does exceed what the person planned or hoped to eat. As a result, in a social setting, the person may feel intense anxiety after eating a normal amount of food—an anxiety that he or she knows can be eliminated only by vomiting. People cannot simply tell a dinner host or fellow guests that they need to use the restroom to vomit up their meal, so they must come up with other plausible explanations for their sudden disappearance from the dinner table. This type of dishonesty is closely related to the emotional and interpersonal effects of bulimia nervosa. Interpersonal Effects of Bulimia Nervosa

People with bulimia nervosa often report having interpersonal difficulties. It is hard to tell whether this is a cause or an effect of the eating disorder. The reason some experts believe it is an effect is that people generally do not engage in bulimic behaviors in front of others. Thus, the frequency of binge eating and purging episodes dictates how often a person with the disorder will need to be alone. The need to be alone to engage in bulimic behavior can interrupt their participation in social events, as they have to excuse themselves for as long as they need to purge and then get rid of any evidence of purging. The secretive nature of the disorder can drive a wedge between people with bulimia and others because the person with the disorder knows they are hiding something from friends and relatives. Often, people with bulimia nervosa believe that others will judge them extremely harshly for their behavior. Since they don’t allow others to know about and react to the eating disorder, patients may imagine the social rejection and isolation that might result would be much worse than would be the case if they asked for help.

Bulimia Nervosa

RECOGNIZING BULIMIA NERVOSA

Because most people with bulimia nervosa have a normal body weight, there is no outward physical sign of the disorder. However, there are behavioral signs of the disorder. For example, if a person seems to avoid eating meals with other people yet retains a normal body weight, this suggests that he or she is consuming most meals alone. Although people may eat normal meals by themselves, it is also possible that they choose to eat alone so they can prevent others from seeing what and how much they eat. If a person makes frequent visits to the bathroom—particularly to brush his or her teeth—this may be a sign of attempts to mask the smell of vomit on the breath. Long bathroom visits may also be the result of attempts to rid the bathroom of the smell of vomit or may be caused by the effects of laxatives on bowel movements. If you live with a person with bulimia nervosa, you may notice that food disappears without explanation. Alternatively, it may seem like food supplies are reduced in ways that are designed to prevent anyone from noticing that food is being eaten. For example, a carton of ice cream may appear to have a relatively smooth surface. However, under that flat surface there may be a cavern from which ice cream has been precisely scooped. Brownies, cakes, and pies may be recut to give them their original appearance, while the equivalent of several pieces has actually been removed. Other signs of bulimia nervosa include skipping meals and excessive exercise routines, since both fasting and exercise can be ways people try to counteract the effects of binge eating. In a person of normal weight, these types of behaviors may not cause much concern. However, if it seems that a person spends too much time exercising and never seems to eat, then he or she may follow a pattern of engaging in one large binge and then compensating for it with exercise and fasting.

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•

•

•

•

•

•

•

SUMMARY

As we discussed in Chapter 2, it is important to remember that suspicions of an eating disorder are just that—suspicions. There may be other reasons behind behavior that resembles that described above. Different people follow different eating patterns. The best way to appreciate how much variability exists in normal eating is to look at eating patterns in different cultures. In the United States, we usually follow a three-meal-perday pattern (breakfast, lunch, and dinner), with the last meal usually being the largest. Many people eat snacks between meals, with midafternoon snacks probably being the most common, followed by both evening and then mid-morning snacks. In England, these meals are supplemented by another meal (called tea) in the late afternoon. This late afternoon meal allows for a later, smaller dinner and reduces the tendency to eat an afternoon and evening snack. In Spain, the midday meal is the largest. In fact, it is so large that people take a period of rest (called a siesta) after eating it. The evening meal is light, similar to the evening meal in other European countries. Clearly, no single society’s eating patterns is necessarily “natural.” As a consequence, there may be a great deal of normal variation within a culture. Some people in the United States may choose to skip breakfast and just eat lunch and dinner (a two-meal pattern). Others may choose to eat three small meals and three snacks (a six-small-meal pattern). Because of this variation, it can be tough to uncover abnormal patterns among normal variation. Therefore, it is important to take great care in responding to suspicions that a person may have bulimia nervosa. It is more likely that a person will become suspicious that someone has anorexia nervosa without ever speaking directly

Bulimia Nervosa

to the affected person. In contrast, with bulimia nervosa, the person who has the disorder will often confide about binge eating and purging to an unsuspecting friend or relative. Sometimes, the person’s confession will come with requests that the information be kept strictly confidential. This is an unreasonable request, because it is a request to take some of the anxiety the person is feeling about the eating disorder upon yourself. This is unhealthy both for you and for the person with the eating disorder. If you learn that a person has an eating disorder and you do nothing, the person may take this as permission to continue the dangerous behavior. Instead, it would be better to talk to someone who will keep the information confidential and who is trained to help individuals in need, such as a school counselor or nurse. You should be honest with your friend that you cannot keep this information secret because of the health risks associated with your friend’s behavior.

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Binge Eating Disorder and Eating Disorders Not Otherwise Specified

Most people who have eating disorders do not suffer from either

anorexia nervosa or bulimia nervosa. This may seem strange, since these are often the only two eating disorders most people know about. However, there are a lot of clinically significant eating disorders other than anorexia nervosa and bulimia nervosa. These are known as eating disorders not otherwise specified (EDNOS). Binge eating disorder, for example, is a specific type of EDNOS. Any clinically significant disorder of eating that does not meet full criteria for anorexia nervosa or bulimia nervosa would be diagnosed as an EDNOS. So, what makes a disorder “clinically significant?” Clinical significance is defined by the presence of one of three qualities: 1. present distress; 2. disability (defined as impairment in important life functions such as relationships with others, work, or school performance); 3. increased risk of death, pain, loss of freedom, or disability. Anorexia nervosa and bulimia nervosa both meet the requirement of clinical significance because of their medical complications. In the case of binge eating disorder, the definition for the

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disorder actually requires that people express present distress over their pattern of binge eating. BINGE EATING, OVEREATING, AND OVERWEIGHT/OBESITY

Chapter 1 discussed how eating disorders were problems of eating, not problems of weight. However, many people continue to believe that a person who is morbidly obese must have an eating disorder. If obesity is associated with an increased risk for death and represents a physical disability, then this would seem to be an EDNOS, as defined above. However, there is one important factor to remember before you jump to this conclusion: Obesity is a consequence of something that is wrong. For some people, obesity may be linked to binge eating disorder (BED) or an EDNOS marked by binge eating. For many people, though, obesity is a result of simple overeating. What is the difference between binge eating and overeating? The answer is control. By definition, people experience a loss of control during binge eating episodes (Figure 4.1). They feel they cannot control what or how much they are eating. This is similar to people with depression feeling they cannot control being down in the dumps or people with panic disorder feeling that they cannot control their sense of anxiety. These people experience these events as something that is happening to them rather than something they are choosing to do. In contrast, overeating is something that almost everyone chooses to do from time to time. Overeating is not healthy—but then, there are many behaviors that people engage in that are not healthy, from smoking cigarettes to driving too fast to talking on a cell phone while driving. People often engage in unhealthy behaviors with full knowledge of how and why the behavior is unhealthy. Similarly, people will occasionally choose to overeat. This is not a sign of a mental disorder. Instead, there must be some sense in which the mental disorder is non-volitional. Otherwise, every

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Figure 4.1 Binge eating is an example of an eating disorder not otherwise specified (EDNOS). Those who have this disorder experience a loss of control during binge eating episodes.

person who engages in risky behaviors would be diagnosed with a mental disorder. Comparisons of obese individuals without BED and obese individuals with BED indicate that BED is associated with increased depression and dissatisfaction with the body. People who have BED may be less likely to respond to weight control programs and more likely to go through dramatic fluctuations

Binge Eating and Other Eating Disorders

in their weight. Thus, understanding whether or not a person feels control over eating holds important implications for understanding his or her psychological health and how he or she may respond to programs designed to improve physical health. The following cases illustrate BED and one other possible EDNOS, known as purging disorder. These are not, however, the only types of EDNOS a person may have. CASE STUDY 1

Ben had always been a big eater. He could remember eating more than anyone else in school and in camp when he was a child. He had always been heavy as well. Ben was also very funny. Not only could he make his friends laugh, he could make kids who didn’t even know him laugh, and he could make teachers laugh. So, Ben was always popular in school. He was elected class vice president and had a leading role in the school musical. However, even though girls always wanted to be his friend, none of them seemed interested in being his girlfriend. Ben felt that girls didn’t find him attractive because of his weight, but he decided that it was okay not to have a girlfriend since he was going away to college after high school anyway. In college, Ben’s reputation as a funny guy grew. He joined the staff of a humorous monthly college journal and started doing stand-up comedy on open mike nights at the local comedy clubs. Ben developed a small following and decided to drop out of college to pursue a career in comedy. Between high school and dropping out of college, Ben gained 75 pounds (34 kg). He attributed this to a lot of beer and late-night eating at pizza places. Ben decided to join Overeaters Anonymous (OA) to try to lose some weight because it was free. In OA, Ben heard others give testimonials that mirrored

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his own life. People talked about how they reacted to food differently from other people. They said that certain foods changed the way they felt and thought, like a powerful drug. Looking around the room, Ben saw a lot of people who had lost a ton of weight by following the OA guidelines. There was also a lot of support within the room as people shared their successes and failures. Each meeting started with a person telling his or her story, and Ben found it very liberating. He had never felt so free to simply “be” without being funny. Ben was able to follow the OA program for a while, and during that time, he lost a lot of weight. However, one late night, after a particularly good comedy set, Ben felt like he deserved a celebration. He went out with some other comedians and ordered beers and pizza. That night, Ben consumed more beer and pizza in one sitting than he had ever eaten before. He felt horrified when he realized what he had done. At the next OA meeting, he described what happened, and other people in the group offered their support and encouraged him to get back on the program. However, from that point on, Ben found it difficult to resist urges to go back to his old eating habits. He alternated between good days and days when he would binge, and his weight crept back up and over what it had been when he joined OA. After six months of binge eating every other day, Ben decided to drop out of OA and seek medical help for his eating problems.

CASE STUDY 2

Pearl was a petite girl whose mother was Korean and father was American. Her mother was a stay-at-home mom and her dad was a college professor who specialized in East Asian History. He had met Pearl’s mother while he was doing research in Korea.

Binge Eating and Other Eating Disorders

Pearl was large for an Asian girl because her father was tall, but she was not overweight. She felt uncomfortable with her size, and her mother emphasized the importance of not overeating and staying thin. Before holiday meals, Pearl’s mother gave her “thinning tea”—an herbal tea that had a laxative and diuretic effect. This tea made Pearl feel thinner and lighter and seemed to offset the effects of holiday meals. After a bout of stomach flu, Pearl discovered that the vomiting and diarrhea of her illness also made her “feel light.” She started experimenting with vomiting after meals to re-create this feeling. By the age of 17, Pearl was vomiting once a day, immediately after dinner, so that she could go to bed with an empty stomach. Although Pearl was thin, her weight remained within a normal range for her height. She never had binge eating episodes. At most, she might eat junk food with school friends. However, she never ate more than others were eating in the same situation. In many respects, Pearl felt very normal. She did not even realize that vomiting after meals was considered unusual because she felt that it was a very clever way to stay thin, which more people would use if it occurred to them. The only time Pearl felt distress was when she was prevented from vomiting. She would become very anxious because she was terrified of gaining weight. It was very important to her to remain thin because she already felt uncomfortable about her height.

On the face of it, Ben and Pearl appear to have very different problems. Ben cannot control what or how much he eats. In contrast, Pearl does not seem to have any notable problems with her food intake. Ben does not engage in any inappropriate compensatory behaviors. Pearl uses self-induced vomiting and drinks tea that acts as a diuretic and laxative. Ben is obese. Pearl

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is thin. Ben’s patterns seem to represent problems with impulsive behaviors. Pearl’s patterns seem to represent problems with compulsive behaviors. However, both of them engage in disordered patterns around eating that increases their risk of health problems. In addition, these patterns are associated with distress, either when they cannot avoid the behavior (like Ben) or when they are prevented from engaging in the behavior (like Pearl). Thus, both have EDNOS even though their circumstances differ greatly. EFFECTS OF EDNOS

The effects of EDNOS depend upon the symptoms. If EDNOS is associated with starvation, then the effects can be similar to those observed with anorexia nervosa. If EDNOS is associated with binge eating and purging, then the effects can be similar to those observed in bulimia nervosa. In the case of binge eating disorder, some effects of the disorder are attributable to obesity (Table 4.1). However, many people who recover from binge eating disorder do not necessarily lose significant amounts of weight. In contrast, a person cannot recover fully from anorexia nervosa without returning to a normal weight. Thus, Table 4.1 HEALTH CONSEQUENCES OF OBESITY High Blood Pressure High Cholesterol Levels Heart Disease Diabetes Mellitus Gallbladder Disease

Binge Eating and Other Eating Disorders

although binge eating may contribute to obesity, it is not the sole cause of obesity for most individuals (Table 4.1). RECOGNIZING EDNOS

Recognizing an EDNOS is probably more difficult than recognizing anorexia nervosa or bulimia nervosa. There may not be dramatic behavioral differences between a person with an EDNOS and a person who has some unhealthy but normal eating patterns. The key factors are personal distress, disability, and increased risk. In Ben’s case, his distress over his pattern of eating is apparent from his attempts to seek help to change. Pearl, on the other hand, has no personal distress because of her eating. Ben’s pattern of eating may play a role in his ability to form relationships with others. For Pearl, there is no evidence of interpersonal problems. In Ben’s case, his eating patterns increase his risk of various medical complications related to obesity. However, he might still face these risks even if he stopped binge eating. Pearl’s vomiting, laxative, and diuretic Table 4.2 BINGE EATING DISORDER (BED) STATISTICS

• The prevalence of BED is estimated to be approximately 1–5% of the general population. • BED affects women slightly more often than men— estimates indicate that about 60% of people struggling with BED are female, 40% are male (Smith, et al., 1998). • People who struggle with BED can be of normal or heavier than average weight. • BED is often associated with symptoms of depression. • People struggling with BED often express distress, shame, and guilt over their eating behaviors.

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use put her at significant medical risk for heart, kidney, and intestinal disorders, but it would not be possible to detect Pearl’s problem unless her behavior was closely monitored after each meal to note how long she takes in the bathroom and whether she suffers distress if she cannot get to a bathroom after dinner (Table 4.2). RESPONDING TO EDNOS

Responses to suspicions of EDNOS should resemble those for anorexia nervosa or bulimia nervosa. However, reactions on the

The Future of Eating Disorders Not Otherwise Specified (EDNOS) Based on studies of binge eating disorder, many researchers in the field of eating disorders support making binge eating disorder a fully recognized eating disorder, like anorexia nervosa and bulimia nervosa. This would increase the proportion of people with eating disorders who receive an official diagnosis. However, most people who suffer from eating disorders would continue to be diagnosed with an EDNOS. Other forms of EDNOS include purging disorder and night eating syndrome. Purging disorder occurs in normal weight individuals who purge to control their weight but do not have large binge episodes. Night eating syndrome is similar to binge eating disorder in that people eat large amounts of food and feel a loss of control over their eating but do not engage in inappropriate compensatory behaviors. However, food consumption occurs primarily at night and is associated with disturbances in sleeping patterns. The inclusion of other EDNOS as categories for further research will make it easier to characterize the full range of eating disorders from which people suffer.

Binge Eating and Other Eating Disorders

part of the person affected will depend greatly upon what he or she is doing. Ben, for example, is likely to respond well to friends’ attempts to support and help him because he is already eager to find a way to control his eating. Pearl, in contrast, is likely to deny that she has any problems related to food or eating and will probably avoid other people’s attempts to prevent her from purging. Both cases will require patience because their patterns—while deliberate for Pearl and not for Ben—feel beyond their control.

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5

Causes of Eating Disorders

Just as eating disorders impact a person’s physical body, mind,

and social life, biological, psychological, and social factors are all important in understanding the causes of eating disorders. This chapter begins by reviewing evidence that social factors contribute to the development of eating disorders, then discusses the importance of psychological factors, and ends with a discussion of biological factors that increase risk for eating disorders. SOCIAL FACTORS

While watching the 2004 Miss Teen USA competition, I was struck by contestants’ comments that they were concerned about the pressure teenage girls experience to conform to media images of the ideal body. In a series of clips from interviews with ten contestants, three of them mentioned the negative effects the media had on girls’ self-esteem and their eating. In the case studies of Ashley, Beth, Nina, and Pearl, the girls all reported some level of concern about their weight or shape. Ashley began her diet and exercise regimen specifically to lose weight. Beth initially went on her diet to go from a size 12 to a size 6, and her response to binge eating was specifically motivated by a desire to avoid gaining weight. Nina would not eat before 8:00 P.M. and used several methods of purging to keep her weight down, and

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Pearl felt that she had to vomit after eating normal amounts of food to stay thin. To what extent are eating disorders caused by the desire to achieve a thin physique? As described in Chapter 1, anorexia nervosa and bulimia nervosa became more common during the second half of the 20th century. At the Clarke Institute of Psychiatry, David Garner and colleagues hypothesized that the increase in rates of anorexia nervosa reflected an increasing idealization of thinness for women.6 To test their hypothesis, they examined time trends for three different sources of information about beauty ideals: the Miss America Pageant, Playboy magazine, and women’s magazines (Harper’s Bazaar, Vogue, McCall’s, Good Housekeeping, Ladies’ Home Journal, and Woman’s Day). From 1959 to 1978, they found that both Miss America contestants and winners became increasingly thinner. In fact, in the last year they examined, the winner of Miss America weighed less than 78% of what would be expected for her height. Recall that deliberately maintaining a weight less than 85% of what is expected for height is the first criterion for a diagnosis of anorexia nervosa. During the same period of time, Playboy centerfolds became thinner as well, and their overall figures shifted from a womanly hourglass shape to a more adolescent tubular shape. Finally, the number of articles on weight loss diets doubled in popular women’s magazines. Based on these trends, Garner and his group concluded that increasing rates of anorexia nervosa were a consequence of America’s increasing obsession with thinness. These trends have continued into recent years. A number of experimental studies have examined the impact of thin media images on women’s body image. Leslie Heinberg and J. Kevin Thompson recruited female participants for a study on the effects of media images on body perception at the Johns Hopkins University School of Medicine.7 Participants were randomly assigned to view either television commercials

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that contained appearance-related images or television commercials that did not contain appearance-related images. Women who viewed appearance-related commercials reported significantly greater body dissatisfaction after seeing the commercials compared to women who saw non-appearance-related commercials. At Arizona State University, Eric Stice and Heather Shaw randomly assigned women to view magazine pictures of very thin models, average-sized models, or no models.8 Women who saw pictures of very thin models reported significantly greater body dissatisfaction than women who saw pictures of average models or no models. Both studies provided evidence that media images portraying the thin ideal contribute to body dissatisfaction. Notably, neither study demonstrated that these images directly cause eating disorders. A recent study looked at how television affected the beliefs, values, and behaviors of girls in Fiji.9 Assessments were conducted within one month of the time that televisions were placed in the homes of Fijian girls. Follow-up assessments were conducted three years later with a new group of girls. At the start of the study, girls reported very little body dissatisfaction, dieting, or purging, and did not report that being thin was important. This was consistent with traditional Fijian cultural values. Three years later, however, after much more exposure to television, the new group of Fijian girls reported beliefs that success, wealth, and independence were related to being thin, and said that they had a desire to be thin. Self-induced vomiting to control weight increased from 0% of girls at the start of the study to 11% of girls three years later. This study provided strong evidence that the introduction of the thin ideal is associated with the development of eating disorders. Given that the ideal female body is much thinner than most women’s bodies are naturally, it is not surprising that most women feel dissatisfied with their weight and have attempted to

Causes of Eating Disorders

lose weight by dieting. Among high school girls, 63% reported that they are currently attempting to lose weight,10 and 73% reported trying to lose weight in the past.11 Among college women, 76% reported dieting at some point and 76% reported desiring to lose weight currently, but only 43% described themselves as currently overweight, and only 3% were actually overweight.12 Girls who diet are eight times more likely to develop anorexia nervosa or bulimia nervosa than girls who do not diet. When dieting leads to significant weight loss, as in Ashley’s case, then anorexia nervosa may develop. When dieting contributes to binge eating, as in Beth’s case, then bulimia nervosa may develop. PSYCHOLOGICAL FACTORS

If three-quarters of college women have tried to lose weight by dieting and most were normal weight when they started their diets, then why isn’t anorexia nervosa more common? Recall that anorexia nervosa only affects about 1 in 100 women. Clearly, the vast majority of girls who attempt to lose weight do not develop anorexia nervosa. One reason for this is that dieting contributes to binge eating, and binge eating causes weight gain, as seen in Beth’s case. Why would attempts to restrict food intake result in the exact opposite behavior? Dieting and Binge Eating

When a person goes on a diet, she uses the diet to decide what she should eat, when she should eat, and how much she should eat. Dietary rules replace physical sensations such as hunger and satiety in determining food intake. For most people, diets lead to initial weight loss, as it did for Beth. However, most people eventually break their diets. Now, if a person simply deviated from the diet slightly, for example, by eating a piece of birthday cake at a friend’s party, but otherwise remained on the diet, then

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the person would still be eating less than normal. As a consequence, his or her weight would be lower than it would be if he or she were not dieting. However, this is not what typically happens when people break their diets. Many people respond by eating more than they would normally eat. Some people eat much more. For example, after eating a piece of cake, the person might have a second piece of cake, some potato chips, some candy, or some crackers and cheese, and continue to eat until feeling stuffed. Why would a person do this? Janet Polivy and Peter Herman from the University of Toronto argued that dieters replaced physical cues for eating with cognitive rules about eating.13 When a rule was broken, there was no difference between a slight deviation (one piece of cake) and a huge deviation (two pieces of cake, a bowl of potato chips, three handfuls of candy, half a plate of cheese and crackers). A broken rule was a broken rule, and as long as the rule was broken, the person might as well enjoy all of the foods forbidden by their diet. Polivy and Herman referred to this phenomenon as cognitive disinhibition. Thoughts about eating (cognitions) acted to release dietary restrictions (disinhibition). These researchers and others have conducted numerous experimental studies that support this hypothesis. The classic design compares responses to experimental manipulations in individuals with high versus low scores on a measure of dietary restraint. For example, individuals will be asked to participate in a “taste test;” however, prior to this they are randomly assigned to consume a milkshake or nothing (the experimental manipulation). When asked to consume nothing prior to the taste test, dieters consume less than nondieters, consistent with their being on a diet. When asked to consume a milkshake prior to the taste test, dieters consume a lot more during the taste test than nondieters. This effect has been demonstrated and replicated by a number of labs. Thus, these studies show that a

Causes of Eating Disorders

milkshake will cause a dieter to eat an unusually large amount of food. Polivy and Herman argued that binge episodes were triggered when dieters encountered cognitive disinhibitors, when using drugs or alcohol, or when feeling emotionally overwhelmed. Essentially, anything that challenged a dieter’s ability to follow the diet left him or her vulnerable to a complete loss of control over eating, resulting in a binge eating episode. Although binge eating episodes offer a temporary release from dietary restriction; give people the opportunity to eat almost unlimited amounts of delicious foods; and can help some individuals “zone out” when they are feeling depressed, anxious, or angry, binge episodes also cause a lot of distress once they are over. When the food is gone and eating stops, the person bingeing is left with the realization that he or she has lost control over eating, which leads to feelings of helplessness, disgust, and self-loathing. In addition, there is terror over the effects that the binge will have on body weight and shape. Purging and other compensatory behaviors are designed to undo these negative effects of binge eating episodes. Purging has the immediate effects of relieving anxiety and stomach discomfort. For a lot of patients who develop bulimia nervosa, the initial cycle often does not seem very bad. Many patients describe feeling that their binge/purge cycles are a perfect solution for an otherwise impossible problem. However, this feeling generally fades when the frequency of binge/purge episodes increases and the realization that the pattern is beyond their control sets in. Treatments for bulimia nervosa have used the premise that dieting causes binge eating, and so they encourage patients to stop dieting. Cognitive behavioral therapy for bulimia nervosa prescribes a pattern of regular eating of three meals and three snacks per day so that patients eat something every two to three hours. These treatments have proved highly successful in eliminating

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binge eating episodes and helping patients recover from bulimia nervosa. If dieting causes binge eating, then why don’t more people suffer from bulimia nervosa and binge eating disorder? Bulimia nervosa only affects about 1 in 33 women, far less than the 3 out of 4 who have dieted at some point in their lives. Clearly, dieting does not cause binge eating in all people. Researchers have suggested that certain personality features determine whether dieting will increase the risk of binge eating. The personality features that are associated with the risk of binge eating are negative emotions, impulsiveness, and perfectionism. Personality and Eating Disorders

Most people who suffer from eating disorders also suffer from depression. This has been attributed to their increased tendency to experience negative emotions such as depression, anxiety, and low self-esteem. Studies have shown that a tendency to have these negative emotions predicts the future development of eating disorders. Interestingly, levels of body dissatisfaction are more strongly associated with depression than they are with bulimic symptoms, which suggests that body dissatisfaction may emerge as a consequence of depression, and, in a subset of individuals, may then contribute to the development of an eating disorder. Why would depression lead to body dissatisfaction? First, depression emerges in people who feel that they are lacking in some way. Those who are depressed often feel that they are not smart enough, social enough, or attractive enough. Thus, feeling overweight may be just one of several ways that a depressed person feels inadequate. Focusing attention on a perceived weight problem may give the person a false sense of control. He or she may come to believe that, by controlling weight and body shape, he or she will feel better.

Causes of Eating Disorders

Hilde Bruch of Baylor College of Medicine noted that many of her patients with anorexia nervosa tended to be straight-A students with many accomplishments.14 In addition, they were less likely to drink alcohol, use drugs, or be sexually active— suggesting that they have higher levels of constraint. Before the onset of their illness, they hid their negative feelings. In contrast to their happy external appearance, Bruch’s patients experienced significant anxiety, sadness, and concern about disappointing others. Many of these features can be seen in Ashley’s case. In contrast to early clinical descriptions of anorexia nervosa, Gerald Russell characterized patients with bulimia nervosa as having antisocial behaviors (abusing drugs, stealing, and sexual promiscuity), having problems with social anxiety, depression, and poor social adjustment.15 Much of this is apparent in Nina’s case. In many ways, her eating disorder seems to be just one more expression of her problems with impulse control and selfregulation. Nina does not seem to care about her own safety. She only seems to care about seeking immediate pleasure in her life, regardless of the long-term consequences. Research has supported that a constricted/overcontrolled personality is characteristic of restricting anorexia nervosa, while an impulsive/emotionally dysregulated personality is characteristic of binge eating in both anorexia nervosa and bulimia nervosa. However, Drew Westen and Jennifer Harnden-Fischer at Boston University reported that a high-functioning/perfectionistic personality style was present in both anorexia nervosa and bulimia nervosa.16 Thus, perfectionism may increase risk of developing both eating disorders. Perfectionism combined with inhibition may contribute to developing restricting anorexia nervosa. Perfectionism combined with impulsiveness may contribute to the development of bulimic symptoms. Perfectionism likely increases risk for eating disorders by

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contributing to dichotomous thinking—the kind of black-andwhite thinking described for when people break their diet. Foods are seen as either good or bad. Losing weight is good, and gaining weight is bad, no matter how emaciated the person becomes. Perfectionism increases selective abstraction—a cognitive distortion in which part of something comes to stand for the whole. For example, a person may believe that because her thighs are too fat, her entire body is too fat, even if her body is actually emaciated. Many of the thought processes that contribute to eating disorders likely arise from perfectionism. Perfectionism, combined with low self-esteem and a belief that one is overweight, has been shown to predict future development of bulimic symptoms. Individuals with eating disorders tend to score higher on measures of perfectionism compared to individuals who do not have eating disorders. BIOLOGICAL FACTORS

Because eating disorders affect mostly women, have become more common over recent years, and are more common in Western nations, social factors have been given the greatest emphasis in their etiology. Because only a very small number of girls in modern Western societies develop eating disorders, researchers increased their focus on psychological factors that might make one individual more vulnerable to cultural messages compared to another individual. What makes a person perfectionistic? Why is one person vulnerable to feeling depressed and anxious while another feels secure and happy? Why did Ashley feel that she needed to cheat on her exam in order to do well? Why does Nina crave danger? Why does Ben have urges to eat such large amounts of food? Genes and Eating Disorders

Early explanations for psychological factors focused on people’s

Causes of Eating Disorders

childhood—how did their parents raise them? However, more recent research has begun to examine not only the contribution of family to rearing environments but also the genetics of children in determining psychological makeup. A gene is a sequence of deoxyribonucleic acid (DNA) that codes for proteins. For example, a gene could code for eye color. Allele refers to one of several forms of the same gene. For a given gene, children receive a single allele from each parent. The resulting combination of alleles for a given gene is called a genotype. When the alleles received from each parent are the same, this results in a homozygous genotype. When the alleles received from each parent differ, this is referred to as a heterozygous genotype (Figure 5.1). The effects of different genotypes (i.e., different combinations of alleles for a given gene) can range from differences in eye color to differences in risk for developing an eating disorder. The observable manifestation of a genotype is referred to as a phenotype. Eating disorders are phenotypes in studies of their getetic bases. One approach to disentangling the effects of rearing environments from genes is to use twin studies. Identical twins (monozygotic twins) have the exact same genetic material, whereas fraternal twins (dizygotic twins) are not genetically identical. Population-based twin studies have shown greater similarity between identical twins for personality features, weight, and eating disorders than between dizygotic twins. These studies provide clear evidence that genes play an important role in the development of eating disorders. Molecular genetic studies identify the specific genes that may increase risk for developing eating disorders. For example, one way to identify specific genes is by using a candidate gene study. Candidate gene studies compare the frequency of alleles for specific genes (“candidate genes”) between individuals affected with a disorder and those unaffected. If individuals with eating

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Mom's Genotype (Homozygous) b

b

Genotype = Bb Phenotype = brown eyes

Genotype = Bb Phenotype = brown eyes

Genotype = bb Phenotype = blue eyes

Genotype = bb Phenotype = blue eyes

B

Dad's Genotype (Heterozygous)

b

Figure 5.1 The Punnett Square is a tool used to determine the possible traits that two parents will pass on to their offspring. Since each individual has one pair of each chromosome, each has two copies of the gene (one on each chromosome). There are four variations of gene pairs for the blue/brown-eyed trait. An individual can have a genotype of BB (homozygous dominant), Bb (heterozygous), or bb (homozygous recessive). The combination that the individual receives will determine his or her eye color.

disorders are more likely than individuals without eating disorders to have a specific allele or genotype, then this supports an association between the function of this candidate gene and risk for developing an eating disorder. Such studies suggest that

Causes of Eating Disorders

genes may contribute to eating disorders by impacting serotonin function.17 Serotonin Function in Eating Disorders Serotonin (also called 5-hydroxytryptamine, or 5-HT) is a neuro-

transmitter that influences mood, sleep, and appetite. Neurotransmitters are chemicals that facilitate communication between brain cells (neurons). So, neurotransmitters influence how the brain works. Specifically, increased 5-HT activity in a

Twin Studies Twin studies take advantage of the natural occurrence of two types of twins—identical (monozygotic) and fraternal (dizygotic). When twins are raised by their biological parents, then both members of a twin pair will share 100% of their rearing environment (called their shared environment). Because monozygotic twins come from one fertilized egg that has split in two, they share 100% of their genes. In contrast, dizygotic twins occur when two separate eggs have been fertilized by two different sperm at the same time. That means that dizygotic twins are just like regular siblings who have been born at the same time and share, on average, 50% of their genes. Twin studies examine the similarity within twin pairs for a characteristic (such as a personality feature, weight, or a disorder). Twin concordance is the similarity within twin pairs. If twin concordance is similar between monozygotic and dizygotic twins, then the similarity between twins is attributed to their shared environment. If monozygotic twins show greater concordance for a disorder compared to dizygotic twins, then the similarity is attributed to genes.

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Figure 5.2 Serotonin (also called 5-HT) is a neurotransmitter that influences mood, sleep, and appetite. Serotonin is made in a small group of brain areas and is carried to other areas of the brain such as the cortex, hippocampus, and hypothalamus. Increased 5-HT activity in the hypothalamus decreases food intake.

part of the brain called the medial hypothalamus decreases food intake (Figure 5.2). Because mood and appetite are altered in patients with eating disorders, 5-HT became a prime candidate in attempting to understand the biological causes of anorexia nervosa and bulimia nervosa. Specifically, research on bulimia nervosa has focused on the possibility that inadequate 5-HT

Causes of Eating Disorders

function may explain binge eating, and recent research on anorexia nervosa has focused on of the idea that too much 5-HT explains self-starvation. An early hypothesis proposed that inadequate 5-HT function produced “carbohydrate craving” that caused binge-eating episodes.18 Dieting was thought to contribute to carbohydrate craving because many weight loss diets of the 1970s emphasized restricting carbohydrate intake. An amino acid required to make 5-HT, tryptophan, is found in food. Diets that diminish tryptophan intake decrease 5-HT production in the brain. Low 5-HT function would certainly explain the depressed mood and large appetites demonstrated by most women with bulimia nervosa. Binge eating episodes that consist of high-carbohydrate foods (such as cookies, cakes, and chips) were thought to represent an attempt at self-medication for low 5-HT function. Supporting this hypothesis, Walter Kaye and colleagues at Western Psychiatric Institute and Clinic found that cessation of binge/purge episodes among women with bulimia nervosa appeared to be related to the extent to which binge episodes increased tryptophan in their blood.19 Women who reached their “desired effect” spontaneously stopped within one to three binge/purge cycles and demonstrated greater increases in tryptophan, compared with women who did not stop their binge/purge cycles spontaneously. More recent research has examined emotional and behavioral responses to changes in blood tryptophan levels. Research participants were given a liquid meal that caused a significant decrease in their tryptophan levels. This diminished the brain’s ability to make 5-HT. Participants with and without bulimia nervosa demonstrated similar changes in blood concentrations of tryptophan; however, only those who had bulimia nervosa reported significant increases in dysphoria, anxiety, and urges to eat following tryptophan depletion. Thus, dieting may cause

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binge eating in people whose brains react differently to decreased tryptophan. Biological studies indicate that genes contribute to the development of eating disorders.17 Genes that influence serotonin function have been implicated in the etiology of anorexia nervosa.17 Studies of serotonin suggest decreased function in patients with bulimia nervosa20,21,22 and possibly increased function in patients with anorexia nervosa.23 •

•

•

•

•

•

•

SUMMARY

Eating disorders are caused by multiple factors, and no single factor alone can completely explain all eating disorders. For example, genes clearly contribute to the risk for developing an eating disorder, but genes do not create a fate. Among monozygotic twins who share 100% of their genes, concordance rates for eating disorders have ranged from 23%24 to 83%.25 If genes fully explained the occurrence of eating disorders, then concordance rates would be 100% in identical twins. Similarly, social pressures to be thin cannot explain eating disorders. Although eating disorders have clearly increased as a consequence of media exposure to the thin ideal of beauty, eating disorders are actually quite rare, considering how common anorexic-looking beauty ideals are in our culture. Finally, psychological factors are important but do not fully explain the onset of eating disorders. There are many perfectionistic girls who struggle with selfdoubt and feel overweight who will never develop an eating disorder. In addition to appreciating the role of different factors in increasing risk for eating disorders, it is also important to recall that different factors may provide protection against the development of eating disorders. It is quite likely that the vast major-

Causes of Eating Disorders

ity of people could never develop anorexia nervosa simply because their bodies would not allow them to sustain a dangerously low weight. This same phenomenon may explain why weight loss diets are so difficult to maintain. Similarly, there may be people for whom vomiting does not come easily, so that occasional binge episodes do not become a pattern. Two people may have the same genetic risk for developing an eating disorder, but one never goes on a diet because she grows up in a household or community that bases self-worth on qualities other than weight. Thus, to understand the emergence of an eating disorder in a particular individual, one must consider all the different forces that both placed him or her at risk or protected him or her at various times during life.

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6

Treatment

Just as biological, psychological, and social factors are all important

in understanding the causes of eating disorders, these factors play important roles in the successful treatment of eating disorders. This chapter describes different treatments that have proven successful in helping girls and women overcome their eating disorders. BIOLOGICAL TREATMENTS

Medication is the main form of biological treatment used for eating disorders. Medications change the way brain cells communicate with each other. Several different medications have been studied for the treatment of anorexia nervosa, bulimia nervosa, and binge eating disorder. For example, the primary component of marijuana has been tested in the treatment of anorexia nervosa in the hopes that the commonly known side effect—increased hunger, or “the munchies”—would induce patients to eat. This did not prove to be successful. Other tested medications include antidepressants, mood stabilizers, opioid antagonists, antipsychotics, and stimulants. Of this impressive array of medications, antidepressants have become the clear medication of choice in the treatment of bulimia nervosa, and some data support their efficacy in the treatment of binge eating disorder. In particular, fluoxetine (commonly known by the

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Treatment

Methods for Evaluating Whether Medications Work To test how well a medication works to treat a problem, known as its efficacy, researchers randomly assign research participants to either receive the medication or to receive a placebo. A placebo is a substance that is known to have no real effect on the problem; however, the placebo is shaped to look exactly like the medication so that neither the research participants nor the physicians prescribing the medication for the study know which participants are receiving medication and which are receiving the placebo. This kind of study design is needed because a great deal of research has shown that people will spontaneously get better when they simply believe they have been given medication for a problem. This phenomenon has been demonstrated in patients being treated for everything from depression to cancer (and for eating disorders, too). In addition, it may be difficult for a physician who knows that one patient is receiving active medication not to perceive the person as getting better compared to another who is receiving placebo. For this reason, preventing the physician from being able to tell who is receiving medication versus placebo eliminates any possibility of bias in reporting the patients’ responses. This is called a doubleblind study because both the patient and the physician are blind to what the patient is receiving. At the end of data collection, coordinating researchers, who do not interact with patients and do not disclose information to physicians, reveal which patients were receiving medication and which were receiving the placebo. The response to the two treatment conditions can then be compared.

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trade name Prozac®) is the only drug that currently has Food and Drug Administration (FDA) approval for treating bulimia nervosa. Most antidepressants work by increasing the activity of monoamines, a class of neurotransmitters that includes serotonin, norepinephrine, and dopamine. However, fluoxetine is a selective serotonin reuptake inhibitor (SSRI). This means that it specifically increases the activity of serotonin without significantly impacting the activity of other monoamines. For the brain to work, brain cells need to communicate with each other. Brain cells “talk” to each other by passing small chemical messengers back and forth, much like passing notes in class. In order for one brain cell to get a message from another brain cell, the first brain cell must release the small chemical messenger, called a neurotransmitter. The second brain cell receives the message when the neurotransmitter binds to a receptor. Neurotransmitters fit into receptors like a key fits into a lock (Figure 6.1). One way of decreasing the activity of a neurotransmitter is to use medications that block the receptor so that they cannot receive the message. One way of increasing the activity of a neurotransmitter is to prevent a process known as reuptake—a process in which the first cell that released the neurotransmitter also reabsorbs some of the neurotransmitter. Reuptake inhibitors prevent this from happening. By preventing the first cell from reabsorbing the neurotransmitter it just released, these medications increase the amount of neurotransmitter that can be received by the second brain cell. A particular benefit of fluoxetine is its low risk of side effects. Serotonin is not just found in the brain, it is also found in other parts of the body, most notably the intestines. As a consequence, one side effect of fluoxetine is gastrointestinal (GI) discomfort. However, this problem usually goes away within four weeks of beginning treatment. Fluoxetine can also cause sleep

Treatment

Presynaptic nerve ending

Neurotransmitter-containing vesicle Neurotransmitter

Synapse Neurotransmitter receptor on postsynaptic neuron

Postsynaptic neuron

Figure 6.1 Brain cells communicate by sending small chemical messengers called neurotransmitters to bind to receptors. Neurotransmitters fit into receptors like a key fits into a lock.

difficulties—particularly at the doses that are required for treatment of bulimia nervosa. For this reason, another medication will sometimes be prescribed along with fluoxetine to improve sleep. Fluoxetine can cause dry mouth and has been associated with a decreased sex drive. In contrast to fluoxetine for treating bulimia nervosa, another antidepressant, bupropion (trade name Wellbutrin®), is not recommended for the treatment of eating disorders because of evidence that it may increase the likelihood of seizures among

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patients. Bupropion is a norepinephrine reuptake inhibitor. It increases the amount of norepinephrine available to the receptors of a neuron by decreasing the amount that is reabsorbed by the axon of the communicating neuron. There is some limited evidence that selective serotonin reuptake inhibitors may decrease risk of relapse among women with anorexia nervosa who have achieved weight recovery. PSYCHOLOGICAL TREATMENTS

Psychological therapies tend to be evaluated by two criteria. First, does a person receiving a particular therapy do better than someone who received no therapy? Second, does a person receiving a particular therapy do better than someone who received a different therapy? Several types of psychological treatment have been tested for eating disorders, and almost all satisfy the first criterion. That is, almost any psychological treatment is better than no treatment. However, only one treatment has received strong support as being superior to alternative treatments—cognitive behavioral therapy. Cognitive-behavioral therapy views eating disorder symptoms as a combination of irrational thoughts that need to be elicited, challenged, and replaced, and behaviors that are reinforced (through positive and negative reinforcement) by immediate consequences. For example, a cognitive-behavioral therapist may get a statement from a patient concerning the importance of being thin, such as: “People will only love me if I’m thin.” This belief can be challenged in several ways that are based on the patient’s own observations. First, the patient can be asked to notice couples in public settings and observe that many overweight people appear to be in happy relationships. Second, the patient can be invited to question the value of love from an individual who places so much importance on physical appearance. Third, the patient can be asked whether there is anyone he or

Treatment

she loves who is not thin (for example, a grandparent or close friend). In the end, the patient may come to adopt a belief that corresponds more closely to reality: “People who truly care about me as a person will love me no matter what I weigh.” One widely used cognitive-behavioral therapy, developed by Christopher Fairburn of Oxford University in England, is divided into three stages.26 The first stage establishes control over eating with behavioral techniques. These techniques include: 1. self-monitoring of food intake, binge eating and inappropriate compensatory behavior with a diary; 2. prescription of a regular pattern of eating at least 3 meals and 2 to 3 snacks per day (going no more than 2 to 3 hours between eating); 3. stimulus control (identifying triggers for binge-eating episodes and avoiding these); and 4. education about weight regulation, dieting, and the risks of purging. The second stage reduces dieting and body image disturbance through a combination of behavioral and cognitive techniques and trains the patient to engage in problem-solving. The steps of problem-solving include: 1. identifying the problem as soon as possible 2. specifying the problem as accurately as possible 3. identifying as many alternative responses to the problem as possible 4. examining the consequences associated with each alternative response 5. choosing the best response (or combination of responses) available, based upon anticipated consequences 6. acting on the selected response.

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The third stage works towards maintenance of progress and reduction of risk for future relapse. For example, patients are encouraged to recognize and challenge dichotomous thinking in order to differentiate a lapse from relapse. Eliminating all-ornothing thinking allows patients to have slips without having a full return of the eating disorder. Cognitive behavioral therapy emphasizes work that patients complete outside of sessions, since most of patients’ lives go on outside of the therapy setting. Therefore, homework assignments, such as maintaining a diary and writing out stages of problem-solving, are featured prominently in each stage of therapy. Numerous studies support the efficacy of cognitive-behavioral therapy in the treatment of bulimia nervosa and binge eating disorder. At this time, cognitive-behavioral therapy is considered the treatment of choice for bulimia nervosa. Unfortunately, cognitive-behavioral therapy has not demonstrated superior efficacy in the treatment of anorexia nervosa. SOCIAL TREATMENTS

So far, this chapter has discussed the failure to find treatments that are successful for patients who are actively suffering from anorexia nervosa. Although selective serotonin reuptake inhibitors may be helpful in preventing relapse among patients who have regained weight, it has not proven helpful in treating underweight patients to achieve weight gain. One treatment has emerged that appears to be helpful in treating adolescent patients with anorexia nervosa—family therapy. Family therapy is more often used when the patients are children or adolescents who live at home. For these reasons, it may be more appropriate for patients with anorexia nervosa than patients with bulimia nervosa because of the age differences between diagnostic groups. Traditional family therapy involves evaluating the entire family as the patient.27 This family systems

Treatment

approach viewed the child with anorexia nervosa as being the identified patient—the person whose behaviors revealed prob-

lems in the social interactions of the family. According to the family systems model, all families are made up of subsystems (e.g., spousal, parental, and sibling) in which different roles and responsibilities occur. Boundaries between subsystems can range from enmeshed (too weak) to disengaged (too strong). Enmeshment represents poorly differentiated boundaries. For example, children are invited into transactions that would typically remain between husband and wife (spousal subsystem). Disengagement represents boundaries that create isolation among family members. Clarity of boundaries may differ across family members and may change within a family over time. Indeed, family systems are required to change in response to the normal processes of development (i.e., as children become adults) and in response to external events (e.g., the family moves). Salvador Minuchin and his colleagues at the New York University Medical School proposed that families in which anorexia nervosa arose were marked by the following characteristics: enmeshment within the family, overprotection of children resulting in rigid boundaries separating family members from extrafamilial relationships, conflict avoidance, and concern about bodily functions, including physical symptoms, eating, and diets. According to this model, family conflict had no means for outlet because distress was suppressed behind a façade of closeness. The lack of boundaries among family members triggered conflict as girls approached adolescence. Girls in enmeshed families were stifled in their attempts to achieve independence and establish relationships outside the family. Because there was no viable option for expressing interpersonal conflict, conflicts were somaticized. That is, conflicts were expressed as physical conditions. Within Minuchin and

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colleagues’ framework, the conflict could be revealed in any number of physical maladies within any member of the family. Traditional family therapy sought to help family members recognize family conflicts, reinforce the boundaries of subsystems, and increase acceptance of children’s growing autonomy. A newer approach to family-based therapy invites family members to be members of the treatment team rather than the patient. Following a study indicating the superiority of a family treatment for younger eating disorder patients,28 the Maudsley model of family therapy has received increased attention and empirical support in the treatment of adolescents with anorexia nervosa. As with cognitive-behavioral therapy, there are three phases to family therapy as developed by the Maudsley group: 1. Refeeding the Client: Therapists support and reinforce parents’ efforts to refeed their child and encourage parents to form a united front. Meanwhile, siblings are encouraged to be supportive of the patient, and this reinforces appropriate boundaries between parental and sibling subsystems. Families are encouraged to devise their own plans for refeeding. 2. Negotiations for a New Pattern of Relationships: Once patients show willingness to participate in refeeding and achieve weight gain, weight gain with the least amount of conflict is allowed. Although symptoms remain central to this phase of treatment, other family issues are introduced to therapy. Of note, only issues that impact the parents’ ability to ensure patients’ weight gain are covered, and issues are covered only to the extent that they are relevant to the patients’ symptoms. 3. Termination: After the patient has achieved a healthy weight, the focus shifts to encouraging a healthy

Treatment

relationship between patients and parents. This is particularly important because, until this point, the patients’ illness forms the basis of family interactions. Reflecting the age of patients, themes of increased autonomy, appropriate family boundaries, and preparation for children’s departure from home are often covered in this phase. Two studies have supported the efficacy of family therapy over alternative therapies in patients with anorexia nervosa,29 and sustained benefits of the intervention were supported in a fiveyear follow-up study30 of the original study. •

•

•

•

•

•

•

SUMMARY

This chapter has focused on treatments with the best evidence of effectiveness. However, there are still several important observations that need to be made. First, most people who suffer from eating disorders never seek treatment. So, even though there are treatments that improve outcome compared to doing nothing, most individuals with eating disorders do nothing. Second, even though effective treatments produce responses that are better than alternative treatments, many people who receive the most effective treatments do not respond to treatment. Third, effective treatments have limited applications. At this time, we have no known effective treatment for adolescents who suffer from bulimia nervosa, for adults who suffer from anorexia nervosa, or for any age group suffering from EDNOS, other than binge eating disorder. As a result, despite many impressive gains in treatment over the past 20 years, a lot of work still needs to be done.

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Future Directions

Although eating disorders have existed for centuries, the field of

studying eating disorders is relatively young. There is a great deal of work yet to be done in addressing these problems. DESCRIPTION OF FULL ARRAY OF EATING DISORDERS

Most people who suffer from eating disorders do not meet diagnostic criteria for anorexia nervosa, bulimia nervosa, or binge eating disorder. Their problems fall within the category of eating disorders not otherwise specified (EDNOS). However, one EDNOS can be as different from another EDNOS as anorexia nervosa is different from bulimia nervosa. As a consequence, we know very little about the problems that most people with eating disorders have. There are two possible approaches to characterizing eating disorders. One approach, called the dimensional approach, places all disorders on a spectrum and views associations among different types of eating disorders as being like different musical notes on a scale. The difference between one musical note and another is quantitative—the frequency of vibration causes the specific pitch of a note. Higher frequencies create higher notes. Once you understand the fundamental principles of one note, you have a way to understand the basic principles of all musical notes. In the spectrum of eating disorders, the quantitative dimension might be thought of as the severity of different 84

Future Directions

symptoms. For example, the difference between anorexia nervosa—binge/purge subtype and bulimia nervosa may be represented as a quantitative difference in weight that is directly related to a quantitative difference in severity. Frequency of behaviors such as binge eating or purging may also be viewed in quantitative dimensions, such that no unique threshold exists between people who binge eat twice a week versus once a week—twice is simply more severe than once, and three times a week is more severe than twice a week. The dimensional approach seeks to identify the dimensions that are relevant for understanding the severity of illness but does not attempt to group people into categories. As appealing as this approach may seem, there are problems with it. First, with the example of weight, the association between weight and severity is not linear. People who are emaciated and those who are obese face greater medical risks than individuals who are normal weight (Figure 7.1). Second, with the example of frequency of behaviors, there may be a unique threshold between never engaging in a behavior (e.g., never purging) and purging, such that the relationship between severity and frequency becomes non-linear (Figure 7.2). The categorical approach is an alternative to the dimensional approach. It views eating disorders as falling into distinct types. This approach is similar to the model used in medicine to diagnose diseases. It simply views disorders as existing in unique classes—like different genes contribute to the risk for developing anorexia nervosa versus bulimia nervosa. The extent that anorexia nervosa exists across cultures and through history but bulimia nervosa appears to be a culture-bound syndrome also supports a categorical approach. Like the dimensional approach, the categorical approach has problems. The greatest problem is deciding where to draw

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boundaries between one type of eating disorder and another— particularly with regard to features that lie on a dimension, such as weight or binge frequency. Reflecting the uncertainty of where true boundaries exist, diagnostic criteria for eating disorders have changed over time and differ between the classification systems created by the American Psychiatric Association (APA) and the World Health Organization (WHO). For example, in the third edition of the APA’s diagnostic system, published in 1980, an individual had to lose 25% of his or her previous weight to be diagnosed with anorexia nervosa. In the current edition’s diagnostic criteria, first published in 1994, an individual needs to maintain weight at less than 85% of what

Medical Risk

High

Table 7.1

Low

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Emaciation

Average Weight

Obesity

Future Directions

would be expected for height to be diagnosed with anorexia nervosa. As described in Chapter 1, anorexia nervosa and bulimia nervosa cannot be diagnosed simultaneously in the current APA diagnostic system because a diagnosis of anorexia nervosa trumps a diagnosis of bulimia nervosa. However, the disorders can be diagnosed simultaneously in the WHO’s diagnostic system, and could be diagnosed simultaneously in the 1987 version of the APA’s diagnostic criteria. Thus, even for well-described eating disorders, the point at which one disorder is diagnosed versus another remains unclear.

Table 7.2

None

Low

Severity

High

RELATIONSHIP BETWEEN SEVERITY AND PURGING FREQUENTLY

Never

Once

5 Lifetime Purging Frequency

10

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Consider now the uncertainty surrounding all of the different possible variations one could show in disordered eating. Should Beth, Nina, Ben, and Pearl all be diagnosed with one type of eating disorder? Should they be diagnosed with four different types of eating disorders? To answer these questions, we need studies that examine the following questions: 1. Do people with EDNOS demonstrate all possible variations in symptom combinations with similar frequency? Or do certain sets of symptoms cluster together more often than would be expected by chance? 2. Do specific EDNOS cluster within families—that is, are Pearl’s biological relatives more likely to have an EDNOS that is similar to Pearl’s, or are they just as likely to have an EDNOS that is similar to Ben’s? 3. Do different EDNOS respond to different kinds of treatments? We know that Beth and Ben are likely to get better with medication. Would Pearl be just as likely to respond to these treatments, or does she need something different to help her overcome her eating disorder? 4. Do different EDNOS have different outcomes? Is the likelihood of recovery, relapse, or death different for Ben than for Pearl? 5. Do the biological bases of different EDNOS differ? Does reduced serotonin function contribute to all of the different EDNOS or are some characterized by increased serotonin function or dysfunction in different systems? These types of questions require further research to accurately describe the full array of eating disorders.

Future Directions

TREATMENT OF ANOREXIA NERVOSA

Although anorexia nervosa has arguably existed longer than any other eating disorder and is associated with the greatest risk of death, surprisingly little is known about how to successfully treat this disorder. Features unique to anorexia nervosa make it difficult to examine in controlled treatment studies. First, the disorder is relatively rare. Thus, only centers specializing in the treatment of eating disorders see large enough numbers of patients to conduct controlled treatment trials. Second, the severity of the disorder makes no-treatment control trials unethical. Thus, any controlled study is always comparing two active treatments in an attempt to determine if one is superior to another. Across treatment studies, few have demonstrated any

What Research Would You Fund? If you had $5 million to fund any type of research program for eating disorders, what would you fund? Currently, most research that is conducted on eating disorders in the United States is funded by the National Institutes of Health (NIH). The NIH receives funding from the federal government based on taxes paid by U.S. citizens. To receive funding, researchers write grant proposals in which they describe what kind of study they want to do and why they want to do the study. An independent group of researchers reviews all grant proposals that are submitted for funding. These reviewers evaluate what proposals pose the most important goals and what proposals are most likely to successfully meet their goals. You can influence the types of research that are funded by the NIH by contacting your congressional representatives and expressing your opinions on what types of health problems need more funding.

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significant differences in remission rates. The one set of studies suggesting any superior treatment effect has supported familybased treatments discussed in Chapter 6. However, support for this treatment is limited both in terms of the number of studies supporting the efficacy of family-based therapy and in terms of the population with whom it works. Specifically, family-based therapy may only be helpful for adolescent patients. To address this gap in the field, the National Institutes of Health (NIH) announced a program in 2003 to fund a multisite treatment study for anorexia nervosa. The purpose of the initiative is to encourage collaborative research among different groups specializing in the treatment of anorexia nervosa to recruit large enough numbers of patients to detect what may be modest but important differences in treatment efficacy. PREVENTION

Even if all eating disorders could be appropriately characterized and effective treatments could be developed for all eating disorders, the number of individuals suffering from eating disorders far exceeds the availability of treatment for eating disorders. For this reason, several experts within the field have directed their attention toward the goal of prevention. Simply put, effective prevention would save time, money, and—most importantly— suffering. People have been working on prevention for some time and with some limited success. Most often, prevention efforts have produced improvements in knowledge and attitudes but not behaviors. For example, prevention participants may report less body dissatisfaction, but they will not report reduced dieting. One challenge in preventing eating disorders is that we do not completely understand the risk factors that explain why one person develops an eating disorder and another person does not. Limited understanding of risk factors for eating disorders

Future Directions

reduces the success of prevention programs that attempt to reduce risk factors. The Health Promotion Paradigm is one approach to prevention that does not rely on altering specific risk factors.31 This prevention model emphasizes protective factors rather than focusing on risk factors. Whereas a risk factor promotes illness when present and does nothing when absent, a protective factor promotes wellness when present and does nothing when absent. In addition to focusing on protective factors, the Health Promotion Paradigm targets change in the actions of the community in addition to changes in the behavior of a given individual within that community. For example, within the Health Promotion Paradigm, schools would be encouraged to promote valuing individual differences with regard to race, sex, and weight. This intervention would seek to reduce prejudice in all of its forms (racism, sexism, and overvaluation of thinness/denigration of fatness or “weightism”). The goal of instilling the value of diversity among school children is not specifically related to the goal of preventing eating disorders. However, promoting health in the general population through promoting tolerance may reduce illness in individuals. A second challenge in prevention has been that improvements immediately after intervention tend to disappear over the course of follow-up. Modest improvements of limited duration may be explained by the use of modest interventions of limited duration. Duration of many programs has been limited to three or five sessions. In fact, two prevention studies utilized a single 22-minute videotape as the prevention.32 Given that girls reported watching 3.2 hours of television per day in one study,33 it is unclear how one video could demonstrate any lasting influence on attitudes. The solution to this challenge requires increasing resources for implementing prevention programs. A third challenge in prevention is the limited scope of

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programs. So far, prevention programs have focused almost exclusively on the psychosocial factors described in Chapter 5 (media images, body image, and dieting). In contrast, treatment spans the full range of social, psychological, and biological factors. The primary emphasis on social factors within prevention programs has two implicit assumptions. The first assumption is that social factors have the greatest influence on the development of eating disorders. The second assumption is that social factors are the easiest to change. Perhaps another reason for limited success of prevention programs is the failure to critically evaluate these assumptions. To improve future prevention programs, the following recommendations were provided from a roundtable discussion of experts convened by the National Institute of Mental Health (NIMH): 1. Develop common definitions of symptoms, syndromes, risk factors, and outcomes to better assess progress in epidemiology and prevention trials. 2. Encourage the integration of basic social science research in prevention approaches. 3. Encourage research on neural mechanisms of eating disorders at the animal level. Foster cross-discipline interactions among animal experimentalists, clinicians, and other researchers in the field. 4. Develop guidelines for assessing the scientific merit of eating disorders prevention trials. 5. Develop approaches to assess and minimize harmful effects of interventions. 6. Encourage research in biology, personality traits, family and social groups, and societal norms and values, all of which influence the development of eating disorders.

Future Directions

7. Increase awareness that eating disorders are a public health problem and that prevention efforts are warranted. 8. Adopt an approach that considers public health impact of these disorders.34 These recommendations reflect an expansion of prevention paradigms to examine the full range of etiological risk factors in eating disorders, from biological to sociocultural factors. These recommendations also reflect some of the impediments to developing efficacious prevention programs. These range from deficits in understanding the exact causes of eating disorders to societal stigmatization of eating disorders as problems that people choose to have. Such ill-informed beliefs reduce support for prevention resulting in the limited success of this important endeavor. • • • • • • • SUMMARY

This chapter has focused on future directions for the field of eating disorders by providing a few examples of topics that require further work. However, there is a great deal more work that needs to be done than has been described in this chapter. Until eating disorders are fully eradicated from human experience, there will always be more work to do. Identifying the right questions is as much a part of reaching that goal as getting answers to the questions already posed. As such, the next big break in the field is likely to come from someone who approaches the problem from a fresh perspective—someone like you.

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NOTES

1. Lasegue, Charles. “On Hysterical Anorexia.” Medical Times and Gazette (2) (1873): 265–266. 2. Keel, Pamela K., and Kelly L. Klump. “Are Eating Disorders Culture-bound Syndromes? Implications for Conceptualizing Their Etiology.” Psychological Bulletin 129(5) (2003): 747–769. 3. Halmi, Katherine A., James R. Falk, and Estelle Schwartz. “Binge-eating and Vomiting: A Survey of a College Population.” Psychological Medicine 11(4) (1981): 697–706. 4. Striegel-Moore, Ruth H., Faith A. Dohm, Helena C. Kraemer, C. Barr Taylor, Stephen Daniels, Patricia B. Crawford, and George B. Schreiber. “Eating Disorders in White and Black Women.” American Journal of Psychiatry 160(7) (2003): 1326–1331. 5. Stein, Daniel, Israel Orbach, Mirit Shani-Sela, Dov Har-Even, Amit Yaruslasky, Dina Roth, et al. “Suicidal Tendencies and Body Image and Experience in Anorexia Nervosa and Suicidal Female Adolescent Inpatients.” Psychotherapy & Psychosomatics 72(1) (2003); 16–25. 6. Garner, David M., Paul E. Garfinkel, Donald Schwartz, and Michael Thompson. “Cultural Expectations of Thinness in Women.” Psychological Reports 47(2) (1980): 483–491. 7. Heinberg, Leslie J., and J. Kevin Thompson. “Body Image and Televised Images of Thinness and Attractiveness: A Controlled Laboratory Investigation.” Journal of Social & Clinical Psychology 14(4) (1995): 325–338. 8. Stice, Eric, and Heather E. Shaw.

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“Adverse Effects of the Media Portrayed Thin-ideal on Women and Linkages to Bulimic Symptomatology.” Journal of Social & Clinical Psychology 13(3) (1994); 288–308. 9. Becker, Anne E., Rebecca A. Burwell, David B. Herzog, Paul Hamburg, and Stephen E. Gilman. “Eating Behaviours and Attitudes Following Prolonged Exposure to Television Among Ethnic Fijian Adolescent Girls.” British Journal of Psychiatry 180 (2002): 509–514. 10. Rosen, James C., Janet Gross, and Linda Vara. “Psychological Adjustment of Adolescents Attempting to Lose or Gain Weight.” Journal of Consulting & Clinical Psychology 55(5) (1987): 742–747. 11. Leon, Gloria R., Cheryl L. Perry, Carolyn Mangelsdorf, and Grethe J. Tell. “Adolescent Nutritional and Psychological Patterns and Risk for the Development of an Eating Disorder.” Journal of Youth & Adolescence 18(3) (1989): 273–282. 12. Heatherton, Todd F., Patricia Nichols, Fary Mahamedi, and Pamela Keel. “Body Weight, Dieting, and Eating Disorder Symptoms Among College Students, 1982 to 1992.” American Journal of Psychiatry 152(11) (1995): 1623–1629. 13. Polivy, Janet, and C. Peter Herman. “Dieting and Binging: A Causal Analysis.” American Psychologist 40(2) (1985): 193–201. 14. Bruch, Hilde. The Golden Cage: The Enigma of Anorexia Nervosa. Cambridge, MA: Harvard University Press, 1978.

15. Russell, Gerald. “Bulimia Nervosa: An Ominous Variant of Anorexia Nervosa.” Psychological Medicine 9(3) (1979): 429–448. 16. Westen, Drew, and Jennifer HarndenFischer. “Personality Profiles in Eating Disorders: Rethinking the Distinction Between Axis I and Axis II.” American Journal of Psychiatry 158(4) (2001): 547–562. 17. Becker, Anne E., Pamela Keel, Eileen P. Anderson-Fye, and Jennifer J. Thomas. “Genes and/or Jeans?: Genetic and Socio-cultural Contributions to Risk for Eating Disorders.” Journal of Addictive Diseases 23(3) (2004); 81–103. 18. Wurtman, Richard J., and Judith J. Wurtman. “Carbohydrate Craving, Obesity and Brain Serotonin.” Appetite 7 Suppl. (1986): 99–103. 19. Kaye, Walter H., Harry E. Gwirtsman, Timothy D. Brewerton, David T. George, and Richard J. Wurtman. “Bingeing Behavior and Plasma Amino Acids: A Possible Involvement of Brain Serotonin in Bulimia Nervosa.” Psychiatry Research 23(1) (1988): 31–43. 20. Goldbloom, David S., Lisa K. Hicks, and Paul E. Garfinkel. “Platelet Serotonin Uptake in Bulimia Nervosa.” Biological Psychiatry 28(7) (1990): 644–647. 21. Kaye, W.H., Frank, G.K., Meltzer, C.C., Price, J.C., McConaha, C.W., Crossan, P.J., et al. (2001). Altered serotonin 2A receptor activity in women who have recovered from bulimia nervosa. American Journal of Psychiatry, 158, 1152–1155.

22. Jimerson, David C., Michael D. Lesem, Walter H. Kaye, and Timothy D. Brewerton. “Low Serotonin and Dopamine Metabolite Concentrations in Cerebrospinal Fluid From Bulimic Patients With Frequent Binge Episodes.” Archives of General Psychiatry 49(2) (1992): 132–138. 23. Kaye, Walter H., Harry E. Gwirtsman, David T. George, and Michael H. Ebert. “Altered Serotonin Activity in Anorexia Nervosa After Long-term Weight Restoration. Does Elevated Cerebrospinal Fluid 5-hydroxyindoleacetic Acid Level Correlate With Rigid and Obsessive Behavior?” Archives of General Psychiatry 48(6) (1991): 556–562. 24. Kendler, Kenneth S., Charles MacLean, Michael Neale, Ronald C. Kessler, Andrew Heath, and Lindon Eaves. “The Genetic Epidemiology of Bulimia Nervosa.” American Journal of Psychiatry 148(12) (1991): 1627–1637. 25. Fichter, Manfred M., and Rainer Noegel. “Concordance for Bulimia Nervosa in Twins.” International Journal of Eating Disorders 9(3) (1990): 255–263. 26. Fairburn, Christopher. “A Cognitive Behavioural Approach to the Treatment of Bulimia.” Psychological Medicine 11(4) (1981): 707–711. 27. Minuchin, Salvador, Bernice L. Rosman, and Lester Baker. Psychosomatic Families: Anorexia Nervosa in Context. Cambridge, M.A.: Harvard University Press, 1978. 28. Russell, Gerald F., George I. Szmukler, Christopher Dare, and Ivan Eisler. “An Evaluation of Family Therapy in Anorexia Nervosa and Bulimia

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Nervosa.” Archives of General Psychiatry 44(12) (1987): 1047–1056. 29. le Grange, Daniel, Ivan Eisler, Christopher Dare, and Gerald F. Russell. “Evaluation of Family Treatments in Adolescent Anorexia Nervosa: A Pilot Study.” International Journal of Eating Disorders 12(4) (1992): 347–357; Robin, Arthur L., Patricia T. Siegel, Ann W. Moye, Marcia Gilroy, Amy Baker Dennis, and Anju Sikand. “A Controlled Comparison of Family Versus Individual Therapy for Adolescents With Anorexia Nervosa.” Journal of the American Academy of Child & Adolescent Psychiatry 38(12) (1999): 1482–1489. 30. Eisler, Ivan, Christopher Dare, Gerald F. M. Russell, George Szmukler, Daniel le Grange, and Elizabeth Dodge. “Family and Individual Therapy in Anorexia Nervosa: A 5year Follow-up.” Archives of General Psychiatry 54(11) (1997): 1025–1030. 31. Rosenvinge, Jan H., and Runi Borresen. “Preventing Eating Disorders—Time to Change Programmes or Paradigms? Current

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Update and Further Recommendations.” European Eating Disorders Review 7(1) (1999) 5–16. 32. Moreno, Addys B., and Mark H. Thelen. “A Preliminary Prevention Program for Eating Disorders in a Junior High School Population.” Journal of Youth & Adolescence 22(2) (1993) 109–124; Withers, Giselle F., Kylie Twigg, Eleanor H. Wertheim, and Susan J. Paxton. “A Controlled Evaluation of an Eating Disorders Primary Prevention Videotape Using the Elaboration Likelihood Model of Persuasion.” Journal of Psychosomatic Research 53(5) (2002) 1021–1027. 33. Tiggemann, Marika, and Amanda S. Pickering. “Role of Television in Adolescent Women’s Body Dissatisfaction and Drive for Thinness.” International Journal of Eating Disorders 20(2) (1996) 199–203. 34. Pearson, Jane, Dorothy Goldklang, and Ruth H. Striegel-Moore. “Prevention of Eating Disorders: Challenges and Opportunities.” International Journal of Eating Disorders 31(3) (2002) 233–239.

GLOSSARY

Allele—Alternative forms that a gene can take. Amino acid—Basic building block for proteins. Anorexia nervosa—An eating disorder characterized by self-starvation in

which a person refuses to maintain a normal weight and fears weight gain. Antidepressant—Medication that reduces feelings of distress. Antipsychotic—Medication that reduces problems characterized by distortions of reality. Attention—Cognitive ability to maintain mental focus. Axon—Part of a brain cell that sends messages to other cells. Bacteria—Single-celled organisms too small to be seen without a microscope; some bacteria cause disease. Binge eating—Eating, within a limited period of time, an amount of food that is substantially larger than most people would eat under similar circumstances, accompanied by a feeling of a loss of control over eating. Binge eating disorder (BED)—An eating disorder characterized by recurrent binge eating episodes that causes significant distress to the person. Boundary—Demarcation between subgroups in a family and between family and non-family members Bowel function—Workings of the intestines. Bulimia nervosa—An eating disorder characterized by recurrent binge eating episodes coupled with extreme measures to counteract the effects of eating on weight (such as self-induced vomiting). Candidate gene study—Investigation that examines whether a specific gene is associated with the presence of illness. Categorical approach—View of disorders as being distinct from one another. Cerebrospinal fluid—Liquid in ventricles in which by-products of brain activity are flushed out of the brain. Chemotherapy—The use of chemical agents to treat or control a disease, most commonly cancer. Cognitive abilities—Mental abilities such as thinking. Cognitive disinhibition—Loss of control over behavior that is triggered by thoughts. 97

Compulsive—Refers to a drive to reduce anxiety or threat. Confidentiality—The protection of privacy by not sharing information. Constipation—Reduced ability to defecate. Constraint—Control over behavior. Culture-bound syndromes—Disorders that occur only in certain cultures

and not in others. Decision-making—The cognitive ability to make a choice. Deoxyribonucleic acid (DNA)—The substance that serves as the building

blocks for genes. Diagnosis—Categorization of physical or mental illness by defining core features of the illness and providing a name for the illness. Diagnostic criteria—The core features of an illness that make up its definition. Dichotomous thinking—Black-and-white thinking in which things are evaluated as either all good or all bad. Dimensional approach—View of disorders as existing on a continuum. Disability—Loss of function in an important area of life. Disengagement—When boundaries are too rigid within families. Diuretic—An agent that produces loss of water by excess urination. Dizygotic twins (fraternal twins)—Twins formed by the fertilization of two separate eggs by two separate sperm; dizygotic twins share, on average, 50% of their genes, like regular siblings born in multiple births. Dopamine—Neurotransmitter that influences the experience of reward. Double-blind study—Study in which neither the patient nor the doctor knows if the patient is receiving active treatment. Dysphoria—The state of feeling unhappy or unwell. Eating disorder not otherwise specified (EDNOS)—An eating disorder that does not meet diagnostic criteria for either anorexia nervosa or bulimia nervosa. Efficacy—Ability of a treatment to produce superior outcomes compared to a control condition. Ego-dystonic—Inconsistent with a person’s sense of self. Ego-syntonic—Consistent with a person’s sense of self.

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Electrolytes—Substances in the body that carry an electrical charge, such

as calcium, potassium, and sodium. Emaciated—Extremely underweight. Enmeshment—When boundaries are too weak within families. Epidemiology—The study of rates of a disorder in a population. Esophagus—The muscular tube between the throat and the stomach. Etiology—Cause. Excessive exercise—Physical activity that goes beyond what is required for physical fitness or performance. Family systems approach—Therapy in which the entire family is seen as having an illness, not just the patient. Fasting—Extended periods of avoiding food intake. 5-hydroxytryptamine (5-HT)—Serotonin, a neurotransmitter that influences satiety, mood, and impulse control. Gene—Part of the code for building the body. Genotype—Basic code from which the body is built. Gluttony—Excessive food intake. Gray matter—Part of the brain that contains brain cells. Heterogeneous—Differing. Heterozygous genotype—Two different alleles comprising a gene. Homozygous genotype—Two of the same alleles comprising a gene. Hyperglycemia—Excessive concentrations of sugar in the blood. Hypokalemia—Insufficient concentrations of potassium in the body. Hypothalamus—Brain structure that influences weight and appetite regulation. Medial hypothalamus refers to inner portions of hypothalamus. Identified patient—Family member identified as having an illness within a family in a family systems approach. Impulsive—Referring to drives to increase reward or gratification. Insomnia—Inability to sleep. Insulin-dependent diabetes mellitus—Chronic disease caused by the body’s inability to properly produce or use insulin. Lanugo—Fine, downy hair that typically is present on fetuses before birth to regulate body temperature. Lanugo can occur in anorexia nervosa. 99

Lapse—A return of symptoms that represents a slip but not a return of

the disorder. Laxative—An agent that produces loss of matter by excess defecation. Memory—Cognitive ability to store information in the mind. Menstrual period—Monthly shedding of uterine lining (appears to be bleeding) in post-pubertal females. Molecular genetic study—Investigation that examines specific genes in relation to illness. Monoamine—Class of neurotransmitters. Monozygotic twins (identical twins)—Twins that share 100% of their genes. Mood stabilizer—Medication that reduces extreme emotional fluctuations. Negative reinforcement—Consequence of behavior that increases frequency of behavior by removing something unpleasant. Neuron—Brain cell. Neurotransmitter—Chemical released from brain cells that allows brain cells to communicate with other cells. Non-volitional—Not of one’s own choosing. Norepinephrine—Neurotransmitter that influences activity level and appetite. Obese—Extremely overweight. Opioid antagonist—Medication that reduces the function of pain-relieving neurotransmitters. Overeating—Consuming an excessive amount of food but not feeling a loss of control of eating. Parotid glands—Glands that produce saliva. Perfectionistic—Having a tendency to strive toward flawlessness. Phenotype—The observable expression of genes. Placebo—An inactive substance made to look like active medication and used as a control condition. Planning—Cognitive ability to organize a series of future actions. Positive reinforcement—Consequence of behavior that increases frequency of behavior by providing something rewarding. Problem-solving—Cognitive ability to resolve difficulties or puzzles. Protective factors—Factors that reduce probability of developing illness. 100

Purge—Extreme method of weight control/compensation for binge

episodes that involves forceful evacuation of matter from the body, including self-induced vomiting, laxative use, and diuretic use. Recall—Cognitive ability to retrieve information stored in memory. Relapse—A return of symptoms that represents the return of the disorder. Remission—Reduction in the severity of symptoms. Reuptake—When the brain cell that is releasing a neurotransmitter reabsorbs the neurotransmitter before it binds to a second brain cell’s receptors. Risk factors—Factors that increase probability of developing illness. Satiety—The feeling of fullness. Selective abstraction—Thinking that substitutes one part of something for its whole. Selective serotonin reuptake inhibitors (SSRIs)—Medications that prevent a brain cell that released serotonin from reabsorbing serotonin before it can bind to the receptor of another cell. Serotonin (5-HT)—Neurotransmitter that influences satiety, mood, and impulse control. Shared environment—External influences that are common to twins reared together (regardless of whether they are identical or fraternal twins). Somaticize—Express emotional distress as bodily complaints. Stimulant—Medication that increases sense of energy, euphoria, and reduces appetite. Subsystem—Subgroup within a family. Symptoms—Features of an illness. Tryptophan—Amino acid that is needed to create serotonin. Twin concordance—Similarity between twins. Ventricles—Fluid-filled core of the brain. White matter—Part of the brain that contains axons. Withdrawal—Effects that result from removing substance to which the body has developed tolerance.

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FURTHER READING

Abraham, S., and D. Llewellyn-Jones. Eating Disorders: The Facts, 5th ed. New York: Oxford University Press, 2001. Apostolides, M. Inner Hunger: A Young Woman’s Struggle Through Anorexia and Bulimia. New York: W. W. Norton and Company, 1998. Bode, J. Food Fight: A Guide to Eating for Preteens and Their Parents. New York: Simon & Schuster, 1997. Costin, C. The Eating Disorder Sourcebook. Los Angeles: Lowell House, 1997. Heller, T. Eating Disorders: A Handbook for Teens, Families and Teachers. Jefferson, NC: McFarland and Co., 2003. Hesse-Biber, S. J. Am I Thin Enough Yet?: The Cult of Thinness and the Commercialization of Identity. London: Oxford University Press, 1996. Hornbacher, M. Wasted: A Memoir of Anorexia and Bulimia. New York: Harper Collins, 1998. Kalodner, C. R. Too Fat or Too Thin?: A Reference Guide to Eating Disorders. Westport, CT: Greenwood Press, 2003. Kaminker, L. Exercise Addiction: When Fitness Becomes an Obsession. New York: Rosen Publishing Group, 1998. Keel, P. K. Eating Disorders. Upper Saddle River, NJ: Prentice Hall, 2005. Kolodny, N. The Beginner’s Guide to Eating Disorders Recovery. Carlsbad, CA: Gurze Books, 2004. Sacker, I. M., and M. A. Zimmer. Dying to Be Thin: Understanding and Defeating Anorexia Nervosa and Bulimia—A Practical, Lifesaving Guide. New York: Warner Books, Inc., 1987. Sandbek, T. J. The Deadly Diet: Recovering From Anorexia and Bulimia. Oakland, CA: New Harbinger Publications, 1993. Schmidt, U., and J. Treasure. Getting Better Bite by Bite: A Survival Kit for Sufferers of Bulimia Nervosa and Binge Eating Disorders. Hove, East Sussex, UK: Psychology Press, 1993. Weeldreyer, L. Body Blues: Weight and Depression. New York: Rosen Publishing Group, 1998. 102

WEBSITES

National Institute of Mental Health http://www.nimh.nih.gov/publicat/eatingdisorders.cfm

Eating Disorders Foundation of Victoria http://www.eatingdisorders.org.au

American Psychiatric Association http://healthyminds.org/

National Eating Disorders Association http://www.nationaleatingdisorders.org

Archives of Family Medicine http://archfami.ama-assn.org/cgi/content/full/9/1/88

Science Central http://www.sciencentral.com

Eating Disorders Information Network http://www.edin-ga.org/index.asp

US Department of Health and Human Services: Anorexia http://www.4woman.gov/faq/easyread/anorexia-etr.htm

International Eating Disorder Referral Organization http://www.edreferral.com/

US Department of Health and Human Services: Bulimia http://www.4woman.gov/faq/Easyread/bulnervosa-etr.htm

The Nation’s Voice on Mental Illness: Bulimia Nervosa http://www.nami.org

Ohio State University FactSheet. Eating Disorders Awareness: Bulimia Nervosa http://ohioline.osu.edu/ed-fact/1003.html

Something Fishy: Website on Eating Disorders http://www.somethingfishy.org/whatarethey/ednos.php

Healthier You: Binge Eating Disorder http://www.healthieryou.com/binge.html

Weight-control Information Network http://win.niddk.nih.gov/publications/binge.htm

A Weigh Out http://www.aweighout.com/binge/binge_overview.html

Overeaters Anonymous http://www.overeatersanonymous.org/

Healthy Within http://www.healthywithin.com/causes.htm

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Eating disorders in Figure Skaters and Non-skaters http://www.angelfire.com/il2/figskating/issues/ed.html

Anorexia Nervosa and Related Eating Disorders, Inc. http://www.anred.com/welcome.html

Helpguide: Eating Disorders: Types, Risk Factors and Treatments http://www.helpguide.org/mental/eating_disorder_treatment.htm#treatments

National Eating Disorder Screening Program http://www.mentalhealthscreening.org/events/nedsp/index.aspx

The Center for Young Women’s Health Eating Disorders: A General Guide for Teens, Children’s Hospital Boston http://www.youngwomenshealth.org/eating_disorders.html

Eating Disorders Association http://www.uq.net.au/eda/documents/eatingdisordershealthpromotion.html

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INDEX

5-hydroxytryptamine (5-HT). See Serotonin American Psychiatric Association (APA), 86–87 Amino acid, 71 Anorexia nervosa, 5, 7, 48, 72 case studies, 1, 3, 11–14 behavioral effects, 20–21,25 cognitive effects, 17–20, 42 defined, 3 diagnosis, 8, 84, 87 effects of, 14–22, 54 emotional effects, 17, 19, 64 history of, 6 interpersonal effects, 21–22, 26 mortality, 6, 16–17, 26, 28–30, 89 physical effects, 15–16, 24 recognizing, 22–25, 55 remission, 90 research studies on, 18–19, 65, 89–90 response to, 26–28, 56 at risk for, 6, 9, 29, 59, 65, 69, 71–72, 85 statistics, 6, 23, 61 symptoms and signs, 3–6, 11–15, 17–26, 30, 35, 58, 64–65, 70, 85 Antidepressants action, 76 treatment of binge eating disorder, 74 treatment of bulimia nervosa, 74, 76–78 Antipsychotics, 74 APA. See American Psychiatric Association Bell, Rudolph, 5 Binge eating disorder case studies, 51–52 defined, 48–49 diagnosis, 84 history of, 8 research on, 56, 61–65, 71

at risk, 8–9, 65, 70, 72 statistics, 8 symptoms and signs, 1, 8, 49–55, 61, 63, 71–72, 85 treatments, 74, 80, 83 Biological causes of eating disorders, 66–72, 74, 92–93 genes and eating disorders, 66–69, 72 serotonin function and eating disorders, 69–72 Biological treatments of eating disorders, 74–78 medications antidepressants, 74 antipsychotics, 74 marijuana, 74 mood stabilizers, 74 opioid antagonists, 74 stimulants, 74 Bruch, Hilde, 65 Bupropion. See Wellbutrin® Bulimia nervosa, 48 case study, 31–34 behavioral effects, 43–44 cognitive effects, 42–43 diagnosis, 8, 84, 87 effects of, 35–44, 54 emotional effects, 30–31, 33, 38–42, 44 interpersonal effects, 30, 44–45 mortality, 29–31, 36, 38 recognizing, 45, 55 research, 65, 71 response to, 56 at risk, 7–9, 29, 59, 63, 65–66, 69, 72, 85 statistics, 7, 61 symptoms and signs, 1, 7, 29–38, 40–45, 54, 58, 61, 63–66, 71 treatments, 63–64, 74, 76–77, 80, 83 Cognitive behavioral therapy, 82 and treatment of eating disorders, 63, 78–80

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Cognitive disinhibition, 62–63 Culture-bound syndrome, 85 Dieting, 3, 23, 31, 79, 92 and binge eating, 61–64 and carbohydrate craving, 70–71 failures, 44, 62 industry, 10 physical effects of, 14 Dysphoria, 71 Eating disorders case studies, 1, 3, 11–14, 31–34, 51–53 causes, 9, 42 characterizing and diagnosing, 84–88 categorical approach, 85–87 dimensional approach, 84–85 future of, 84–93 history of, 4–5 prevention, 90–93 signs and symptoms, 1–8 statistics, 23 study of, 84 treatment, 74–83 Eating disorder not otherwise specified (EDNOS) case studies, 51–53 causes of, 58–74 defined, 48–49 diagnosis, 8, 56, 84, 88 effects of, 54–55 future of, 56 recognizing, 55–56 response to, 56–57 symptoms and signs, 8, 48–50, 54–55 EDNOS. See Eating disorder not otherwise specified Ego-dystonic disorder, 30 Ego-syntonic disorder, 27 Electrolytes, 34

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Family therapy boundaries, 81 disengagement, 81 for eating disorders, 80, 90 enmeshment, 81 identified patient, 81 phases, 82–83 subsystems, 81 systems approach, 80–81 Fairburn, Christopher, 79 FDA. See Food and Drug Administration Fluoxetine. See Prozac Food and Drug Administration (FDA), 76 Garner, David, 59 Genes coding, 67–68 and eating disorders, 66–69, 72–73 Gluttony, 8, 40 Gull, Sir William, 6 Health Promotion Paradigm protective factors, 91 risk factors, 91–93 Heinberg, Leslie, 59 Herman, Peter, 62–63 Heterogeneous disorder, 31 Hyperglycemia, 38 Hypokalemia, 36 Hypothalamus, 69–70 Insulin-dependent diabetes mellitus, 38 Kaye, Walter, 71 Keys, Ancel, 18 Lasegue, Charles, 6 Marijuana, 74 Maudsley model of family therapy, 82–83 Minnesota starvation study, 18–20

Minuchin, Salvador, 81 Monoamines, 76 Mood stabilizers, 74 National Institutes of Health (NIH), 89–90 National Institute of Mental Health (NIMH), 92–93 Neurotransmitters, 77 dopamine, 76 norepinephrine, 76, 78 serotonin, 69–72, 76 Night eating syndrome, 56 NIH. See National Institutes of Health NIMH. See National Institute of Mental Health Non-volitional disorder, 49 OA. See Overeaters Anonymous Obesity, 8, 10, 20 causes, 55 and eating disorders, 49–50, 54–55 health consequences of, 54, 85 statistics, 55 Opioid antagonists, 74 Overeaters Anonymous (OA), 51–52 Overeating, 3 Perfectionism and increased risk for eating disorders, 64–66, 72 Polivy, Janet, 62–63 Prozac® (Fluoxetine), 74 side effects, 76–77 and the treatment of bulimia nervosa, 76–77 Psychological causes of eating disorders, 61–66, 74, 92 dieting and binge eating, 61–64 personality and eating disorders, 64–66, 72

Psychological treatments of eating disorders, 78–80 cognitive behavioral therapy, 63, 78–80 Purging disorder, 56 case study, 52–53 symptoms and signs, 53–57, 59, 85 Reinforcement negative, 78 positive, 78 Research on anorexia nervosa, 65, 72, 80, 89–90 on binge eating disorder, 56, 61–65, 71, 80 on bulimia nervosa, 65, 71, 80 on cognitive-behavioral therapy, 79 on family therapy, 80–83, 90 funding, 89 future of, 88 on genes and eating disorders, 66–70, 72–73 on media images of the ideal body, 59–60 on medications, 75 on starvation effects, 18–20 on twin studies, 68–69, 72 Russell, Gerald, 7, 65 Selective serotonin reuptake inhibitor (SSRI), 76 and relapse prevention in anorexia nervosa, 78, 80 Serotonin function, 76 in eating disorders, 69–72 Shaw, Heather, 60 Social causes of eating disorders, 58–61, 74, 92–93 media images of the ideal body, 58–60, 72, 92 Social treatments of eating disorders, 80–83 family therapy, 80–83

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SSRI. See Selective serotonin reuptake inhibitor Starvation effects, 20, 22, 24–25, 54 depression, 19 withdrawal, 19 St. Catherine of Siena, 4–5 Stice, Eric, 60 Stimulants, 74

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Thompson, J. Kevin, 59 Tryptophan, 71 Wellbutrin® (Bupropion), 77–78 WHO. See World Health Organization World Health Organization (WHO), 86–87

PICTURE CREDITS

page:

2: © Grace/Zefa/CORBIS 4: © Bass Museum of Art/CORBIS 15: Associated Press, THE GRAND ISLAND INDEPENDENT 19: © Time Life Pictures/Getty Images 23: Associated Press AP 36: © HFS Imaging

37: Scherer Illustration 39: Scherer Illustration 50: © Zave Smith/CORBIS 68: Scherer Illustration 70: © HFS Imaging 77: © HFS Imaging

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TRADEMARK

Atkins is a registered trademark of Atkins Nutritionals, Inc.; Prozac is a registered trademark of Eli Lilly and Company; Wellbutrin is a registered trademark of GlaxoSmithKline.

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AUTHOR

Dr. Pamela K. Keel received a B.A. in anthropology from Harvard University

in 1992 and received a Ph.D. in clinical psychology from the University of Minnesota in 1998. She completed her internship at Duke University Medical Center in 1999. From there she joined the faculty in the Department of Psychology at Harvard University. In 2003, she left Harvard to join the faculty in the Department of Psychology at the University of Iowa. Dr. Keel began conducting research on eating disorders as an undergraduate. She has published more than 50 journal articles from research she has conducted. In addition, she authored a book on eating disorders in 2005 for college students.

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