Anorexia Nervosa And Bulimia Nervosa: New Research

ANOREXIA NERVOSA AND BULIMIA NERVOSA: NEW RESEARCH No part of this digital document may be reproduced, stored in a retrieval system or transmitted in any form or by any means. The publisher has taken reasonable care in the preparation of this digital document, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained herein. This digital document is sold with the clear understanding that the publisher is not engaged in rendering legal, medical or any other professional services.

ANOREXIA NERVOSA AND BULIMIA NERVOSA: NEW RESEARCH

PAMELA I. SWAIN EDITOR

Nova Science Publishers, Inc. New York

Copyright © 2006 by Nova Science Publishers, Inc.

All rights reserved. No part of this book may be reproduced, stored in a retrieval system or transmitted in any form or by any means: electronic, electrostatic, magnetic, tape, mechanical photocopying, recording or otherwise without the written permission of the Publisher. For permission to use material from this book please contact us: Telephone 631-231-7269; Fax 631-231-8175 Web Site: http://www.novapublishers.com NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book, but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book. The Publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance upon, this material. This publication is designed to provide accurate and authoritative information with regard to the subject matter covered herein. It is sold with the clear understanding that the Publisher is not engaged in rendering legal or any other professional services. If legal or any other expert assistance is required, the services of a competent person should be sought. FROM A DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS. Library of Congress Cataloging-in-Publication Data Anorexia nervosa and bulimia nervosa : new research / Pamela I. Swain (editor). p. ; cm. Includes bibliographical references and index. ISBN 978-1-61668-120-3 (E-Book) 1. Eating disorders. 2. Anorexia nervosa. 3. Bulimia. [DNLM: 1. Anorexia Nervosa. 2. Bulimia. WM 175 A615 2005] I. Swain, Pamela I. RC552.E18A55 2005 362.2'5--dc22 2005005548

Published by Nova Science Publishers, Inc. New York

Contents Preface

vii

Chapter I

Suicide in Anorexia Nervosa and Bulimia Nervosa Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

Chapter II

Psychopathological Aspects of Body Image Disturbance on Anorexia and Bulimia Nervosa Simone Mancini Castilho

Chapter III

Chapter IV

Chapter V

Chapter VI

Experiences of ‘Control’ in Anorexia Nervosa Treatment: Delayed Coercion, Shadow of Law, or Disseminated Power and Control? Terry Carney, Mim Ingvarson and David Tait

1

27

41

Secondary Anorexia: A Neglected Issue in the Optimal Management of Patients Suffering from Acute and Chronic Diseases Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli

63

"I Couldn´t Find the Food I Liked" Anorexia in Boys. Three Case Reports B. Bräutigam and M. Herberhold

91

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake, Eating Patterns, Eating Attitudes and Body Image of Brazilian Bulimic Patients Marle dos Santos Alvarenga, Fernanda Baeza Scagliusi and Sonia Tucunduva Philippi

105

vi Chapter VII

Chapter VIII

Chapter IX

Index

Pamela I. Swain Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept in Women with Bulimia Nervosa and Binge Eating Disorder Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh, Monique Potvin-Kent and Hany Bissada

145

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

159

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health Alex Milosevic

185 205

Preface The abundance of food in the developed countries of the world has seemingly spawned an epidemic of disorders connected to the food. Extremes such as intensive concern about one’s body image and total disregard for it have resulted in countries which contain enormous segments of the population who are either obese and proud of it or bordering on anorexia nervosa. This new book gathers state-of-the-art research from leading scientists throughout the world which offers important information on understanding the underlying causes and discovering the most effective treatments for eating disorders. Suicide in anorexia nervosa and bulimia nervosa is a major cause of death as reported in chapter I. Meta-analytic studies have shown that individuals suffering from anorexia nervosa and bulimia nervosa commit suicide more often than their counterparts in the general population. The percentage of suicide among patients with eating disorders (not differentiated) ranges from 1.8% to 7.3%. Risk factors for suicide and attempted suicide (which in many cases results in successful suicide) in anorexia nervosa and bulimia nervosa include: purging type, chronic disease, obsessive symptoms, drug abuse, major depression, lack of impulse control, and low body mass index (BMI) at presentation (for anorexia nervosa). A few studies have suggested that suicide is the major cause of death among patients with anorexia nervosa, refuting the assumption that inanition generally threatens the life of these patients. Data concerning suicide in bulimia nervosa, on the other hand, are still scarce, as more long-term follow-up studies need to be completed before the risk for bulimia nervosa may be compared with that for anorexia nervosa. Suicide attempts are easily found among cohorts of patients with bulimia nervosa, which constitutes a risk factor for completed suicide. Comorbidity between anorexia nervosa or bulimia nervosa and other psychiatric disorders is a frequent event, as in the case of affective disorders and personality disorders. No doubt suicidal behavior is underestimated amongst patients with anorexia nervosa and bulimia nervosa. Young women are heavily represented among these patients; therefore suicidal behavior is gender-related. An effort to reconcile with the subject of suicide and a better evaluation of these patients’ psychopathology should improve suicide prevention strategies among these individuals. According to World Health Organization estimates, suicidal behavior and eating disorders are alarming phenomenon among young people. Preventive strategies of suicide among these patients should include pharmacological

viii

Pamela I. Swain

treatments, psychotherapy and school-based interventions involving crisis management, selfesteem enhancement and the development of coping skills and healthy decision making. Body image disturbance is an important clinical feature on eating disorders and was characterized by the Diagnostic and Statistical Manual of Mental Disorders, fourth Edition (DSM-IV), as one of the diagnostic criteria for these pathologies. Although the presence and importance of body image disturbance in eating disorders are well established, the psychopathological nature of this symptom is not yet defined. Chapter II explores the presence of obsessive-compulsive and delusional features of the ‘Body Image Disturbance’ in anorexia and bulimia nervosa. Sixteen women with anorexia nervosa and eleven women with bulimia nervosa were compared regarding their responses to the Yale-Brown Obsessive Compulsive Scale (Y-BOCS) and to the Delusional Features Assessment Scale. Variables were analyzed with the Fisher’s Exact Test and Mann-Whitney non-parametric test (U). Patients with anorexia nervosa had scores significantly higher than bulimic patients in the Delusional Features Assessment Scale and no differences were found between the groups regarding obsessive-compulsive features. The analysis of the psychopathological differences of ‘Body Image Disturbance’ in anorexia and bulimia nervosa has diagnostic implications. Anorexia nervosa is often chronic, with one of the highest death rates for psychological conditions. Law can compel treatment, but is rarely invoked, at least formally (though the strategic possibilities of orders confers internal authority within the clinical setting). Instead, ‘control’ (or management) is exercised diffusely, through disciplinary practices embedded in everyday clinic life, such as daily routines of eating and washing, behavioural ‘contracts’, regular surveillance and measuring, interactions with staff, visits and activities. The regulatory regime not only touches on such ‘practices’ but also targets ‘identities’ (including self-image, and attitudes to the body) and what Goffman called the ‘moral career’ of the patient (eg learning to play the ‘patient role’, to ‘be’ an ‘anorexic’). Chapter III argues that it is not the clumsiness of the law, or the success of less restrictive options which explains why law is so infrequently engaged. Rather, based on an interpretation of Foucault, the authors conclude that the regulatory regime that shapes treatment of anorexia nervosa, is ‘the law’, in a sense. The regime of governmentality within the clinic is shaped by practices which operationalise ‘duty of care’, or translate medical expertise into medical authority, or show how interactions between ‘experts’, ‘carers’ and patients are mediated through conventions and rules, or which conscript ‘empowerment’ as control. The patient learns to provide consent ‘freely’, to make the ‘correct’ choices, to accept the ‘empowerment’ regime that is made even more convincing by the threat of legal intervention. In time the constraints learned in this way become part of the new role, that of the ‘recovering’ patient. The ‘fiction’ of acting ‘responsibly’, employed so hesitantly at first, becomes part of the new identity. The patient has become an active participant in the governance of self. Anorexia and reduced food intake are relevant issues in the management of patients suffering from acute and chronic diseases, including sepsis, cancer, chronic liver failure, chronic renal failure, etc. In acute diseases, anorexia does not represent a primary therapeutic target, since effective treatment of the underlying disease rapidly ameliorates food intake. In chronic diseases, anorexia impacts on patients’ prognosis, since it contributes to the development of malnutrition, thereby increasing morbidity and mortality, and impinges on quality of life. Accumulating evidence indicate that anorexia associated to different diseases

Preface

ix

is multifactorial in its pathogenesis, and suggest that most of the hypothalamic neuronal signalling pathways modulating energy intake are involved. Chapter IV reports a number of factors are considered mediators of anorexia, including hormones [e.g., leptin], neuropeptides [e.g., NPY], cytokines [e.g., IL-1, IL-6, TNF] and neurotransmitters [e.g., serotonin and dopamine]. Their modes of action do not appear to be separate and distinct, rather they are closely inter-related. However, convincing evidence suggest that a hierarchical organization exists in which cytokines play a key role, triggering the complex neurochemical cascade which leads to the onset of anorexia. Cytokine increased expression during disease inhibits the hypothalamus to appropriately respond to peripheral signals, by persistently activating anorexigenic systems and/or inhibiting prophagic pathways. Hypothalamic monoaminergic neurotransmission may significantly contribute to these effects. Thus, the optimal therapeutic approach to anorectic patients should be based on both changes in dietary habits, achieved via nutritional counselling, and drug therapy, aimed at interfering with cytokine expression or hypothalamic monoaminergic neurotransmission. The number of boys affected by eating disorders is increasing. The fact that the numbers for eating disorders among boys are so low is probably due in part to underdiagnosis. Although adolescent girls are still the group primarily affected by eating disorders, nearly every tenth person suffering from an eating disorder is male. The lifetime prevalence of any eating disorder has been reported as 17.9% among women and 6.5% among men. There are triggers for the disorders among boys that are different from those that have been identified among girls. These include excessive physical activity, a fragile sexual identity, demanding requirements or expectations in the areas of competitive sports, muscle building, and ideals of physical perfection. There are also differences in the pathologies. For example, boys often exhibit a different form of body image distortion, one that is more focused on masculine muscular form. They also show less shame concerning binge eating. The fact that anorexia and bulimia are much more difficult to diagnose among boys has led to a situation in which only the most severe cases are successfully diagnosed. This situation is exacerbated by the fact that bulimia is perceived by the public as a disease that only affects girls, with the result that affected boys often have to struggle with emotions of shame and denial. Chapter V reports on three clinical cases that illustrate some of the differences between male and female anorexia and other aspects like the wide range of psychological and physical symptoms, the different therapeutic approaches, and kinds of treatment. The authors focus on the patients’ personal histories and the psychological conditions in the parents. Discussion of the results encompasses psychodynamic and systemic issues. Eating disorders (ED) have been treated in Brazil since 1992 with the creation of the ED Unit of the University of São Paulo, a public service that has treated 1,794 patients, mainly white, reasonable educated and aged between 21 and 40 years. Food intake and eating patterns and behaviors are disturbed in bulimia nervosa (BN). Food intake is defined as the food and nutrients that compose the diet, while eating patterns are the meal frequency, regularity and schedules, and eating behaviors are the attitudes, beliefs and relationship with food. In Brazil, the effect of multiprofessional treatment in BN had never been examined. Even in developed nations, only the frequency of bulimic symptoms has been evaluated. In chapter VI, the Eating Disorder Inventory, Three-Factor Eating Questionnaire, Dutch Eating Behavior Questionnaire and Restraint Scale were used to analyze eating behaviors, although

x

Pamela I. Swain

these questionnaires focus especially in dietary restraint, leaving the other eating behaviors’ aspects uncovered. Thirty-nine women with BN (according to DSM-IV criteria) were followed. Treatment was composed by 12 weeks of cognitive-behavior therapy, pharmacotherapy and nutrition counseling. Measurements were made before and after treatment, and after three months. Patients recorded their food intake and occurrence of compulsions and purges in a diary. They fulfilled the EAT, BITE and BSQ, and also an eating attitudes questionnaire, especially developed for this research. Non-parametric statistics were used to test for differences among the three moments. The authors observed an improvement in clinical symptoms; at the end of following 97.5% of the patients did not fulfill criteria for BN anymore. Scores of EAT, BSQ and BITE-symptoms decreased after treatment and even more after the later following. Nutrients intake did not alter, even though energy content of the meals followed by vomit decreased. Number of meals increased and patients did more meals seated, with company and less anxious. The belief of automatically gaining weight after a meal, and guilty and worry after eating a “forbidden” food decreased. Nevertheless, most of them remained hating the hunger sensation, having difficulties with food choices and not believing that they could have a normal diet and a normal weight. Based on the questions used to assess eating attitudes, they are now developing an eating attitudes questionnaire, which will be psychometrically tested. This study supports the idea of the importance of food issues and behaviors in ED, because even the patients that had a clinical improvement remained with a complicated relationship with food, which can contribute to relapses. As described in chapter VII, it was hypothesized that higher levels of actual-desired BMI discrepency (ADBD) would be associated with higher binge eating symptoms, lower self concept, and higher body dissatisfaction for a clinical sample of women with Bulimia Nervosa (BN) and Binge Eating Disorder (BED). A theoretical frame for ADBD was put forward based on self discrepancy theory. Also hypothesized was that women with BN would have greater eating and self related pathology than those with BED. Fifty-one participants diagnosed with BN and 41 with BED drawn from a clinical sample completed questionnaires assessing eating disorder and general psychopathology. Greater ADBD was related to greater body dissatisfaction for the BN and BED groups, and lower self concept for the BN group. Those with BN had more self-related pathology. ADBD can be easily assessed by clinicians and may be used as an index of body dissatisfaction and overall self concept. ADBD may be a vulnerability factor for developing an eating disorder for women. Heritability studies provide a general framework for understanding risk for bulimia nervosa (BN): liability is a function of both genetic and environmental factors. Chapter VIII proposes a specific model that integrates identified heritable and environmental risk factors for BN. Trait urgency, the tendency to act rashly in response to distress, is a heritable risk factor that increases the likelihood that one will engage in some form of rash, maladaptive behavior pattern (such as BN). The specific form of one’s maladaptive behavior is a function of learned experiences from one’s environment. Individuals who learn to expect alleviation of negative mood from eating, and overgeneralized life improvement from thinness, are more likely to engage in bulimic behaviors. Thus, the general, heritable risk from high levels of urgency is likely to become expressed as BN when one learns to expect benefits from eating

Preface

xi

when distressed and extreme benefits from thinness. The proposed process is empirically supported and consistent with findings from heritability research. The dental and oral health of individuals with an eating disorder has been largely underinvestigated and ignored as health care professionals focus on the general medical, dietary and psychiatric/psychological needs of patients. Disordered eating and chaotic lifestyle may affect patterns of caries (decay) and gum disease. Oral microbial flora, either in dental plaque or saliva, could theoretically differ to normal flora as a consequence of repeatedly low intraoral pH secondary to self-induced vomiting (SIV). Parotid salivary gland enlargement and altered salivary composition have been described. The presence of gastric acid in the mouth can result in acid erosion, with disfiguring consequences to the dentition. The impact of anomalous behaviours such as chaotic eating and self-induced vomiting upon the dental health of eating disordered subjects may not be apparent to the subjects themselves or their carers, be they physicians, psychiatrists, psychologists, nurses or relatives. Nonetheless, the effects upon the teeth can be significant such that it has been postulated that the dentist may be the first health care professional to suspect an eating disorder in an otherwise healthy individual. The mouth is the first part of the digestive system and commonly exhibits signs of disease occurring elsewhere. Chapter IX reviews the literature and illustrates the clinical problems faced by real cases. Prevention will also be discussed.

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 1-26 © 2006 Nova Science Publishers, Inc.

Chapter I

Suicide in Anorexia Nervosa and Bulimia Nervosa Maurizio Pompili1, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli Department of Psychiatry – Sant’Andrea Hospital University of Rome “La Sapienza” - Italy

Abstract Suicide in anorexia nervosa and bulimia nervosa is a major cause of death. Meta-analytic studies have shown that individuals suffering from anorexia nervosa and bulimia nervosa commit suicide more often than their counterparts in the general population. The percentage of suicide among patients with eating disorders (not differentiated) ranges from 1.8% to 7.3%. Risk factors for suicide and attempted suicide (which in many cases results in successful suicide) in anorexia nervosa and bulimia nervosa include: purging type, chronic disease, obsessive symptoms, drug abuse, major depression, lack of impulse control, and low body mass index (BMI) at presentation (for anorexia nervosa). A few studies have suggested that suicide is the major cause of death among patients with anorexia nervosa, refuting the assumption that inanition generally threatens the life of these patients. Data concerning suicide in bulimia nervosa, on the other hand, are still scarce, as more long-term follow-up studies need to be completed before the risk for bulimia nervosa may be compared with that for anorexia nervosa. Suicide attempts are easily found among cohorts of patients with bulimia nervosa, which constitutes a risk factor for completed suicide. Comorbidity between anorexia nervosa or bulimia nervosa and other psychiatric disorders is a frequent event, as in the case of affective disorders and personality disorders. No doubt suicidal behavior is underestimated amongst patients with anorexia nervosa and bulimia nervosa. Young women are heavily represented among these patients; therefore suicidal behavior is gender-related. An effort to reconcile

1

Maurizio Pompili, M.D.Sant’Andrea Hospital – Dep. of Psychiatry,University of Rome “La Sapienza”,Via di Grottarossa, 1035-1039, 00189 Roma – Italy, [email protected]

2

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli with the subject of suicide and a better evaluation of these patients’ psychopathology should improve suicide prevention strategies among these individuals. According to World Health Organization estimates, suicidal behavior and eating disorders are alarming phenomenon among young people. Preventive strategies of suicide among these patients should include pharmacological treatments, psychotherapy and school-based interventions involving crisis management, self-esteem enhancement and the development of coping skills and healthy decision making.

Introduction Suicidal behavior is identified as a major public health problem and a considerable drain on resources in both primary and secondary health care settings in many countries worldwide. Suicide is the ninth leading cause of death in the United States for all ages. Among teenagers and young adults, it is the third most frequent cause of death. Approximately 40,000 to 50,000 Americans die every year by their own hand. According to World Health Organization estimates, approximately 1 million people died from suicide, and 10 to 20 times as many attempted suicide worldwide in the year 2000 (WHO, 2000a). This averages out to one death every 40 seconds and one attempt every three seconds. Youth suicide, the third leading cause of death among teenagers and young adults, accounts for more deaths in the United States than natural causes combined for 15 to 24-years-olds, according to the National Center for Health Statistics (2000). In Europe, according to the WHO Databank, suicidal behavior among young people has increased over the past thirty years and statistics match with those of the U.S. Each suicide has a serious impact on at least six other people and the psychological, social and financial impact of suicide on the family and community is immeasurable. The World Health Organization (2000b) recognizes suicide as a complex problem for which there is no single cause, no single reason. It results from a complex interaction of biological, genetic, psychological, social, cultural and environmental factors. Shneidman (1985), who is considered the father of suicidology, has proposed the following definition of suicide: “Currently in the Western world, suicide is a conscious act of selfinduced annihilation, best understood as a multidimensional malaise in a needful individual who defines an issue for which the suicide is perceived as the best solution”. We shall continue with another citation by Edwin Shneidman (1993) who suggested “that suicide is best understood not so much as a movement toward death as it is a movement away from something and that something is always the same: intolerable emotion, unendurable pain, or unacceptable anguish. Reduce the level of suffering and the individual will choose to live”. Profound psychic pain is a major part of the clinical picture, so much so that self-harming thoughts and behaviors, including self-mutilation, suicidal ideation, gestures and attempts, may become a way of attempting to cope with this pain and the marked social isolation that results from eating disorders (Manley and Leichner, 2003). The best way to prevent suicide is to learn what is causing the distress, the tension and anguish – and the work to treat these emotions within the suicidal person. Several governments around the world have established suicide prevention programs. A major reason for this has been the very large increase in suicide in young people, especially males, seen in many countries. Retrospective studies indicate that the absolute majority (81-100%) of suicides occurs in subjects with a psychiatric

Suicide in Anorexia Nervosa and Bulimia Nervosa

3

illness, depression being the most common diagnosis (Lonnqvist, 2000). There has been recent recognition of a very definite increased risk for suicide in girls with eating disorders (Apter et al., 1995). A few studies suggested that suicide is the major cause of death among patients with anorexia nervosa (Toltrup et al. 1985; Patton, 1988; Santonastaso, et al. 1991); refuting the assumption that inanition generally threatens the life of these patients. The analysis of suicide and attempted suicide in patients suffering from anorexia nervosa and bulimia nervosa constitutes a focal point for an appropriate comprehension of the psychopathology of these individuals. People with eating disorders usually evoke the idea of self-wounding features, aiming at destroying the body slowly rather than through a suicidal act. This misconception often leads to ignoring the risk of suicide. Few studies, in fact, analyzed suicidal behavior in-depth among patients with eating disorders, in particular in patients with anorexia nervosa and bulimia nervosa, and there is no doubt that suicidal behavior is an underestimated phenomenon. Great importance can be placed upon the course of the illness and the follow-up period considered for a correct evaluation of the suicidality among this class of patients (Theander, 1985). According to various authors, suicide occurs not only in the late phases of the illness but above all in periods of symptomatic remission (Jeammet et al., 1984; Bruch, 1988). Frequent hospitalizations and, in the case of the anorexic patients, a lower weight at the first consultation are two predictive factors of suicidal behavior (Morgan and Russell, 1975; Hsu et al., 1979; Patton, 1988); also, an important risk factor is a later onset of illness (Patton, 1988). Eating disorders are often comorbid with depression, a feature identifiable in histories of suicidal individuals (Russell, 1979). Some scholars believe that eating disorders represent a form of affective disorder (Cantwell et al., 1977; Winokur et al., 1980; Hudson et al., 1983) and antidepressant medications have been employed. Viesselman and Roig (1985) suggested that response to an antidepressant does not necessarily mean that the disorder being treated is depression; patients with eating disorders may be responding to the anti-panic nature of the drugs rather than to their antidepressant characteristics. Most authors believe that suicidal behavior among patients with eating disorders is independent of the existence of mood disorders and stress the existence of suicidal behavior among patients with eating disorders. It has been suggested that depressive disorders in anorexia nervosa are, in general, secondary to eating disorders (Ivarsson et al., 2000). It has been stressed that another cause of depression secondary to anorexia nervosa is reactive distress related to disturbed eating behavior, concerns about body-image, poor self-esteem, shame and guilt (Halmi et al., 1991; Cooper, 1995). Depression disorders in patients with anorexia nervosa may be related to personality disorders, which have been shown to have high prevalence in anorexia nervosa patients (Gartner et al., 1989; Kennedy et al., 1990; Wonderlich et al., 1990; Herzog et al., 1992; Skodol et al., 1993; Braun et al., 1994; Halmi, 1995), in particular, avoidant, borderline and obsessive compulsive personality disorders (Piran et al., 1985; Braun et al., 1994; Gillberg et al., 1995; Halmi et al., 1999). Milos et al. (2004a) investigated comorbidity of psychiatric disorders with eating disorders. They found that the most common Axis I disorders were affective, anxiety and substance-related disorders; for Axis II, most common were personality disorders of cluster C; only subscale B of the Eating Disorder Inventory was associated with the presence of cluster B disorders. According to these authors the symptomatology of cluster

4

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

B patients often impairs patients’ ability to perceive and recognize their own emotional states and processes, which may in turn decrease the probability that they will endorse items describing psychopathology. This assumption may explain why these patients are not represented in studies employing questionnaires, requiring concentration, reading items carefully, and deciding the most appropriate answer. Spindler and Milos (2004) found that among bulimic subjects, axes II comorbidity, especially cluster B disorders and to a lesser degree depressive/negative personality disorders, was associated with a history of inpatient treatment. History of suicide attempts was also linked to inpatient experience, but not to a history of underweight. Van Hanswijck de Jonge et al. (2003) reported results of an investigation among patients with eating disorders. They found that there was a continuum of severity in borderline personality disorder pathology between the groups of patients with bulimia nervosa, binge eating and obesity. They observed that personality disorder difficulties are particularly represented in patients who binge eat. Karwautz et al. (2003) investigated personality disorders and personality dimensions in anorexia nervosa and found that cluster analysis based on their Temperament and Character Inventory (TCI) identified a subgroup of patients characterized by low levels of novelty seeking, self-directedness, and cooperativeness and high levels of harm avoidance. Bruce et al. (2004) found that women with bulimia nervosa and comorbid avoidant personality disorder may be characterized by interpersonal submissiveness and avoidance, affective instability, self-harm and behavioral inhibition in response to threat. A history of suicide attempts is frequent in women with diagnosis of anorexia nervosa or bulimia nervosa and major depression. Bulik et al. (1999) found that in the bulimia nervosa group of their sample, suicide attempts were significantly more common in subjects with a lifetime diagnosis of major depression; women with anorexia nervosa, on the other hand, were equally likely to attempt suicide, regardless of the presence of lifetime major depression. The authors concluded that depression may be a contributing factor to suicide attempts in bulimia, but previous suicide attempts in the sample of women with anorexia nervosa presented in the study appear independent of affective disorders. Women suffering from bulimia nervosa also showed a statistical trend to report a less severe intention to die. Russell (1979) reported that 87% of patients with eating disorders also had depressive symptoms and 37% of them had attempted suicide; 45% of these attempts were serious suicidal gestures. Similar percentages have been reported by Vasselman and Roig (1985). A higher frequency of death wishes and suicidal feelings in the bulimarexic group may be due to their feeling more out of control because of the vomiting behavior and its attendant fear of discovery, shame, secret, or disgust; or it may be a clinical consequence of the possible increase of bipolar and secondary depression in this group. Also, among patients of this sample, there was a higher frequency of conduct, antisocial, and hysterical diagnosis. Patients had planned and carefully thought out their suicide attempts and they told no one of their plans. Both anorexia nervosa and bulimia nervosa share the disturbance in the way in which one’s body or shape is experienced. The body is experienced with intense fear because it may gain weight or become fat or, as in the case of bulimia nervosa, self-evaluation is unduly influenced by body shape and weight. Orbach et al. (2001) pointed out that the body is a source of satisfaction and pleasure that enhances the tendency for life preservation and attraction to life and serves as a shield against self-destruction, while bodily dissatisfaction

Suicide in Anorexia Nervosa and Bulimia Nervosa

5

may increase suffering and intensify self-destructive attitudes. Extreme negative life events, such as physical and mental traumas, can result in great alteration in perception, attitudes, feelings, and experiences of the body in the form of body rejection, body hate, bodily detachment, insensivity and indifference to sensation, sense of lack of control, and loss of bodily boundaries. Such changes may facilitate self-destructive behavior when under stress. Orbach et al. (2001) investigated a sample of adolescents to examine the relationship between cognitive and affective attitudes toward the body, body experiences and suicide. They found that attitudes and feelings toward the body, protection of the body, and body aberration were the three factors that differentiated the suicidal group and the two nonsuicidal groups. Also, the sense of lack of control over the body also distinguished the suicidal group from the normal group. Among this sample, an interrelationship between attraction to death, lack of body protection, and body aberration emerged. The authors interpreted this result, indicating that inability or unwillingness to protect the body and dissociative bodily tendencies (body aberration) are strongly associated with suicidal tendencies. They proposed that enjoyment in life is strongly linked to good feelings about the body and vice versa. Lack of enjoyment in life and death wishes are strongly associated with a hateful relationship and lack of comfort with the body. Suicidal tendencies and body image and experience have been investigated in a sample of patients with anorexia nervosa and compared to suicidal female adolescent inpatients (Stein et al., 2003). The authors found that female anorexia inpatients with no evidence of overt suicidal behavior demonstrated elevated suicidal tendencies that are similar to those of suicidal psychiatric inpatients. These self-destructive tendencies are highly associated with a pervasive sense of disturbance of body image and experience. Many patients with borderline personality disorder suffer from a sense of body alienation that results from the domination of their body representation by hostile introjects (Maltsberger, 1986). Individuals with anorexia nervosa and bulimia nervosa show a very peculiar attitude toward their bodies. In one way, they believe that their body is the most precious and important thing that surrounds them, in another, they fear their body and struggle with it as an ominous enemy that has to be killed, which deserves a suicidal gesture. Mazza and Reynolds (2001) investigated self-reported psychopathology in a school-based sample of 456 suicidal and non-suicidal adolescents. They found that females who engaged in suicidal behavior reported experiencing significant levels of symptomatology associated with anorexia nervosa; this led the authors to suggest that body-and self-image may be important factors for clinicians and mental health professionals to examine when working with suicidal female adolescents.

Suicide and Attempted Suicide in Anorexia Nervosa According to Patton (1988) suicide is the main cause of death among individuals with anorexia nervosa, typically performed with drug overdose and alcohol. Norring and Sohlberg (1993) have pointed out that death in anorexia is very often caused by a self-inflicted act rather than inanition typically performed with drug overdose and alcohol. Sullivan (1995) derived a crude rate of mortality due to all causes of death of 5.9 % for individuals with

6

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

anorexia nervosa. This author analyzed 42 studies (178 deaths in 3066 individuals). In the 38 studies in which the cause of death was specified (N=164), 89 (54%) of the deaths could be attributed to the complications of an eating disorder, 44 (27%) to suicide, and 31 (19%) to unknown or other causes. Herzog et al. (2000) found that anorexia nervosa carries a substantial risk of premature death, and suicide in their sample was significantly higher than expected. Harris and Barraclough (1997) selected thirteen studies which described cohorts of anorexic and bulimic patients and performed a meta-analysis. They found that the suicide risk was 23 times that expected for the combined group, ranging between zero and 100 times. The suicide risk for anorexia nervosa increased 23 times. Pompili et al. (2004a) also performed a meta-analytic investigation of cohorts of patients with anorexia nervosa. These authors selected 10 studies (see table I) and identified suicides which occurred in the follow-up period of each cohort. They calculated expected suicides in a year in 100,000 individuals if they all suffered from anorexia nervosa. The authors searched the World Health Statistics Annual published by the World Health Organization and identified expected suicides in a year in a population of 100,000 individuals. For each study selected the authors identified suicide statistics for a specific year and country and used only data applicable to females in the 14-25 age group. A comparative analysis was performed to ascertain whether suicide among subjects with anorexia nervosa may be considered a more frequent phenomenon in comparison to suicide among the general population. The meta-analysis showed that suicide in anorexia nervosa was, except in one study (Crisp et al., 1992 – St. George’s cohort), a more frequent phenomenon than their counterparts in the general population. Apter et al. (1995) found that 10% of their adolescent inpatients met the diagnostic criteria for anorexia nervosa and that suicidal behavior scores were significantly higher in those with anorexia nervosa (and conduct disorder) compared to those with anxiety disorders and schizophrenia. Great differences exist among sub-groups of anorexics. The overall risk of suicide range from 1.8% (Patton, 1988) to 7.3% (Ratnasuriya et al., 1991). Patients with binge eating and purgative behavior usually have a weak control over impulsivity associated with the eating disorder. Among these individuals alcohol and drug abuse is also widespread. Also, mood disorders seem to affect those who manifest such behavior more than they do restrictive anorexics (Vandereychen and Pierloot, 1983). In literature, anorexics with purging behavior are described as those more vulnerable to affective disorders and poor outcome compared with individuals without purging behavior (Vandereychen and Pierloot, 1983; Garner et al., 1993). Suicide attempts are also a prerogative of patients with anorexia nervosa. The WHO/EURO (Platt et al., 1992) multicenter study defines suicide attempts as “an act with non fatal outcome, in which the individual deliberately initiates a non-habitual behavior that, without intervention from others, will cause self-harm, or deliberately ingests a substance in excess of the prescribed or generally recognized therapeutic dosage, and which is aimed at realizing changes which the subject derived via actual or expressed physical consequences”. According to Shneidman (1985) the term attempted suicide should be used only for those events in which there has been a failure of a conscious effort to end the life. All others – selfmutilations, excessive dosage of drugs, and other events of this ilk – are, properly speaking, “quasi-suicidal attempts” or probably, more accurately, “non-suicidal attempts”. Milos et al. (2004b) found a lifetime prevalence of suicide attempts of 26%, which is four times higher

Suicide in Anorexia Nervosa and Bulimia Nervosa

7

than the lifetime prevalence found in the general female population in Western countries (ca. 6%) (Weissman et al., 1999; Choquet, 1994) and is comparable to rates previously reported for eating disorder samples (Corcos et al., 2002; Bulik et al., 1999; Viesselman and Roig, 1985). These authors found that a history of attempted suicide was significantly more frequent in participants with a purging type disorder (anorexia nervosa and bulimia nervosa), which is also consistent with the result of the study by Favaro and Santonastaso (1997). The same study outlined the fact that anorexia nervosa participants were more likely to engage in suicidal ideation than bulimia nervosa participants. The authors suggested that in anorexia nervosa, starvation is a form of chronic self-harming behavior and continuously maintaining underweight generates considerable distress, which might contribute to higher levels of suicidal ideation in this group. Self-destructive behavior, suicide attempts included, has often been associated with traumatic experiences in childhood, such as sexual and physical abuse. In patients with anorexia nervosa suicide attempts and other self-injuring behavior are more frequently represented in those patients who present binge eating and purging behavior. In Favaro and Santonastaso’s study (1997), those patients who had attempted suicide were older than non-attempters, had a longer duration of illness and a greater number of previous failed treatments. These patients seemed to have a more serious form of anorexia, with lower body mass index, higher levels of obsessionality and more frequent drug and/or alcohol abuse than non-attempters. The personality of anorexic patients has been described as obsessive-compulsive, introverted, socially insecure and dependent; moreover it has been reported that patients with anorexia nervosa have typical personality clusters. In a study performed in Japan, Matsunaga et al. (1998) found that if anorexia nervosa alone was taken into account, DSM-III-R cluster C was more prevalent; if, instead, anorexia nervosa and bulimia nervosa were considered together in patients who had both, cluster B and cluster C were both represented; this points to the role of bulimia nervosa in the identification of individuals belonging to cluster B. Comorbidity between personality disorders and eating disorders is frequent and it is a major issue, since the two conditions seem to increase the risk of suicide dramatically. In fact, at least one-third (31-62%) of people who have committed suicide (Henriksson et al., 1993; Brent et al., 1994; Lesage et al., 1994; Cheng et, 1997; Foster et al., 1997; Foster et al., 1999) and up to 77% of suicide attempters (Suominen et al., 1996; Engström et al., 1997; Nimeus et al., 1997; Ferreira de Castro et al., 1998) have suffered from personality disorders. Suicide attempters with personality disorders have the highest level of repetition. Comorbidity of personality disorder with other psychiatric disorders contributes to suicidality, and may markedly elevate suicide risk (Suominen et al. 2000). Modestin et al. (1997) reported that in their sample of patients with personality disorders, sexual abuse, physical abuse and the witnessing of violence were found to be associated with self-destructive and suicidal behavior of different kinds, including suicide attempts. Virtually all kinds of childhood traumatic experiences were found to be associated with a history of suicide attempts, even though the strongest association was found with sexual abuse. The results of this study confirm these findings in women; only rarely were such associations found in men. The rates of personality disorders among adolescents who died by suicide have been studied (Links et al., 2003). In the comprehensive Psychological Autopsy Study in Finland, Marttunen and colleagues (1994) estimated that 17% of the adolescents aged 13 to 19 years who died by

8

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

suicide met criteria for conduct disorder or antisocial personality disorder. Marttunen et al. (1994) examined adolescents with nonfatal suicidal behavior, and found that approximately 45% of male adolescents and 33% of female adolescents were characterized by antisocial behavior. Milos et al. (2004b) in their sample of patients with eating disorders found that cluster B disorders showed a strong association with a history of suicide attempts. Wonderlich and Swift (1990) reported an association between borderline personality disorder (which belongs to cluster B) and suicide gestures in eating disorders. Youssef et al. (2004) investigated a sample of young women through the MMPI-2 and observed that some scales were risk indicators for suicide. They found that anorexic patients with antisocial practices are at serious risk for suicide; more subjects have this trait in the anorexia nervosa restrictive type with suicide attempts than in the same sub-group of anorexia without suicide attempts. The same authors reported that in the case of anorexia nervosa purging type, they found the following traits as risk factors for suicide: “hysteria”, “psychopathic deviate”, “shyness/self-consciousness”, “antisocial practices”, “obsessiveness”, and “low self-esteem”. Guillon et al. (2003) investigated self-esteem in a sample of adolescent psychiatric patients. They pointed out that self-esteem can be defined as an individual’s opinion of him/or herself, or the degree to which one holds attitudes of acceptance or rejection of oneself. These authors reported that self-esteem has a different role among the various types of mental disorders. Psychotic disorders were associated with a relatively intact self-esteem when they were characterized by positive symptoms, whereas low self-esteem was associated with depression. In this study adolescents with a history of suicide attempts showed significantly lower self-esteem. This is consistent with Pinto and Whisman’s (1996) investigation which reported that adolescents who have attempted suicide have been found to have significantly lower self-esteem than non-suicidal inpatients. Given the fact that patients with eating disorders usually present low self-esteem we can hypothesize that rejection of oneself exposes the individual, especially the young one, to a greater risk of suicide. Table I – Suicides among various cohorts of patients with anorexia nervosa. (Pompili et al., 2003 – modified) Study Patton, 1988, (UK) Eckert et al.,1995, (USA) Herzog et al., 2000, (USA) Toltrup et al., 1985, (Denmark) Deter and Herzog, 1994, (Germany) Corem and Hewitt, 1998, (USA) Crisp et al.,1992 (St George's) Crisp et al.,1992, (Aberdee), (UK) Emborg, 1997 (Denmark) Kreipe et al., 1989 (USA)

Sample 332 76 136 151 84 571 105 63 47 9

Follow-up 10 10 11 16 12 5 20 20 23 6

Suicides 6 0 3 6 2 8 1 4 5 1

Suicide in Anorexia Nervosa and Bulimia Nervosa

9

Table II Attempted suicides (A.S.) among cohorts of patients with anorexia nervosa. The table shows the number of patients that attempted suicide at least once during the follow-up period or the number of patients that attempted suicide at least once in their clinical histories (ascertained by scales or questionnaires). (Pompili et al., 2003 – modified) Study Viesselman and Roig,1985 (USA) Favaro and Santonastaso, 1997 (Italy) Favaro and Santonastaso, 1996 (Italy) Bulik et al., 1999 (USA) Wiederman and Pryor, 1996 (USA) Kreipe et al., 1989 (USA)

Sample 13 167 164 70 59 6 49

Follow-up

3

A.S 3 15 13 19

6

2

6

Suicide and Attempted Suicide in Bulimia Nervosa Suicide is one of the main causes of death among individuals with bulimia nervosa (Keel and Mitchell, 1997). These patients have an extraordinarily high rate of suicide (Favaro and Santonastaso, 1999). Several studies have reported a lifetime frequency of suicide attempts in bulimics between 15% and 40% (Favaro and Santonastaso, 1997; Bulik et al., 1999; Lewinsohn et al., 2000). In a study which investigated 205 bulimic patients, 25% of those that attempted suicide also had at least one past suicide attempt (1997), which is a major risk factor for completed suicide. (Kotila and Lönnqvist, 1987). Corcos et al. (2002) presented a sample of 295 women with bulimia nervosa (202 with BN purging type, 68 with BN nonpurging type and 25 with anorexia nervosa binge eating purging type). These authors found that the bulimics who had attempted suicide reported suicidal ideation more often during adolescence and had made their first attempt at this period. They found that more than twothirds had suicidal ideation during adolescence and their age at onset of the first eating disorder had been, on average, one and a half years younger than for subjects with no history of suicide attempts. Also, those who had been suicidal had a more frequent incidence of live events such as separation from their family or separation in their family (parental separation or divorce). Patients with a history of suicidal attempts used laxatives and diuretics more frequently, had more lifetime depressive disorders, and more lifetime frequencies of substance use and disorders of conduct (self-injurious behavior, risk-taking behavior, stealing, running away, pathological lying, or hetero-aggressive behavior. As stated for anorexia nervosa, the body of evidence suggests that depressive symptoms reported by patients with bulimia nervosa are secondary, rather than primary phenomena (Cooper and Fairburn, 1986). Kent et al. (1997) suggested that low self-esteem, which is a characteristic feature of bulimia nervosa occurring independently of depression and associated with poor body image, is the factor associated with increased levels of internally directed irritability. In bulimic patients with a history of suicide attempts, the onset of psychopathology seemed to have been particularly precocious.

10

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

Data concerning suicide in bulimia nervosa are still scarce, as more long-term follow-up studies need to be completed before the risk for bulimia nervosa may be compared with that for anorexia nervosa. Yet in some studies suicide seems to be the main cause of death (Mitchell et al., 1988; Vandereychen and Pieters, 1992). Among bulimic patients a number of clinical variables have been linked to a greater risk of suicide, such as late onset, purging behavior, affective disorders, substance and alcohol abuse and borderline personality characteristics including impulsiveness. Patients with purging behavior seem to have more severe suicidality and show a greater number of suicide attempts and self-injurious acts compared with bulimic patients who do not purge (Viesselman and Roig, 1985; Mitchell, 1992; Shearer et al., 1988). Viesselman and Roig (1985) found that 20% of the bulimic patients analyzed who had attempted suicide, also had a diagnosis of major depressive disorder; 11% of these individuals were drug and alcohol abusers. Sheares et al. (1988) found that suicide attempts were more serious in those patients who had a borderline personality disorder comorbid with the eating disorder. As stated above, comorbidity between personality disorders and eating disorders is frequently found among cohorts of patients. Borderline personality disorder is no doubt extremely frequent in patients suffering from bulimia nervosa. The incidence of completed suicide in borderline personality disorder has been unknown until recently (Paris et al., 1989). In two long term follow-up studies of borderline patients treated in residential settings, McGlashan (1986) and Stone (1987) found that 3% and 9%, respectively, of borderline go on to complete suicide. Soloff et al. (2000) found that patients with borderline personality disorder or comorbid disorders attempted suicide for the first time earlier in life than the depressed patients; no significant difference in age at the first suicide attempt was found in patients with borderline personality disorder and patients with comorbid disorders. The suicide intent of the pooled group of patients with borderline personality disorder had a greater lifetime level of lethality than those of the depressed patients. In this study, the patients with borderline personality disorder differed from the depressed patients in having an earlier onset of suicidal behavior, consistent with the natural history of the disorder, and a higher lifetime number of attempts. Comorbidity of personality disorder and major depressive episode was associated with an increased number of suicide attempts. Also, among patients with borderline personality disorder, impulsivity, assessed as a diagnostic criterion, is associated with the number of suicide attempts independent of comorbid depression or substance use disorder. Some authors call for the recognition of a distinct diagnostic subgroup of bulimia nervosa, such as “multi-impulsive bulimia” or “multi-impulsive personality disorder” (Lacey, 1993; Fichter et al., 1994). This subgroup is usually defined by the existence of at least three (Lacey, 1993; Fichter et al., 1994) or at least one (Fahy and Eisler, 1993) of the following behaviors: alcohol or drug abuse, suicide attempts, repeated self-mutilation, sexual disinhibition, shoplifting. Nagata et al. (2000) investigated a sample of patients with eating disorders and found that 18% of the 114 bulimic patients showed multi-impulsivity; 80% of the patients with this features had a history of suicide attempts or self-mutilation prior to the onset of bulimia nervosa. The authors questioned the hypothesis that impulsivity in bulimia nervosa is not necessarily part of a comorbid borderline personality disorder; in fact, in their sample only 27% of the multi-impulsive bulimics met the borderline personality disorder criterion.

Suicide in Anorexia Nervosa and Bulimia Nervosa

11

Youssef et al. (2004) found among women with bulimia nervosa purging type a number of personality traits associated with suicide risk. They observed through the employment of the MMPI-2 that in bulimic women with suicidal attempts the following scales were risk indicators: “psychasthenia”, “anger” and “fear”. Favaro and Santonastaso (1997) underlined the fact that suicide attempts among bulimic patients did not appear to be linked to the severity of bulimic symptoms in terms of frequency of binge eating and vomiting, but rather to the presence of purging behavior. Suicide attempts were associated with more serious psychiatric symptoms and with higher levels of obsessionality. Patients with purging behavior have a more serious course of illness, as they more frequently experience depressive symptoms, weight and shape of body preoccupations and have a history of suicide attempts, drug and alcohol abuse and self-injurious behavior. (Favaro and Santonastaso, 1997; Da Costa and Halmi, 1992; Dulit et al., 1994; Viesselman and Roig, 1985; Mitchell, 1992). Suicidality among these patients seems to be increased by the number of compensatory behaviors that the patients engage in, in order to reduce weight; the more strategies utilized, the greater the risk of suicide (Favaro and Santonastaso, 1996). Bulimia nervosa is without doubt linked to self-injury (Dulit et al., 1994; Favazza et al., 1989; Herpertz, 1995). A typical symptom of bulimia nervosa is self-injuring and self-mutilation; purgative behavior might be considered a sort of self-wounding action. Patients, in fact, describe this behavior as an invincible impulse to self-inflict punishment. Van der Kolk et al. (1991) have considered eating disorders a form of self-destructive behavior similar to suicide attempts and selfcutting. Self-mutilation should not be considered a feature of suicide behavior but a way to reduce tension and induce relief (Root and Fallon, 1991); this behavior has also been linked to a number of dissociative symptoms (Everill et al., 1995). Nevertheless, patients have the chance to experience their body and look for a sense of reality and their own identity. However, impulsivity does predict suicidal behavior (Favaro and Santonastaso, 1998). Table III Attempted suicides (A.S.) among cohorts of patients with bulimia nervosa. The table shows the number of patients that attempted suicide at least once during the follow-up period or the number of patients that attempted suicide at least once in their clinical histories (ascertained by scales or questionnaires). (Pompili et al., 2003 – modified) Study Viesselman and Roig 1985 (USA) Garfinkel et al., 1980 (Canada) Favaro and Santonastaso,1997 (Italy) Favaro and Santonastaso, 1996 (Italy) Bulik et al., 1999 (USA) Wiederman and Pryor, 1996 (USA) Favaro and antonastaso,1998 (Italy) Favaro and Santonastaso, 1999 (Italy) Raynes et al., 1983 (USA)

sample 36 155 210 161 152 58 125 175 15

follow-up 8 6 3 2

A.S. 36 38 28 47 18 23 29 6

12

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

Risk Taking Behavior as Part of Suicide in Anorexia Nervosa and Bulimia Nervosa Owing to the dissatisfaction with their bodies, many children and adolescents not only try to lose weight and are concerned about what they should and should not eat, but also engage in high risk behaviors, which underline their inner struggle with the body. In this section we analyze high risk behavior among teenagers and point out its role as a consistent part of suicidal behavior. High risk behavior is strictly linked to indirect self-destructive behavior, which is defined by The Encyclopedia of Suicide (2003) as “A group of behaviors that is distinguishable from overt self-destructive behavior by the criteria of time and awareness. The effect of the behaviors is long-term, and the person is usually unaware of or does not care about the effect of the behavior”. Farberow (1980) persuasively presented the following features of such behaviors: 1) undermining physical health; 2) need to gratify the present and to overcome feelings of inadequacy; 3) lack of future orientation and little maturity; 4) no immediate action taken towards stress; 5) need of stimulating actions and games; 6) various coping mechanisms (denial, suppression, regression, narcissism); 7) lack of messages and communication with others; 8) superficial and casual relationship. Some investigators argued that risk taking is a part of normal adolescence (Baumrind, 1987). They distinguish developmentally constructive risk taking (adaptive experimentation to build confidence, enhance competence and develop initiatives, i.e., behavior promoting autonomy, mastery, and skills essential for transition to adulthood) from pathogenic, deviant, life-threatening risk taking that potentially jeopardizes health and life. According to Jessor (1991), behavior such as smoking, drinking, illicit substance use and risky driving are methods to gain acceptance and respect among peers, establishing independence from parental authority. Individuals in crisis often resort to indirect self destructive behavior as a coping mechanism, but when conflicts are solved, such behavior is given up. When repetitive and habitual, indirect self-destructive behavior endangers life. As Litman (1980) put it, “When painful psychological states, especially depression, are chronic rather than transitory, and the need for repression is also chronic, the symbolic replacement or symbolic partial expression of the problem in its own turn becomes chronic and fixed. Many forms of indirect selfdestructive behavior that developed as coping mechanisms have often also been a source of temporary pleasure. To give up the indirect self-destructive behavior is not an easy task, since it means the loss of pleasure and reactivation of painful depression”. Dysfunctional behavior in the family environment may undermine development during adolescence and lead to indirect self-destructive behavior. Unfortunately, it is a chronic process, necessitating longterm adjustment. Caplan (1964) states: “A crisis is an upset in a steady state or disturbance of homeostasis”. Eventually, some kind of adaptation is achieved which may or may not be in the best interest of that person and his fellows (Farberow, 1967). In the case of adolescent “crisis”, we recognize this as a time-limited condition; nevertheless, behavior patterns adopted during this period may constitute dysfunctional behavior in adulthood, if problems were not adequately worked through, thus persisting for a long time and impairing intrafamily relationships.

Suicide in Anorexia Nervosa and Bulimia Nervosa

13

Suicide is a leading cause of death in developed countries; lifetime prevalence of attempted suicide is about 4% in a United States population attending a primary care clinic, and its risk, as assessed through the Adverse Childhood Experiences (ACE) scores, increases with increasing ACE scores (Dube et al., 2001). These scores also correlate with risk-related behavior, such as alcohol or illicit drug abuse. Onset of problem behavior is at 12 years, rises to peak until 15 years, and plateaus thereafter (Reynolds and Rob, 1988). Adolescent suicide attempters report lower levels of parental interest and involvement and belong to more disrupted families than their nonsuicidal counterparts (Flouri and Buchanan, 2002). A recent paper (Borawski et al., 2003) investigated two different parenting practices (parental monitoring and negotiated unsupervised time) and perceived parental trust in the reporting of health risk behaviors among adolescents. This study clearly stressed the importance of parents in induction of health risk behavior. Adolescents’ rating their parents as “affectionless” on the Parental Bonding Instrument (PBI) doubles their risk for suicidal ideation and triples it for deliberate self-harm. Taken together, these data point at a healthy, traditional-style family, as the major determinant of protection from risk-related behavior, which is linked to suicide attempts. Coordinated efforts are needed when dealing with children or adolescents with suicidal ideation. Compliance with prescription, either pharmacological or behavioral, is a major issue in decreasing suicidal risk and this must be assessed and addressed from the first contact with the patient (Litt et al., 1983). Various approaches were suggested to treat suicidal children and adolescents; a holistic family technique focuses on children and their parents and aims at increasing appropriateness of child-parent communication (Pfeffer, 1982); metatherapy, a psychotherapy based on the collaboration of the parental couple, is supposed to reduce perceived stigma in children and adolescents, as well as to increase satisfaction with parental role in parents (Vaz-Leal, 1989). Furthermore, modifying the youth’s perception of his own parents may be critical in reducing both suicidal thoughts and deliberate self-harm (Martin and Waite, 1994). Finally, techniques aiming at correction of pathogenic beliefs may prove useful for adolescents and adults (Weiss and Sampson, 1986). Self-destructive and risk-taking behavior, although they cannot be classified as suicide sensu strictu, from part of a broad suicide continuum that may increase premature death in individuals conforming to this spectrum. Even minimal manifestations of this continuum, such as drug or alcohol exposure, unprotected sex, and risky driving, displayed to comply with peer pressure, should not be disregarded, as they could give rise to successful suicide attempts or impair the organism’s defenses and render the individual more vulnerable to various noxae. The role of parents is a critical one in this respect. Hence, in managing youths exhibiting such behavior, care should be taken to involve and educate parents. Another open issue is those deaths called subintentioned deaths, which may be represented in individuals with anorexia nervosa and bulimia nervosa. Shneidman et al. (1961) suggested that motivation is present in some deaths and a comprehensive taxonomy of death must include components that reflect the role of the individual in his own death. In particular, an intentioned death is any death in which the decedent plays a direct, conscious role in affecting his own demise; an unintentioned death is any death in which the decedent plays no effective role in effecting his own demise. In this discussion it is paramount to define a subintentioned death, namely a death in which the decedent plays some partial,

14

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

covert, or unconscious role in hastening his own demise. Subintentioned deaths are often identifiable in individuals who manifest poor judgment, excessive risk-taking, abuse of alcohol, misuse of drugs, self-destructive style of life, disregard of prescribed lifesaving medical regimen, unprotected sex, driving after alcohol abuse. One may wonder how to identify deaths from accidents and from suicide, bearing in mind that individuals who die after an accident may actually have had a role in the occurrence of that accident, acting more like a suicidal person than a victim of adverse circumstances. Often risk-taking behavior and adverse circumstance act synchronically and it is very difficult to ascertain whether a death was suicide or accident (Pompili et al., 2004b). However, in the case of undetermined death, a conscious act may be lacking or may not be recognized, especially when the individual is ambivalent in his decision. This leads to a distinction between suicide and subintentional deaths even if they share various elements. Shneidman (1991, 1993) hypothesized a spectrum of intentional deaths in which unequivocal completed suicide is the most extreme form of self-destructive behavior and self-inflicted death should also be recognized in a wide variety of behaviors which share a dimension called lethality, defined as the probability of a specific individual’s killing himself (i.e. bringing about his own death) in the immediate future (today, tomorrow, the next day, the next month). Given the fact that patients with eating disorders manifest a number of behaviors that do reflect lethality towards themselves and high risk behaviors, we should emphasize the need to improve recognition of all manifestations of the suicide spectrum. People who engage in high risk behaviors may paradoxically be protected from suicide per se, as if they preferred a slow lethal action rather than a sudden death (Pompili et al., 2004c). Individuals with eating disorders may in some cases interchange their suicidal wishes with high risk-behaviors, or their unconscious wish to be dead may play a role in all those deaths that belong to the subintentional category. Deaths from suicide are underreported because of the tendency to group them as accidental deaths or deaths from undetermined causes.

Prediction and Prevention of Suicide Among Patients with Eating Disorders Suicide prevention among children and adolescents is a high priority due to the fact that suicide ranks first or second as a cause of death among both boys and girls in the 15 to 19year age group in many countries. Given the fact that in many countries and regions most people in this age group attend school, this appears to be an excellent place to develop appropriate prevention action. Eating disorders are becoming more prevalent and observable across cultures. These difficult-to-treat disorders also demonstrate a continuity between adolescent onset and adult risk for the presence of an eating disorder (Kotler, 2001). The promotion of children’s health through school is recognized at the international level as an important means of influencing health behavior. The World Health Organization (2000a; 2000c) defines a “Health-Promoting School” as a school that is constantly strengthening its capacity to be a healthy setting for living, learning and working. Specifically, these programs aim to build healthy public policies, create supportive environment, strengthen community action, foster the development of personal skills, and reorient health services to embrace

Suicide in Anorexia Nervosa and Bulimia Nervosa

15

health promotion in addition to clinical and curative services (WHO, 2000). HealthPromoting Schools also help pupils, parents and community members work together to set priorities and plan actions. They use information about the determinants of health and wellbeing, as well as leading causes of death and disease and they foster healthy behavior as well as those that prevent the initiation of important health risks, such as risk taking behavior in individuals with eating disorders and suicidality among them. During adolescence, girls have a much higher prevalence of depression and eating disorders and engage more in suicidal ideation and suicide attempts than boys. Adolescence is not an easy time psychologically, and adjustment indicators are important, especially in suicide prevention. Unfortunately, mass media do not help in either the prevention of suicide or eating disorders. It is believed that a contributing factor in the rise of eating disorders is the exposure to Western media and its influence on desirable body characteristics. The power of mass media has been investigated in connection with suicidal behavior. In fact, numerous studies have considered the association between media reporting and portrayal of suicide and actual suicidal behavior and ideation (Pirkis and Blood, 2001a,b). Research finds an increase in suicide by readers or viewers when 1) the number of stories about individual suicide increases; 2) a particular death is reported at length or in many stories; 3) the story of an individual death by suicide is placed on the front page or at the beginning of a broadcast; 4) the headlines about specific suicide death are dramatic (a recent example: “Boy, 10, kills himself over poor grades”). The media can play a powerful role in educating the public about suicide prevention as well as in eduating youth about eating disorders. It might be speculated that those people who are the most vulnerable to mass media’s presentation of desirable body characteristics are also the most easily influenced by media portrayals of suicide.

Psychotherapy with Suicidal Anorexic and Bulimic Patients Psychotherapy with suicidal patients is a real challenge for any clinician. Psychotherapy has also been employed in the treatment of anorexia nervosa and bulimia nervosa especially in conjuction with pharmacotherapy. Nevertheless, international literature does not provide definitive results on the efficacy of psychotherapy in the treatment of such diseases. There are relatively few evidence-based findings, particularly for the treatment of anorexia nervosa. In the few studies that have shown the statistical effectiveness of a certain approach, the rate of failure to respond is typically high and not readily explained by current scientific knowledge (Hsu, 2004). Psychotherapy may offer a key opportunity to reduce pain. Shneidman (1993) described what he called “psychache”, meaning an ache in the psyche and suggested that the key questions to ask a suicidal person are “Where do you hurt?” and “How may I help you?”. If the function of suicide is to put a stop to an unbearable flow of painful consciusness, then it follows that the therapist’s main task is to mollify that pain. Shneidman (1993) also pointed out that the main sources of psychological pain, such as shame, guilt, rage, loneliness, hopelessness, and so forth, stem from frustrated or thwarted psychological needs. These psychological needs include the need for achievement, for affiliation, for autonomy, for counteraction, for exhibition, for nurturance, for order, for understanding. The healing effects

16

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

of careful listening to the patient’s story and the development of empathy, so that the patient feels truly understood, cannot be over-emphasized in this respect. A sound therapeutic relationship, or working alliance, will go a long way toward preventing repeated suicidal behavior as the adolescent experiences the feeling of being heard in an important interpersonal relationship (Manley and Leichner, 2003). Many authors have written about psychotherapy for patients with anorexia nervosa. Despite different approaches, they believe that the therapist should be active and should function in the therapeutic encounter as a parent, teacher, guide and coach. The personality of the therapist is a major therapeutic element in the treatment of patients with anorexia nervosa (Hsu, 2004). The main goal of a psychotherapy with anorexic patients is to help the patient get in touch with inner feelings and experiences, to identify and verbalize them; also therapy should change dysfunctional thinking which plays an important role in the psychopathology of this disorder. Psychotherapy with bulimic patients is also a key element of the therapeutic armamentarium; various therapeutic approaches have been employed, but cognitive behavioral therapy seems the most effective strategy for these patients. Treatment is active, problem-oriented, semistructured, and concerned more with the patient’s present and future than with the past. Yet, psychotherapy with suicidal patients must take into serious consideration the need of these patients to escape from unbearable psychological pain and provide a safe and accepting environment. Also, countertransference reactions play an important role in the management of suicidal patients. Due to their ability to cause strong emotional feelings, the suicidal patienta are particularly prone to provoking countertransference reactions. Suicidal patients generate more anxiety and more feelings of anger. Doctors usually treat patients who desperately want to live; suicidal patients, in contrast, undermine the very core of the medical profession by wishing to be dead and by struggling with the therapist who is trying to prevent this action. Not evey therapist may be an appropriate therapist for suicidal patients. Insufficient control over counter-transference problems may increase suicide risk in the patient and suicide may result from an iatrogenic event (Andriola, 1973). In fact, therapists that are unable to handle strong feelings provoked by suicidal patients cannot conduct proper therapeutic work with these patients who do not have the opportunity to externalize thei inner negative feelings to a strong therapeutic figure. Therapists may fear the death of the patient but at the same time may enhance the risk of a suicidal death. Anorexic and bulimic patients may be hospitalized especially in the case of severe medical complications. Hospitalization may carry an extra risk for suicide and staff should always keep an open mind throughout the entire stay of the patients. A lesson may be learned from the studies devoted to suicide among inpatients. Crammer (1974) pointed to the potentially disruptive effects of transitions – for example, initial acclimation toward life or plans for discharge or rehabilitation. He also emphasized the environmental impact of staff variables, such as low morale or the absence of key personnel, as well as the need for effective communication among relevant staff about patients judged as having an increased risk of suicide. Adverse circumstances such as single-occupancy rooms or the return to a family in which the patient’s presence represents a severe emotional or financial strain, most probably add to the suicide risk for a schizophrenic patient. Poor communications about risk between medical and nursing staff, change in staff, and ward layout have been suggested as risk factors. According to Crammer (1974) an anti-suicidal ward is one with calm routine,

Suicide in Anorexia Nervosa and Bulimia Nervosa

17

carried out daily by staff who are themselves unworried and confident of the immediate future. Their calm is, so to speak, infectious.

Pharmacotherapy and Suicididality in Anorexia Nervosa and Bulimia Nervosa Pharmacotherapy plays an important role in the treatment both of patients with anorexia nervosa or bulimia nervosa and suicide. Yet, pharmacological studies have not yet identified any medication resulting in definitive improvement of the core symptoms of anorexia nervosa. In the international literature several clinical trials employing various molecules versus placebo led to the conclusion that only rarely does pharmacotherapy have some definitive results in the treatment of anorexia nervosa. Molecules showing more efficacy than placebo were amitriptyline (Halmi et al., 1986), cyroheptidine (Halmi et al., 1986), and fluoxetine (Kaye et al., 1998). Nevertheless, several recent studies have examined the use of olanzapine (Mehler et al., 2001; Powers et al., 2002), haloperidol (Cassano et al., 2003), sertraline (Santonastaso et al., 2001), fluoxetine, chlorpromazine and amisulpride (Ruggiero et al., 2001). Suicide risk is strongly linked to the persistence of severe symptomatology; that is why prevention of relapses and amelioration of symptoms through proper pharmachotherapy is a key feature. However, pharmacological treatments, especially those employing antidepressant medications, should be used very carefully in suicidal patients. Despite the fact that these medications do reduce overall suicide rates, they should be avoided during suicidal crises as patients may become more energized and thus able to put their suicidal plans into action (Baldessarini et al., 2005; Pompili et al., 2005). Antidepressant medications can reduce binge eating and purging independent of the presence of a mood disorder; this is of great benefit since compensatory behaviors are associated with increased risk of suicide. Over the past twenty years a considerably controlled trials have been devoted to bulimia nervosa compared with those devoted to anorexia nervosa. A deatailed review of these trials is beyond the purpose of this papar, we will therefore list molecules that showed efficacy versus placebo with the sole purpose of drawing a general picture: imipramine (Pope et al., 1983), desimipramine (Hughes et al., 1986; Blouin et al., 1988), bupropion (Horne et al., 1988), isocaboxazide (Kennedy et al., 1988), phenelzine (Walsh et al., 1988), trazodone (Pope et al., 1989), fluoxetine (Fichter et al., 1991; FBNC, 1992; Goldstein et al., 1995; Romano et al., 2002), brofaromine (Kennedy et al., 1993), ondansetron (Faris et al., 2000). The first-line medication is probably fluoxetine at high dose (20-80 mg). Recent evidence points to the role of topiramate, which has been found to have both antibinge and weight loss properties (McElroy et al., 2003). As stated above, antidepressant medications such as fluoxetine and imipramine should be used very carefully in case of suicidal ideation (Baldessarini et al., 2005; Pompili et al., 2005). Treating suicidal patients with eating disorders without any question a clinical challenge that requires great confidence in one’s own body of knowledge. A continous balance of the medication employed might be necessary in certain periods. Suicidal patients need to be sedated, and treatment of the main disorder should be a second target of the therapeutic intervention.

18

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

References Andriola J. A note on the possible iatrogenesis of suicide. Psychiatry 1973;36:213-218. Apter A, Gothelf D, Orbach I, Weizman R, Ratzoni G, Har-Even D, Tyano S. Correlation of suicidal and violent behavior in different diagnostic categories in hospitalized adolescent patients. J Am Acad Child Adolesc Psychiatry 1995;34:912-8. Baldessarini RJ, Pompili M, Tondo L, et al. (2005). Antidepressants and suicidal behavior: Are we hurting or helping? Clinical Neuropsychiatry 2005 (in press). Baumrind D. A developmental perspective on adolescent risk taking in contemporary America. New Dir Child Dev 1987;37:93-125. Beautrais AL, Joyce PR, Mulder RT. Psychiatric illness in a New Zealand sample of young people making serious suicide attempts. N Z Med J 1998;111:44-8. Blouin AG, Blouin JH, Perez EL, Bushnik T, Zuro C, Mulder E.Treatment of bulimia with fenfluramine and desipramine. Clin Psychopharmacol 1988;8:261-9. Borawski EA, Ievers-Landis CE, Lovegreen LD, Trapl, ES.. Parental monitoring, negotiated unsupervised time, and parental trust: the role of perceived parenting practices in adolescent health risk behaviors. Journal of Adolescence Health 2003;33:60-70. Braun DL, Sunday SR, Halmi KA. Psychiatric comorbidity in patients with eating disorders. Psychol Med 1994;24:859-67. Brent DA, Johnson BA, Perper J, Connolly J, Bridge J, Bartle S, Rather C. Personality disorder, personality traits, impulsive violence, and completed suicide in adolescents. J Am Acad Child Adolesc Psychiatry 1994;33:1080-6. Bruce KR, Steiger H, Koerner NM, Israel M, Young SN. Bulimia nervosa with co-morbid avoidant personality disorder: behavioural characteristics and serotonergic function. Psychol Med 2004;34:113-24. Bruch H. Anoressia mentale: casi clinici. Raffaello Cortina, Milano, 1988 Bulik CM, Sullivan PF, Joyce PR. Temperament, character and suicide attempts in anorexia nervosa, bulimia nervosa and major depression. Acta Psychiatr Scand 1999;100:27-32. Cantwell DP, Sturzenberger S, Burroughs J, Salkin B, Green JK. Anorexia nervosa. An affective disorder? Arch Gen Psychiatry 1977;34:1087-93. Caplan G. Principles of Preventive Psychiatry. New York: Basic Books, 1964 Cassano GB, Miniati M, Pini S, Rotondo A, Banti S, Borri C, Camilleri V, Mauri M. Sixmonth open trial of haloperidol as an adjunctive treatment for anorexia nervosa: a preliminary report. Int J Eat Disord 2003;33:172-7. Cheng AT, Mann AH, Chan KA. Personality disorder and suicide. A case-control study. Br J Psychiatry 1997;170:441-6. Choquet M, Ledoux S. Adolescents. Enquete nationale. Paris, Edition Inserim, 1994. Cooper PJ, Fairburn CG. The depressive symptoms of bulimia nervosa. Br J Psychiatry 1986;148:268-74. Cooper PJ. Eating disorders and their relashionship to mood and anxiety disorders. In: Brownell KD, Fairburn CG (eds.). Eating disorders and obesity. The Guilford Press, New York 1995, p. 199-206.

Suicide in Anorexia Nervosa and Bulimia Nervosa

19

Corcos M, Taieb O, Benoit-Lamy S, Paterniti S, Jeammet P, Flament MF. Suicide attempts in women with bulimia nervosa: frequency and characteristics. Acta Psychiatr Scand 2002;106:381-6. Coren S, Hewitt PL. Is anorexia nervosa associated with elevated rates of suicides? Am J Public Health 1998;88:1206-1207 Crammer JL. The special characteristics of suicide in hospital inpatients. Br J Psychiatry 1984;145:460-463. Crisp AH, Callender JS, Halek C, Hsu LKG. Long-term mortality in anorexia nervosa. A 20year follow-up of the St George’s and Aberdeen cohorts. Br J Psychiatry 1992;161:104107 Da Costa M, Halmi KA. Classifications of anorexia nervosa: question of subtypes. Int J Eat Disord 1992;11:305-313 Deter HC, Herzog W. Anorexia nervosa in a long-term perspective: results of the Heildelberg-Mannheim study. Psychol Med 1994;56:20-27 Dowson J. Associations of the severity of depressive disorders in women with psychogenic low weight. J Affect Disord 2004;78:279-84. Dube SR, Anda RF, Felitti VJ, Chapman DP, Williamson DF, Giles WH. Childhood abuse, household dysfunction, and the risk of attempted suicide throughout the life span: findings from the Adverse Childhood Experiences Study. JAMA 2001;286:3089-3096. Dulit RA, Fyer MR, Leon AC, Brodsky BS, Frances AJ. Clinical correlates of self-mutilation in borderline personality disorder. Am J Psychiatry 1994;151:1305-1311 Eckert ED, Halmi KA, Marchi P, Grove W, Crosby R. Ten-year follow-up of anorexia nervosa: clinical course and outcome. Psychol Med 1995;25:143-156 Emborg C. Mortality and causes of death in eating disorders in Denmark 1970-1993: a case register study. Int J Eat Disord 1999;25:243-251 Engstrom G, Alling C, Gustavsson P, Oreland L, Traskman-Bendz L. Clinical characteristics and biological parameters in temperamental clusters of suicide attempters. J Affect Disord 1997;44:45-55. Evans G, Farberow NL, Kennedy Associates. (Eds). The Encyclopedia of Suicide. New York, Fact On File, 2003 Everill JT, Waller G, MacDonald W. Dissociation in bulimic and non-eating disordered women. Int J Eat Disord 1995;17:127-134 Fahy T, Eisler I. Impulsivity and eating disorders. Br J Psychiatry. 1993 Feb;162:193-7. Farberow NL. Crisis, disaster, and suicide: theory and therapy. In E.S. Shneidman (Ed). Essays in self-destruction New York: Science House 1967, p. 373-398. Farberow NL. Indirect self-destructive behavior. Classification and characteristics. In The Many Faces of Suicide. New York: McGraw-Hill, 1980: 15-27. Faris PL, Kim SW, Meller WH, Goodale RL, Oakman SA, Hofbauer RD, Marshall AM, Daughters RS, Banerjee-Stevens D, Eckert ED, Hartman BK. Effect of decreasing afferent vagal activity with ondansetron on symptoms of bulimia nervosa: a randomised, double-blind trial. Lancet 2000 4;355:792-7. Favaro A, Santonastaso P. Purging behavior, suicide attempts, and psychiatric symptoms in 398 eating disordered subjects. Int J Eat Disord 1996;20:99-103

20

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

Favaro A, Santonastaso P. Suicidality in eating disorders: clinical and pscyhological correlates. Acta Psychiatr Scand 1997;95:508-514 Favaro A, Santonastaso P. Impulsive and compulsive self-injurious behavior in bulimia nervosa: prevalence and psychological correlates. J Nerv Ment Dis 1998;186;157-165 Favaro A, Santonastaso P. Different types of self-injurious behavior in bulimia nervosa. Compreh Psychiatry 1999;40:57-60 Favazza AR, De Rosear L; Conterio K. Self-mutilation and eating disorders. Suicide Life Treat Behav 1989;19:352-361 FBNC. Fluoxetine in the treatment of bulimia nervosa. A multicenter, placebo-controlled, double-blind trial. Fluoxetine Bulimia Nervosa Collaborative Study Group. Arch Gen Psychiatry 1992;49:139-47. Ferreira de Castro E, Cunha MA, Pimenta F, Costa I.Parasuicide and mental disorders. Acta Psychiatr Scand 1998;97:25-31. Fichter MM, Leibl K, Rief W, Brunner E, Schmidt-Auberger S, Engel RR. Fluoxetine versus placebo: a double-blind study with bulimic inpatients undergoing intensive psychotherapy. Pharmacopsychiatry 1991;24:1-7. Fichter MM, Quadflieg N, Rief W. Course of multi-impulsive bulimia. Psychol Med 1994;24:591-604. Fitcher MM, Pirke KM. Starvation models and eating disorders. In: Szmukler D, Dare C, Treasure J (eds.). Handbook of eating disorders: theory, treatment and research. John Wiley, Chirchester, 1995, p. 83-107. Flouri E, Buchanan A. The protective role of parental involvement in adolescent suicide. Crisis 2002;23:17-22. Foster T, Gillespie K, McClelland R. Mental disorders and suicide in Northern Ireland. Br J Psychiatry 1997;170:447-52. Foster T, Gillespie K, McClelland R, Patterson C. Risk factors for suicide independent of DSM-III-R Axis I disorder. Case-control psychological autopsy study in Northern Ireland. Br J Psychiatry 1999;175:175-9. Garfinkel PE, Moldofsky H, Garner DM. The eterogeneity of anorexia nervosa. Arch Gen Psychiatry 1980;37:1036-1040 Garner DM, Garner MV, Rosen LW. Anorexia nervosa “restricter” who purge: implication for subtyping anorexia nervosa. Int J Eat Disord 1993; 13:171-185 Gartner AF, Marcus RN, Halmi K, Loranger AW. DSM-III-R personality disorders in patients with eating disorders. Am J Psychiatry 1989;146:1585-91. Gillberg IC, Rastam M, Gillberg C. Anorexia nervosa 6 years after onset: Part I. Personality disorders. Compr Psychiatry 1995;36:61-9. Goldstein DJ, Wilson MG, Thompson VL, Potvin JH, Rampey AH Jr. Long-term fluoxetine treatment of bulimia nervosa. Fluoxetine Bulimia Nervosa Research Group. Br J Psychiatry 1995;166:660-6. Guillon MS, Crocq MA, Bailey PE. The relationship between self-esteem and psychiatric disorders in adolescents. Eur Psychiatry 2003;18:59-62. Gunderson JG, Triebwasser J, Phillips KA, Sullivan CN. Personality and vulnerability to affective disorders. In: Cloninger CR (eds.). Personality and Psychopathology. American Psychiatric Press, London, 1999, p. 3-32.

Suicide in Anorexia Nervosa and Bulimia Nervosa

21

Halmi KA, Eckert E, LaDu TJ, Cohen J. Anorexia nervosa. Treatment efficacy of cyproheptadine and amitriptyline. Arch Gen Psychiatry 1986;43:177-81. Halmi KA, Eckert E, Marchi P, Sampugnaro V, Apple R, Cohen J. Comorbidity of psychiatric diagnoses in anorexia nervosa. Arch Gen Psychiatry 1991;48:712-8. Halmi KA, Kleifield EI, Braun DL, Sunday SR. Personality correlates of aeting disorder subtypes. In: Cloninger S (ed.). Personality and Psychopathology. American Psychiatric Press, London, 1999, p. 67-82. Halmi KA. Current concepts and definitions. In: Szmukler G, Dare C, Treasure J (eds.). Handbook of asting disorders: theory, treatment and research. John Wiley, Chirchester, 1995, p. 29-44. Henriksson MM, Aro HM, Marttunen MJ, Heikkinen ME, Isometsa ET, Kuoppasalmi KI, Lonnqvist JK.Mental disorders and comorbidity in suicide. Am J Psychiatry. 1993;150:935-40. Herpertz S. Self injurious behavior. Psychological and nosological characteristics in subtypes of self-injurers. Acta Psychiatr Scand 1995;91:57-68 Herzog DB, Keller MB, Lavori PW, Kenny GM, Sacks NR. The prevalence of personality disorders in 210 women with eating disorders. J Clin Psychiatry 1992;53:147-52. Herzog DB. Greenwood DN, Dorer DJ. Mortality in eating disorders: a descriptive study. Int J Eat Disord 2000;28: Hirschfeld RMA, Shea MT. Personality. In: Paykel ES (ed.) 2nd Edition. Handbook of affective disorders. Churchill Livingstone, London, p. 185-194. Horne RL, Ferguson JM, Pope HG Jr, Hudson JI, Lineberry CG, Ascher J, Cato A. Treatment of bulimia with bupropion: a multicenter controlled trial. J Clin Psychiatry 1988;49:2626. Hsu L, Crisp A, Harding B. Outcome of anorexia nervosa. Lancet 1979;I:61-65. Hsu LK. Eating disorders: practical interventions. J Am Med Womens Assoc 2004;59:113-24. Harris EC, Barraclough B. Suicide as an outcome for mental disorders. A meta-analysis. Br J Psychiatry 1997;170:205-28. Hudson JI, Pope HG Jr, Jonas JM, Yurgelun-Todd D. Family history study of anorexia nervosa and bulimia. Br J Psychiatry 1983;142:133-8. Hughes PL, Wells LA, Cunningham CJ, Ilstrup DM. Treating bulimia with desipramine. A double-blind, placebo-controlled study. Arch Gen Psychiatry 1986;43:182-6. Ivarsson T, Rastam M, Wentz E, Gillberg IC, Gillberg C. Depressive disorders in teenageonset anorexia nervosa: a controlled longitudinal, partly community-based study. Compr Psychiatry 2000;41:398-403. Jeammet P, Jayle D, Terrasse-Brechon G, George A. Le devenir de l’anorexie mentale. Neuropsychiatrie de l’enfance 1984;32:97-113 Jessor R. Risk behavior in adolescence: a psychosocial framework for understanding and action. J Adolesc Health 1991;12:597-605. Karwautz A, Troop NA, Rabe-Hesketh S, Collier DA, Treasure JL. Personality disorders and personality dimensions in anorexia nervosa. Personal Disord 2003;17:73-85. Kaye W, Gendall K, Strober M. Serotonin neuronal function and selective serotonin reuptake inhibitor treatment in anorexia and bulimia nervosa. Biol Psychiatry. 1998 1;44:825-38. Keel PK, Mitchell JE. Outcome in bulimia nervosa. Am J Psychiatry. 1997;154:313-21.

22

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

Keel PK, Mitchell JE, Miller KB, Davis TL, Crow SJ. Long-term outcome of bulimia nervosa. Arch Gen Psychiatry 1999;56:63-9. Kennedy SH, Piran N, Warsh JJ, Prendergast P, Mainprize E, Whynot C, Garfinkel PE. A trial of isocarboxazid in the treatment of bulimia nervosa. Clin Psychopharmacol 1988;8:391-6. Kennedy SH, McVey G, Katz R. Personality disorders in anorexia nervosa and bulimia nervosa. J Psychiatr Res 1990;24:259-69. Kennedy SH, Goldbloom DS, Ralevski E, Davis C, D'Souza JD, Lofchy J. Is there a role for selective monoamine oxidase inhibitor therapy in bulimia nervosa? A placebo-controlled trial of brofaromine. J Clin Psychopharmacol 1993;13:415-22. Kent A, Goddard KL, van den Berk PA, Raphael FJ, McCluskey SE, Lacey JH. Eating disorder in women admitted to hospital following deliberate self-poisoning. Acta Psychiatr Scand 1997;95:140-4. Kotila L, Lönnqvist J. Adolescent who make suicide attempts repeatedly. Acta Psychiatr Scand 1987;76:386-393 Kotler LA, Cohen P, Davies M, Pine DS, Walsh BT. Longitudinal relationships between childhood, adolescent, and adult eating disorders. J Am Acad Child Adolesc Psychiatry 2001;40:1434-40. Kreipe RE, Churchill BH, Strauss J. Long-term outcome of adolescents with anorexia nervosa. AJDC 1989;143:1322-1327 Lacey JH. Self-damaging and addictive behaviour in bulimia nervosa. A catchment area study. Br J Psychiatry 1993;163:190-4. Lesage AD, Boyer R, Grunberg F, Vanier C, Morissette R, Menard-Buteau C, Loyer M. Suicide and mental disorders: a case-control study of young men. Am J Psychiatry 1994;151:1063-8. Lewinsohn PM, Striegel-Moore RH, Seeley JR. Epidemiology and natural course of eating disorders in young women from adolescence to young adulthood. J Am Acad Child Adolesc Psychiatry 2000;39:1284-92. Links PS, Gould B, Ratnayake R. Assessing suicidal youth with antisocial, borderline or narcissistic personality disorder. Can J Psychiatry 2003;48:301-310. Links PS, Heslegrave RJ, Mitton JE, van Reekum R, Patrick J. Borderline personality disorder and substance abuse: consequences of comorbidity. Can J Psychiatry 1995;40:9-14. Litman RE. Psychodynamics of indirect self-destructive behavior. In:. Farberow NL. (Ed). The Many Faces of Suicide. Indirect Self-Destructive Behavior. New York: McGrawHill, 1980 , p. 28-40. Litt IF, Cuskey WR. Rudd S. Emergency room evaluation of the adolescent who attempts suicide: compliance with follow-up. J Adolesc Health Care 1983, 4,106-8. Lönnqvist JK. Psychiatric aspects of suicidal behaviour: depression. In: Hawton K, van Heeringen K, eds.. Suicide and attempted suicide. Chichester England, Wiley Ltd, 2000:107-20. Maltsberger JT. Suicide risk. The formulation of clinical judgment. New York University, New York, 1986, p. 31-48.

Suicide in Anorexia Nervosa and Bulimia Nervosa

23

Manley RS, Leichner P. Anguish and despair in adolescents with eating disorders--helping to manage suicidal ideation and impulses. Crisis. 2003;24:32-6. Martin G, Waite S. Parental bonding and vulnerability to adolescent suicide. Acta Psychiatr Scand 1994;89:246-254. Marttunen MJ, Aro HM, Henriksson MM, Lonnqvist JK. Antisocial behaviour in adolescent suicide. Acta Psychiatr Scand 1994;89:167-73. Matsunaga H, Kiriike N, Nagata T, Yamagami S. Personality disorders in patients with eating disorders in Japan. Int J Eat Disord 1998;23:399-408. Mazza JJ, Reynolds WM. An Investigation of psychopathology in nonreferred suicidal and non suicidal adolescents. Suicide Life Threat Behav 2001;31:282-302. McElroy SL, Arnold LM, Shapira NA, et al. Topiramate in the treatment of BED associated with obesity. Am J Psychiatry 2003;160:255-261. McGlashan TH. The Chestnut Lodge follow-up study. III. Long-term outcome of borderline personalities. Arch Gen Psychiatry 1986;43:20-30. Mehler C, Wewetzer C, Schulze U, Warnke A, Theisen F, Dittmann RW. Olanzapine in children and adolescents with chronic anorexia nervosa. A study of five cases. Eur Child Adolesc Psychiatry 2001;10:151-7. Milos G, Spindler A, Schnyder U. Psychiatric comorbidity and Eating Disorder Inventory (EDI) profiles in eating disorder patients. Can J Psychiatry. 2004a;49:179-84. Milos G, Spindler A, Hepp U, Schnyder U. Suicide attempts and suicidal ideation: links with psychiatric comorbidity in eating disorder subjects. Gen Hosp Psychiatry. 2004b;26:12935. Mitchell JE, Pyle RL, Hatsukami D, Goff G, Glotter D, Harper J. A 2-5 year follow-up study of patients treated for bulimia. Int J Eat Disord 1988;8:157-165 Mitchell JE. Subtyping of bulimia nervosa. Int J Eat Disord 1992;11:327-332 Modestin J, Oberson B, Erni T. Possible correlates of DSM-III-R personality disorders. Acta Psychiatr Scand 1997;96:424-430 Morgan G, Russell G. Value of family background and clinical features as predictors of longterm outcome in anorexia nervosa. Four years follow-up study of 41 patients. Psychol Med 1975;5:335-371 Nagata T, Kawarada Y, Kiriike N, Iketani T. Multi-impulsivity of Japanese patients with eating disorders: primary and secondary impulsivity. Psychiatry Res 2000 17;94:239-50. Fahy T, Eisler I. Impulsivity and eating disorders. Br J Psychiatry 1993;162:193-7. National Center for Health Statistics. Death: final data for 1998. U.S. Department of Health and Human Services. In S.L Murphy. (Ed.) Vol. 48, No. 11, 2000. Nimeus A, Traskman-Bendz L, Alsen M.Hopelessness and suicidal behavior. J Affect Disord 1997;42:137-44. Norring CEA, Sohlberg SS. Outcome, recovery, relapse and mortality across six years in patients with clinical eating disorders. Acta Psychiatr Scand 1993;87:437-444. Orbach I, Stein D, Shan-Sela M, Har-Even D. Body attitudes and body experiences in suicidal adolescents. Suicide Life Threat Behav 2001;31:237-49. Paris J, Nowlis D, Brown R. Predictors of suicide in borderline personality disorder. Can J Psychiatry 1989;34:8-9. Patton GC. Mortality in eating disorders. Psychol Med 1988;18:947-951.

24

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

Pfeffer CR. Interventions for suicidal children and their parents. Suicide Life Threat Behav 1982;12:240-248. Pinto A, Whisman MA. Negative affect and cognitive biases in suicidal and nonsuicidal hospitalized adolescents. Am Acad Child Adolesc Psychiatry 1996;35:158-65. Piran N, Kennedy S, Garfinkel PE, Owens M. Affective disturbance in eating disorders. Nerv Ment Dis 1985;173:395-400. Pirkis J, Blood RW. Suicide and the media. Part I: Reportage in nonfictional media. Crisis 2001a;22:146-54. Pirkis J, Blood RW. Suicide and the media. Part II: Portrayal in fictional media. Crisis 2001b;22:155-62. Platt S, Bille-Brahe U, Kerkhof A, et al. Parasuicide in Europe: the WHO/EURO multicentre study on parasuicide. I, introduction and preliminary analysis for 1989. Acta Psychiatr Scand 1992;85:97-104. Pompili M, Mancinelli I, Girardi P, Accorrà D, Ruberto A, Tatarelli R. Suicide and attempted suicide in anorexia nervosa and bulimia nervosa. Ann Ist Sup Sanita 2003;39:275-281. Pompili M, Mancinelli I, Girardi P, Ruberto A, Tatarelli R. Suicide in anorexia nervosa. A meta-analysis. Int J Eat Dis 2004a;36:99-103. Pompili M, Mancinelli I, Girardi P, Tatarelli R. Toward better understanding of equivocal deaths and suicides. Croat Med J 2004b;45:103-104. Pompili M, Girardi P, Ruberto A, Tatarelli R. Risk taking behavior and suicide in a non clinical sample of 312 university students. Submitted for publication, 2004c Pompili M. Tondo L, Baldessarini RJ. Suicidal risk emerging during antidepressant treatment: Recognition and intervention. Clinical Neuropsychiatry 2005 (in press). Pope HG Jr, Keck PE Jr, McElroy SL, Hudson JI. A placebo-controlled study of trazodone in bulimia nervosa. J Clin Psychopharmacol 1989;9:254-9. Pope HG, , Hudson JI, Jonas J, Yergelun-Todd D. Bulimia treated with imipramine: a placebo-controlled, double-blind study. Am J Psychiatry 1983;140:554-558. Powers PS, Santana CA, Bannon YS. Olanzapine in the treatment of anorexia nervosa: an open label trial. Int J Eat Disord 2002;32:146-54. Ratnasuriya R, Eisler I, Szmukler G, Russell G. Anorexia nervosa and prognostic factors after 20 years. Br J psychiatry 1991;158:495-502. Raynes Weiss S, Erbert MH. Psychological and behavioral characteristics of normal-weight bulimics and normal-weight controls. Psychol Med 1983;45:293-303. Reynolds I, Rob MI. The role of family difficulties in adolescent depression, drug-taking and other problem behaviours. Med J Austr 1988;149:250-256. Romano SJ, Halmi KA, Sarkar NP, Koke SC, Lee JS. A placebo-controlled study of fluoxetine in continued treatment of bulimia nervosa after successful acute fluoxetine treatment. Am J Psychiatry 2002;159:96-102. Root MPP, Fallon P. Treating the victimized bulimic: the function of bing-purge behavior. J Interpers Viol 1989;4:90-100. Ruggiero GM, Laini V, Mauri MC, Ferrari VM, Clemente A, Lugo F, Mantero M, Redaelli G, Zappulli D, Cavagnini F. A single blind comparison of amisulpride, fluoxetine and clomipramine in the treatment of restricting anorectics. Prog Neuropsychopharmacol Biol Psychiatry 2001;25:1049-59.

Suicide in Anorexia Nervosa and Bulimia Nervosa

25

Russell G. Bulimia nervosa: an ominus variant of anorexia nervosa. Psychol Med 1979;9:429-448. Santonastaso P, Friederici S, Favaro A. Sertraline in the treatment of restricting anorexia nervosa: an open controlled trial. Child Adolesc Psychopharmacol 2001;11:143-50. Santonastaso P, Pantano M, Panarotto L, Silvestri A. Follow-up study on anorexia nervosa: clinical features and diagnostic outcome. Eur Psychiatry 1991;6:177-185. Shearer S, Peter C, Quaitman M, Wadman B. Intent and lethality of suicide attempts among female borderline inpatients. Am J Psychiatry 1988;145:1424-1427. Shneidman ES, Farberow NL, Litman RE. A Taxonomy of death- a psychological point of view. In: Farberow NL, Shneidman ES, editors. The cry for help. New York: McGrawHill; 1961, p.129-135. Shneidman ES. A life in death: notes of a committed suicidologist. An epistolary autobiography. In: Walker CE (ed.). The history of clinical psychology in autobiography. Pacific Groove, CA: Brooks/Cole; 1991, p. 225-292. Shneidman ES. Definition of suicide. Northvale: Aronson; 1985. Shneidman ES. Suicide as psychache. A clinical approach to self-destructive behavior. Nortvale: Aronson; 1993. Skodol AE, Oldham JM, Hyler SE, Kellman HD, Doidge N, Davies M. Comorbidity of DSM-III-R eating disorders and personality disorders. Int J Eat Disord 1993;14:403-16. Soloff PH, Lynch KG, Kelly TM, Malone KM, Mann JJ. Characteristics of suicide attempts of patients with major depressive episode and borderline personality disorder: a comparative study. Am J Psychiatry 2000;157:601-8. Spindler A, Milos G. Psychiatric comorbidity and inpatient treatment history in bulimic subjects. Gen Hosp Psychiatry 2004;26:18-23. Stein D, Orbach I, Shani-Sela M, Har-Even D, Yaruslasky A, Roth D, Meged S, Apter A. Suicidal tendencies and body image and experience in anorexia nervosa and suicidal female adolescent inpatients. Psychother Psychosom 2003;72:16-25. Stone MH, Stone DK, Hurt SW. Natural history of borderline patients treated by intensive hospitalization. Psychiatr Clin North Am 1987;10:185-206. Sullivan PF. Mortality in anorexia nervosa. Am J Psychiatry 1995;152:1073-1074. Suominen K, Henriksson M, Suokas J, Isometsa E, Ostamo A, Lonnqvist J.Mental disorders and comorbidity in attempted suicide. Acta Psychiatr Scand 1996;94:234-40. Suominen KH, Isometsa ET, Henriksson MM, Ostamo AI, Lonnqvist JK. Suicide attempts and personality disorder. Acta Psychiatr Scand 2000;102:118-125. Theander S. Outcome and prognosis in anorexia nervosa and bulimia: some results of previous investigastions, compared with those of a swedish long-term study. J Psychiatr Res 1985;19:493-508. Toltrup K, Brinch M, Isanger T. Long term outcome 151cases of anorexia nervosa. The Copenhagen anorexia nervosa follow-up study. Acta Psychiatr Scand 1985;71:308-387. Van der Kolk BA, Perry JC, Herman JL. Childhood origins of self-destructive behavior. Am J Psychiatry 1991;148:1665-1671. van Hanswijck de Jonge P, Van Furth EF, Lacey JH, Waller G. The prevalence of DSM-IV personality pathology among individuals with bulimia nervosa, binge eating disorder and obesity. Psychol Med 2003;33:1311-7.

26

Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli

Vandereychen W, Pierloot R. The significance of subclassification in anorexia nervosa: a comparative study of clinical features in 141 patients. Psychol Med 1983;13:543-549. Vandereycken W, Pieters G. A large-scale longitudinal follow-up study of patients with eating disorders. In: Herzog et al., (Ed.). The course of eating disorders. Berlin: Springer-Verlag, 1992. p. 182-197. Vaz-Leal FJ. Psychotherapeutic management of suicide attempts in children and early adolescents: working with parents. Psychother Psychosom 1989;52:125-132. Viesselman JO, Roig M. Depression and suicidality in eating disorders. J Clin Psychiatry 1985;46:118-124 Walsh BT, Gladis M, Roose SP, Stewart JW, Stetner F, Glassman AH. Phenelzine vs placebo in 50 patients with bulimia. Arch Gen Psychiatry 1988;45:471-5. Weiss J, Sampson H. The Psychoanalytic Process: Theory, Clinical Observation, and Empirical Research. New York: Guilfor Press, 1986. Weissman MM, Bland RC, Canino GJ, et al. Prevalence of suicide ideation and suicide attempts in nine countries. Psychol Med 1999;29:9-17. Wiederman MW, Pryor T. Multi-impulsivity among women with bulimia nervosa. Int J Eat Disord 1996;;20:359-365. Winokur A, March V, Mendels J. Primary affective disorder in relatives of patients with anorexia nervosa. Am J Psychiatry 1980;137:695-8. Wonderlich SA, Swift WJ, Slotnick HB, Goodman S. DSM-III-R personality disorders in eating-disorder subtypes. Int J Eat Disord 1990;9:607-616. Wonderlich SA, Swift WJ. Borderline versus other personality disorders in the eating disorders: a clinical description. Int J Eat Disord 1990;9:629-628. World Health Oorganization. Preventing suicide. A resource for primary health care workers. WHO, Geneva, 2000b. World Health Organization. Figure and facts about suicide (adaptation of the 1999 document). WHO, Geneva, 2000 World Health Organization. Preventing suicide. A resource for teacher and other school staff. WHO, Geneva, 2000c. Youssef G, Plancherel B, Laget J, Corcos M, Flament MF, Halfon O. Personality trait risk factors for attempted suicide among young women with eating disorders. Eur Psychiatry 2004;19:131-9.

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 27-39 © 2006 Nova Science Publishers, Inc.

Chapter II

Psychopathological Aspects of Body Image Disturbance on Anorexia and Bulimia Nervosa Simone Mancini Castilho Instituto de Psiquiatria, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brasil Faculdade de Psicologia, Universidade São Judas Tadeu, São Paulo, Brasil

Abstract Body image disturbance is an important clinical feature on eating disorders and was characterized by the Diagnostic and Statistical Manual of Mental Disorders, fourth Edition (DSM-IV), as one of the diagnostic criteria for these pathologies. Although the presence and importance of body image disturbance in eating disorders are well established, the psychopathological nature of this symptom is not yet defined.

Objective This study explores the presence of obsessive-compulsive and delusional features of the ‘Body Image Disturbance’ in anorexia and bulimia nervosa.

Method Sixteen women with anorexia nervosa and eleven women with bulimia nervosa were compared regarding their responses to the Yale-Brown Obsessive Compulsive Scale (YBOCS) and to the Delusional Features Assessment Scale. Variables were analyzed with the Fisher’s Exact Test and Mann-Whitney non-parametric test (U).

Simone Mancini Castilho

28

Results Patients with anorexia nervosa had scores significantly higher than bulimic patients in the Delusional Features Assessment Scale and no differences were found between the groups regarding obsessive-compulsive features. Discussion The analysis of the psychopathological differences of ‘Body Image Disturbance’ in anorexia and bulimia nervosa has diagnostic implications.

Introduction Body image disturbance is an important clinical feature on eating disorders and was characterized by the Diagnostic and Statistical Manual of Mental Disorders, fourth Edition, (DSM-IV) (APA, 1994) as one of the diagnostic criteria for these pathologies. The severest abnormalities occur in anorexia nervosa, whose diagnostic criterion according to the DSM-IV requires a ‘disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or denial of the seriousness of the current low body weight’ (APA, 1994). For the diagnosis of bulimia nervosa the DSM-IV requires that “self-evaluation is unduly influenced by body shape and weight’ (APA, 1994). Dissatisfaction with body weight and shape seems to motivate several of the behaviors found on subjects with these pathologies. For example, the essential feature of anorexia nervosa according to the DSM-IV is ‘a refusal to maintain body weight at or above a minimally normal weight for age and height’, what means an attempt to correct a perceived defect in the physical appearance (APA, 1994). The essential feature of bulimia nervosa are the recurrent episodes of lack of control over eating. At first, these episodes would apparently represent the opposite of the excessive eating restriction and fasting seen in anorexia nervosa. However, bulimic episodes are mostly originated in the dissatisfaction with the body and in the attempts to reduce body weight. Although the presence and importance of body image disturbance in eating disorders are well established, the psychopathological nature of this symptom is not yet defined. Despite the fact that the features of obsessiveness in eating disorders have been studied (Pigott et al., 1991; Zubieta, J.K.; Demitrack, M.A.; Fenick, A.; Krahn, D.D., 1995), the research on delusional features or the interface between obsessions/delusions in eating pathologies has to be better explored.

Review of the Literature Meyer and Weinroth (1957) noted that patients with anorexia nervosa are excessively concerned with their shape, especially with their abdominal features, which they consider as protuberant, despite the evident cachexia. Next, Bruch (1962) stated that ‘a disturbance in body image of delusional proportions’ would be the central aspect of anorexia nervosa.

Psychopathological Aspects of Body Image Disturbance on Anorexia …

29

Controlled studies identify high rates of obsessiveness among patients with anorexia and bulimia nervosa, and there are studies showing increased diagnostic proportions of obsessivecompulsive disorder (OCD) in eating disorders (Pigott et al., 1991; Kaye et al., 1992; Solyom, L.; Freeman, R.J.; Miles, J.E., 1982; Bulik, C.M.; Beidel, D.C.; Duchmann, E.; Weltzin, T.E.; Kaye, W.H., 1992). The inverse relationship, that is, an increased frequency of eating disorders or symptoms in patients with OCD has been also documented (Thornton, C.; Russel, J., 1997; Thiel, A.; Broocks, A.; Ohlmeier, M.; Jacoby, G.E.; Schussler, G., 1995; Pigott et al., 1991; Rubenstein, C.S.; Pigott, T.A.; L’heureux, F.; Hill, J.L.; Murphy, D.L., 1992). On the other hand, we noted that systematized studies assessing the degrees or rates of psychotic symptomatology in patients with eating disorders are scarce. Hsu et al. (1981) described the clinical features of six patients with anorexia nervosa who had developed associated schizophrenia or schizophreniform disorder. In a retrospective study, Grounds (1982) showed that 5% of patients with anorexia nervosa had brief psychotic episodes. Of note, in these studies structured diagnostic instruments were not used. Hudson et al. (1984) detected psychotic symptoms, according to the DSM-III criteria (APA, 1980), in 17 (13%) out of 130 patients with lifetime diagnosis of anorexia nervosa and/or bulimia nervosa. Among 16 patients these symptoms seemed attributable to an affective or schizoaffective disorder, whereas in one of them they seemed to represent a factitious psychosis. Cases of schizophrenia or organic psychosis were not identified. We also found studies in the literature which comment on the clinical features present in eating disorders and comorbid psychotic conditions (Ferguson, J.M.; Damluji, N.F., 1988; Lyketsos, G.C.; Paterakis, P.; Beis, A.; Lyketsos, C.G., 1985).

Objectives This study aimed at: 1. Assessing obsessive, compulsive or delusional features of body image disturbance in patients with anorexia and bulimia nervosa. 2. Comparing both diagnostic groups regarding the mentioned psychopathological features.

Method Twenty-seven female patients were interviewed, all being followed up in the Ambulatory of Bulimia and Eating Disorders (AMBULIM) of the Psychiatric Institute of the Medical School of the University of São Paulo. They were selected according to DSM-IV criteria (APA, 1994), and 16 met criteria for the diagnosis of anorexia nervosa and 11 for bulimia nervosa. All anorexic and 3 bulimic patients were hospitalized at the time of the interview.

Simone Mancini Castilho

30

After giving their written Informed Consent, we proceeded to accomplish the interviews, that were performed in the first week of treatment. All interviews were performed by the same psychiatrist who used the following instruments, applied in the presented order: 1. Free anamnesis. It included a description of body image disturbance. 2. Eating Disorders Questionnaire Developed by Mitchell et al. (1985), it provides the main clinical features of these eating disorders. 3. Beck Depression Inventory (Beck, A.T.; Ward, V.H.; Mendelson, M.; Mock, J.; Erbaugh, G., 1961). We used the Brazilian version of this scale, which was validated by Gorenstein and andrade (1996).

Body Image Questionnaire This self-reporting questionnaire, developed by Cooper et al. (1987), provides a measure of the concerns with body image together with the antecedents and consequences of these concerns. The groups of anorexic and bulimic patients were compared regarding their demographic and clinical features, based on the answers to the Eating Disorders Questionnaire as well as regarding the total scores of the other above-mentioned instruments.

Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), Developed by Goodman et al. (1989 A,B) For this study we elaborated a list of target symptoms encompassing concerns and behaviors specifically related to body image. The Y-BOCS (questions 1 to 10) was used to assess the obsessive and compulsive aspects of these target symptoms.

Examples of Concerns Concern with the physical appearance, fear of being or becoming fat, imagining that a determined part of the body is disproportionate, thinking excessively in the numeric value of one’s weight or in the calories of food, concern with cellulite or flaccidity, thinking of becoming thinner, thinking that one’s body might be observed and assessed.

Examples of Behaviors Looking at oneself on the mirror, weighing oneself, making physical exercises to lose weight or to change the appearance, eating less than usual or fasting, measuring parts of the

Psychopathological Aspects of Body Image Disturbance on Anorexia …

31

body, using lotions for striae or flaccidity, wearing clothes in order to assess gain or loss of weight.

Delusional Features Assessment Scale Using an adaptation of an instrument developed by Lelliot et al. (1988), we assessed the delusional features of body image disturbance which were considered by patients as the most important (extracted from the list of target symptoms). We assessed the conviction – three questions with responses rated from 0 to 8 measured the strength with which the belief was sustained (degree of conviction, irreducibility and insight), the fourth question assessed the bizarreness of the belief (discrepancy between what is informed by the patient and what is observed by the psychiatrist) and the fifth one, the patient’s concern regarding her belief.

Statistical Analysis Regarding the statistical methodology, the qualitative categories were analyzed with the Fisher’s Exact Test. Qualitative variables with many categories were codified as 0, 1, etc., and the distribution of notes of the groups was analyzed with the Mann-Withney nonparametric test (U). As they had great variability, scalar variables and the sum of the items were analyzed with the Mann-Withney non-parametric test (U). We adopted the .05 significance level (α= 5%). Descriptive levels (P) below this value were considered significant and were represented by *.

Results Demographic Data There were no statistically significant differences between the group of patients with anorexia nervosa and that of patients with bulimia nervosa, except for the schooling, that was lower in the anorexic group compared to the bulimic one. A hundred per cent of the sample were females, and mostly single.

Clinical Features As expected, anorexic patients had lower Body Mass Indexes than bulimic patients and also lower frequencies of bulimic episodes, self-induced vomiting and lower use of appetite suppressants.

Simone Mancini Castilho

32

Beck Depression Inventory (Beck et al., 1961) Both diagnostic groups were not different regarding the total punctuation of this scale (P = .3111). There was a significant difference in three questions, two of them related to the eating aspect: total lack of appetite reported by 37.5% of anorexic while none of the bulimic patients and weigh loss higher than 7.5 Kg in 56.2% of the anorexics while in no one of the bulimic patients. The other question with different responses between the groups was question number three, in which 43.7% of anorexic patients chose the statement ‘I feel that I’m a total failure as a person’ in contrast with no patient with bulimia nervosa choosing this alternative.

Body Image Questionnaire The Body Image Questionnaire was similarly punctuated by patients with anorexia and bulimia nervosa, except for the question ‘Have you already vomited in order to feel thinner?’ that was answered as ‘very frequently’ or ‘always’ by 63.6% of bulimic, compared to 12.5% of anorexic patients. There were no significant differences in the questions about alteration of body perception proper, such as, ‘Do you think your thighs, hips or buttocks are too big regarding the rest of your body?’, which was answered as ‘very frequently’ or ‘always’ by 53.7% of anorexic patients and 54.5% of bulimic ones. There was also no difference between groups regarding answers to questions about possible triggers or consequences of the symptom ‘body image disturbance’, such as ‘Being naked, for instance, during a bath, makes you feel fat?’ (50% of anorexic and 36.3% of bulimic patients answered ‘very frequently’ or ‘always’) or ‘Have you been avoiding wearing clothes that make the forms of your body noticeable?’, answered as ‘very frequently’ or ‘always’ by 43.7% of anorexic and by 36.3% of bulimic patients. There was also no significant difference between groups in the total punctuation of this instrument (P = .92).

Psychopathological Features (Obsessive and Delusional) Obsessive Features According to the Y-BOCS Both diagnostic groups showed obsessive features in the symptom ‘body image disturbance’ and for 75% of anorexic and 54.5% of bulimic patients concerns related to the body took 3 hours or more per day (P=.22). Slightly more than half of both diagnostic groups reported as intense or extreme the social or professional interference provoked by concerns related to body image (P=.95), and half of anorexic and 27.2% of bulimic patients described as intense or incapacitating the associated distress (P= .27). Similar frequencies of both groups resist to the concerns always or most of the times (56.2% of anorexic and 45.4% of bulimic patients; P= .93) and have slight or no control over them (75% of anorexic and 72.7% of bulimic patients; P= .77).

Psychopathological Aspects of Body Image Disturbance on Anorexia …

33

Compulsive Features According to the Y-BOCS The frequency of patients with anorexia nervosa who spend three hours per day or more with behaviors related to the physical appearance is significantly higher when compared to patients with bulimia nervosa (81.2% and 27.2%, respectively; P= .05*). The same thing occurs with the social or professional interference, which was intense or extreme in 43.7% of anorexic, compared to 9.0% of bulimic patients (P= .008*), with intense or extreme distress (75% of anorexic and 27.2% of bulimic patients; P= .01*) and small or null degree of control, reported by 81.2% of anorexic and 36.3% of bulimic patients (P= .007*). There was no difference between both groups regarding the resistance to the behaviors, reported as always present or most of the times, in 25% of anorexic and 36.3% of bulimic patients (P= .14). The group of anorexic patients showed a significantly higher total score in the sum of questions 1 to 10 of the Y-BOCS (i.e., in the assessment of the obsessive and compulsive features of body image disturbance), compared to the group of bulimic patients (P = .0398*). When groups were compared regarding the total score for the questions 1 to 5 (obsessive features), there were no differences between them (P = .656). Regarding the total score for questions 6 to 10 (compulsive features) there was a statistically significant predominance of compulsive features in the group of anorexic patients (P = .0032*). This difference disappears when we take away ‘fasting’ from the list of target symptoms from which the YBOCS questions were made.

Delusional Features Nearly half of the patients pointed out as the central target symptom of body image disturbance the ‘concern of being fat or of gaining weight’, and, thus, we applied the delusional features assessment scale. The group of patients with anorexia nervosa had a significantly higher total score in the sum of questions of delusional features, when compared to the group of bulimic patients (P = .0082*). The answers to the five questions of this scale were: the anorexic patients, with higher frequency, were certain about their belief when compared to the bulimic patients (50% and 18.1%, respectively; P= .05*), and the same occurred with the concern with the central target symptom, which was extreme for 68.7% of anorexic and 27.2% of bulimic patients (P= .01*). In 81.2% of anorexic patients, the bizarreness of the belief was extreme when compared to the 18.1% of bulimic ones, and all these differences were statistically significant (P= .0002*). There was no difference between the groups regarding the item that states that other people did not share the same belief with them due to ignorance (56.2% of anorexic and 45.4% of bulimic patients; P= .03) and also regarding the question which assessed the irreducibility of the belief (56.2% of anorexic and 45.4% of bulimic patients; P= .85). Even when we exclude the question 4 from the delusional features assessment scale (How bizarre is the belief, according to the interviewer), the total score of the remaining questions which assess delusional features is significantly higher in the anorexic group (P = .05*).

34

Simone Mancini Castilho Table 1 Obsessive, Compulsive and Delusional Features in the diagnostic groups

Obsessive Features Time spent with obsessions(more than 3 hours per day) (question 1 of Y-BOCS) Social or professional interference (intense or extreme) (question 2 of Y-BOCS) Associated anxiety (intense or extreme) (question 3 of YBOCS) Resistance to obsessions always or most times (question 4 of Y-BOCS) Degree of control (mild or none) question 5 of Y-BOCS Compulsive features Time spent with compulsions (more than 3 hours per day) (question 6 of Y-BOCS) Social or professional interference (intense or extreme) (question 7 of Y-BOCS) Associated anxiety (intense or extreme) (question 8 of YBOCS) Resistance to obsessions always or most times (question 9 of Y-BOCS) Degree of control (mild or none) question 10 of Y-BOCS Delusional features Conviction (being sure regarding the occurrence of her belief) Question 1 of scale for assessment of delusional features Conviction (the ignorance of people does not allow them to share her beliefs) Question 2 of scale for assessment of delusional features Conviction (patient remains defending completely their belief when contrary evidence and arguments are offered) Question 3 of scale for assessment of delusional features Extreme bizarreness (question 4 of scale for assessment of delusional features) Extreme concern (Question 5 of scale for assessment of delusional features) * Statistically significant difference between groups, P < .05.

Anorexia nervosa N = 16

Bulimia nervosa N = 11

P

75%

54.54%

.2240

56.25%

54.54%

.9594

50%

27.27%

.2747

56.25%

45.45%

.9394

75%

72.72%

.7741

81.25% *

27.27% *

.0032*

43.75% *

9.09% *

.0081*

75% *

27.27% *

.0174*

25%

36.36%

.1492

81.25% *

36.36% *

.0075*

50% *

18,18% *

.0551*

25%

18,18%

.3048

56.25%

45,45%

.8520

81.25% *

18,18% *

0,0002*

68.75% *

27,27% *

0,0130*

Discussion A complex interaction of physiological and psychological factors, cultural pressures and family demands is involved in the appearance of anorexia nervosa and bulimia nervosa. Conditions that increase the probability of going on a diet or fasting, such as the concern regarding body shape, weight and eating seem to be important risk factors for these pathologies (Fairburn, C.G.; Welch, S.L.; Doll, H.A.; Davies, B.A.; O'connor, M.E., 1997).

Psychopathological Aspects of Body Image Disturbance on Anorexia …

35

Once started, behaviors related to weight loss (e.g., fasting, purging behaviors) cause physiological alterations, some of which are probable maintainers of the disease (Walsh, B.T.; Devlin, M.J., 1998). In this context, the ‘body image disturbance’ becomes a risk and maintenance factor for the disease, as it stimulates the performing of a diet. The symptom ‘body image disturbance’ shares several similarities with obsessions as it is characterized by the recurrent and persistent idea of being fat or the presence of distorted images about one’s body. These concerns or images are frequent or almost constant and cause remarkable anxiety in the patients, who try but are not always able to resist to their occurrence. Sometimes, however, patients do not show resistance or insight regarding these thoughts or images, experiencing them as natural and reasonable. Similarly to the compulsions there are repeatedly performed voluntary behaviors such as fasting, making physical exercises, weighing oneself or provoking vomits, aiming at relieving the discomfort caused by the idea of being fat. Such behaviors are clearly excessive and interfere with the socio-occupational performance of the patients. Behaviors related to body weight and image differ from compulsions when patients do not consider them exaggerate and defend the fact of performing these behaviors instead of feeling compelled to accomplish them. Not all obsessive or compulsive features are always found in one idea or behavior. For example, the lack of insight or resistance may make a belief or a behavior different from classical obsessions or compulsions, as can be observed, for instance, in patients with chronic OCD (Insel; Akiskal, 1986). Mayer-Gross et al. (1969) described the obsession as a ‘mental event with a subjective feeling of compulsion overcoming an internal resistance’ , but added that if the personality as a whole identifies itself with the idea, then this idea could be deemed overvalued or delusional. Therefore, if patients cease to recognize their idea as irrational or egodystonic, that is, intellectually and emotionally identify themselves with it, we could be facing a different notion of a typical obsession (Insel,T.R.; Akiskal, H.S., 1986). Mullen (1979) also noted that the resistance to an obsession could fluctuate and suggested that, in such cases, the phenomenon could be considered an overvalued idea or a delusion if the lack of resistance not be only occasional, but a constant feature of the experience. The symptom ‘body image disturbance’ may have some features that deviate from the obsessive concern and bring it closer to overvalued ideas. The lack of resistance offered against thoughts and behaviors and the non-intrusive way of experiencing them, that is, the emotional syntony or egosyntony with which patients experience it are some of these features. The concept of an overvalued idea was established by Wernicke (1900) apud McKenna (1984) who defined it as a solitary belief that determines the subject’s actions at a morbid degree, whereas, at the same time, it is considered as justified and a normal expression of its nature. Wernicke was the first one to distinguish overvalued ideas from obsessions showing that an overvalued idea may arise form adverse experiences that makes them understandable, differing from the obsessive concern for being a natural, non-intrusive idea, accepted without resistance and which is not seen as senseless by the patient. If we transport this concept to the

36

Simone Mancini Castilho

symptom ‘body image disturbance’ we may perceive that the resistance of patients to the idea of being fat might not be present in all cases. In this case, the idea of being fat or having a big belly would be accepted and defended by patients, and it could appear in the mind for understandable reasons, such as the fear of gaining weight among subjects with professional requirements of weight control, previous history of obesity or the presence of obese family members. In that case, patients might not consider their behaviors dedicated to weight loss excessive, reaching to the point of defending this practice, what attenuates its compulsive character and make them more similar to the actions stemming from an overvalued idea. Jaspers (1963) provides a formal distinction between prevalent ideas and delusions. The latter, he says, are the result of a specific abnormal process whose basis is unknown but that seems to involve a radical transformation in the way by which meanings are associated to events. Its quality is, therefore, entirely distinct from normal beliefs. By contrast, an overvalued idea is, in fact, an isolated idea, loaded and accentuated by a very strong affective state, understandable by the personality and life of the subject, and that, due to this strong affective load, is erroneously considered as true, as the personality is identified with the idea. Therefore, its quality is similar to strong political, religious or ethical convictions, differing from them only in degree. Hamilton (1974) adds that in delusions there is often a discrepancy between the degree of conviction and the extension in which the belief guides the action, and patients with a prevalent idea inevitably act on it, in a determined and repeated way. Since the hey-day of phenomenology at the end of the 19th and the beginning of the 20th centuries, delusion has been defined in several ways, without a consensus regarding its nature, origin and taxonomy (Butler; Braff, 1991; Roberts, 1992). The study of Jaspers (1963) was incorporated in the current definitions, delusions having determined features: (a) its content is deemed false or fantastic; (b) the degree of conviction is firm and absolute; (c) beliefs are idiosyncratic to the patients’ cultural context and (d) they are kept despite evidence or experiences in the opposite sense. However, some problems to apply these criteria have arisen and Strauss (1969) suggested that the dichotomic classification of beliefs in delusive and non-delusive was not adequate. He argued that delusions would be better conceived as extreme points along certain dimensions of beliefs, such as the degree of conviction, resistance and insight. Delusions were thus proposed to be studied as a phenomenon that could vary along several dimensions instead of being considered as an allor-nothing phenomenon (Garety, P.A.; Hemsley, D.R., 1987). The symptom ‘body image disturbance’ has delusional features which, in our study, were assessed according to the following dimensions: concern with the belief, conviction, irreducibility, insight and bizarreness. Of note, the great concern, high degree of conviction and irreducibility of the belief shown by some patients. Other remarkable aspect is the bizarreness of the belief or its lack of compatibility with reality, regarding the high degree of current malnutrition and weight loss. Anorexic and bulimic patients presented high scores in the assessment of obsessive, compulsive, and delusional features of the body image disturbance symptom. Although both groups had high values in the questions which investigated how obsessive their concerns related to body image were, there was no difference between the groups in the total scores of these questions (1 to 5 in the Y-BOCS). On the other hand, anorexic patients had higher scores in the questions that assessed compulsive features (6 to 10 in the

Psychopathological Aspects of Body Image Disturbance on Anorexia …

37

Y-BOCS) and delusive characteristics (conviction, bizarreness and concern) than bulimic patients. Therefore, behavioral aspects of body image disturbance (weighing oneself, looking at the mirror, fasting or doing physical exercises to lose weight, etc.) seem to have a greater compulsive quality (questions 6 to 10 in the Y-BOCS) in patients with anorexia nervosa, compared to bulimic patients . However, it is interesting that if we take away the practice of fasting from the list of target symptoms of body image disturbance, there is no difference between the groups regarding the quality of compulsions. This analysis seems relevant to us as fasting would be more similar to an avoidant behavior than to a compulsive behavior proper. Other difference between the groups was the fact that anorexic patients punctuate higher in the total of questions which assessed delusional features when compared to bulimic ones. A more careful analysis demonstrated that the components conviction (question 1), bizarreness and concern were those responsible for such difference. As the assessment of the bizarreness of the belief was performed only by the interviewer, what could be a source of bias, the groups were compared again after the exclusion of this component of the scale, but, nevertheless, the difference between them remained. Summing up, body image disturbance in anorexic and bulimic patients has the same quality in obsessive and compulsive aspects and in anorexia nervosa this symptom shows also some delusional features in higher degree, such as having a lower correspondence with reality, being more vigorously defended by patients and being more concerning for them. These findings can be related, in part, to the severity of the clinical picture of anorexic patients in this study. Prospective studies with greater samples and are needed to prove this.

References American Psychiatry Association (1980). Diagnostic and statistical manual of mental disorders. 3rd.ed. Washington, DC: The Association. American Psychiatry Association (1987). Diagnostic and statistical manual of mental disorders. 3rd.ed., revised. Washington, DC: The Association. American Psychiatry Association (1994). Diagnostic and statistical manual of mental disorders. 4th.ed. Washington, DC: The Association. Beck, A.T.; Ward, V.H.; Mendelson, M.; Mock, J.; Erbaugh, G. (1961) An inventory for measuring depression. Archives of General Psychiatry, v.4, p.53-63. Bruch, H. (1962). Perceptual and conceptual disturbance in anorexia nervosa. Psychosomatic Medicine, v.24, p.187-94. Bulik, C.M.; Beidel, D.C.; Duchmann, E.; Weltzin, T.E.; Kaye, W.H. (1992). Comparative psychopathology of women with bulimia nervosa and obsessive-compulsive disorder. Comprehensive Psychiatry, v.33, p.262-8. Butler, R.W.; Braff, D.L. (1991). Delusions: a review and integration. Schizophrenia Bulletin, v.17, p.633-47.

38

Simone Mancini Castilho

Cooper, P.J.; Taylor, M.J.; Cooper, Z.; Fairburn, C.G. (1987). The development and validation of the Body Shape Questionnaire. International Journal of Eating Disorders, v.6, p.485-94. Fairburn, C.G.; Welch, S.L.; Doll, H.A.; Davies, B.A.; O'Connor, M.E. (1997). Risk factors for bulimia nervosa. A community-based case-control study. Archives of General Psychiatry, v.54, p.509-17. Ferguson, J.M.; Damluji, N.F. (1988). Anorexia nervosa and schizophrenia. International Journal of Eating Disorders, v.7, p.343-52. Garety, P.A.; Hemsley, D.R (1987). Characteristics of delusional experiences. European Archives of Psychiatry and Neurological Sciences, v.236, p.294-8. Goodman, W.K.; Price, L.H.; Rasmussen, S.A.; Mazure, C.; Fleischmann, R.L.; Hill, C.L.; Heninger, G.R.; Charney, D.S. (1989a). The Yale-Brown obsessive compulsive scale, I: development, use and reliability. Archives of General Psychiatry, v.46, p.1006-11. Goodman, W.K.; Price, L.H.; Rasmussen, S.A.; Mazure, C.; Delgado, P.; Heninger, G.R.; Charney, D.S. (1989b). The Yale-Brown obsessive compulsive scale, II: validity. Archives of General Psychiatry, v.46, p.1012-16. Gorenstein, C; Andrade, L. (1996). Validation of a Portuguese version of the Beck Depression Inventory and the State-Trait Anxiety Inventory in Brazilian subjects. Brazilian Journal of Medical and Biological Research, v.29, p.453-57. Grounds, A. (1982). Transient psychoses in anorexia nervosa: A report of 7 cases. Psychological Medicine, v.12, p.107-13. Jones, E.; Watson, J.P. (1997). Delusion, the overvalued idea and religious beliefs: a comparative analysis of their characteristics. British Journal of Psychiatry, v.170, p.3816. Hamilton, M. (1974). Fish’s clinical psychopathology. Bristol: John Wright. Hsu, L.K.; Meltzer, E.S.; Crisp, A.H. Schizophrenia and anorexia nervosa. (1981). The Journal of Nervous and Mental Disease, v.169, p.273-6. Hudson, J.I.; Pope,H.G., Jr.; Jonas, J.M. (1984). Psychoses in anorexia nervosa and bulimia. British Journal of Psychiatry, v.145, p.420-3. Insel,T.R.; Akiskal, H.S. (1986). Obsessive-compulsive disorder with psychotic features: a phenomenological analysis. American Journal of Psychiatry, v.143, p.1527-33. Jaspers, K. (1963). General Psychopathology. Chicago: University of Chicago Press. Kaye, W.H.; Weltzin, T.E.; Hsu, L.K.G.; Bulik, C.; Mcconaha, C.; Sobkiewicz, T. (1992). Patients with anorexia nervosa have elevated scores on the Yale-Brown ObsessiveCompulsive Scale. International Journal of Eating Disorders, v.12, p.57-62. Keys, A.; Brozek, J.; Henschel, A.; Mickelsen, O.; Taylor, H.L. (1950). The biology of human starvation. Minneapolis: University of Minnesota Press. Lelliot, P.T.; Norshivani, H.F.; Basoglu, M.; Marks, I.M.; Monteiro, W.O. (1988). Obsessivecompulsive beliefs and treatment outcome. Psychological Medicine, v.18, p.697-702. Lyketsos, G.C.; Paterakis, P.; Beis, A.; Lyketsos, C.G. (1985). Eating disorders in schizophrenia. British Journal of Psychiatry, v.146, p.255-61. Mayer Gross, W.; Slater, E.; Roth, M. (1969). Clinical psychiatry. 3. ed. London: Baillière, Tindall and Cassell.

Psychopathological Aspects of Body Image Disturbance on Anorexia …

39

Meyer, B.C.; Weinroth, L.A. (1957). Observations on psychological aspects of anorexia nervosa. Psychosomatic Medicine, v.19, p.389-98. Mitchell, J.E.; Hatsukami, D.; Eckert, E.; Pyle, R. (1985). Eating Disorders Questionnaire. Psychopharmacology Bulletin, v.21, p.1025-43. Mullen, P. (1979). Phenomenology of disordered mental function. In: Hill, P.; Murray, R.; Thorley, G., ed. Essentials of postgraduate psychiatry. London: Academic Press. Pigott, T.A.; Altemus, M.; Rubenstein, C.S.; Hill, J.L.; Bihari, K.; L’Hereux, F.; Bernstein, S.; Murphy, D.L. (1991). Symptoms of eating disorders in patients with obsessivecompulsive disorder. American Journal of Psychiatry, v.148, p.1552-7. roberts, g. The origins of delusion. (1992). British Journal of Psychiatry, v.161, p.298-308. Rubenstein, C.S.; Pigott, T.A.; L’heureux, F.; Hill, J.L.; Murphy, D.L. (1992). A preliminary investigation of the lifetime prevalence of anorexia and bulimia nervosa in patients with obsessive-compulsive disorder. Journal of Clinical Psychiatry, v.53, p.309-14. Solyom, L.; Freeman, R.J.; Miles, J.E. (1982). A comparative psychometric study of anorexia nervosa and obsessive neurosis. Canadian Journal of Psychiatry, v.27, p.282-6. Strauss, J.S. Hallucinations and delusions as points on continua function. (1969). Archives of General Psychiatry, v.21, p.581-6. Thiel, A.; Broocks, A.; Ohlmeier, M.; Jacoby, G.E.; Schussler, G. (1995). Obsessivecompulsive disorder among patients with anorexia nervosa and bulimia nervosa. American Journal of Psychiatry, v.152, p.72-5. Thornton, C.; Russel, J. (1997). Obsessive compulsive comorbidity in the dieting disorders. International Journal of Eating Disorders, v.21, p.83-7. Walsh, B.T.; Devlin, M.J. (1998). Eating disorders: progress and problems. Science, v.280, p.1387-90. Wernicke, C. (1900). Grundriss der psychiatrie. Leipzig, Verlag von Georg Thieme, apud McKenna, P.J. (1984). Disorders with overvalued ideas. British Journal of Psychiatry, v.145, p.579-85. Zubieta, J.K.; Demitrack, M.A.; Fenick, A.; Krahn, D.D. (1995). Obsessionality in eating disorder patients: relationship to clinical presentation and two-year outcome. Journal of Psychiatric Research, v.29, n.4, p.333-42.

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 41-61 © 2006 Nova Science Publishers, Inc.

Chapter III

Experiences of ‘Control’ in Anorexia Nervosa Treatment: Delayed Coercion, Shadow of Law, or Disseminated Power and Control? Terry Carney, Mim Ingvarson and David Tait Sydney Law School, University of Sydney NSW 2006 Australia

Abstract Anorexia nervosa is often chronic, with one of the highest death rates for psychological conditions. Law can compel treatment, but is rarely invoked, at least formally (though the strategic possibilities of orders confers internal authority within the clinical setting). Instead, ‘control’ (or management) is exercised diffusely, through disciplinary practices embedded in everyday clinic life, such as daily routines of eating and washing, behavioural ‘contracts’, regular surveillance and measuring, interactions with staff, visits and activities. The regulatory regime not only touches on such ‘practices’ but also targets ‘identities’ (including self-image, and attitudes to the body) and what Goffman called the ‘moral career’ of the patient (eg learning to play the ‘patient role’, to ‘be’ an ‘anorexic’). We argue that it is not the clumsiness of the law, or the success of less restrictive options which explains why law is so infrequently engaged. Rather, based on an interpretation of Foucault, we conclude that the regulatory regime that shapes treatment of anorexia nervosa, is ‘the law’, in a sense. The regime of governmentality within the clinic is shaped by practices which operationalise ‘duty of care’, or translate medical expertise into medical authority, or show how interactions between ‘experts’, ‘carers’ and patients are mediated through conventions and rules, or which conscript ‘empowerment’ as control. The patient learns to provide consent ‘freely’, to make the ‘correct’ choices, to accept the ‘empowerment’ regime that is made even more convincing by the threat of legal intervention. In time the constraints learned in this way become part of the new role, that of the ‘recovering’ patient. The ‘fiction’ of acting ‘responsibly’, employed so

42

Terry Carney, Mim Ingvarson and David Tait hesitantly at first, becomes part of the new identity. The patient has become an active participant in the governance of self.

Introduction Anorexia nervosa joins other ‘syndromes’ listed in psychiatric manuals like the DSMlV(R) or the ICD 10. Along with many psychiatric conditions, it is identified by ‘clusters of symptoms and behaviours considered clinically meaningful in terms of course, outcome and response to treatment’, rather than by objective anatomical features (Bruce, 1999: 37; Further: Beumont and Carney, 2003). The literature is divided about whether anorexia is mainly a pathological condition, or may in some contexts be understood as a ‘rational’ form of behaviour (For a review: Dresser, 1984: 302-308). Some writers highlight long historical traditions of ascetism, where fasting is associated with religious merit and definition of the ‘self’. On this view, intense fasting, like self-flagellation, embarking on crusades and other forms of extreme self-discipline, may connote a display of devotion and sacrifice (Tait, 1993). Others focus on the family and relational context in which the anorexic ‘identity’ is constructed (Young, 1998), seeing eating disorders as one of a series of responses to familial traumas. Feminists point to socio-political dimensions of anorexia (patriarchy, disempowerment) to explain the reported loss of self esteem and ‘powerlessness’ (Gilmore, 1994; Bray, 1996). And resistance to assuming an adult female identity may be reflected in attempts to delay the onset of puberty, specifically menstruation (Tomkiewicz, 2003). Culture too may play a part, either in shaping the form in which body image conditions express themselves in different countries (Abusah, 1993), or pre-disposing some young people to greater risk of anorexia.1 Whatever its true ‘character’, or its social and familial origins, severe anorexia nervosa is experienced by half to 1 percent of women over their lifecourse (Steiger and Séguin, 1999). And even if some fasting originates in a rational decision, its escalation into severe anorexia nervosa is usually accompanied by physiological changes that then limit the person’s awareness of the risks they face. Anorexia nervosa is life-threatening, with one of the highest death and morbidity rates among cognate conditions,2 complicated by treatment resistance and low rates of success (Ben-Tovim, 2001).

1

2

One Australian study which examined the family backgrounds of people with anorexia found an overrepresentation of parents from Asia or Europe, and fewer from the Middle East, leading the authors to suggest that, while it is a myth to believe that some cultures immunise against the condition, those young people from cultures where the condition is rare may experience a heightened risk of the condition (Alexander, Kohn, Feeney and Clarke, 2000). Mortality among people diagnosed with anorexia ranges from a low of 4 percent to a more widely accepted figure of up to one in five (Dresser, 1984: 297; Griffiths, 1996; Draper, 2000: 120). However its low prevalence, peaking at about 0.5% (or 1% in some US studies) of women aged 15-19 age band (Griffiths, 1996), means that aggregate mortality figuresof perhaps 1 death annually per million women aged 15-65 (Draper, 2000)pales against the equivalent statistic of 61 female suicides per million Australian women (ABS Year Book 1997). 3 ‘Control’ is an apt term from the sociological perspective, but it has strong pejorative overtones. A more neutral term, like ‘management’ highlights the positive contribution to therapeutic outcomes, but masks the exercise of legal and social power which brings about that result.

Experiences of ‘Control’ in Anorexia Nervosa Treatment

43

Clinicians sometimes turn to law for assistance in compelling hospitalisation of people with treatment resistant or life-threatening severe anorexia nervosa, or to require involuntary nasogastric feeding. Some patients are scheduled/committed under mental health laws while others are covered by adult guardianship legislation (Carney, 2002). When mental health law is used, the head psychiatrist of the service where a person is receiving treatment makes the decisions about treatment. Under guardianship laws the substitute decision-maker can be any person from a statutory guardian to a member of the person’s family. Different laws may be invoked at different times during episodes of hospitalisation or increased management over the course of their treatment (Carney and Saunders, 2003; Carney, Tait, Saunders, Touyz, Wakefield et al., 2003). Previous work (Carney, Tait, Saunders, Touyz, Wakefield et al., 2003) analysed the experience of anorexia patients, revealing the importance of the ‘context’ (or the social/clinical setting) in understanding their perception of ‘institutional’ choices about the type of legal order (and administering tribunal) used to coerce treatment. This Chapter reports our data about the way ‘control’ is conceptualised and experienced during the lifecourse of anorexia,3 both in formal (legal orders) and ‘informal’ settings where it is synonymous with clinical management regimes like ‘assertive treatment’ (Davis, 2002) or ‘close management’ (Drake, Bartels, Teague, Noordsy and Clark, 1993; Noordsy, Mercer and Drake, 2002). We argue that control is mainly extra-legal (a product of family and clinical rather than legal transactions), is very diverse in its deployment (ranging from suasion to coercion), andmost cruciallyoften involves transformation of the identity of the patient within the particular social environment in which control finds expression. This arises at a previously neglected intersection between the personal ‘career stage’ of the condition (as expressed by Erving Goffman and others) and the disseminated forms of expression of power as postulated by Michael Foucault.

Diverse Clinical Configurations of Management and Control: Where does Formal Coercion Fit in? The first main insightthat the instruments of social control are quite diverseis derived from our data on the pattern of deployment of the formal and ‘informal’ measures of social control of anorexia nervosa patients (Carney, Saunders, Tait, Touyz and Ingvarson, 2004). Law is invoked only when other, less restrictive, measures prove inadequate. Moreover in the case of anorexia, those legally sanctioned interventions account for comparatively small proportions (or ‘slices’) of the lifecourse4 of the condition (Carney and Saunders, 2003). Given the legislative and clinical preference for voluntary treatment, legislatively

4

Our focus is on sociological insights revealed by taking a lifecourse perspective on the life domains of anorexia, and the trajectories and transitions associated with it (See: George, 1999), including notions of illness as ‘career’ (Aneshensel, 1999), coupled with insights derived from the work of Erving Goffman and Michael Foucault.

44

Terry Carney, Mim Ingvarson and David Tait

sanctioned coercion,5 tends to be a measure of ‘last resort’; informal ‘suasion’ is both much more common and more nuanced in its impact on the young woman (Tait, Ingvarson, Wakefield, Touyz and Carney, 2003). This is unsurprising, since responsibility for assisting with the management of adverse effects of severe anorexia primarily lies with the medical profession, not the legal system, just as in mental health generally. Legal coercion, as Hiday et al observed, ‘does not tell the whole story of coercion’ in mental health (Hiday, Swartz, Swanson, Borum and Wagner, 2002: 122). Individuals are ‘”pushed” into care by friends, relatives and co-workers’ (Pescosolido, Boyer and Lubell, 1999: 449).

A Gradient of Forms of Suasion/coercion. The diversity in the forms of social control able to be deployed in mental health by clinicians or the law is illustrated by the range of different expressions it may take, running from: [M]ild persuasive attempts and pleas, through inducements with offers of desired objects or services …. through threats of negative consequences such as involuntary hospitalisation or being put out of the house, to strong application of physical force (Hiday, Swartz, Swanson, Borum and Wagner, 2002: 124).

Even ‘informal persuasion’ takes many forms in the case of anorexia management, ranging from ‘mere invitations’ to ‘verbal brow-beating’ or moral blackmail, as Rathner observed, [T]here are various social pressures that family, friends, relatives, schools and (mental) health care personnel use in an attempt to get the sufferer to accept the idea of seeking help: request, reasoning, persuasion, barter, bargaining, gentle prodding, enticement, selective information, manipulation, deceiving, blackmail, … (Rathner, 1998: 185-86).

Among clinicians, a frequent next step up the compliance ladder is to encourage compliance by employing a legal concept like a ‘contract’ (Harlow, 1998: 51), with its notion of ‘mutual obligations’ of clinician/patient (Dresser, 1984: 323). This may be followed in mental health settings by a ‘shadow-land’ where people are encouraged into treatment through ‘foreshadowing’ (or even ‘threatening’) to invoke formal legal measures. Thus 40 percent of ‘voluntary’ patients studied in the MacArthur Coercion Study in the US believed that they would have been involuntarily committed had they not signed themselves in (Pescosolido, Boyer and Lubell, 1999: 450). As discussed further below, stronger again in its impact on the person with anorexia are cases of ‘strategic’ use of law. This entails strategic lodgement of legal action to compel 5

Perceptions of legal coercion do not necessarily coincide with the legal status of being a voluntary or involuntary patient, and coercion may be ‘experienced’ in community as well as in hospital settings, depending among other things on the perceived ‘fairness’ of the process (Hiday, Swartz, Swanson, Borum and Wagner, 2002).

Experiences of ‘Control’ in Anorexia Nervosa Treatment

45

treatment (such as adult guardianship), only to be later followed by its subsequent withdrawal once this ‘leverage’ has achieved the desired goal of ‘voluntary’ acceptance of treatment. Of these, the least popular choice among anorexia clinicians is to obtain a formal legal order to compel treatment (Carney and Saunders, 2003; Carney, Tait, Saunders, Touyz and Beumont, 2003). As revealed in the next section, if both adult guardianship and mental health laws are available, guardianship tends to be favoured over mental health, with committal retained as the last port of call.

Use of Formal ‘Control’ in a Typical Specialist Anorexia Unit. A clearer picture of the relationship between formal and informal measures of clinical management of anorexia is provided by data collected from a specialist Australian anorexia in-patient facility in the state of New South Wales (‘NSW’).6 The facility utilised a ‘progressive’ regime that minimised the level of coercion (Carney, Wakefield, Tait and Touyz, 2004),7 within a state jurisdiction where adult guardianship options were available, and reportedly used mainly to ‘initiate’ rather than coerce treatment (Newman, Russell and Beumont, 1995). On entry to the program clinicians implicitly assessed the required patient ‘status’, deciding if legal coercion was needed, and whether to go ahead with obtaining legal backing, and what form of order to seek (Saunders, 2001; Carney, 2002). This provided a particularly useful case study of how power is exercised within a relatively low-coercion environment. a. Legally-backed coercion is the exception As more fully reported elsewhere (Carney, Saunders, Tait, Touyz and Ingvarson, 2004), the study found low rates of resort to formal (legally mandated) coercion. Almost two thirds of admissions (63 of 96) took place without any indication of clinical consideration of a possible need for coercion, even though 15 of these cases (28% of the sub-sample), were second admissions, and in another three cases (5%) it was their third admission.8

6

7

8

Data was extracted for all 119 admissions to the specialist anorexia program of the Royal Prince Alfred hospital (RPA, a major public teaching hospital in Sydney, in the state of New South Wales), over a period of four and a half years, mapping various factors such as case flows, characteristics of patients, duration of treatment stays and use of legally mandated coercion. Twenty five cases with another eating disorder or co-morbid diagnosis were discarded, leaving 96 admissions relating to 75 individuals. Slightly over a third (36%) were under the age of 20, while 19% were people over the age of 30. Approximately 40% of admissions were for less than three weeks, with a mean stay of 49 days (and a maximum of 344 days). One third of the admissions were isolated events within the sample frame, while for a quarter of the sample there were 4 or more admissions in the period. Even lower proportions of coercion (approximately 16% of the samples) were found in the Iowa (US) and Maudsley (UK) studies (Ramsay, Ward, Treasure and Russell, 1999; Watson, Bowers and Andersen, 2000). Formal coercion might have been mentioned by treating doctors, or foreshadowed strategically (Carney, Saunders, Tait, Touyz and Ingvarson, 2004).

Terry Carney, Mim Ingvarson and David Tait

46

b. Coercion is most likely to be considered for chronic cases Formal coercion is understandably considered in more chronic, treatment-resistant cases,9 but it was sometimes utilised for a first admission to a specialist unit as well (accounting for one in five cases of formal coercion). As revealed in the table below, 16 of the formally coerced cases involved patients on their 3rd or subsequent admission (72% of this subsample). Of those where formal coercion was not considered or used, 40 cases (62%) were patients on their first or second admission. Number and coercion status of admissions. Status Not coerced Considered coercion Coerced Total

Number of Admissions (%age of total by coercion status) 1 2 3 4+ Unknown TOTAL 25 (40) 15 (24) 3 (5) 11 (17) 9 63 2 (29) 1 (14) 0 (0) 1 (14) 3 7 5 (19) 32 (33)

1 (4) 17 (18)

4 (15) 7 (7)

12 (46) 24 (25)

4 16

26 96

c. Guardianship is seldom used on its own, but mental health committal is popular. When formal coercion was canvassed by clinicians, as it was in 27 percent of cases, it usually led to an application for an order. But adult guardianship, on its own, was the exception: only 3 admissions (11.5% of 26 admissions backed by a legal order) solely involved adult guardianship. Mental health committal orders were much more popular with clinicians as a ‘standalone’ order, accounting for 44% of all such admissions. Slightly more than half of these were based on the medical complications of anorexia itself (6 of 11 cases), while the others were grounded in supervening factors such as depression, delusional behaviour or threats to the health and safety of the person. d. Mental health committal is also commonly used in conjunction with/after guardianship. The study data revealed that mental health committal is also quite commonly used in conjunction with guardianship, or subsequent to an earlier order for adult guardianship. Forty two percent of legally coerced admissions were of this character.10

9

10

If age is a proxy for ‘maturity’ (or insight) it would appear that this is not a factor in deciding to obtain a legal order. The mean age at admission was almost identical for the coerced (24.5 yrs) and the non-coerced group (24.2 yrs). By contrast, those for whom coercion was considered but not invoked were older (average age 29.6 yrs). Guardianship allows appointment of a third party to provide consent to medical treatment (one third of the ‘mixed’ order cases), or to make decisions about proposed behavioural therapies (two thirds of such cases in the study).

Experiences of ‘Control’ in Anorexia Nervosa Treatment

47

Tracing ‘Strategic’ (or Shadow of Law) Uses of Formal Coercion The normative character of transactions taking place in the ‘shadow’ of the law has long intrigued researchers (Eg Mnookin and Kornhauser, 1979 on divorce bargaining), with recent examples including the strategic influence of law on negotiation of child custody disputes (Jacob, 1992), the management of alleged promiscuous sexual ‘delinquency’ of young women (Ajzenstadt and Steinberg, 1995), or procedural rules impacting on pre-trial civil settlements (Main and Park, 2000; 2002), and even law/power influencing World Trade Organisation bargaining (Steinberg, 2002). This phenomenon was detected in anorexia cases by members of the adult guardianship tribunal in the state of New South Wales, Australia (‘NSW’). Members observed that guardianship applications were being lodged strategically to persuade patients reluctant to consent to proposed treatment regimes, and were then allowed to lapse once cooperation was forthcoming.11 This was confirmed by initial data showing that nearly a third (four of 13 people, 2 then to be heard) of applications and reviews dealt with in the 2000-2001 period were withdrawn prior to hearing.12 It was further refined by a more detailed review, tracking the history of guardianship applications in respect of anorexia nervosa patients. a. Guardianship is lightly used Data for the ten year period 1994-2003,13 indicated that the tribunal has been lightly used for anorexia cases over much of its history. As shown in the next table, applications are patchy at best. Guardianship (GO) Applications 1994-2003. STATUS OF APPLICATIONS

Withdrawn Adjourned Dismissed GrantedGO

Total

Year ‘94 1 1 0 0 0

‘95 1 1 0 0 0

‘96 1 0 1 0 0

‘97 1 0 0 1 0

‘98 1 0 0 0 1

‘99 4 2 0 0 2

‘00 7 0 0 0 7

‘01 4 2 0 0 2

‘02 3 0 0 0 3

‘03 3 0 0 0 3

26 6 1 1 18

It can be seen that guardianship was rarely used in the first half of the decade, with only an average of one application a year. Indeed, apart from a peak of seven applications in 2000, only three or four applications were made each year in the latter part of the decade. Seven (27%) of the applications over the decade involved more than one application, however.

11 12 13

Personal communication with NSW Guardianship Board members, Thurday 11 October 2001. Statistics supplied by the NSW Guardianship Tribunal. De-identified data extracted by Esther Cho of the Guardianship Tribunal on 8 August 2003.

48

Terry Carney, Mim Ingvarson and David Tait

b. Strategic withdrawals are not always the end of the story Fewer applications were withdrawn than was expected: just six of 26 applications (or 23%). Closer study, however, revealed that several withdrawn cases reappeared in later years. Thus the sole case from 1994 (‘Abigail’, not her real name) appeared on three occasions in all. She had a guardianship application lodged and withdrawn in 1994. She reappeared in 1996 when a financial management order was granted (and guardianship adjourned). And in 1997 another guardianship order was sought (but denied by the Tribunal). Likewise ‘Eve’, the sole case in 1995, had her application withdrawn in that year. But she was placed on guardianship when she reappeared six years later in 2001. For her part, ‘Hanna’ saw two applications withdrawn in 1999 and 2001, before finally being placed on an order in 2003. ‘Martha’ (withdrawn 1999, granted 2000) and ‘Rebecca’ (granted 2000, withdrawal in 2001) round out these cases of an apparently ‘strategic’ resort to the Tribunal. The remaining two cases where multiple appearances are recordedRachel (GO orders in 1998 and 2003) and Leah (orders in 1999 and 2003)were the only ones where all applications are recorded as having proceeded as lodged. Fieldwork reports by ‘Fiona’ (not her real name) of another otherwise unrecorded episode suggests that this may understate such cases, however, with paperwork mobilised to trigger acceptance of admission without leading to a ‘listing’ of the case for hearing: There was actually an application for an order to appear before a tribunal and all the rest of it….. Yeah, well it’s funny ‘cos it said on the envelope it had been delivered by the bailiff and it was in my mail box. And I thought oh great, and so I thought well I don’t want to go through all that crap and it was at that time that I didn’t really, you know, really my head wasn’t there and I really wasn’t there. The first time I was already in hospital when I got the letter so it was a bit late but this time I got the letter here and that’s when I got my friends who are lawyers and I was saying ‘what can I do? What can I do?’ They were saying ‘that we don’t think you should resist. We just think you should go to the hospital’. I said say ‘I’m not going to; how can I appeal this or whatever’. And they said ‘you’ll have to go to the tribunal’ and yeah …

What we term the ‘strategic context’, then, is pertinent to choice of pathway, including whether to rely on the ‘shadow of law’, as in the case of lodging proceedings which are later withdrawn.14 Another feature of guardianship applications deserves mention: almost all of these were lodged by (or more usually) on the instigation of the treatment team.15 Unlike most other types of adult guardianship application, very few applications appear to have been lodged by

14

15

As indicated previously, an alternative explanation can be made in terms of regimes such as clinical regimes such as ‘close monitoring’ or ‘assertive treatment’, often adopted with ‘dual disorder’ patients, where such forms of ‘intensive supervision [are] at times provided with the client’s consent and at other times is provided involuntarily’ (Noordsy, Mercer and Drake, 2002). Indeed such regimes may occupy the hinterland between community treatment orders and more ‘voluntary’ programs (Davis, 2002). Clinicians were named as applicants in 14 cases, while family members were the nominal or actual applicants in 8 cases (in 4 withdrawn matters the applicant was ‘to be advised’, implying that clinicians had a hand in initiating the matter): data referred to at n 15 above.

Experiences of ‘Control’ in Anorexia Nervosa Treatment

49

friends or family members on their own volition. This suggests that the applications were seen as something that would enable treatment rather than as a challenge to medical authority (also: Newman, Russell and Beumont, 1995: 58). C. Disseminated Power and Control: Towards self-management/control? As we have already seen, clinicians, and the services with which they are associated, are key players too. As one commentator observed, [d]ealing with any health problem is a social process that is managed through contacts or social networks that individuals have in the community, the treatment system, and social service agencies, including self-help groups, churches and jails (Pescosolido, Boyer and Lubell, 1999: 455).

So an analysis from the standpoint of managers and regulators alone, without regard to the wider context and web of relationships within which a patient operatesis likely to be unduly simplistic. Our second main insightthat power and control is a product of interaction between patient identity and the broader social environmentis best shown in one of our case studies. ‘Felicity’s’ reaction to one episode is described as follows: I was being seen as an outpatient at [X hospital] by a doctor that I’d … seen at the Children’s Hospital … And I hated the doctor there … hated him with a passion …. So they said, ‘Right. We’re going to tube feed you’. And they got the guardianship order out against me … Because they knew I’d fight it [being tube fed] and pull it out and do whatever. They threatened to send me to a locked ward where I would be physically restrained … They threatened to send me to … to the psychiatric unit [at a nearby hospital]. And that was enough for me … to comply with what they wanted for the time being. (Emphasis added).

There are several factors in play here. First, Felicity is driven by her violent dislike of a particular clinician at an alternative facility. Despite being tube fed, and despite being coerced into acceptance of this course by a legal order (adult guardianship), her ‘hatred’ of that other clinician was apparently the more powerful force motivating her (reluctant) compliance. Second, she was fearful of the loss of control of being placed in a locked ward and then physically ‘restrained’, and of the prospect of the stigma of transfer to a ‘psychiatric’ unit, as foreshadowed by her treatment team. This combination of disciplinary influencesthe interplay between dislike of a particular clinician, threats to switch service settings, and the foreshadowing of psychiatric committalwas sufficient to win her grudging compliance. She decided to ‘comply with what they wanted’; at least ‘for the time being’. As Foucault demonstrated, power is dynamic rather than static, and is often highly disseminated rather than always channelled through particular structures. Institutions not commonly thought of as part of the law, such as the home or the hospital, may become sites for expression of such poweroften linked in with complex social networks, and shaped by its point in history. His focus is on the ‘techniques’ for the exercise of power, and the

50

Terry Carney, Mim Ingvarson and David Tait

dialectic of the dialogue of application and resistance to that power. It is a truism that law is power, but that its power is mediated in many ways. Power is shifting and unstable, and it takes various forms other than the classical ‘disciplinary’ form so sharply expressed in anorexia management in the form of legally compelled detention for treatment, or imposition of nasogastric feeding (Carney, 2002). For Foucault, power was not so well captured by such metaphors of ‘command and control’. Instead it was located in the ‘governmentality’ space. A space lying between mere gameplaying contestation and the ‘state of domination’ constituted by its expression in legal coercion, or as the ‘sovereignty’ of power (Rabinow, 1997: xvii). In this view, a regulatory regime may be experienced as beneficent, indeed sometimes even pleasurable, and freely chosen (Shearing and Stenning, 1984). Shearing and Stenning show how Disney World is constructed to ensure that consumers are complicit in their own security (347), that selfregulation (assisted when necessary by staff dressed up as Mickey Mouse or other characters from the Walt Disney imaginary) combines freedom and security. The treatment of anorexia nervosa is harder to deliver without coercion than a plunge down Splash Mountain, but the question posed is still relevant: how can governance be exercised in a way that is experienced as freely chosen?

Power in ‘Pastoral’ Settings Power may also take a ‘pastoral’ form of course, as in the carer relationship in nursing: Nurses … are in direct contact with individuals, groups, communities, and populations [constituting] a powerful group of experts …. Working at the junction of the individual and collective body within power relations that promote and recuperate life, nurses are able, through their interventions, to mold, conduct or affect people as well as to construct, with the help of other health care professionals, people's subjectivities. (Holmes and Gastaldo, 2002).

These ‘subjectivities’ (sometimes called ‘bio-power’) principally include the ‘self’ or ‘identity’ of the patient. So self-images are shaped by these exchanges. Exchanges which are never neutral but which may be advantageous or ‘controlling’ in character. As Powers has recently argued, even as superficially attractive a goal as pursuit of ‘empowerment’ in therapy can constitute a technique for the exercise of power. This is because clinicians may subtly ‘privilege’ the preferred option supposedly ‘chosen’ by the patient (Powers, 2003). Nursing too involves deploying techniques ranging from ‘disciplining’ to ‘promoting discourses that construct desirable subjectivities’ (Holmes and Gastaldo, 2002). Of course care must be taken not to oversimplify the application of this analysis (Cheek and Porter, 1997). While therapeutic interventions lend themselves to analysis from this perspective, this does not displace the legitimate role played by the psychodynamics of some conditions (Glass, 2000). Nor does it mean that power and control are inimical to the interests of the patient: processes of socialisation and formation of identities are shaped by power, and such acculturation may facilitate social functioning or the capacity to manage chronic

Experiences of ‘Control’ in Anorexia Nervosa Treatment

51

conditions like anorexia (Aneshensel, 1999: 597). Indeed, given that lack of ‘insight’ (denial) is a central ingredient of anorexia, the role of access to ‘normalising’ social interactions and supports may be central to its satisfactory management (White, Bebbington, Pearson, Johnson and Ellis, 2000). In-patient care for psychiatric conditions has altered quite dramatically over the last several decades, however. The hospital setting is no longer the primary ‘place of observation, of diagnosis, of clinical and experimental identification [and] immediate intervention’, that once was the case when the ‘infection’ model of health was dominant (Foucault, 1997: 4041). Hospitals (and medicine) no longer serve as the primary agents for ‘clarifying and purifying’ the disease entity. That role has been undermined both by the problematic status of ‘disease’ within psychiatry (Dawson, 1996; Beumont and Carney, 2004), and by the relegation of hospitals to brief interludes in the management of conditions like anorexia (Carney, Tait, Saunders, Touyz, Wakefield et al., 2003).

Power as Experienced by Anorexia Patients Consequently, the ‘community/family’ space is now much more central. This is the new site where power and control is experienced by sufferers of conditions like anorexia (Hiday, Swartz, Swanson, Borum and Wagner, 2002: 123). Power in the case of anorexia management, we suggest, tends to find its expression in the fluidity of the ‘negotiations’ about the relationships forged both in this societal space, and those within the hospital setting. Moreover the currency used in negotiations within the setting (hospital or community) where the person with anorexia is currently residing, frequently harks back to, or anticipates, life in the other sphere. So conditions of life in the community loom large in the life of hospitalised patients. And in similar vein, the prospect of a return to hospital also shapes the lives of those currently living in the community. One of our qualitative interviews illustrates this interpenetration of the two ‘worlds’, but also brings out the multiple levels of that relationship. It shows that sometimes the legacy of past experience, however unpleasant, can leave a more positive legacy of ‘control’ for the future. Kelly’s opinion of the outcome of a previous period of hospitalisation is a case in point: I think hospital was good in a way, as I wouldn’t want to ever go there again. That’s the only good thing about the hospital experience. I’m terrified of ever going there again. (Emphasis added).

Turning to her ongoing issues with her weight management, she brought out the sense of being caught in a kind of systemic ‘limbo-land’ or twilight zone in terms of her weight, when she said: I know where this is going to end up, in hospital again. That terror of having control taken off me. It’s almost like um, I think a lot of people do it, who have had an eating disorder, or anorexia and have been under weight. You can kind of keep yourself

52

Terry Carney, Mim Ingvarson and David Tait between these safe weights that aren’t perhaps as healthy as they should be but aren’t going to get you put in hospital. It‘s a pretty miserable way to live. Look, you know, it’s hard because I think the system makes it almost like, because of the way you’re treated in hospital you kind of afterwards get stuck. I guess there are times where I feel like that. I get stuck in this: ‘I’m not totally over it or totally well’. Not going to, um way too terrified to [end up in] hospital again. (Emphasis added).

As can be seen from this passage, previous unhappy experiences (in this case of hospitalisation) maintain an element of on-going control or influence over the life course of the patient with anorexia on return to community living. Kelly’s experience is that this is both empowering and controlling: empowering in the sense of reminding her of the unpleasant consequences of an acute episode, but paradoxically ‘controlling’ as well, in the sense of maintaining its thrall over her life and her management of the condition. So power and control can be very subtle and highly nuanced. The interview with ‘Tess’, the sister of ‘Kate’ (the patient), where she is describing their mother visiting Kate in the hospital, shows the way other more intimate worlds can interrelate with each other – [E]ven in hindsight again you could probably imagine her sense of failure and everything. And she couldn’t even come to the hospital. And when she did she was hostile. And Kate used to dread her visits. (Emphasis added).

Kate’s mother, then was a powerful part of this woman’s ‘social context’. Blaming herself for ‘failing’ her daughter, she found it a great ordeal to visit her in hospital. When she did so, she projected her ‘hostility’. As a result, Kate ‘dreaded’ visits. As elaborated by Tess when she was asked how she herself came to understand that her sister was suffering from anorexia, she recalls how her mother presented herself as the ‘victim’ of Kate’s vindictive or ‘attention seeking’ behaviour: But Mum was also, Mum didn’t know how to deal with it. She didn’t have the emotional ability or any type of insight to deal with it. Um, and just saw it as, my mother has always been a victim, and she thought Kate was doing something to her and directly punishing her for something. So you know, it was ‘the little bitch is only doing it for attention’. That sort of thing, which exacerbated the problem. Kate bought home a Foundation form saying there’s an information night on anorexia and Mum said ‘what do I want to learn about that shit for’ and she ripped it up in front of her. Which is another kick in the guts.

So in Kate’s case, one of the most powerful set of forces operating in her social environment was the presence of her mother and the negative images and tension stemming from her lack of insight into her daughter’s condition. This was a major complicating or compounding influencea control or constraint standing in the way of a more therapeutic acceptance or resolution of her condition. Likewise in the case of ‘Kelly’, who described the onset of her issues with food in the following way:

Experiences of ‘Control’ in Anorexia Nervosa Treatment

53

Mum’s very controlling about food with all of me and my sisters. You weren’t allowed to eat at, like, when you got home from school or like you weren’t – she was just really really controlling. So we would all of us sneak food from the kitchen from between when we got home from school and she got home from work and so we’d all like cut the slice carefully and take it into our room and hide it in the desk draw and hide it for later. It was like a little game with my family so I guess we’d all sort of had… Food was just a big issue. I’ve tried to talk to my mum. I’ve tried to work it out with her why it was such a big issue for her. She had her own problems.

Here the pattern of family ‘culture’ or rules about access to food within the family is identified as a contributing factor in the emergence and continuation of Kelly’s anorexia. Again the ‘family food discipline’ is continuing to operate as a form of control into the present day.

Moral Career When a young woman does appear to gain greater insight into the anorexia and become more accepting of treatment interventions and maintenance of minimum weights, there is a tendency to see this as ‘progress’, and a lessening of the web of ‘control’. But is it really that she is ‘getting better’ or is she becoming more ‘managed’ and accepting the authority of her doctors? a. The ‘stage’ of the life-course of the illness ‘career’? ‘Time’ is a somewhat neglected variable in the sociology of mental health, the incorporation of which enables a richer understanding to be gained of: [H]ow social factors interact with the risk, expression, course, and outcomes of mental illness, taking into account the longer term context, at least in terms of age of onset, duration of the episode, history of past episodes, time to recovery and so forth (Bruce, 1999: 53).

Given its often chronic, fluctuating pattern, anorexia is one where the ‘stage’ of the condition is significant. Goffman's term ‘moral career’ is therefore an apt one to apply in studying this aspect of the changing experience reported by patients over the course of treatment (Aneshensel, 1999), just as has proved to be the case with another eating disorder, that of compulsive eating (O'Brien and Bankston, 1984). The concept of career traditionally focuses on the external attributes of the professional ‘position’ a person holds, its legal authority, the associated lifestyle, or the relationship to the ‘significant society’ or institutional complex. But for Goffman it was the personal interior which was significant, such as the ‘image of self and felt identity’. Or as he wrote in the essay on the ‘moral career of the mental patient’: [My] main concerns will be with the moral aspects of careerthat is, the regular sequence of changes that career entails in the person's self and in his framework of imagery for judging himself and others (Goffman, 1961: 119).

54

Terry Carney, Mim Ingvarson and David Tait

b. The ‘pre-patient’ and the ‘patient’ phases of identity. Goffman distinguished between the ‘pre-patient’ and the ‘patient’ phases of a sociological transition which he argues can serve to construct one’s ‘self identity’ (Goffman, 1961; 1968). Our data does not directly capture the early stages of the management of the pre-patient phase, but the resistance to acceptance of anorexia which characterised the state of mind of patients admitted to the RPA unit offered rich data on the possible transitions from pre-patient to patient and ‘managed patient’ phases (Pescosolido, Boyer and Lubell, 1999: 458). Goffman shows that the reaction of others to a person’s condition, once this reaction is internalised, can displace a person’s previous identity and see that identity reconceived (and processed) according to the expectations and requirements of more powerful players, such as clinicians and other networks (Aneshensel, 1999: 596). For instance a former mental patient residing in supported boarding accommodation may develop ‘classifications’ of those who can, and who cannot, readily take the next step back into fully independent living (Shaw, 1991). Part of that process for a person with anorexia entails convergence towards a new image of the ‘self’, including the constraints of the role and expectations about how to act as a group of fellow sufferers, and in relationships to staff (whose transition from general to say psychiatric nursing may exemplify a 'moral career': Caygill, 1993). One aspect of the pre-patient stage that Goffman identifies is the formation of an alliance, or even conspiracy, between the medical staff and the family. The latter are persuaded to take on the view of the person presented to them by medical authorities. This could lead to the person feeling further isolated and betrayed, as those who were believed to be supporters become revealed to be allies of psychiatrists (1961, 129). Families were torn between their desire to ‘support’ the family member or to ally themselves with the doctors. Guardianship can offer one way of addressing this dilemma, by appointing a person, independent of both family and treatment team, who can participate in treatment and lifestyle decisions. In his book on Stigma, Goffman wrote of the duality of self-images which emerge, one representing the viewpoint and values of so-called ‘normal’ society, the other the subjective experience of the person with the condition (Goffman, 1968: 45), and the four common ‘patterns’ of response to that dissonance: i) dual acquisition of both perspectives; ii) family insulation from outside perspectives serving to delay appreciation of societal attitudes; iii) late-in-lifecourse discovery of a devalued identity (either prospectively, leaving the past intact; or retrospectively, involving reconstruction of past identities; and iv) those socialised in the ‘alien’ community and who make the transition to values shared by the community at large (id, 45-49). Likewise Talcott Parsons’ work on the ‘illness career’, starting with perceptions of undifferentiated ‘symptoms’ (such as lack of good health), leading on into possible adoption of a social condition or ‘sick role’, and development of (medical practitioner-validated’) ‘patient’ roles. A trajectory culminatingat its most optimisticin ‘recovery’ following

Experiences of ‘Control’ in Anorexia Nervosa Treatment

55

treatment (Pescosolido, Boyer and Lubell, 1999: 443). But one where the network of family, friends and significant ‘others’ may mediate the choice of pathways taken (or resisted) at any one time (Pescosolido, 1991). c. Fieldwork illustrations of compromised identity. These frameworks provide a useful lens for understanding the way some anorexia patients ‘mould’ their behaviour to accommodate preservation of relationships with significant others, such as family, partners or therapists. Thus ‘Kate’, when discussing her relationship with her previous therapist, said: And so I was always used to keeping things to myself because ‘Mary’ said I was being provocative by voicing how I was feeling or just voicing how I felt about something, my perception of things, so that in the end I just had to tell her what she wanted to hear to keep her happy. (Emphasis added).

It is clear that Kate managed the way she presented her ‘public’ self in order not to unduly offend her therapist. Rather than fully express her feelings and thoughts, she kept certain things to herself. Obviously this avoided the tension and trauma of what she described as her more ‘provocative’ behaviour. But it also entailed a moulding of her relationship with the therapist, so thaton a superficial level at leastit was a ‘happier’ interaction. And, as a result of this internalisation of more negative thoughts, perhaps also a more ‘therapeutic’ relationship as well, in that there was more chance for mutual respect to build? Sometimes there is an intersection with the ‘suasive/coercive’ narrative as well however. Thus Kate also talked about conforming to clinicians expectations to avoid transfer into the public system: So I’ll just never forget that, of having to prove, and then that whole admission was one I think I mentioned where I was constantly, I was putting all my effort into trying to be such a good patient. I had to make sure that um, you know, that my reputation somehow had to be salvaged, even just a little bit. And that, um, went against me further down the track big time in myself. In my own, on my way to recovery really, set me back in my own way. It was just that if they didn’t accept me then they would transfer me to Royal Melbourne [Hospital]. I felt desperate, I didn’t want to be in there, but I knew I couldn’t leave. So, and I remember trying to leave once, and they put in a psychiatrist in front of me, she was Chinese, and she said she’d make me involuntary. So it was like I have to do this, be the good patient. (Emphasis added).

There are at least two forces at work in Kate’s mind here. First, she was concerned to preserve her ‘reputation’; her reputation as a ‘good patient’. Her identification with herself as a patient reflects an important transition: no longer a person in denial of being ‘ill’, she has been socialised into acceptance of the ‘sick role’. Consistent with the medical model of diagnosis, identification of cause and application of curative treatment’, Kate is at least prepared to talk the language of illness/recovery. Not only did she want to be good at ‘anorexia’ she also wanted to be good at being treated for ‘anorexia’. Good enough at ‘anorexia’ to need intensive inpatient care but good enough to be able to stay at her preferred inpatient care facility and to be considered a ‘good patient’.

56

Terry Carney, Mim Ingvarson and David Tait

Yet even this is a qualified acceptance: her identity is partly that of the cooperative patient, but it also has strong connotations of acceptance of her present place and regimen of treatment as an appropriate management of her ‘slightly deviant’ condition. Her language here seems little different to that of a person on probation, who has reconciled themselves to the advantage of being a ‘good’ probationer (just as people who are incarcerated usually become acculturated to being a ‘model’ prisoner). The second force at work is even more consistent with an analysis in terms of power, stigma and social control. For Kate is articulating a coldly rational analysis of the ‘least worst option’. She may not have enjoyed treatment where she was, but she was fearful of a ‘transfer to Royal Melbourne’. The threat of a transfer, playing on what she knew about that facility as well as on her uncertainty about the ‘unknown’, was a subtle but very effective expression of power which helped control her current compliance with her treatment. Because these future scenarios were playing on her mind at the time, Kate decided to be more cooperative. She internalised the disseminated forms of control operating in her clinical environment. This case is a classic illustration of what we mean when we say that power is a product of the intersection between personal identity (the ‘good patient’) and the highly disseminated ways in which power is dispersed in society, outside the formal legal system and authority structures usually the focus of attention by lawyers.

Conclusion Anorexia nervosa remains one of the difficult and frustrating conditions for medical staff, in part because of the resistance of patients to therapies intended to cure them. This may be experienced as ingratitude not just from patients themselves (who may be presumed to ‘lack insight’), but by feminist groups raising civil liberties objections. Obtaining informed consent is an ongoing concern, and developing compliance strategies becomes a major focus of the intervention. From the perspective of patients, enduring the regulatory regime imposed on them becomes a challenge and can be experienced as harsh and threatening. Issues of power and control are therefore major ongoing issues in the treatment of the condition. And yet, the law is rarely invoked, at least formally. Control is exercised not through the majesty of a court or tribunal order but through the routine practices of the clinic, through disciplinary practices embedded in everyday life. This includes daily routines of eating and washing, informal or written ‘contracts’ and other behavioural measures, regular surveillance and measuring, interactions with staff, visits and activities, and all the other rituals of institutional living. The regulatory regime does not just touch on practices; it is also explicitly targeted at identities. This includes self-image, and the attitudes to the body. It also shapes what Goffman refers to as the ‘moral career’ of the patient. This includes learning to play the ‘patient role’, to ‘be’ an ‘anorexic’, a credible exemplar of a condition. This role may be learned by observing and modeling oneself on peers, or by responding to the reactions of others. But a moral career may also lead to displaying signs of being on the road to recovery, whether through compliance with therapies or screening information suitable for the ears of

Experiences of ‘Control’ in Anorexia Nervosa Treatment

57

therapists. The language of ‘cure’ and ‘recovery’ providing a framework for an ongoing reshaping of identity. If intrusive medical and behavioural intervention to re-shape both practices and identities rarely engages the law, the question must be asked – why not? After all this is precisely the sort of situation where fundamental principles of right to life and right to control over one’s body come most acutely into collision. Is the law so clumsy that it fails to provide a mechanism for handling these issues in a timely and sensitive way? Or is the law being avoided because less restrictive options work most of the time? Our answer to these questions, based on an interpretation of Foucault, is that the regulatory regimes that shape the treatment of conditions such as anorexia nervosa, constitute, and in a sense, are ‘the law’. How ‘duty of care’ is operationalised in a hospital environment, how medical expertise has been translated into medical authority, how therapies are developed and tested through a scientific process, how interactions between ‘experts’, ‘carers’ and patients are mediated through conventions and rules, indeed how ‘empowerment’ is conscripted in the service of control―these practices and many more help to shape the regimes of governmentality that operate within the setting of the eating disorder clinic or hospital. Some of the ‘rules’ are based in part on legislation, or codes of ethics grounded in international covenants. But many of them are ‘informal’ in the sense that they operate outside, or ‘in the shadow of’, the formal legal system. What was perhaps most interesting about the use of the law for those included in this study was the way the possibility of legal orders provided a source of authority within the clinical setting. This could include foreshadowing, strategic lodging or withdrawal of applications, or use of guardianship to provide substitute consent rather than the more extensive mental health orders. Rather than ‘the law’ being something external that imposed itself upon patients and clinicians, it became instead a new source of power for medical therapists. Such a role for the law could perhaps be seen as ‘professional capture’ by those supposedly regulated by a legal regime, or an example of how a system set up to protect patient rights had the unintended consequence of strengthening medical authority. However there is another interpretation, based on Goffman’s understanding of the complicity involved in sustaining a role. Taking on the role of the patient involves ‘participating in reciprocally sustained fictions’ (1961, 142). The ‘fiction’ of acting ‘responsibly’ without coercion is an important part of the therapeutic framework in many contemporary treatments, and this fiction can best be sustained when legal coercion is not formally employed. Indeed the availability of legal measures may ironically reduce the need for physical constraints. The patient learns to provide consent ‘freely’, to make the ‘correct’ choices, to accept the ‘empowerment’ regime that is made even more convincing by the threat of legal intervention. In time the constraints learned in this way become part of the new role, that of the ‘recovering’ patient. The fiction employed so hesitantly at first becomes part of the new identity. The patient has become an active participant in the governance of self. The question posed by the therapeutic jurisprudence literature on the work of tribunals and other institutions (McMahon and Wexler, 2002/3; Freckelton, 2003) is whether this somewhat duplicitious alliance between law and medicine really does promote therapeutic outcomes (Wexler and Winick, 1996; Wexler, 2000; Winick, 2003). If tribunals and courts

58

Terry Carney, Mim Ingvarson and David Tait

have become an adjunct to medical authority rather than an independent check on it, how can we be sure that this authority is subject to appropriate accountability procedures? ‘Control’ so far as anorexia nervosa patients are concerned, is a highly nuanced, and quite diffuse and diverse concept. It is neither formal legal control, time-delayed imposition of coercion, nor social control achieved under the thrall (or in the ‘shadow’) of law. It is at times all of those things and much more. However the experiences reviewed here might we think best be captured by the label of ‘disseminated power and control’.

References Abusah, P. (1993). "Multicultural Influences in Case Management Transcultural Psychiatry." Mental Health in Australia, 5: 67-75. Ajzenstadt, M. and O. Steinberg (1995). "The Elasticity of the Law: Treating girls in distress in Israel through the shadow of the law." British Journal of Criminology, 35(2): 236-247. Alexander, N., M. Kohn, K. Feeney and S. Clarke (2000). "The Changing Faces of Anorexia Nervosa". In: M. Bashir, Bennett, D. (ed) Deeper Dimensions - Culture, youth and mental health. Parramatta, NSW, NSW Transcultural Mental Health Centre: 119-122. Aneshensel, C. (1999). "Mental Illness as a Career". In: C. Aneshensel, Phelan, J. (ed) Handbook of the Sociology of Mental Illness. New York, Kluwer Academic/Plenum: 585-603. Ben-Tovim, D. (2001). "Outcomes in Patients with Eating Disorders: A 5 year study." The Lancet, 357: 1254-57. Beumont, P. and T. Carney (2003). "Conceptual Issues in Theorising Anorexia Nervosa: Mere matters of semantics?" International Journal of Law and Psychiatry, 26(6): 585598. Beumont, P. and T. Carney (2004). "Can Psychiatric Terminology be Translated into Legal Regulation: The anorexia example." Australian and New Zealand Journal of Psychiatry, 38(10): 819-829. Bray, A. (1996). "The Anorexic Body: Reading disorders -The feminist interpretation of self starvation." Cultural Studies, 10: 413-419. Bruce, M. (1999). "Mental Illness as Psychiatric Disorder". In: C. Aneshensel, Phelan, J. (ed) Handbook of the Sociology of Mental Health. New York, Kluwer Academic/Plenum: 3755. Carney, T. (2002). "Regulation of Treatment of Severe Anorexia Nervosa: Assessing the options?" Australian Health Law Bulletin, 11(3): 25-32. Carney, T. and D. Saunders (2003). "Therapeutic Jurisprudence and Anorexia: A synergy?" Law in Context, 20(2): 54-73. Carney, T., D. Saunders, D. Tait, S. Touyz and M. Ingvarson (2004). "Therapeutic Pathways in Treatment of Severe Anorexia Nervosa." Contemporary Issues in Law, 7: 100-118. Carney, T., D. Tait, D. Saunders, S. Touyz and P. Beumont (2003). "Institutional Options in Management of Coercion in Anorexia Treatment: The Antipodean experiment." International Journal Law and Psychiatry, 26(6): 647-675. Carney, T., D. Tait, D. Saunders, S. Touyz, A. Wakefield and P. Beumont (2003). "Therapeutic Pathways in Treatment of Severe Anorexia Nervosa?" A paper delivered at

Experiences of ‘Control’ in Anorexia Nervosa Treatment

59

the conference: 28th Congress of the International Academy of Law and Mental Health, Sydney, 29 September- 3 October 2003. Carney, T., A. Wakefield, D. Tait and S. Touyz (2004). "Clinical and Demographic Dimensions of Coercion in the Treatment of Severe Anorexia Nervosa". A paper delivered at the conference: 39th RANZP Congress, Christchurch New Zealand, 10-13 May 2004. [Alison Wakefield presenting author] Caygill, J. (1993). "The Moral Career of the Psychiatric Nurse." New Zealand Sociology, 8(2): 137-165. Cheek, J. and S. Porter (1997). "Reviewing Foucault: Possibilities and problems for nursing and health care." Nursing Inquiry, 4(2): 108-19. Davis, S. (2002). "Autonomy versus Coercion: Reconciling competing perspectives in community mental health." Community Mental Health Journal, 38(3): 239-50. Dawson, J. (1996). "Psychopathology and Civil Commitment Criteria." Medical Law Review, 4: 62-83. Drake, R., S. Bartels, G. Teague, D. Noordsy and R. Clark (1993). "Treatment of Substance Abuse in Severely Mentally ill Patients." Journal of Nervous and Mental Disease, 181(10): 606-11. Draper, H. (2000). "Anorexia Nervosa and Respecting a Refusal of Life-prolonging Therapy: A limited justification." Bioethics, 14(2): 120-33. Dresser, R. (1984). "Feeding the Hunger Artists: Legal issues in treating anorexia nervosa." Wisconsin Law Review, [1984]: 297-374. Foucault, M. (1997). "Psychiatric Power". In: P. Rabinow (ed) Michael Foucault 'Ethics': Subjectivity and Truth. London, Penguin: 39-50. Freckelton, I. (2003). "Mental Health Tribunal Decisionmaking: A therapeutic jurisprudence lens." Psychiatry, Psychology and Law, 10(1): 44-62. George, L. (1999). "Life-course Perspectives on Mental Health". In: C. Aneshensel, Phelan, J. (ed) Handbook of the Sociology of Mental Health. New York, Kluwer/Plenum: 565583. Gilmore, J. (1994). "Young Women and Eating Issues: A feminist perspective." Youth Issues Forum, Summer: 14-16. Glass, J. (2000). "Counseling and the Therapeutic State." Journal of Nervous and Mental Disease, 188(8): 549-550. Goffman, E. (1961). Asylums: Essays on the social situation of mental patients and other inmates. New York, Doubleday. Goffman, E. (1968). Stigma: Notes on the management of a spoiled identity. Harmondsworth, UK, Penguin. Griffiths, R. (1996). "Compulsory Treatment and Anorexia Nervosa." Australian Journal of Forensic Sciences, 28: 35-38. Harlow, C. (1998). "Public Service, Market Ideology, and Citizenship". In: M. Freeland and S. Sciarra (ed) Public Services and Citizenship in European Law. Oxford, Clarendon: 4956. Hiday, V., M. Swartz, J. Swanson, R. Borum and H. Wagner (2002). "Coercion in Mental Health Care". In: P. Backlar, Cutler, D. (ed) Ethics in Community Mental Health Care: Commonplace concerns. New York, Kluwer/Plenum: 117-136.

60

Terry Carney, Mim Ingvarson and David Tait

Holmes, D. and D. Gastaldo (2002). "Nursing as Means of Governmentality." Journal of Advanced Nursing, 38(6): 557-565. Jacob, H. (1992). "The Elusive Shadow of the Law." Law and Society Review, 26(3): 565590. Main, B. G. M. and A. Park (2000). "The British and American rules: An experimental examination of pre-trial bargaining in the shadow of the law." Scottish Journal of Political Economy, 47(1): 37-60. Main, B. G. M. and A. Park (2002). "The Impact of Defendant Offers into Court on Negotiation in the Shadow of the Law: Experimental evidence." International Review of Law and Economics, 22(2): 177-192. McMahon, M. and D. Wexler, Eds. (2002/3). Therapeutic Jurisprudence. Special Issue: Law in Context. Sydney, Federation Press. Mnookin, R. and L. Kornhauser (1979). "Bargaining in the Shadow of the Law: The case of divorce." Yale Law Journal, 88: 950-997. Newman, L., J. Russell and P. Beumont (1995). "Issues in the Treatment of Very Low Weight Anorexics". In: D. Kenny and R. SoamesJob (ed) Australia's Adolescents: A health psychology perspective. Armidale, University of New England Press: 53-58. Noordsy, D., C. Mercer and R. Drake (2002). "Involuntary Interventions in Dual Disorders Programs". In: P. Backlar, Cutler, D. (ed) Ethics in Community Mental Health Care. New York, Kluwer Academic/Plenum: 95-114. O'Brien, M. and W. Bankston (1984). "The Moral Career of the Reformed Compulsive Eater: A study of conversion to charismatic conformity." Deviant Behavior, 5(1-4): 141-150. Pescosolido, B. (1991). "Illness Careers and Network Ties: A conceptual model of utilization and compliance." Advances in Medical Sociology, 2: 161-184. Pescosolido, B., C. Boyer and K. Lubell (1999). "The Social Dynamics of Responding to Mental Health Problems". In: C. Aneshensel and J. Phelan (ed) Handbook of the Sociology of Mental Health. NY, Kluwer Academic/Plenum: 441-460. Powers, P. (2003). "Empowerment as Treatment and the Role of Health Professionals." Advances in Nursing Science. Health Variables: Economics and Class., 26(3): 227-237. Rabinow, P. (1997). "Introduction: The History of Systems of Thought". In: P. Rabinow (ed) Michael Foucault 'Ethics' Subjectivity and Truth. London, Penguin. 1: xi-xlii. Ramsay, R., A. Ward, J. Treasure and G. Russell (1999). "Compulsory Treatment in Anorexia Nervosa." British Journal of Psychiatry, 175: 147-153. Rathner, G. (1998). "A Plea Against Compulsory Treatment of Anorexia Nervosa Patients". In: W. Vandereycken, Beumont, P. (eds) (ed) Treating Eating Disorders: Ethical, legal and personal issues. London, The Athlone Press. 1: 179-215. Saunders, D. (2001). "Treatment of Severe Anorexia: A role for law in therapy?" Law Institute Journal, 11: 69-71. Shaw, L. (1991). "Stigma and the Moral Careers of Ex-Mental Patients Living in Board and Care." Journal of Contemporary Ethnography, 20(3): 285-305. Shearing, C. and P. Stenning (1984). "From the Panopticon to Disney World: The development of discipline". In: A. Doob and E. Greenspan (ed) Perspectives in Criminal Law: Essays in Honour of John LL.J Edwards. Ontario., Canada Law Book: 335-349.

Experiences of ‘Control’ in Anorexia Nervosa Treatment

61

Steiger, H. and J. Séguin (1999). "Eating Disorders: Anorexia nervosa and bulimia nervosa". In: T. Million, Blaneyu, P., David, R. (ed) Oxford Textbook of Psychopathology. New York, Oxford University Press: 365-88. Steinberg, R. (2002). "In the Shadow of Law or Power? Consensus-based bargaining and outcomes in the GATT/WTO." International Organisation, 56(2): 339-374. Tait, D., M. Ingvarson, A. Wakefield, S. Touyz and T. Carney (2003). "Experiences of Coercion: The stories of young women with anorexia nervosa". A paper delivered at the conference: 28th Congress of the International Academy of Law and Mental Health, Sydney, 29 September-3 October 2003. Tait, G. (1993). "Anorexia Nervosa: Asceticism, differentiation, government." Australian and New Zealand Journal of Sociology, 29: 194-208. Tomkiewicz, S. (2003). "Entretien avec Stanislav Tomkiewicz". In: M. Balinska (ed) Retour a la vie: quinze ans d'anorexie. Paris, Odile Jacob: 251-260. Watson, T., W. Bowers and A. Andersen (2000). "Involuntary Treatment of Eating Disorders." American Journal of Psychiatry, 157: 1806-1810. Wexler, D. (2000). "Therapeutic Jurisprudence: An Overview." Thomas Cooley Law Review, 17: 125-134. Wexler, D. and B. Winick, Eds. (1996). Law in a Therapeutic Key: Developments in therapeutic jurisprudence. Durham, NC, Carolina Academic Press. White, R., P. Bebbington, J. Pearson, S. Johnson and D. Ellis (2000). "The Social Context of Insight in Schizophrenia." Social Psychiatry and Psychiatric Epidemiology, 35(11): 5007. Winick, B. (2003). "A Therapeutic Jurisprudence Model for Civil Commitment". In: K. Diesfeld and I. Freckelton (ed) Involuntary Detention and Therapeutic Jurisprudence. Aldershot, Ashgate: 23-54. Young, S. (1998). "Body Talk: Some thoughts on anorexia." Australian and New Zealand Journal of Family Therapy, 19(2): 63-67.

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 63-90 © 2006 Nova Science Publishers, Inc.

Chapter IV

Secondary Anorexia: A Neglected Issue in the Optimal Management of Patients Suffering from Acute and Chronic Diseases Alessandro Laviano*, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli Department of Clinical Medicine, University La Sapienza, Rome, ITALY Department of Surgery, University Hospital, SUNY Upstate Medical University, Syracuse, NY, USA

Abstract Anorexia and reduced food intake are relevant issues in the management of patients suffering from acute and chronic diseases, including sepsis, cancer, chronic liver failure, chronic renal failure, etc. In acute diseases, anorexia does not represent a primary therapeutic target, since effective treatment of the underlying disease rapidly ameliorates food intake. In chronic diseases, anorexia impacts on patients’ prognosis, since it contributes to the development of malnutrition, thereby increasing morbidity and mortality, and impinges on quality of life. Accumulating evidence indicate that anorexia associated to different diseases is multifactorial in its pathogenesis, and suggest that most of the hypothalamic neuronal signalling pathways modulating energy intake are involved. A number of factors are considered mediators of anorexia, including hormones [e.g., leptin], neuropeptides [e.g., NPY], cytokines [e.g., IL-1, IL-6, TNF] and neurotransmitters [e.g., serotonin and dopamine]. Their modes of action do not appear to be separate and distinct, rather they are closely inter-related. However, convincing *

Correspondence: dr. Alessandro Laviano, Department of Clinical Medicine, University La Sapienza, viale dell'Università 37, 00185 Rome, ITALY; tel: +39-06-49973902; Fax: +39-06-4440806; E-mail: [email protected]

64 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli evidence suggest that a hierarchical organization exists in which cytokines play a key role, triggering the complex neurochemical cascade which leads to the onset of anorexia. Cytokine increased expression during disease inhibits the hypothalamus to appropriately respond to peripheral signals, by persistently activating anorexigenic systems and/or inhibiting prophagic pathways. Hypothalamic monoaminergic neurotransmission may significantly contribute to these effects. Thus, the optimal therapeutic approach to anorectic patients should be based on both changes in dietary habits, achieved via nutritional counselling, and drug therapy, aimed at interfering with cytokine expression or hypothalamic monoaminergic neurotransmission.

Key Words: anorexia, food intake, malnutrition, chronic diseases, brain monoamines, hypothalamus

Introduction Anorexia is a very well-known word among general audience. Very often newspapers and TV news report dramatic stories about young girls who let themselves starve to death because they could no longer stand their physical shape, whose perception has become pathologically deranged. Therefore, common people, but some physicians as well, believe not only that anorexia and anorexia nervosa are synonymous, but more importantly that there is no clinically relevant syndrome characterized by reduced food intake other than anorexia nervosa. Actually, the clinical problem of reduced appetite and food intake is much more pervasive than that represented by anorexia nervosa alone. Indeed, almost every disease, either acute or chronic, is associated with the loss of appetite. In this light, although the prevalence of anorexia nervosa is raising among young girls in western countries, it is much smaller than the prevalence of secondary anorexia, i.e., the anorexia occurring in patients suffering from acute or chronic diseases. If we consider that secondary anorexia characterizes highly prevalent diseases (cancer, liver cirrhosis, chronic renal failure, chronic obstructive pulmonary disease, ) while secondary anorexia occurs in specific populations, the overall magnitude of the clinical issue represented by secondary anorexia becomes self-evident, anorexia nervosa thus representing the tip of the iceberg. Also, an important difference between anorexia nervosa and secondary anorexia should not be overlooked: young girls suffering from anorexia nervosa do feel hunger, but they force themselves not to eat; anorectic cancer patients, or uremic patients, or liver cirrhosis patients really would like to eat, but they can’t because they lost their appetite.

Definition In medicine, diagnosis is made based on specific combinations of symptoms and signs. However, symptoms or constellations of symptoms [i.e., syndromes] per se may not be specific of a single disease. In this light, the anorexia syndrome represents a suitable example, since it characterizes the clinical course of different diseases. Therefore, anorexia is a highly prevalent syndrome which heavily impacts on the prognosis of patients suffering

Secondary Anorexia

65

from acute (i.e., sepsis) and chronic diseases (i.e., cancer, liver cirrhosis, chronic renal failure, COPD). Anorexia is defined as the loss of the desire to eat, leading very often to reduced food intake. As a consequence, reduced calorie intake should not be considered as being part of the clinical definition of anorexia, rather its consequence. However, based on their strict interdependence, they are often used as synonymous. Anorexia is among the physiologic responses, including immune system activation and increased energy expenditure, prompted in the host by internal/external insults. Initially, all these changes are believed to help the host organism to fight back the invasion. As far as anorexia is concerned, the beneficial effect is usually supposed to be related to a number of mechanisms. First, the host saves energy by not moving around in search for food, and this also reduces heat loss that would otherwise occur from increased convection. The conserved energy is then available for the body’s fight against disease. Second, the suppression of food intake during disease may be important in reducing the availability of nutrients essential for invading organisms and reducing energy expenditure for digestion. The beneficial effect of the initial anorexia during disease is supported by a classic study in which force-feeding of experimentally infected mice increased mortality rate [1]. Nevertheless, despite being beneficial in the beginning, long lasting anorexia compromises host defence and ultimately delays recovery. As a consequence, the clinical relevance of anorexia varies according to the time course of the underlying diseases. In acute clinical states [i.e., sepsis or influenza infection], anorexia does not represent a therapeutic target, since the quick and effective treatment of the underlying disease is the main goal inevitably leading to amelioration of eating behaviour. In chronic clinical states, anorexia should be considered and treated because its long lasting effects on food intake and quality of life impact on patient’s nutritional and psychological status, and therefore on his/her prognosis. Despite the well-known effects of anorexia on patients’ prognosis, the interest of clinicians toward this syndrome is much less than it should be deserved. As an example, cancer anorexia is highly prevalent and clinically relevant. Yet, very often oncologists do not consider it as a symptom deserving investigation and treatment. An insight on the reasons for their negative attitude toward anorexia, and more broadly toward supportive care, can be drawn by a recent survey of the European Society of Medical Oncology [2]. Approximately 900 oncologists responded to the survey, the large majority of them being from Europe and involved with advanced cancer patients. Interestingly, almost all of the responding oncologists agreed that all advanced cancer patients should receive concurrent supportive care, even if they are receiving antitumour therapy, and that medical oncologists should be expert in the management of physical and psychological symptoms of advanced cancer. Yet, only a minority of respondents reported to collaborate often with a supportive care specialist, while 42% felt that they were inadequately trained to this task. Surprisingly, 15% of respondents still believed that palliative care begins when medical oncology ends, while an astonishing 30% did not disagree with the statement “palliative care specialists steal patients who would otherwise benefit from medical oncology”. Therefore, it appears that most oncologists recognize the importance of supportive care for patients with advanced cancer. Despite this, many are prepared inadequately for these tasks, and actual participation levels

66 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli commonly are suboptimal. On a broader perspective, it could be concluded that clinicians may be aware of the clinical impact of anorexia, but their training to recognize and treat anorexia is not sufficient.

Diagnostic Tools It is still difficult to clearly define and diagnose anorexia. Sometimes, a visual analogue scale is used, which is a useful tool in epidemiological or prospective studies but may prove quite unreliable if small changes in appetite need to be detected [3]. Very often, the diagnosis of anorexia is based on the presence of reduced energy intake, even if this procedure could be misleading, since the reduction of ingested calories might be the consequence of dysphagia or depression rather than the sign of anorexia, as previously mentioned. To reliably assess the presence of anorexia, a number of symptoms interfering with food intake and likely related to changes in the central nervous system control of energy intake has been identified (Table I)[4]. Patients reporting at least one of these symptoms are defined as anorectic. The use of questionnaires to diagnose anorexia is rapidly increasing, thus highlighting their feasibility and reliability in different clinical settings. However, considering that questionnaires provide only a qualitative assessment of the presence of anorexia, it may appear advisable to also quantify the degree of anorexia via the administration to the patient of a visual analogue scale. Table I: Symptoms interfering with food intake and related to changes in the central nervous system regulation of energy intake. Patients reporting at least one of these symptoms are defined as anorectic [see ref. 4]. SYMPTOMS early satiety taste alterations smell alterations meat aversion nausea/vomiting

Prevalence As a consequence of the difficulties in clearly defining and diagnosing anorexia, its prevalence in different clinical conditions is yet to be precisely assessed. A clear example is given by the anorexia of cancer. In 300 cancer patients, Geels et al. identified the nine most common symptoms using patients’ responses to a quality-of-life questionnaire as well as using graded toxicity data collected on case report forms [5]. By using case report forms, which closely reflect the attitude of clinicians in investigating specific symptoms, anorexia

Secondary Anorexia

67

was detected in approximately 13% of patients, while using the quality-of-life questionnaire 55% of patients were diagnosed as anorectic [5].

Cancer An acceptable estimate of the prevalence of cancer anorexia can be derived from a number of papers which show that approximately 50% of cancer patients upon diagnosis report abnormalities of eating behaviour [6, 7]. This figure might slightly overestimate the actual prevalence of cancer anorexia, but it must be reminded that it is generally acknowledged that anorexia and reduced food intake are frequently encountered in cancer patients [7]. Moreover, anorexia is usually the symptom urging the patients to refer to their physicians, and its alleviation is perceived as a sign of benign evolution of the disease. Prevalence data are more reliable in terminally ill cancer patients. In this subset of patients, the prevalence of anorexia ranges between 60% and 65% [8, 9]. Based on these alarming figures and considering that 20% of cancer deaths are due to malnutrition per se [10], it is reasonable to conclude that many cancer patients are starving to death.

Liver Cirrhosis Similarly to what is observed in the course of neoplastic disease, patients suffering from chronic liver failure frequently experience anorexia. In a recent paper, Marchesini et al. assessed the presence of anorexia in 174 patients with advanced liver cirrhosis (Child-Pugh score ≥7; Class B or C), using the guiding symptoms previously mentioned. Data obtained show that more than 50% of patients were anorectic [11].

Chronic Renal Failure In this clinical setting, anorexia is among the most important causes of malnutrition. It is pervasive in patients on conservative treatment and very common in patients on hemodialysis [12]. Indeed, Kalantar-Zadeh et al. studied a cohort of 331 maintenance hemodialysis outpatients and demonstrated that diminished appetite was reported by 128 patients, i.e., 38% of the entire cohort [13].

Chronic Obstructive Pulmonary Disease [COPD] In COPD patients, the prevalence of anorexia is particularly high, since most patients suffer from breathlessness which affects food intake. Recent data indicate that 67% of chronic lung disease patients experience anorexia during the last year of life, this figure not being much different from the prevalence of anorexia among lung cancer patients, i.e. 76% [14]. More striking, however, are data showing that despite COPD patients have physical and

68 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli psychosocial needs at least as severe as lung cancer patients, their symptoms, including anorexia, receive much less attention from health care professionals [14].

Congestive Heart Failure [CHF] In this clinical setting, the assessment of the prevalence of anorexia is made difficult by the high proportion of patients suffering from dyspnea, peaking at 90% in the last stages of the disease [15]. Severe nausea has been reported affecting approximately 10% of CHF patients [16], but the actual prevalence of anorexia may well be higher [17].

Clinical Impact The onset of anorexia significantly impacts on the clinical course of the disease. It contributes to the development of malnutrition and cachexia, since it reduces the oral intake of calories thus further promoting skeletal muscle wasting. Also, it exacerbates the detrimental effects of disease-related alterations of protein metabolism on nutritional status, eventually leading to increased morbidity and mortality [18]. On the other hand, the metabolic dysregulation of cachexia [19] sustains and corroborates the neurochemical alterations responsible of anorexia. The clinical relevance of anorexia is underscored by its role as an independent prognostic factor in terminally ill cancer patients, being as reliable in predicting survival as well-defined prognostic factors, including Karnofsky Performance Status and Clinical Prediction of Survival [9, 20]. Similar data have been obtained in chronic renal failure: in maintenance hemodialysis patients, diminished appetite is associated with poor clinical outcome, including a 4-fold increase in mortality and a greater hospitalization rates [13]. Finally, anorexia and reduced energy intake impinge on quality of life, which is now becoming a critical endpoint in the management of patients as well as in designing clinical trials [21]. An interesting and emerging aspect of the clinical impact of anorexia is its influence on patients’ quality of life. This issue has been specifically raised in cancer patients, in whom anorexia is pervasive and much effort has been devoted to improve food intake. It is selfevident that in humans, food and food intake are much more than calories, nutrients and digestion. Special events are celebrated with food, people often discuss of economic opportunities while eating, friendship is strengthened by sharing the same food. Consequently, cancer patients, and patients suffering from other chronic diseases as well, point to anorexia as one of the most psychologically disturbing symptoms of cancer and anorexia is frequently found as a major contributor to reduced quality of life. Therefore, cancer anorexia should represent a major therapeutic goal and its alleviation should lead to improved quality of life. Since cancer anorexia can be effectively treated or at least its severity dampened [22], it would be expected that the alleviation of anorexia should be associated with significantly improved quality of life. Unfortunately, as recently outlined by Jatoi et al. [23], almost none of the clinical trials reporting improvements in appetite

Secondary Anorexia

69

following drug therapy also reported improved quality of life, as assessed by a number of different tools. Many possible explanations have been proposed for this apparent inconsistency, including undesirable effects of appetite stimulants, insufficient reliability and/or complexity of quality of life assessing tools, insufficient statistical power of the available data, the “soretooth-tight-shoe” phenomenon, i.e., cancer patients complain of different symptoms and relief of anorexia would simply shift symptomatology [23]. Alternatively and provocatively, it could be questioned whether cancer anorexia and starvation to death represent horrifying symptoms to the surviving relatives rather than to the dying patients. Ganzini et al. recently conducted a survey to characterize the experience of dying among terminally-ill patients who make the choice to stop eating and drinking to hasten death, this experience somewhat resembling severe anorexia [24]. The authors mailed all nurses employed by hospice programs in Oregon, USA, and analyzed the results. On the basis of reports by nurses, patients in hospice care who voluntarily choose to refuse food and fluids usually die a “good” death within two weeks after stopping food and fluids. Considering that anorexia alleviation has never been demonstrated to lead to enhanced quality of life, or improved morbidity and mortality, should we care about anorexia in cancer patients? Certainly yes, because of the psychological value of appetite rather than for its caloric sequelae. As brilliantly pointed out by Jatoi et al., anorexia “is important in its own right—independent of global quality of life, independent of survival, and independent of any other clinical end point” [23].

Pathogenesis of Anorexia The pathogenesis of anorexia is multifactorial and related to disturbances of the central physiological mechanisms controlling food intake, but the precise neurochemical mechanisms are still matter of debate. However, by understanding how energy intake is physiologically controlled, insights might be obtained. Under normal conditions energy intake is controlled within the hypothalamus by specific neuronal populations which integrate peripheral signals conveying information on energy and adiposity status [25]. In particular, the arcuate nucleus of the hypothalamus transduces these inputs into neuronal responses and, via second order neuronal signalling pathways, into behavioural responses (Figure 1). Intuitively, anorexia might be secondary to defective signals arising from the periphery, due to an error in the transduction process, or to a disturbance in the activity of the second order neuronal signalling pathways.

Role of Peripheral Signals The hypothesis that peripheral signals are involved in the pathogenesis of anorexia is intriguing. Among the large series of peripheral signals [Table II], the hormone leptin exerts a strong negative influence on food intake.

70 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli

Hypothalamus

NPY/AgRP peripheral signals

modulation of food intake POMC/CART arcuate nucleus

Figure 1: in the hypothalamus, the arcuate nucleus receives information from the periphery and intergrates these inputs to modulate food intake [NPY: neuropeptide Y; AgRP: agouti-related protein; POMC: proopiomelanocortin; CART: cocaine-amphetamine related transcript].

Table II: Signals arising from the periphery and influencing food intake SIGNALS Adiposity signals Gut-derived signals

Energy signals

leptin insulin CCK ghrelin PYY glucagon-like peptide-1 oxyntomodulin intracellular malonyl-CoA

Hormones a) Leptin Leptin is produced primarily by adipocytes in proportion to body fat. It reaches the brain and a raise in its circulating levels results in inhibition of energy intake. Thus, leptin is an intuitive likely mediator of anorexia, particularly because its synthesis and secretion appear to be stimulated by cytokines, recognized anorexigenic factors [26]. However, results from animal and clinical studies are controversial [27-29], and do not seem to support this hypothesis. More recently, Bing et al. significantly contributed to the debate by showing in

Secondary Anorexia

71

an animal model that anorexia develops despite the normal regulation of leptin synthesis [30]. Consistently with animal data, Mantovani et al. showed that in anorectic cancer patients, circulating leptin levels are lower than those of healthy individuals, while no difference exists between cancer patients and healthy individuals in the production of leptin by peripheral blood mononuclear cells [31]. Similar data questioning the role of circulating leptin in the pathogenesis of anorexia of chronic renal failure patients undergoing dialysis have been recently published [32, 33]. Rather, they suggest that leptin in these patients may represent a marker of inflammation [32]. Supporting a common pathogenic mechanism for the anorexia associated with different diseases, Ben-Ari et al. showed that in chronic liver disease serum leptin appears a passive marker and not a cause of anorexia [34]. When considered together, these data suggest that peripheral leptin synthesis is preserved during disease, and point to a central dysregulation of the physiological feedback loop. b) Insulin Food intake triggers a complex cascade of neurochemical events that signal nutrient and energy availability in the central nervous system, down regulate stimulators, activate anorexigenic factors, including brain insulin, and result in reduced eating. Insulin reaches the brain from the periphery, but intracerebral insulin synthesis has been also demonstrated. Brain insulin has anorexigenic effects, but its mechanism of action needs to be further elucidated. However, consisting evidence show that brain insulin interacts with different anorexigenic and orexigenic pathways to modulate their activity and thus food intake [for review, see ref. 35]. Similarly, different factors are able to regulate insulin release directly in the hypothalamus. Particularly, leptin and melanocortins, anorexigenic peptides, are highly interactive with insulin in the central nervous system, probably via the neurotransmitter serotonin. In the hypothalamus, insulin and leptin share a common signaling pathway involved in food intake, namely the insulin receptor substrate, phosphatidylinositol 3-kinase pathway. Disrupted brain insulin signalling in obesity and diabetes has been proposed, but its involvement in secondary anorexia received less attention by reasearchers. However, Sato et al. recently demonstrated a possible role for insulin in cytokine-induced anorexia, using an experimental model [36]. c) Cholecystokinin (CCK) CCK is probably the most extensively studied satiety signal, i.e., an endogenous factor that causes a sensation of fullness and reduces the size of an ongoing meal [for review, see ref. 37]. CCK is secreted from duodenal cells in response to nutrients in the lumen, but intracerebral CCK synthesis has been described. Some of the secreted CCK enters the blood and stimulates the secretion of appropriate enzymes into the duodenum to facilitate digestion. However, CCK influence food intake and particularly meal size, via a more complex mechanism. Some of the CCK released after nutrients stimulus into the duodenum acts in a local paracrine manner to stimulate CCK1 receptors on the sensory fibers of the vagus nerves, which is simultaneously sensitive to both CCK and other stimuli such as gastric distension, via other branches emanating from the gastric wall. Therefore, individual vagal neurons are able to integrate different kinds of signals relevant to ingestion. Then, the CCK signal enters

72 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli the hindbrain, where it initiates local reflexes and interacts with central pathways to modulate food intake. The involvement of CCK in secondary anorexia is debated: it appears unlikely in cancer anorexia, while contrasting results have been obtained in the anorexia of aging [38, 39]. d) Ghrelin More recently, the prophagic hormone ghrelin has received considerable interest as a putative mediator of cancer anorexia. Ghrelin is produced by gastric cells and under physiological conditions its circulating levels raise before feeding and stimulate food intake via intra-hypothalamic effects [40]. Consequently, it is conceivable to hypothesize that during tumour growth ghrelin circulating levels may drop leading to the onset of anorexia. Unfortunately, recent data obtained in cancer patients show that plasma ghrelin levels are higher than in healthy individuals, being even higher in patients with cachexia [41]. These data suggest that anorectic cancer patients might be resistant to the appetite-stimulating effects of ghrelin. Also, animal data obtained with ghrelin-deficient mice appear to suggest that ghrelin is not a critical orexigenic factor and, rather, support the hypothesis that ghrelin’s principle physiological role may be in the determination of the type of metabolic substrate (i.e., fat vs. carbohydrate) that is used for maintenance of energy balance, particularly under conditions of high fat intake [42]. Therefore, the impaired ability of target organs, including the hypothalamus, to respond to ghrelin, rather than the actual circulating levels of the hormone, appears to mediate cancer anorexia. However, this suggestion does not imply that supraphysiologic doses of exogenous ghrelin may not be effective in ameliorating anorexia, although it is likely that this therapeutic approach may progressively worsen ghrelin resistance of anorectic patients. e) PYY PYY is a peptide secreted from the entire gastrointestinal tract [40]. However, the number of PYY immunoreactive cells increases in the most distal sections of the gastrointestinal tract, being at a very high level in the rectum. Food intake, but also CCK, trigger the release of PYY, whose circulating concentrations peak at 1–2 h post ingestion and are influenced by both the number of calories and the composition of the food consumed. PYY is present in two forms, PYY [1–36] and PYY [3–36], the latter being the major circulating form. PYY [3–36] has been shown in normal-weight human volunteers and in obese subjects to reduce caloric intake by 30%. Interestingly, the effects of PYY are orexigenic when administered centrally. Considering its anorexigenic properties, PYY represents a suitable mediator of anorexia, but its role in secondary anorexia has not been investigated yet. f] Glucagon-like peptide-1 (GLP-1) and oxyntomodulin (OXM) GLP-1 and OXM are proglucagon-derived peptides, i.e., derive from the cleavage of the preproglucagon gene, which is expressed in the central nervous system, in the small intestine and in the pancreas. OXM and GLP-1 are satiety signals, and they are rapidly released after food ingestion at levels in proportion to calorie intake [40]. Their anorexigenic effects are likely mediated by the vagal nerve, as discussed for CCK. However, both GLP-1 and OXM

Secondary Anorexia

73

reduce food intake when administered centrally, thus suggesting a direct anorexigenic effect. The mechanism of action need to be better elucidated, but GLP-1 and OXM interact with a number of pathways to modulate food intake, including ghrelin and insulin. Both GLP-1 and OXM are thought to exert their effects via the GLP-1 receptor [GLP-1R]. Interestingly, GLP1 and OXM, which are structurally distinct, differentially regulate food intake and energy expenditure by interacting with a GLP-1R-dependent pathway [43]. Therefore, ligandspecific activation of a common GLP-1R increases the complexity of gut-brain pathways regulating energy homeostasis. The involvement of GLP-1 and OXM in secondary anorexia has not been investigated, nor in experimental or human models.

Energy Signals Similarly to changes in fat mass, also changes in energy metabolism influence energy intake in a leptin-independent manner via energy signals. Conceptually, energy signals differ from classic peripheral signals, since they are generated within the hypothalamic neurons controlling energy intake. A number of studies suggest that a metabolic control of food intake also exists, in which the biochemical partitioning between fatty acid oxidation and synthesis represents a key signal indicating catabolic or anabolic energy status [44]. Energy signals are independent from leptin pathway and they inform the brain on the metabolic switch occurring at a subcellular level between fatty acid oxidation and synthesis [45]. Under physiological conditions, food intake is accompanied by increased intracellular levels of malonyl coenzyme A (malonyl-CoA)[46], which is a potent signal reducing food intake, via inhibition of the synthesis of the prophagic factor neuropeptide Y (NPY)[45]. It is therefore tempting to speculate that energy signals could contribute to anorexia, possibly via a deranged "sensing" of the energy metabolism during disease. Supporting evidence show that during tumour growth, fat metabolism is altered leading to decreased fatty acid oxidation [47] and possibly increased intracellular malonyl-CoA levels. Also, the supplementation of carnitine, which is involved in fatty acid oxidation, ameliorates anorexia in pathophysiological conditions [48]. However, more studies are needed to verify the involvement of energy signals in anorexia.

Role of Second Order Neuronal Signalling The hypothalamic arcuate nucleus, where peripheral signals mainly converge, projects to other hypothalamic areas, thus interacting with a number of neuronal populations [25]. Many pathways have been described serving as second order neuronal signalling pathways, including orexins A and B, but their involvement in the pathogenesis of anorexia has so far received little attention, but it cannot be excluded. In a recent study, Li et al. showed that the loss of renal function in Wistar rats reduces hypothalamic orexin A, a prophagic mediator [49], which in turn may contribute to the development of anorexia. Evidence exist suggesting that disease-associated metabolic changes, and particularly alterations of protein turnover, may impact on the neurochemistry in localized brain areas

74 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli [50]. However, they appear to have a role in sustaining and corroborating anorexia, while its onset seems to be secondary to the inability of the hypothalamus to recognize and respond appropriately to consistent peripheral signals [51].

Role of Neuropeptides Consistent and convincing evidence suggest that disease-associated anorexia is brought about by the derangement of the hypothalamic system transducing peripheral signals into neuronal responses. Under normal conditions, peripheral signals interact with two separate neuronal populations within the arcuate nucleus: the NPY/Agouti-related peptide (AgRP) neurons, stimulating food intake, and the pro-opiomelanocortin [POMC]/cocaine- and amphetamine-regulated transcript (CART) neurons, inhibiting food intake [for review see ref. 25]. As a consequence, when energy intake needs to be initiated, peripheral signals activate the NPY/AgRP pathway, simultaneously inhibiting the POMC/CART pathway. When energy intake needs to be inhibited, peripheral signals inhibit the NPY/AgRP pathway while simultaneously activating POMC/CART neurons and thus upregulating the expression of a number of POMC/CART pathway-related factors, including α-melanocyte stimulating hormone [α-MSH] and corticotropin releasing hormone (CRH). Because of the central role of these neuronal pathways, they were postulated as putative mediators of anorexia. A number of studies investigated the role of the prophagic signal NPY in the pathogenesis of anorexia. In cancer, the results obtained in animal models and humans are conflicting [52-55]. However, it seems that a dissociation exists between NPY mRNA levels and actual NPY levels, which appear decreased. Indeed, recent data show a decrease of NPY and NPY-immunoreactive neurons in the hypothalamus of anorectic tumour bearing rats [56, 57]. These data suggest that NPY is involved in cancer anorexia, but it is difficult to assess the extent of the involvement. In chronic renal failure, animal and human studies consistently show a reduction of NPY [49, 58]. However, and similarly to cancer, it is not clear whether NPY should be considered as a mediator or a marker of anorexia. Results from studies investigating the role of the hypothalamic anorexigenic pathway POMC/CART in anorexia appear more convincing. Unfortunately this line of investigation has been pursued in cancer anorexia only, but it is likely that the pathogenic mechanisms hypothesized for cancer anorexia might well be operating during the clinical course of other diseases. It has been repeatedly demonstrated that by blocking the hypothalamic melanocortin system, using either its physiological inhibitor (i.e., AgRP) or the synthetic compound SHU9119, food intake is restored in tumour bearing animals, and the development of cachexia is prevented [59, 60]. Similar results have been obtained in melanocortin 4 receptor (MC4-R) knock-out mice. In these mutants, POMC/CART neurons cannot be completely activated because of the lack of this class of receptors, and tumour growth is not accompanied by the development of anorexia and cachexia, which occur in wild type mice [59] Thus, it appears that secondary anorexia is related to the inability of the hypothalamus to respond appropriately to consistent peripheral signals, primarily due to the hyperactivation of the melanocortin system. This derangement could be triggered by cytokines.

Secondary Anorexia

75

Role of Cytokines A number of studies indicate that cytokines are involved in anorexia [61, 62]. In the Fischer rat/MCA sarcoma model, brain interleukin-1 (IL-1) levels inversely correlate with food intake [63] while intra-hypothalamic IL-1 receptor antagonist microinjection increases energy intake [64]. In Lobund-Wistar rats bearing prostate adenocarcinoma tumour cells, early anorexia is associated with an upregulation of brain IL-1β mRNA [54]. In chronic renal failure patients, several groups have found increased levels of cytokines [13, 58, 65]. In cancer patients, cytokines and anorexia are intuitively connected, but compelling evidence are lacking, since cytokines biological effects are largely mediated by paracrine and autocrine influences. Thus, cytokine circulating levels may not reliably reflect their role in determining specific biological responses [66], rather they suggest their involvement. However, it must be acknowledged that studies also exist, which failed to demonstrate a direct role of cytokines in experimental models of cancer anorexia, while suggesting the involvement of the nitric oxide system and systemic or local production of eicosanoids [67, 68].

Hypothalamic Neuro-Immune Interactions: The Role of Brain Monoamines The mechanisms by which cytokines negatively influence energy intake are currently under investigation. As proposed by Inui, cytokines may play a pivotal role in long-term inhibition of feeding by mimicking the hypothalamic effect of excessive negative feedback signalling [69]. This could be done by inhibition of the NPY/AgRP orexigenic network, as well as by persistent stimulation of the POMC/CART anorexigenic pathway. In the complex scenario of mutual interactions existing between different peripheral and central factors, brain monoamines and particularly brain serotonin appears to play a pivotal role. A simplistic view of energy intake regulation is that ingested nutrients are sensed at different levels of the gastrointestinal tract, including the liver. This information, together with that arising from adipose tissue, is transmitted to the brain via a series of routes [neuronal input, hormones, peptides], and is integrated in the hypothalamus, where the appropriate behavioral response is triggered. Actually, the picture is far more complex, since the hypothalamus consists of different areas and nuclei, and within each of them a set of effectors [neurotransmitters, neuromodulatory peptides and transmembrane proteins] interact [25]. For several decades, hypothalamic serotonin systems have been implicated in the suppression of feeding [70]. Serotonin is a monoamine acting as neurotransmitter and involved in different biological responses. Although the exact role of serotonin in the central regulation of food intake and body weight still awaits further clarification, its involvement in this process has been repeatedly confirmed. Now it is clear that serotonin acts in conjunction with neuropeptides and peripheral hormones to bring about physiological states such as hunger, satiation and satiety.

76 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli Beside its role in influencing food intake, hypothalamic serotonin appears to impact also energy expenditure. In a recent report, Ohliger-Frerking et al. studied dorsal raphe nucleus serotonergic neurons, projecting to the hypothalamus to influence feeding [71]. They showed that the neurons from obese Zucker rats exhibit both a larger depolarization and increased firing rate in response to phenylephrine than did cells from lean rats, thus suggesting that dorsal raphe nucleus serotonergic neurons of obese rats have an enhanced adrenergic drive. Furthermore, serotonin reduces food intake and augment sympathetic activity, thus promoting weight loss [72]. Recent data suggest that during disease, hypothalamic serotonergic neurotransmission may be critical in linking different central anorexigenic pathways, and particularly cytokines and the melanocortin system. Fenfluramine is a serotonin agonist once widely prescribed in the treatment of obesity. It has been recently shown that fenfluramine raises hypothalamic serotonin levels, which in turn activate POMC/CART neurons in the arcuate nucleus, therefore inducing anorexia and reduced food intake [73]. On the other hand, it is well documented that cytokines, and particularly IL-1, stimulate the release of hypothalamic serotonin [74]. Thus, it could be speculated that during disease, cytokines increase hypothalamic serotonergic activity, which in turn contributes to persistent activation of POMC/CART neurons, leading to the onset of anorexia and reduced food intake. Supporting the role of serotonin in the pathogenesis of anorexia, we demonstrated that in anorectic tumour-bearing animals hypothalamic serotonin levels are increased when compared with control rats [75]. After tumour removal, hypothalamic serotonin levels normalize and food intake improves [75]. In the same experimental model, intrahypothalamic microinjections of mianserin, a serotonin antagonist, improves food intake [64]. In humans, the demonstration of the involvement of brain serotonin in anorexia is more difficult since serotonergic activity cannot be easily measured in-vivo. Thus, the activity of hypothalamic serotonergic system is inferred by cerebro-spinal fluid (CSF) levels of tryptophan. Tryptophan is the precursor of serotonin, whose synthesis is strictly dependent on the availability of tryptophan [76]. In anorectic cancer patients, plasma and particularly CSF concentrations of tryptophan are increased when compared to controls and non anorectic cancer patients [4, 77]. After tumour removal, plasma typtophan normalizes and food intake improves [66]. Similar data suggesting increased serotonergic activity in the presence of anorexia have been obtained in patients suffering from chronic renal failure [12, 50, 62] and liver cirrhosis [78], thus supporting the view that anorexia associated with different diseases may share a similar pathogenic mechanisms. It must be acknowIedged that partial brain serotonin depletion and antagonism did not result in improved food intake of tumour bearing animals [68, 79]. However, it is not clear whether the failure in influencing food intake in these models could be secondary to the incomplete brain serotonergic depletion or to the lack of any involvement of serotonin in cancer anorexia [80]. When considered together, we believe that these data suggest that brain serotonin could represent is a key factor involved in the pathogenesis of disease-associated anorexia and thus provide an interesting therapeutic target.

Secondary Anorexia

77

Therapy The detrimental effects of anorexia on nutritional status and quality of life can be counteracted by a well designed therapeutic strategy which includes both nutritional counselling and pharmacological approach (Table III). Table III: Therapeutic strategies in cancer anorexia DIETARY COUNSELLING Small but frequent meals Energy-dense food Limit fat intake Avoid extremes in taste Avoid extremes in smell Pleasant environment Presentation of food

DRUGS Progestagens [MA, MPA] Cannabinoids [dronabinol] Corticosteroids [dexamethasone]

Dietary Habits In anorectic patients, nutritional counselling may significantly improve food intake. Food intake can be improved by providing small and frequent meals that are energy-dense and easy to eat. Patients should eat in pleasant surroundings and attention should be given to the presentation of food. It is advisable to avoid high-fat food, since fat delays gastric emptying and thus it may worsen anorexia symptoms. Since changes in taste/smell may occur in anorectic patients, extremes in temperature and flavour should be avoided [7].

Drug Therapy The optimal therapeutic approach to anorexia should be aimed at counteracting its pathogenic mechanisms. Therefore, considering that cytokines appear to represent the factor initiating the complex cascade of neurochemical events eventually leading to the onset of anorexia, it would be advisable to target their synthesis and/or activity to effectively treat anorexia and reduced food intake in cancer patients. Animal studies support this approach, by showing that intrahypothalamic IL-1 blockade as well as systemic TNF inhibition result in amelioration of anorexia and improved food intake [64, 81]. In humans, cytokine therapeutic targeting is achieved via agents interfering with their synthesis and release. They include progestagens [82], cannabinoids [83] and corticosteroids [84]. Progestagens [megestrol acetate and medroxyprogesterone acetate] are the first-line therapy for cancer anorexia [69]. They are highly effective in relieving the symptoms of cancer anorexia. In a recent systematic review of randomised clinical trials, high-dose progestagens have been shown to improve food intake and to a less extent body weight [85].

78 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli Their prophagic effect appears to be mediated by the down-regulation of the synthesis and release of cytokines [86], leading to an increase of NPY hypothalamic levels [87] and a possible inhibition of serotonergic activity [88]. However, they are contraindicated in hormone-dependent tumours, and their use may lead to fluid retention, deep venous thrombosis, vaginal spotting and sexual dysfunction. Cannabinoids are derivatives of marijuana and particularly dronabinol has been demonstrated to alter cytokine production by human immune cells [89]. In cancer patients, dronabinol at a dose of 2.5 mg twice a day increases food intake, but its prophagic effects are less evident than those obtained by megestrol actetate [83]. Corticosteroids are widely used to dampen immune response and cytokine activity. Exploiting their immunomodulatory effects, they have been used in the treatment of cancer anorexia. Their effects are similar to those obtained by megestrol acetate, but corticosteroids have a higher rate of drug discontinuation because of toxicity and/or patient refusal [84].

Therapy of Anorexia: What’s Next? Omega-3 Fatty Acids The n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid [DHA] have been shown to suppress production of proinflammatory cytokines and arachidonic acid-derived mediators [90]. Thus, EPA supplementation may represent an effective therapeutic strategy to ameliorate cancer anorexia [91]. Jatoi et al. recently compared the orexigenic effects of megestrol acetate and of a caloric supplement enriched with EPA and DHA in weight losing, anorectic cancer patients [92]. More than 400 patients were studied over a period of approximately 3 months. Data obtained show that megestrol acetate and EPA supplement are equally effective in improving body weight. Appetite is similarly enhanced by the two treatments when it is assessed via North Central Cancer Treatment Group Questionnaire, but megestrol acetate appears superior when appetite is assessed via 4-week Functional Assessment of Anorexia/Cachexia score. Combination of both treatments does not increase response rate.

Anti-Cytokine Agents Other molecules exhibit anti-cytokine activity. Pentoxifylline, thalidomide, suramin have been demonstrated to significantly reduce cytokine release, thus prompting their testing as anti-anorexia/cachexia agents [82]. Unfortunately, the results obtained appear modest, while the potential side effects discourage their clinical use. In particular, recent data show that suramin inhibits chemotherapy-induced apoptosis [93]. Similarly, the infusion of adenosine 5’-triphosphate [ATP] in cancer patients modestly increased weight, improved strength and slowed the decline in quality of life [94, 95]. Newly synthesised molecules, dubbed “cytokine traps” after their ability to block cytokines, appear more promising. Cytokine traps consist of fusions between the constant region of IgG and the extracellular domains of two distinct

Secondary Anorexia

79

cytokine receptor components involved in binding the cytokine. Traps potently block cytokine in vitro and in vivo, and represent a substantial advance in creating novel therapeutic candidates for cytokine-driven diseases [96].

Anti-Serotonergic Agents Cancer anorexia might be therapeutically approached by interfering with the neurochemical events downstream cytokine activation. Serotonergic hypothalamic neurotransmission may represent a suitable example. Hypothalamic serotonin synthesis depends on the brain availability of its precursor, the amino acid tryptophan [76]. Tryptophan crosses the blood-brain barrier via a specific transport mechanism shared with the other neutral amino acids, including the branched-chain amino acids. Thus, by artificially increasing the plasma levels of the competing amino acids, a reduction of tryptophan brain entry could be achieved, leading to a reduction of hypothalamic serotonin synthesis and release, which in turn would result in amelioration of cancer anorexia. To test this hypothesis, tumor-bearing rats were fed with a BCAA-enriched diet, and their feeding behaviour compared with that of tumor-bearing rats receiving an isocaloric, isonitrogenous standard diet. The results obtained showed that BCAA-enriched diet delayed the development of anorexia by 2 days when compared to standard diet [unpublished observations]. To further test the clinical relevance of BCAA, anorectic cancer patients were orally supplemented with branched-chain amino acids or placebo for 7 days, while simultaneously recording their energy intake [97]. Anorexia significantly improved after 3 days of treatment only in cancer patients receiving branched-chain amino acids, leading to a significant improvement of energy intake. These encouraging results must be considered as preliminary, since they were obtained in a small population during a short study period, and need to be validated in larger trials. However, they confirm the feasibility of interfering with hypothalamic neurotransmission to influence energy intake. Indeed, more fascinating results were later obtained in uremia and in liver cirrhosis. During chronic renal failure, derangements of plasma amino acid profile occur and a reduction of circulating levels of BCAA is frequently observed. Interestingly, the reduction of plasma BCAA is associated with the presence of anorexia [12]. It is therefore tempting to speculate that by supplementing uremic patients with BCAA, energy intake and nutritional status can be improved. Hiroshige et al. studied 44 elderly patients on chronic hemodialysis [12]. Among them, 28 patients with low plasma albumin levels [<3.5 g/dL] were classified as the malnourished group; they also suffered from anorexia. The other 16 patients did not complain of anorexia and were classified as the well-nourished group. Then they performed a 12-month, double-blind, placebo-controlled study on the malnourished group. Fourteen patients each received daily oral BCAA supplementation [12 g/day] or a placebo in random order in a cross-over trial for 6 months. Lower plasma levels of BCAA and lower protein and caloric intakes were found in the malnourished group as compared to the well-nourished group. In BCAA-treated malnourished patients, anorexia and poor oral protein and calorie intakes improved within a month concomitant with the improvement of plasma BCAA levels over the values in well-nourished patients. After 6 months of BCAA supplementation,

80 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli anthropometric indices [body fat percentage, lean body mass] showed a statistically significant increase and mean plasma albumin concentration increased form 3.3 g/dL to 3.9 g/dL. After changing BCAA for a placebo, spontaneous oral food intake decreased, but the favourable nutritional status persisted for the next 6 months. In 14 patients initially treated with placebo, no significant changes in nutritional parameters were observed during the first 6 months. However, positive results were obtained by BCAA supplementation during the subsequent 6 months, and mean plasma albumin concentration increased from 3.2 g/dL to 3.8 g/dL. These data are particularly important because demonstrate that BCAA supplementation results not only in improved food intake but also in improved nutritional status. Such encouraging results were replicated also in cirrhotic patients. A multicenter, randomized study comparing 1-year nutritional supplementation with BCAA against lactoalbumin or maltodextrins was recently performed in 174 patients [11]. Primary outcomes were the prevention of a combined end point [death and deterioration to exclusion criteria], the need for hospital admission, and the duration of hospital stay. Secondary outcomes were nutritional parameters, laboratory data and Child-Pugh score, anorexia, health-related quality of life, and need for therapy. Interestingly, treatment with BCAA significantly reduced the combined event rates compared with lactoalbumin. The average hospital admission rate was lower in the BCAA arm compared with control treatments. In patients who remained in the study, nutritional parameters and liver function tests were, on average, stable or improved during treatment with BCAA and the Child-Pugh score decreased. Also, anorexia and health-related quality of life [as assessed by the SF-36 questionnaire] improved. In particular, anorexia was reported in more than 50% of all cases and was not different between groups. Its prevalence decreased with BCAA from 52% to 25% and remained unchanged with lactoalbumin and maltodextrins. Treatment groups did not score differently on SF-36 questionnaire at baseline. Treatment with BCAA had a significant effect on role limitation/physical, and other scales improved significantly when compared with baseline. Physical functioning and role limitation/emotional also improved. No significant changes were observed in subjects treated with lactoalbumin or maltodextrins. Finally, there was a shift toward better scoring of health only in subjects actively treated with BCAA, with the percent of patients scoring health as poor decreasing from 19% to 3%. Similarly, after 1 year of continuous treatment with BCAA, the percentage of patients believing that their health had improved during the preceding 12 months had increased from 29% to 52%, and the percentage believing that their health had worsened had decreased from 43% to 18%. When considered together, these data suggest that the anti-serotonergic approach to the treatment of disease-associated anorexia is effective and results in significant clinical outcomes, far beyond mere increase of energy intake. The observed improvement of nutritional status and particularly of lean body mass could be explained at least in part by the excitatory effects of serotonin on hypothalamic melanocortin receptors [73], whose function has been linked to cachexia [98]. By reducing brain serotonergic activity via BCAA, it is conceivable that melanocortin receptors are less activated, leading to reduced peripheral muscle wasting. Considering the role of brain serotonin in the pathogenesis of disease-associated anorexia and cachexia, antiserotonergic drugs might be as effective as BCAA in improving food intake

Secondary Anorexia

81

and nutritional status. However, this approach bears some limitations. Firstly, antiserotonergic drugs must target the specific serotonin receptor involved in the pathogenesis of anorexia, the best candidate to this role being the 5-HT(2C) receptor. The need for selectivity may explain the failure of cyproheptadine in the treatment of anorexia in cancer patients [for review see ref. 99]. Secondly, provided that the given antiserotonergic drug selectively targets 5-HT(2C) receptors, then it must reach the hypothalamus in adequate concentrations to block the receptors. This may be difficult to achieve, particularly if adequate brain concentrations are reached only when using suprapharmacologic peripheral doses, which may lead to the development of side-effects. Promising and in early clinical trials is blockade of type 3 serotonergic receptors, which appear more involved in mediating nausea and emesis rather than in controlling energy balance [70]. Ondansetron is a type 3 serotonergic receptor antagonist widely used in cancer patients in the prevention and treatment of chemotherapy-induced nausea and vomiting. Edelman et al. [100] studied 27 patients with advanced cancer and weight loss. Patients were not receiving antineoplastic treatment, but received oral ondansetron. Unfortunately, weight loss continued, but after 1 month of treatment patients scored better on an hedonic scale, suggesting that they were enjoying food more. However, large and placebo controlled trials are needed to establish whether these positive results reflected a true orexigenic effect attributable exclusively to ondansetron, thus prompting more interest on this class of drugs. More data support a role for hypothalamic neurotransmission as an effective therapeutic target in the treatment of cancer anorexia. Using in vivo microdialysis, Blaha et al. showed that intrahypothalamic serotonin concentrations are increased in anorectic tumor bearing rats [75]. In the same study, they also showed a more complex derangement of hypothalamic monoaminergic neurotransmission, since dopamine levels were also found depressed [75]. This evidence may give the neurochemical explanation for the results obtained in anorectic cancer patients, whose food intake has been restored and quality of life improved by the administration of dopamine (L-DOPA) at a dosage ranging from 375 mg/d to 750 mg/d [101, 102]. Although not obtained in prospective randomized clinical trials, these data are very intriguing and further support the “monoaminergic” approach to the treatment of anorexia.

Ghrelin Considering the orexigenic effects of ghrelin [103], it is tempting to speculate that its administration to anorectic cancer patients may enhance their appetite and improve energy intake. This hypothesis has been recently tested in an acute study [104]. Seven anorectic cancer patients received i.v. ghrelin and their subsequent food intake and meal appreciation recorded. Acute ghrelin infusion resulted in increased energy intake (approximately +30% vs saline infusion) and meal appreciation in all patients studied. Considering the few patients enrolled, these intriguing data should be considered as preliminary and need confirmation by larger trials. Also, the use of ghrelin in cancer patients must be cautiously considered because of the stimulatory effects of this hormone on GH production, which are mediated by the same receptor stimulating appetite [105]. Although it remains to be ascertained whether in humans chronically administered ghrelin sustains

82 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli increased GH production, it must be reminded that acromegalic patients with chronically elevated GH have a small increase in absolute risk of bowel cancer [106]. Also, ghrelin infusion increases plasma glucose and decreases plasma insulin [107]. However, glucose is the preferred substrate for cancer cells [108] and sustained hyperglycemia as in diabetic patients has been shown to represent a risk factor for cancer development and mortality [109]. Finally, animal studies seem to anticipate that chronic treatment with this hormone will have little effect on appetite [105].

Anti-Inflammatory Agents As previously mentioned, the nitric oxide system and the production of eicosanoids might be of importance for the pathogenesis of anorexia, and particularly cancer anorexia. Supporting this view, animal and clinical studies show that nitric oxide synthase and cyclooxigenase inhibitors, including indomethacin, decrease tumour growth and improve anorexia [110, 111]. However, evidence that nitric oxide and eicosanoids act directly on cells in the central nervous system is lacking. Also, nitric oxide mechanism may involve tumour growth and thereby secondarily influence appetite. Finally, nitric oxide and eicosanoid influences on appetite appear related to serotonin metabolism [112, 113], and the prostaglandin E2 receptor EP3 has been identified on serotonergic neuronal cell bodies in the raphe nucleus [114]. Thus, nitric oxide and eicosanoid pathways could not be completely alien from the cytokine-monoamine system.

Conclusion Anorexia is a syndrome which is pervasive among patients suffering from acute and chronic diseases. The pathogenesis is multifactorial, but it appears to be related to the hyperactivation of hypothalamic inhibitory pathways, which in turn seems to be triggered by cytokine-driven stimulation of hypothalamic serotonergic system. Anorexia can be effectively treated, although it is not known whether amelioration of anorexia results in a long-term benefit for patients, leading to reduced morbidity and mortality. However, it should be always remembered that improving anorexia and energy intake has a positive impact on quality of life.

References [1] Murray MJ, Murray AB. Anorexia of infection as a mechanism of host defense. Am J Clin Nutr 1979; 32: 593-6 [2] Cherny NI, Catane R. Attitudes of medical oncologists toward palliative care for patients with advanced and incurable cancer. Cancer 2003; 98: 2502-10 [3] Stubbs RJ, Hughes DA, Johnstone AM, Rowley E, Reid C, Elia M, Stratton R, Delargy H, et al. The use of visual analogue scales to assess motivation to eat in human

Secondary Anorexia

[4]

[5]

[6]

[7] [8]

[9]

[10] [11]

[12]

[13]

[14]

[15] [16]

83

subjects: a review of their reliability and validity with an evaluation of new hand-held computerized systems for temporal tracking of appetite ratings. Br J Nutr 2000; 84: 405-15 Rossi Fanelli F, Cangiano C, Ceci F, Cellerino R, Franchi F, Menichetti ET, Muscaritoli M, Cascino A. Plasma tryptophan and anorexia in human cancer. Eur J Cancer Clin Oncol 1986; 22: 89-95 Geels P, Eisenhauer E, Bezjak A, Benny Z, Day A. Palliative effect of chemotherapy: objective tumor response is associated with symptom improvement in patients with metastatic breast cancer. J Clin Oncol 2000; 18: 2395-405 DeWys WD, Begg C, Lavin PT, Band PR, Bennett JM, Bertino JR, Cohen MH, Douglass HO Jr, et al. Prognostic effect of weight loss prior to chemotherapy in cancer patients. Eastern Cooperative Oncology Group. Am J Med 1980; 69: 491-7 Sutton LM, Demark-Wahnefried W, Clipp EC. Management of terminal cancer in elderly patients. Lancet Oncol 2003; 4: 149-57 Pirovano M, Maltoni M, Nanni O, Marinari M, Indelli M, Zaninetta G, Petrella V, Barni S, et al. A new palliative score: a first step for the staging of terminally ill cancer patients. Italian Multicenter and Study Group on Palliative Care. J Pain Symptom Manage 1999; 17: 231-9 Maltoni M, Nanni O, Pirovano M, Scarpi E, Indelli M, Martini C, Monti M, Arnoldi E, et al. Successful validation of the palliative prognostic score in terminally ill cancer patients. Italian Multicenter Study Group on Palliative Care. J Pain Symptom Manage 1999; 17: 240-7 Daly JM, Redmond HP, Gallagher H. Perioperative nutrition in cancer patients. JPEN J Parenter Enteral Nutr 1992; 16 [suppl. 6]: 100S-5S Marchesini G, Bianchi G, Merli M, Amodio P, Panella C, Loguercio C, Rossi Fanelli F, Abbiati R for the Italian BCAA Study Group. Nutritional supplementation with brached-chain amino acids in advanced cirrhosis: a double-blind, randomized trial. Gastroenterology 2003; 124: 1792-801 Hiroshige K, Sonta T, Suda T, Kanega K, Ohtani A. Oral supplementation of branchedchain amino acid improves nutritional status in elderly patients on chronic haemodialysis. Nephrol Dial Transplant 2001; 16: 1856-62 Kalantar-Zadeh K, Block G, McAllister CJ, Humphreys MH, Kopple JD. Appetite and inflammation, nutrition, anemia, and clinical outcome in hemodialysis patients. Am J Clin Nutr 2004; 80: 299-307 Edmonds P, Karlsen S, Khan S, Addington-Hall J. A comparison of the palliative care needs of patients dying from chronic respiratory diseases and lung cancer. Palliat Med 2001; 15: 287-95 Nordgren L, Sorensen S. Symptoms experienced in the last six months of life in patients with end-stage heart failure. Eur J Cardiovasc Nurs 2003 ; 2: 213-7 Lynn J, Teno JM, Phillips RS, et al. Perceptions by family members of the dying experience of older and seriously ill patients. SUPPORT investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. Ann Int Med 1997; 126: 97-106

84 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli [17] Gibbs JS, McCoy AS, Gibbs LM, Rogers AE, Addington-Hall JM. Living with and dying from heart failure: the role of palliative care. Heart 2002; 88 [suppl. 2]: 36-9 [18] Rossi Fanelli F, Muscaritoli M, Cangiano C, Cascino A, Laviano A, Fava A. The basis for a rational nutritional approach to patients with cancer. In: Abraham NG, Tabilio A, Martelli M, Asano S, Donfrancesco A [eds.], "Molecular Biology of Hematopoiesis 6"; Kluwer Academic/Plenum Publishers, New York, pp. 229-34, 1999 [19] Tisdale MJ. Cachexia in cancer patients. Nat Rev Cancer 2002; 2: 862-71 [20] Maltoni M, Pirovano M, Scarpi E, Marinari M, Indelli M, Arnoldi E, Gallucci M, Frontini L, et al. Prediction of survival of patients terminally ill with cancer. Results of an Italian prospective multicentric study. Cancer 1995; 75: 2613-22 [21] Apolone G, De Carli G, Brunetti M, Garattini S. Health-related quality of life [HRQOL] and regulatory issues. An assessment of the European Agency for the Evaluation of Medicinal Products [EMEA] recommendations on the use of HR-QOL measures in drug approval. Pharmacoeconomics 2001; 19: 1727-9 [22] Davis MP, Dreicer R, Walsh D, Lagman R, Le Grand SB. Appetite and cancerassociated anorexia: a review. J Clin Oncol 2004; 22: 1510-7 [23] Jatoi A, Kumar S, Sloan JA, Nguyen PL. On appetite and its loss. J Clin Oncol 2003; 21: 79s-81s [24] Ganzini L, Goy ER, Miller LL, Harvath TA, Jackson A, Delorit MA. Nurses’ experience with hospice patients who refuse food and fluids to hasten death. N Engl J Med 2003; 349: 359-65 [25] Schwartz MW, Woods SC, Porte D Jr, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature 2000; 404: 661-71 [26] Janik JE, Curti BD, Considine RV, Rager HC, Powers GC, Alvord WG, Smith JW 2nd, Gause BL, Kopp WC. Interleukin-1 alpha increases serum leptin concentrations in humans. J Clin Endocrinol Metab 1997; 82: 3084-6 [27] Chance WT, Sheriff S, Moore J, Peng F, Balasubramaniam A. Reciprocal changes in hypothalamic receptor binding and circulating leptin in anorectic tumor-bearing rats. Brain Res 1998; 803: 27-33 [28] Sato T, Meguid MM, Miyata G, Chen C, Hatakeyama K. Does leptin really influence cancer anorexia? Nutrition 2002; 18: 82-3 [29] Simons JP, Schols AM, Campfield LA, Wouters EF, Saris WH. Plasma concentration of total leptin and human lung-cancer-associated cachexia. Clin Sci 1997; 93: 273-7 [30] Bing C, Taylor S, Tisdale MJ, Williams G. Cachexia in MAC 16 adenocarcinoma: suppression of hunger despite normal regulation of leptin, insulin and hypothalamic neuropeptide Y. J Neurochem 2001; 79: 1004-12 [31] Mantovani G, Maccio A, Mura L, Massa E, Mudu MC, Mulas C, Lusso MR, Madeddu C, et al. Serum levels of leptin and proinflammatory cytokines in patients with advanced-stage cancer at different sites. J Mol Med 2000; 78: 554-61 [32] Stenvinkel P, Lindholm B, Lonnqvist F, Katzarski K, Heimburger O. Increases in serum leptin levels during peritoneal dialysis are associated with inflammation and a decrease in lean body mass. J Am Soc Nephrol 2000; 11: 1303-9

Secondary Anorexia

85

[33] Bossola M, Muscaritoli M, Valenza V, Panocchia N, Tazza L, Cascino A, Laviano A, Liberatori M, et al. Anorexia and serum leptin levels in hemodialysis patients. Nephron Clin Pract 2004; 97: c76-82 [34] Ben-Ari Z, Schafer Z, Sulkes J, Manhaim V, Tur-Kaspa R, Fainaru M. Alterations in serum leptin in chronic liver disease. Dig Dis Sci 2002; 47: 183-9 [35] Gerozissis K. Brain insulin and feeding: a bi-directional communication. Eur J Pharmacol 2004; 490: 59-70 [36] Sato T, Laviano A, Clin Nutr [37] Woods SC. Gastrointestinal satiety signals - I. An overview of gastrointestinal signals that influence food intake. Am J Physiol Gastrointest Liver Physiol 2004; 286: G7-G13 [38] MacIntosh CG, Morley JE, Wishart J, Morris H, Jansen JBMJ, Horowitz M, Chapman IM. Effect of exogenous cholecystokinin [CCK]-8 on food intake and plasma CCK, leptin, and insulin concentrations in older and young adults: evidence for increased CCK activity as a cause of the anorexia of aging. J Clin Endocrinol Metab 2001; 86: 5830-7 [39] Sturm K, MacIntosh CG, Parker BA, Wishart J, Horowitz M, Chapman IM. Appetite, food intake, and plasma concentrations of cholecystokinin, ghrelin, and other gastrointestinal hormones in undernourished older women and well-nourished young and older women. J Clin Endocrinol Metab 2003; 88: 3747-55 [40] Wynne K, Stanley S, Bloom S. The gut and regulation of body weight. J Clin Endocrinol Metab 2004; 89: 2576-82 [41] Shimizu Y, Nagaya N, Isobe T, Imazu M, Okumura H, Hosoda H, Kojima M, Kangawa K, et al. Increased plasma ghrelin level in lung cancer cachexia. Clin Cancer Res 2003; 9: 774–8 [42] Wortley KE, Anderson KD, Garcia K, Murray JD, Malinova L, Liu R, Moncrieffe M, Thabet K, et al. Genetic deletion of ghrelin does not decrease food intake but influences metabolic fuel preference. Proc Natl Acad Sci USA 2004; 101: 8227-32 [43] Baggio LL, Huang Q, Brown TJ, Drucker DJ. Oxyntomodulin and glucagons-like peptide-1 differentially regulate murine food intake and energy expenditure. Gastroenterology 2004; 127: 546-58 [44] Kahler A, Zimmermann M, Langhans W. Suppression of hepatic fatty acid oxidation and food intake in men. Nutrition 1999; 15: 819-28 [45] Loftus TM, Jaworsky DE, Frehywot GL, Townsend CA, Ronnett GV, Lane MD, Kuhajda FP. Reduced food intake and body weight in mice treated with fatty acid synthase inhibitors. Science 2000; 288: 2379-81 [46] Rasmussen BB, Holmback UC, Volpi E, Morio-Liondore B, Paddon-Jones D, Wolfe RR. Malonyl coenzyme A and the regulation of functional carnitine palmitoyltransferase-1 activity and fat oxidation in human skeletal muscle. J Clin Invest 2002; 110: 1687-93 [47] Peluso G, Nicolai R, Reda E, Benatti P, Barbarisi A, Calvani M. Cancer and anticancer therapy-induced modification on metabolism mediated by carnitine system. J Cell Physiol 2000; 182: 339-50

86 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli [48] Laviano A, Meguid MM, Renvyle T, Yang Z-J, Beverly JL. Carnitine supplementation accelerates normalization of food intake depressed during TPN. Physiol Behav 1996; 60: 317-20 [49] Li JL, Zheng FL, Tan HB, Yin SY, Yang JH, Li Y, Bu YF. Orexin A and neuropeptide Y in plasma and hypothalamus of rats with chronic renal failure. Zhonghua Yi Xue Za Zhi 2003; 83: 992-5 [50] Rossi Fanelli F, Cangiano C. Increased availability of tryptophan in brain as common pathogenic mechanism for anorexia associated with different diseases. Nutrition 1991; 7: 364-7 [51] Laviano A, Meguid MM, Yang Z-J, Gleason JR, Cangiano C, Rossi Fanelli F. Cracking the riddle of cancer anorexia. Nutrition 1996; 12: 706-10 [52] Chance WT, Balasubramaniam A, Fischer JE. Neuropeptide Y and the development of cancer anorexia. Ann Surg 1995; 221: 579-87 [53] Chance WT, Sheriff S, Kasckow JW, Regmi, A, Balasubramaniam A. NPY messenger RNA is increased in medial hypothalamus of anorectic tumor-bearing rats. Regul Pept 1998; 75-76: 347-53 [54] Plata-Salaman CR, Ilyin SE, Gayle D. Brain cytokine mRNAs in anorectic rats bearing prostate adenocarcinoma tumor cells. Am J Physiol 1998; 275: R566-73 [55] Jatoi A, Loprinzi CL, Sloan JA, Klee GG, Windschitl HE. Neuropeptide Y, leptin, and cholecystokinin 8 in patients with advanced cancer and anorexia: a North Central Treatment Group exploratory investigation. Cancer 2001; 92: 629-33 [56] Meguid MM, Ramos EJ, Laviano A, Varma M, Sato T, Chen T, Qi Y, Das UN. Tumor anorexia: effects on neuropeptide Y and monoamines in paraventricular nucleus. Peptides 2004; 25: 261-6 [57] Makarenko IG, Meguid MM, Gatto L, Chen C, Ugrumov MV. Decreased NPY innervation of the hypothalamic nuclei in rats with cancer anorexia. Brain Res 2003; 961: 100-8 [58] Aguilera A, Codoceo R, Selgas R, Garcia P, Picornell M, Diaz C, Sanchez C, Bajo MA. Anorexigen [TNF-alpha, cholecystokinin] and orexigen [neuropeptide Y] plasma levels in peritoneal dialysis [PD] patients: their relationship with nutritional parameters. Nephrol Dial Transplant 1998; 13: 1476-83 [59] Marks DL, Ling N, Cone RD. Role of central melanocortin system in cachexia. Cancer Res 2001; 61: 1432-8 [60] Wisse BE, Frayo RS, Schwartz MW, Cummings DE. Reversal of cancer anorexia by blockade of central melanocortin receptors in rats. Endocrinology 2001; 142: 3292-301 [61] Plata-Salaman. Anorexia during acute and chronic disease. Nutrition 1996; 12: 69-78 [62] Aguilera A, Selgas R, Codoceo R, Bajo A. Uremic anorexia: a consequence of persistently high brain serotonin levels? The tryptophan/serotonin disorder hypothesis. Perit Dial Int 2000; 20: 810-6 [63] Opara EI, Laviano A, Meguid MM, Yang Z-J. Correlation between food intake and CSF IL-1α in anorectic tumor bearing rats. NeuroReport 1995; 6: 750-2 [64] Laviano A, Gleason JR, Meguid MM, Yang Z-J, Cangiano C, Rossi Fanelli F. Effects of intra-VMN mianserin and IL-1ra on meal number in anorectic tumor-bearing rats. J Investig Med 2000: 48: 40-8

Secondary Anorexia

87

[65] Pereira BJG, Shapiro L, King AJ, Falagas ME, Strom JA, Dinarello CA. Plasma levels of IL-1b, TNF-a and their specific inhibitors in undialyzed chronic renal failure, CAPD and hemodialysis patients. Kidney Int 1994; 45: 890-6 [66] Cangiano C, Testa U, Muscaritoli M, Meguid MM, Mulieri M, Laviano A, Cascino A, Preziosa I, et al. Cytokines, tryptophan and anorexia in cancer patients before and after surgical tumor ablation. Anticancer Res 1994; 14: 1451-6 [67] Wang W, Lonnroth C, Svanberg E, Lundholm K. Cytokine and cyclooxigenase-2 protein in brain areas of tumor-bearing mice with prostanoid-related anorexia. Cancer Res 2001, 61: 4707-15 [68] Wang W, Danielsson A, Svanberg E, Lundholm K. Lack of effects by tricyclic antidepressant and serotonin inhibitors on anorexia in MCG 101 tumor bearing mice with eicosanoid-related anorexia. Nutrition 2003; 19: 47-53 [69] Inui A. Cancer anorexia-cachexia syndrome: are neuropeptides the key? Cancer Res 1999; 59: 4493-501 [70] Giorgetti M, Tecott LH. Contributions of 5-HT2C receptors to multiple actions of central serotonin systems. Eur J Pharmacol 2004; 488 :1-9 [71] Ohliger-Frerking P, Horowitz JM, Horwitz BA. Enhanced adrenergic excitation of serotonergic dorsal raphe neurons in genetically obese rats. Neurosci Lett 2002; 332: 107-10 [72] Bray GA. Reciprocal relation of food intake and sympathetic activity: experimental observations and clinical implications. Int J Obes Relat Metab Disord 2000; 24 [suppl. 2]: S8-17 [73] Heisler LK, Cowley MA, Tecott LH, Fan W, Low MJ, Smart JL, Rubinstein M, Tatro JB, et al. Activation of central melanocortin pathways by fenfluramine. Science 2002; 297: 609-11 [74] Shintani F, Kanba S, Nakaki T, Nibuya M, Kinoshita N, Suzuki E, Yagi G, Kato R, et al. Interleukin-1beta augments release of norepinephrine, dopamine and serotonin in the rat anterior hypothalamus. J Neurosci 1993; 13: 3574-81 [75] Blaha V, Yang ZJ, Meguid MM, Chai JK, Oler A, Zadak Z. Ventromedial nucleus of hypothalamus is related to the development of cancer-induced anorexia: in vivo microdialysis study. Acta Medica [Hradec Kralove] 1998; 41: 3-11 [76] Diksic M, Young SN. Study of the brain serotonergic system with labelled α-methyl-Ltryptophan. J Neurochem 2001; 78: 1185-200 [77] Cangiano C, Cascino A, Ceci F, Laviano A, Mulieri M, Muscaritoli M, Rossi-Fanelli F. Plasma and CSF tryptophan in cancer anorexia. J Neural Transm [Gen Sect] 1990; 81: 225-33 [78] Laviano A, Cangiano C, Preziosa I, Riggio O, Conversano L, Cascino A, Ariemma S, Rossi Fanelli F. Plasma tryptophan and anorexia in liver cirrhosis. Int J Eating Disord 1997; 21: 181-6 [79] Chance WT, von Meyenfeldt M, Fischer JE. Serotonin depletion by 5,7dihydroxytryptamine or para-chloroamphetamine does not affect cancr anorexia. Pharmacol Biochem Behav 1983; 18: 115-21 [80] Laviano A, Rossi-Fanelli F. Pathogenesis of cancer anorexia. Still doubts after all these years? Nutrition 2003; 19: 67-8

88 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli [81] Torelli GF, Meguid MM, Moldawer LL, Edwards CK 3rd, Carter JL, Laviano A, Rossi Fanelli F. Use of recombinant human soluble TNF receptor in anorectic tumor-bearing rats. Am J Physiol 1999; 277: R850-5 [82] Inui A. Cancer anorexia-cachexia syndrome: current issues in research and management. CA Cancer J Clin 2002; 52: 72-91 [83] Jatoi A, Windschitl HE, Loprinzi CL, Sloan JA, Dakhil SR, Mailliard JA, Pundaleeka S, Kardinal CG, et al. Dronabinol versus megestrol acetate versus combination therapy for cancer-associated anorexia: a North Central Cancer treatment Group study. J Clin Oncol 2002; 20: 567-73 [84] Loprinzi CL, Kugler JW, Sloan JA, Mailliard JA, Krook JE, Wilwerding MB, Rowland KM Jr, Camoriano JK, et al. Randomized comparison of megestrol acetate versus dexamethasone versus fluoxymesterone for the treatment of cancer anorexia/cachexia. J Clin Oncol 1999; 17: 3299-306 [85] Pascual Lopez A, Roque I Figuls M, Urrutia Cuchi G, Berenstein EG, Almenar Pasies B, Balcells Alegre M, Herdman M. Systematic review of megestrol acetate in the treatment of anorexia-cachexia syndrome. J Pain Symptom Manage 2004; 27:360-9 [86] Mantovani G, Maccio A, Lai P, Massa E, Ghiani M, Santona MC. Cytokine involvement in cancer anorexia/cachexia: role of megestrol acetate and medroxyprogesterone acetate on cytokine downregulation and improvement of clinical symptoms. Crit Rev Oncog 1998; 9: 99-106 [87] McCarthy HD, Crowder RE, Dryden S, Williams G. Megestrol acetate stimulates food and water intake in the rat: effects on regional hypothalamic neuropeptide Y concentrations. Eur J Pharmacol 1994; 265: 99-102 [88] Mantovani G, Maccio A, Lai P, Esu S, Massa E, Santona MC, Massa D, Dessi D, et al. Medroxyprogesterone acetate and megestrol acetate reduce cisplatin-induc serotonin release from human peripheral blood mononuclear cells of cancer patients. Oncol Rep 1998; 5: 121-4 [89] Srivastava MD, Srivastava BI, Brouhard B. Delta9-tetrahydrocannabinol and cannabidiol alter cytokine production by human immune cells. Immunopharmacology 1998; 40: 179-85 [90] Calder PC. Dietary modifications of inflammation with lipids. Proc Nutr Soc 2002; 61: 345-58 [91] Bruera E, Strasser F, Palmer JL, Willey J, Calder K, Amyotte G, Baracos V. Effect of fish oil on appetite and other symptoms in patients with advanced cancer and anorexia/cachexia: a double-blind, placebo-controlled study. J Clin Oncol 2003; 21: 129-34 [92] Jatoi A, Rowland K, Loprinzi CL, Sloan JA, Dakhil SR, MacDonald N, Gagnon B, Novotny PJ, et al. An eicosapentaenoic acid supplement versus megestrol acetate versus both for patients with cancer-associated wasting: a North Central Cancer Treatment Group and National Cancer Institute of Canada collaborative effort. J Clin Oncol 2004; 22: 2469-76 [93] Eichorst ST, Krueger A, Muerkoster S, Fas SC, Golks A, Gruetzner U, Schubert L, Opelz C, et al. Suramin inhibits death receptor-induced apoptosis in vitro and fulminant apoptotic liver damage in mice. Nat Med 2004; 10: 602-9

Secondary Anorexia

89

[94] Agteresch HJ, Dagnelie PC, van der Gaast A, Stijnen T, Wilson JH. Randomized clinical trial of adenosine 5’-triphosphate in patients with advanced non-small-cell lung cancer. J Natl Cancer Inst 2000; 92: 321-8 [95] Jatoi A, Loprinzi CL, Sloan J, Golderg RM. Is ATP [adenosine 5’-triphosphate], like STP, a performance-enhancing additive for the tanks of cancer patients? J Natl Cancer Inst 2000; 92: 290-1 [96] Economides AN, Carpenter LR, Rudge JS, Wong V, Koehler-Stec EM, Hartnett C, Pyles EA, Xu X, et al. Cytokine traps: multi-component, high-affinity blockers of cytokine action. Nat Med 2003; 9: 47-52 [97] Cangiano C, Laviano A, Meguid MM, Mulieri M, Conversano L, Preziosa I, Rossi Fanelli F. Effects of administration of oral branched-chain amino acids on anorexia and caloric intake in cancer patients. J Natl Cancer Inst 1996; 88: 550-2 [98] Marks DL, Butler AA, Turner R, Brookhart G, Cone RD. Differential role of melanocortin receptor subtypes in cachexia. Endocrinology 2003; 144: 1513-23 [99] Laviano A, Meguid MM. Nutritional issues in cancer management. Nutrition 1996; 12: 358-71 [100] Edelman MJ, Gandara DR, Meyers FJ, Ishii R, O’Mahony M, Uhrich M, Lauder I, Houston J, et al. Serotonergic blockade in the treatment of the cancer anorexiacachexia syndrome. Cancer 1999; 86: 684-8 [101] Herreros R, Serrat I, Boronat A. L-DOPA and cancer anorexia. Palliat Med 1999; 13: 83-4 [102] Lozano RH, Jofre IS. Novel use of L-DOPA in the treatment of anorexia and asthenia associated with cancer. Palliat Med 2002; 16: 548 [103] Inui A, Asakawa A, Bowers CY, Mantovani G, Laviano A, Meguid MM, Fujimiya M. Ghrelin, appetite, and gastric motility: the emerging role of the stomach as an endocrine organ. FASEB J 2004; 18: 439-56 [104] Neary NM, Small CJ, Alison MW, Lee JL, Druce MR, Palmieri C, Frost GS, Ghatei MA, et al. Ghrelin increases energy intake in cancer patients with impaired appetite: acute, randomized, placebo-controlled trial. J Clin Endocrinol Metab 2004; 89: 2832-6 [105] Sun Y, Wang P, Zheng H, Smith RG. Ghrelin stimulation of growth hormone release and appetite is stimulated through the growth hormone secretagogue receptor. Proc Natl Acad Sci USA 2004; 101: 4679-84 [106] Orme SM, McNally RJ, Cartwright RA, Belchetz PA. Mortality and cancer incidence in acromegaly: a retrospective cohort study. United Kingdom Acromegaly Study Group. J Clin Endocrinol Metab 1998; 83: 2730-4 [107] Broglio F, Arvat E, Benso A, Gottero C, Muccioli G, Papotti M, van der Lely AJ, Deghenghi R, et al. Ghrelin, a natural GH secretagogue produced by the stomach, induces hyperglycemia and reduces insulin secretion in humans. J Clin Endocrinol Metab 2001; 86: 5083–6 [108] Rossi Fanelli F, Cascino A, Muscaritoli M. Abnormal substrate metabolism and nutritional strategies in cancer management. JPEN J Parenter Enteral Nutr 1991; 15: 680-3 [109] Coughlin SS, Calle EE, Teras LR, Petrelli J, Thun MJ. Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults. Am J Epidemiol 2004; 159: 1160-7

90 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli [110] Cahlin C, Gelin J, Delbro D, Lonnroth C, Doi C, Lundholm K. Effect of cyclooxigenase and nitric oxide synthase inhibitors on tumor growth in mouse tumor models with and without cachexia related to prostanoids. Cancer Res 2000; 60: 1742-9 [111] Lundholm K, Gelin J, Hyltander A, Lonnroth C, Sandstrom R, Svaninger G, Korner U, Gulich M, et al. Anti-inflammatory treatment may prolong survival in undernourished patients with metastatic solid tumors. Cancer Res 1994; 54: 5602-6 [112] Squadrito F, Calapai G, Altavilla D, Cucinotta D, Zingarelli B, Arcoraci V, Campo GM, Caputi AP. Central serotoninergic system involvement in the anorexia induced by NG-nitro-L-arginine, an inhibitor of nitric oxide synthase. Eur J Pharmacol 1994; 255: 51-5 [113] Lugarini F, Hrupka BJ, Schwartz GJ, Plata-Salaman CR, Langhans W. A role for cyclooxygenase-2 in lipopolysaccharide-induced anorexia in rats. Am J Phyisiol Regul Integr Comp Physiol 2002; 283:R862-8 [114] Nakamura K, Li YQ, Kaneko T, Kayoh H, Negishi M. Prostaglandin E3 receptor protein in serotonin and catecholamine cell groups: a double immunofluorescence study in the rat brain. Neuroscience 2001; 103: 763-75

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 91-104 © 2006 Nova Science Publishers, Inc.

Chapter V

“I Couldn’t Find the Food I Liked” Anorexia in Boys. Three Case Reports B. Bräutigam and M. Herberhold Klinik fur Kinder und Jugendmedizin der Medizinischen Universitat zu Lubeck, Arbeitsgruppe fur Psychosomatik und Psychotherapie, Ratzeburger Allee 160, 23538 Lubeck.

Abstract The number of boys affected by eating disorders is increasing. The fact that the numbers for eating disorders among boys are so low is probably due in part to underdiagnosis. Although adolescent girls are still the group primarily affected by eating disorders, nearly every tenth person suffering from an eating disorder is male. The lifetime prevalence of any eating disorder has been reported as 17.9% among women and 6.5% among men. There are triggers for the disorders among boys that are different from those that have been identified among girls. These include excessive physical activity, a fragile sexual identity, demanding requirements or expectations in the areas of competitive sports, muscle building, and ideals of physical perfection. There are also differences in the pathologies. For example, boys often exhibit a different form of body image distortion, one that is more focused on masculine muscular form. They also show less shame concerning binge eating. The fact that anorexia and bulimia are much more difficult to diagnose among boys has led to a situation in which only the most severe cases are successfully diagnosed. This situation is exacerbated by the fact that bulimia is perceived by the public as a disease that only affects girls, with the result that affected boys often have to struggle with emotions of shame and denial. We report on three clinical cases that illustrate some of the differences between male and female anorexia and other aspects like the wide range of psychological and physical symptoms, the different therapeutic approaches, and kinds of treatment. We focus on the patients’ personal histories and the psychological conditions in the parents. Discussion of the results encompasses psychodynamic and systemic issues.

92

B. Bräutigam and M. Herberhold “I always wanted you to admire my fasting,” said the hunger artist. “We do admire it,” said the overseer affably. “But you shouldn’t admire it,” said the hunger artist. “Well then we don’t admire it,” said the overseer, “but why shouldn’t we admire it?” “Because I have to fast, I can’t help it,” said the hunger artist. “What a fellow you are,” said the overseer, “and why can’t you help it?” “Because,” said the hunger artist, lifting his head and speaking, with his lips pursed, as if for a kiss, right into the overseer’s ear, so that no syllable might be lost, “because I couldn’t find the food I liked.” “If I had found it, believe me, I should have made no fuss and stuffed myself like you or anyone else.” (Kafka 1924, trans. W and E Muir)

Introduction The number of boys and men suffering from eating disorders is potentially on the rise; currently approximately every tenth person with an eating disorder is male. Some recent studies have placed the ratio as high as 1:5 (see Woodside 2004). In general, the prevalence rates given for the disorders vary from study to study, especially for adolescents. The numbers given for anorexia range from a rate of 19:1 (Jacobs and Isaacs 1987) to 35:13 (Fosson et al. 1987). One current study estimates the risk for a girl to be affected by an eating disorder during her adolescence at 17.9% and that for boys at 6.5%. Overall, the number of young men suffering from a disorder involving binge eating is about four times that of those with anorexia. The data for pre-pubertal anorexia are particularly inconsistent. One paper describes it as rare among boys (Muise et al. 2003); while another describes the pre-pubertal form of male anorexia as the more frequent and the more difficult to treat form of the disease (see Olivry and Corcos 1999). Ohzeki et al. (1993) investigated changes in eating behavior in boys and girls between the ages of 6-18 and discovered that eating-related problems among boys have a tendency to decrease with age while they increase in girls as they get older. Under the DSM IV criteria, anorexia is present when the subject’s body weight is maintained at less than 85% of expected weight and when the subject has a intense fear of gaining weight, despite being underweight; a body image distortion; and amenorrhea. The ICD-10 lists 5 major criteria: 1) a BMI (Body Mass Index kg/m2) under 17.5; 2) self-induced weight loss brought about through the avoidance of high-calorie foods and/or though selfinduced vomiting, purging, excessive exercise, or appetite suppressants; 3) a body-image distortion (see Sack, Henninger and Lamprecht 2002); 4) an endocrine disorder in the hypothalamic-pituitary-gonadal axis, manifest in women as amenorrhea and in men as loss of sexual interest and potency; and 5) in the case of pre-pubertal onset of the disorder the sequence of pubertal events is delayed – in boys the genitals remain juvenile, in girls there is primary amenorrhea. So, the ICD-10 does specify gender-specific disorder symptoms, which are reflected in various studies. In a study of six male youths with anorexia, Toifl et al. (1988) found a hypothalamic pituitary dysfunction and delayed onset of pubertal development. Jacoby et al. (2000) distinguish between physical and psychological changes. The first group includes circulatory regulatory disorders; hypotonia; disorders of the circulatory regulatory system; bradycardia (unusually slow pulse); hypothermia; amenorrhea; and, in advance stages, heart rhythm disorders, electrolyte disorders, and lanugo. The second

“I Couldn’t Find the Food I Liked” Anorexia in Boys. Three Case Reports

93

group includes conspicuous eating behavior; body image distortion, i.e., an altered cognitive perception of the body’s boundaries; extreme self-esteem issues (marked insecurity, feeling of worthlessness); avoidance of intimate sexual contact; and a high performance orientation. The gonadal disorder develops gradually in men and manifests itself in insufficient testosterone secretion and a resulting loss of sexual interest and potency. Medical complications, e.g., osteoporosis, affect men with anorexia to a similar extent that they do women. (Schweiger 2003). The primary age group for the disorder in children and adolescents is that of 11-18 year-olds. Resch (1999) gives the following risk factors: high pressure to perform, an inadequate ability to perceive one’s own emotional state, family conflict situations and overly close bonds, very early onset of puberty, and being a twin. Typical psychological and psycho-social characteristics of female anorexia patients are an above-average I.Q., a clinically relevant depressive pathology, being overly responsive to the needs of others, and conflict avoidance in family relationships, as well as heightened separation anxieties and contact disorders in school (see Walitza et al. 2001). Contrary to previous belief, eating disorders can begin even in pre-pubertal children. As early as kindergarten or primary school years, children can feel too fat and begin restricting eating behavior that may result in their being underweight or growth disorders. Patients with eating disorders report several non-specific food-related symptoms in childhood years, such as the inability to stomach certain foods, limited food selection, frequent nausea, or stomach pains after meals. Thus in the field of child psychology, the adoption of diagnostic criteria less strict than those laid out, for example, in the DSM IV (Schweiger, Peters and Sipos 2003) has been discussed. The DSM-IV distinguishes between restricting-type anorexia and the binge-eating type, i.e., with binging and induced vomiting. The latter differs from bulimia in that the diagnosis of bulimia does not apply to cases where patients are underweight. The ICD-10 refers to an atypical anorexia nervosa in cases where one of the major symptoms is missing, e.g. the body image distortion. The DSM-IV also distinguishes diagnostically among other types of psychogenic appetite loss that can occur when other psychological disorders are present, such as severe depression somatoform autonomic dysfunction (see Rief 1995), acute and chronic stress situations (see Garfinkel, Garner 1982) or post traumatic stress disorder. Bruch described anorexia in 1978 as a typical disease of the daughters of well-to-do, successful families. Eating disorders and anorexia in particular were then and still are considered typically female diseases. In-depth somatic examinations intended to rule out organic diseases are much more likely to be administered when the patients are undernourished boys (Severin, Benden and Menken 1992). In a review article, Muise et al. (2003) state that the diagnosis of an eating disorder under strict ICD-10 and DSM VI criteria raises serious difficulties, in part because in boys and men there is no distinct phenomenon corresponding to amenorrhea. They also point out that a wide and distinct spectrum of subclinical eating disorders does exist. Overall, the majority of studies agree that the similarities between those symptoms associated with eating disorders in male and female patients outweigh the differences (see Schweiger, Peters and Sipos 2003). There are, though, a few characteristics specific to boys and men. A study of body image, weight, and eating behavior in boys identified a strong denial of the presence of excess weight and described the pursuit of the perfect figure as far

94

B. Bräutigam and M. Herberhold

less prominent. Sixty-six percent of girls wanted to achieve a figure under normal weight (1015% underweight), while 82% of boys considered a figure in the normal weight range to be desirable. There was one very significant gender difference observed in an examination of attacks of hunger cravings: 78% of girls reported feelings of guilt, while only 24% of boys mentioned them (Hoffmann-Müller and Amstad 1994). The reason for this may lie in different gender-specific expectations regarding social rolls or it might trace back to different conflicts and conflict-resolution at an internal-psychological level. A premorbid obesity frequently occurs among men and male adolescents. Eating disorders are diagnosed less frequently and in general only when a psychiatric comorbidity is present (Severein, Benden and Menken 1992). These include depression, compulsive disorders and addiction. Eating disorders are more likely to affect boys / men who are involved in physical and sporting activities. In generally, boys / men who suffer from an eating disorder tend to push themselves to the limit physically rather than to fixate mentally on a specific weight. They strive less towards an ideal weight than they do to attain an ideal body, typically one that is muscular and powerful. The issue of sexual orientation, including a fragile sexual identity, seems to be a frequent point of conflict (Chyambry 2002, Dalem 2000). However, there is no definitive indication of a link between homosexual orientation and a more frequent incidence of eating disorders (Woodside 2004). There has been a higher frequency of homosexual orientation reported among men with bulimia nervosa. (Carlat et al. 1997). Homosexual men exhibit more eating disorder psychopathologies and higher depressivity in comparison to heterosexual men (Russel and Keel 2002). A familial constellation described as typical among eating disorder patients is one with an overprotective mother and absent father (Srenivasan 1978; Chambry 2002). In this area too though, we must point out that there is no sufficient indication for a specific familial pattern, though the family dynamics do play a significant roll in treatment of eating disorders. In diagnoses of the families of female eating disorder patients, the crucial evaluation is as to whether the damaging eating behavior has a specific function within the familial system. Characteristics that are often identified among very heterogeneous families with an anorexic family member are the following: a strong norm-referenced and high-performance orientation, “it ought to be done the right way”; the fear of separation, this can be linked with the myth of misfortune; the tendency to over-protectiveness and sacrifice (decisions are always made based on the other person’s interests, actions are always carried out with wellmeaning intentions for the other person and are not open to criticism); ill-defined borders; and the tendency to avoid entanglement. The ‘law of harmony’ (peace at all costs) and conflict avoidance are of special importance (see Cierpka and Reich 1997). Situations of separation or the disruption of attachments are often described as triggers of the disease in both genders. Anorexia among both boys and girls is seen as a way of coping with stress or, in negative terms, as a refusal to confront the conflicts typical of the developmental phase currently being undergone. The affected persons develop a heightened sense for the needs of others and often use it with controlling or manipulative intentions. A childish super-ego persists, as does a tendency on the part of the patient to be demanding, both of him or herself and of others (Schepker 1993). Regarding the pre-pubertal form of anorexia among boys, Olivry and Corcos (1999) allude to the comorbidity and to the case history of the psychological disturbance that

“I Couldn’t Find the Food I Liked” Anorexia in Boys. Three Case Reports

95

evinced itself earlier both through problems with food and through phobic-compulsive disturbances. The authors also describe a high incidence of narcissistic disorders in the primary attachment figures. In this specific form there is a significant presence of depression and auto-aggressive behavior among boys, while the incidence of laxative abuse is described as less probable. All of the studies reviewed stem from the same environment and similar treatment methods for both genders. In the case of in-patient treatment of adolescents, parental agreement and cooperation is of central importance. Since parents often experience the separation as a strain, it is recommended that attending staff work with the parents to set up precise conditions for discharge. Systemic short-term therapy, combined with elements of behavior therapy, is viewed as an especially effective treatment for adolescents (Blank et al. 2002). It is thought that the earlier a treatment begins after the onset of the disease, the better chances it has of success (Romeo 1994; Dalem 2000). The shame affect is seen as a particular problem among male adolescents who suffer from bulimia, because bulimia in general is viewed as an even more typically female disease than anorexia is. Below we have attempted to comprehensively describe the course of therapy and psychodynamics in a case report of a boy of just under 11 who suffers from the restricting type of anorexia. Following that, we have sketched out two vignettes of cases that were treated in another clinic and that fall more into the borderline area of classic eating disorders and hence indicate the broad spectrum of sub-clinical eating disorders that often go unnoticed but nonetheless require treatment.

Case Report 1 Situation at Admission David (10 yr. 11 mo.) was brought in as an emergency patient for in-patient treatment. David’s parents reported that his weight had fallen from 33 to 28 kg over the previous four weeks. He was 149 cm tall. According to his parents, he hadn’t eaten for 2 days and hadn’t drunk anything for one day. He had been given an infusion by his personal physician but had consistently refused to take any other liquids. His parents dated the onset of his weight loss back to a trip taken with his soccer club four months previously. They said David had felt very isolated on this trip, which was the first time he had been separated from his parents. He had, they said, been teased and bullied on the trip. David himself said “nothing in this trip had suited him.” Since that time he had eaten less and less, not because he was less hungry but because he had decided not to. The situation had come to a climax in the preceding month. His parents felt as though they were “hitting a wall” when they admonished him about eating. They reported that David was very concerned about gaining weight, felt guilty about food, and that his need for activity increased dramatically over the same period, but that he was not at all interested in his actual weight. They also noticed that David was extremely thrifty and concerned with cleanliness: he was sickened by the idea of showering at the swimming pool, wanting instead to shower at home because it was cleaner there. They said he would frequently check to see that the door was closed, washed his hands relatively frequently, and needed an unusually long time to perform day-to-day tasks such as tying his

96

B. Bräutigam and M. Herberhold

shoes. In the first conversation David himself reported being sadder than usual; his parents confirmed this. The parents supported the decision to have their son examined due to his poor physical condition and they expressed their agreement with the conditions of the in-patient treatment (participation in family therapy, etc).

Patient History The pregnancy went without complications. David was a planned child. He was breastfed for 10 months and was on the whole a restive and nervous infant. His statomotoric and speech development progressed normally. He suffered from chronic obstipation for about 3 months when he was 4. At 4 1/2 he started kindergarten, where he integrated quickly, although he often reacted aggressively to other children. His behavior overall was very defiant, and he exhibited a markedly strong will that, according to his parents, could not be countered in a strict manner. When he started school at six, David’s aggressive behavior stopped and he adapted very well. At times, in fact, his parents were shocked at how overadapted his behavior seemed. In first or second grade, David suffered from a sleep disorder, but after half a year it receded without any special intervention. Three months before his admission, he had entered secondary school, where he had great difficulties integrating in class. He was a relatively good student in terms of his performance in school. David listed soccer, skateboarding, swimming, cycling, handicrafts, and painting as his hobbies.

Family History David had a 22 year-old sister, a student of education science, who no longer lived at home. At 15, she had suffered from anorexia that abated without therapy. The relationship between David and his sister was good. His mother was employed half time in a white-collar job. The maternal grandparents had died as a result of excessive alcohol consumption: the grandmother when David’s mother was 8 years old, the grandfather one and a half years before David’s treatment began. David’s father was a decorator by profession. He had been an enthusiastic marathon runner, but had had to give this up five years earlier due to multiple pains for which no somatic cause could be found. David’s paternal grandfather committed suicide 22 years earlier; he suffered from multiple sclerosis and, according to David’s father, “couldn’t deal with that.” His paternal grandmother was still alive and there was loose contact with her; she was described as being somewhat inaccessible.

The Inpatient Treatment Environment A multi-discipline team works at the station, made up of pediatric nurses, a therapeutic educational nurse (Heilerziehungspfleger), an art therapist, teachers, and psychiatric and psychological psychotherapists. There are also a physiotherapist and a social worker that can be called in. There are twelve treatment positions available for children and adolescents aged

“I Couldn’t Find the Food I Liked” Anorexia in Boys. Three Case Reports

97

4 to 17. The station specializes in treating somatization and eating disorders. The treatment concept is committed to an integrative method approach; i.e., it draws on behavioral therapy, depth-psychological, systemic, and on elements of the integrative child and adolescent psychotherapy as well. Treatment of eating disorder patients lasts between a minimum six weeks and a maximum six months. As a rule, patients are given a behavioral therapyoriented, individually designed, step-by-step plan to nutritional rehabilitation; they also take part in the depth-psychology oriented group therapy, in art therapy, in physical therapy, and learn yoga, to improve their body awareness. They also receive two individual therapy hours per week, and once a week a parent or family therapy session takes place.

Course of the Therapy Our first impression of David was of a precocious, serious, and in his whole behavior, very stiff boy, who spoke of his illness as something alien. He said he no longer had an appetite and had to count calories, but he didn’t know why that was the case. It was very important to him to be thin though, so that he could be agile. His speech was uniform, with little modulation in his voice, and his facial expression was rigid. The first four weeks of his stay were marked by crises. David often refused to cooperate, pulled out his tube himself, and exerted enormous pressure on his parents to take him back home. After two weeks of inpatient stay, an extreme compulsion to wash manifested itself; after an observation phase this was treated with Anafranil. In the individual therapy sessions we sensed mental disturbances and blocks in the counter-transference, which, as I record later, also were partly responsible for the patient not sensing powerful emotions like rage or powerlessness. In the psychological diagnostics, especially during the projective test procedures, the theme of aggression, and the fear of and defense against it, were dominant with David. Another central theme seemed to be his relationship with his father, to whom David wanted to be close, but with whom he was also in competition. In addition, his fantasies of greatness and high-performance related themes, which he attempted to keep minor, became evident. Work with the parents was initially quite difficult; the collaboration was extremely fragile. It was extremely difficult for both parents to decide definitely on the in-patient treatment. Both preferred the idea that their son not be forced into anything and anxiously predicted resistance from him: resistance that promptly emerged, in all its intensity and despair. On several occasions, David threatened to take his own life if his parents didn’t take him out of in-patient treatment immediately. Understandably, this threw both parents into panic, particularly David’s father, due to the suicide of his own father. The fear that something would happen to David at home or that he might die collided with the fear inspired by David’s threat to harm himself. With strong therapeutic support however, both decided to leave David in the in-patient treatment program. As soon as it became clear to David that this decision was unequivocal, the situation defused itself and he grew increasingly willing to cooperate. A further hurdle in the therapeutic treatment arose in dealing with the paradoxical signals the parents sent David. They constantly sent conflicting messages: obey the rules, but break

98

B. Bräutigam and M. Herberhold

them too. Once the weight situation had become less dramatic, David’s parents began to join forces with him to break the hospital rules: they smuggled food in, over-stayed visiting hours, etc. When confronted with this, the parents behaved like anxious and rebellious children, while the clinic and the therapist took over the roll of the strict, rigid but also life-sustaining mother. The decisive positive shift in the therapeutic treatment occurred on two levels. Initially through a conversation with the parents in which they articulated their anger at the clinic, which had cut their contact with their son. Focusing on this conflict made it possible to transform the opposition into cooperation. There followed an individual therapy session with David, in which he actively demanded therapeutic support in the form of positive signals when something had worked successfully. At this level too, a change occurred, and the patient decided, on his own initiative, to work with the therapist instead of against her. It was only after the conflict with the parents had been resolved that this became possible. The therapeutic relationship then became so stable that it became possible to establish sustainable cooperation with David and to modify the stimuli plans with him. His mood - which up until this time had ranged from despair, to auto-aggression, to aggression directed outwards visibly improved; he gained weight and the compulsive behavior lessened. In individual therapy his behavior developed from that of a precocious, intellectualizing and problemconscious narrative behavior to a more childlike, age-appropriate, playful behavior. He also became better and better at articulating the fact that he had often felt lonely and isolated from other children. By the end of the 10-week treatment, David had gained 8 kg and the compulsive pathology had abated to such an extent that the medication could be tapered off. The latter was primarily understood as an expression of an underlying severe depressive episode. David’s father was advised to seek individual psychotherapeutic support to confront his own fear pathology; his response to this suggestion was positive and he acted upon it.

Family Dynamics In the course of the family therapy, food established itself as a significant topic and relevant arena for action. Both parents were very slender to the point of thinness; during the treatment of her son, David’s mother became even thinner. In the same period, it became clear that she had had only very limited experience with care-giving and continually felt herself to be on the verge of being overburdened within her role as a mother and in her duty to care for others emotionally. The father talked about the unbelievable amount of calories that, he said, he had been able to consume without gaining fat during his marathon running days. The fear, to some extent seemingly paranoid, of the deterioration of his own body – especially before the background of his father’s suicide – was a central theme for him. David’s sister talked about her own anorexic period during a family session. The relationship of the parents to one another came across as very sibling-like in character. There seemed to be almost no partner level that was separate from the children. Both spoke of extreme difficulties in supporting each other and keeping each other grounded. They reported that in the current situation they could neither comfort nor be gentle with one

“I Couldn’t Find the Food I Liked” Anorexia in Boys. Three Case Reports

99

another, because to do so would cause them to feel guilty about feeling good when their son was in the clinic. David, for his part, refused to accept gifts from his parents, claiming that he had not earned them. This is a self-punishing dynamic typical for families with anorexic children, one that could be summed up with the motto: “Do everything for the others, nothing for yourself, a depressive duty-fulfillment without enthusiasm that is driven by guilt” (Schepker 1993, p.12). Once a trusting therapeutic relationship had been established, the themes of separation and the disruption of bonds dominated the family therapy session. Within the family there was a significant amount of fear associated with these themes: separation was viewed as almost equivalent to death and absolute loss. The family sculpture had something about it that struck outside observers as rather oppressive and constricting but which all of the family members perceived as a pleasant density and physical closeness. The sister, who took part in one family session, articulated her feelings of guilt and ambivalence about having moved out; that is when it became obvious just how critical and existentially threatening all family members perceived the physical separation from the sister to be.

Psychodynamics David’s illness must be viewed at different levels. On the one level, it presents a classic autonomy-dependency conflict; on another it symbolizes a trans-generationally-significant theme for the paternal line; and on a third, it fulfils the function of a familial reapprochement. David’s pathology began with his entry into a developmental phase that implied more autonomy. For David and his whole family, autonomy was associated with fear and thus this represented a critical transition. In our view the disease was triggered by the temporary separation from his parents, a situation exacerbated by harassment by the other children and in which David was also confronted with a new environment. David’s self image as that of an athletic boy who wins all competitions also collapsed on this soccer trip. He lost to other boys. David processed this defeat and the separation from his parents with a feeling of guilt. Out of this emerged what was for him an existential question, one that had dominated his father and probably his grandfather as well: can I go on living if I don’t have complete control over my body? This is where the trans-generationally-significant theme expressed itself. According to family lore, David’s grandfather had committed suicide because he could no longer tolerate the physical deterioration brought on by his multiple sclerosis. David’s father had kept physically fit through marathon running for years but was ultimately forced to give that up. He then became preoccupied with the unvoiced question or fear that he might have the same disease his father had had. When David’s disorder appeared, his father was at the same age at which his own father had committed suicide. For David’s father, this represented an extremely critical point of in his life, one that his son picked up on and transformed into a crisis of his own. David confronted the issue of life and death and these existential questions in his father’s place, and by doing so managed to bring his whole family together and cause them to confront such threatening subjects as fear of loss and separation together.

100

B. Bräutigam and M. Herberhold

David’s illness is also an avowal of his loyalty for his father: David identified with his father very much and tried to emulate him in his athletic endeavors, but he was also very much afraid outdoing his father in that arena.

Case Report 2 Over a four-year period, Stefan (13 yr. 3 mo.) received in-patient psychiatric treatment four times under various diagnoses. He was diagnosed under ICD-10 with a social behavior and emotional disorder (F. 91.3) and with a somatoform dysfunction with nausea and vomiting. The early patient history shows normal statomotoric and speech development; toilet training was complete at the end of his first year. As an infant and small child, Stefan suffered from severe sleep disorders: up until his third year he woke up as often as 20 times at night. He also ate and drank very little, reacting with vomiting to milk products in particular. When his father insisted that he eat his entire serving, Stefan reacted by vomiting. In the later patient history, the fact that Stefan initially had many friends and got along fairly well in school seems significant. He had several stays in the pediatric clinic due to undefined stomach pains and refusal to eat. From the beginning of his eleventh year, Stefan’s aggressive behavior in school and at home began to increase. He was often involved in fistfights and verbally aggressive towards his mother. The mother reacted to this at times by accommodating his wishes or by ignoring the behavior, sometimes with blows and rescinding television privileges. With respect to the family history, we know that Stefan grew up with his parents as an only child. His father became unemployed when Stefan was one and developed an alcohol problem. Stefan witnessed acts of domestic violence perpetrated against his mother and there were isolated violent acts directed against Stefan. For years, Stefan’s mother took care of her own ailing mother, who died when Stefan was 12. She herself suffered from a cerebral tumor with facial paralysis. Stefan’s parents separated when he turned 10; the separation was not discussed with Stefan. From then on, contact with his father was sporadic and irregular. From the various courses of treatment, it is apparent that the somatoform dysfunction with vomiting and nausea was not treated directly until around the end of his tenth year, although it was obviously dominant. The disorder developed from an earlier interaction disorder that went unrecognized and untreated. This earlier disorder manifested itself as a sleep and feeding disorder. It is also evident that both parents had, in different ways, withdrawn from the relationship with their son. The only way Stefan could get his parents attention was by refusing to eat and through the stomach aches, accompanied with nausea and vomiting, that cropped up again and again. After he turned 10, with the onset of puberty and his parents’ separation, Stefan’s introverted self-destructive behavior began to decrease and aggression directed outward became more frequent, climaxing in arson and severely destructive behavior during his last in-patient treatment period. This case illustrates the way that a diagnosed but incompletely treated eating disorder, an expression of the hunger for parental attention and security, can be transformed into a dissocial disorder in male adolescents with multiple manifestations.

“I Couldn’t Find the Food I Liked” Anorexia in Boys. Three Case Reports

101

Case Report 3 13 yr. 10 mo. old Michael, who had a learning disability, was treated for three and a half months for a psychogenic eating disorder for which no more exact diagnosis was given; for a nascent personality development disorder with anxiety/avoidance personality traits; and for stereotyped movement disorders in the form of jactation. Michael, who comes from a tall family, is 1.93 m tall and weighed 54 kg (BMI 14.5) at admission. A weight loss of 6 kg and the intensification of a chronic eating disorder triggered his hospitalization. The eating disorder took the form of a daily battle over eating: Michael was said to throw out his food and often vomit after meals. With regard to Michael’s medical history: nicotine and alcohol abuse were known to have taken place during the pregnancy, which went to term, with an umbilical cord entanglement at birth. Nutritional problems arose very early on. His statomotoric development and speech development were delayed. Michael’s parents separated when he was five years old, at which point his paternal grandparents took over his care. Two years later, contact with Michael’s mother broke off completely. He saw his father regularly on weekends. Michael started at a residential school for children with disabilities at age 7. At eleven, the fourteen year-old son of his father’s long-term girlfriend sexually abused him. Michael transferred to another residential school shortly before his hospitalization at the clinic. A few days before his hospitalization, Michael’s father and his girlfriend, with whom Michael had had a good relationship, separated. The over-protective child-raising style of the grandmother was discussed as a problem and the high degree of responsibility borne by his father was also raised as an issue during the in-patient treatment. A recommendation was made that Michael be encouraged to take on more independence and responsibility in the area of practical living. Michael was released after a small weight gain and a decrease in the jactation. The psychogenic eating disorder was considered to be the reaction of a learning-disabled boy who was extremely anxious/unselfconfident, socially less competent and conflict-avoiding, due to psychosocial stress factors on the basis of an early childhood emotional deprivation.

Summary and Discussion The number of boys and men suffering from eating disorders is increasing. Girls run a 17.5% risk of acquiring an eating disorder; boys, 6.5%. The number of boys with a binge eating form of disorder is four times higher than that suffering from anorexia nervosa. When applying the classification system, the criterion of the abnormal gonadal axis (lowered libido, potency, juvenile genitals) is more difficult to operationalize than is amenorrhea. Boys seem to strive for a less underweight ideal figure than that pursued by girls. They do not suffer as much from feelings of guilt regarding food binges. Boys tend to fixate less on a specific weight, and they strive less towards an ideal weight, instead pursuing an ideal physique, usually a muscular and powerful one. Questions of sexual orientation play a role among boys with eating disorders more often than they do among girls. Among men with bulimia, a higher frequency of homosexual orientation has been reported. Overall however, those

102

B. Bräutigam and M. Herberhold

symptoms disorders in both genders have in common outweigh the gender-specific differences. Eating disorders among boys are characterized by a wide spectrum of forms of manifestation and causal factors and by a high frequency of sub-clinical disorders in particular. In the restricting type of anorexia nervosa, the aspect of asceticism and the strength drawn from it is used as a way of establishing borders between the subject and the parents or important attachment persons. The children and adolescents in question use the refusal to eat as a way to try to deal with the general developmental tasks of gradual separation, identity building, and assertion of independence, at the cost of enjoyment, sensuality, sexuality, and intimacy. By refusing to eat, a female anorexic patient is often trying to detach herself from a symbiotic relationship with her mother and thereby to demonstrate – in an extreme and often life-threatening way –having cut the apron strings and gained independence. In describing the case of 10 year-old David, we have attempted to give an example of a seldom described but probably not so very rare kind of case. This is that of a boy who uses his pathology in an attempt to detach himself from a symbiotic relationship with his father and transform a conflict that actually belongs to his father into one of his own, thus making it a family theme more available to examination. The sustainable therapeutic alliance with the parents, which included the general terms set by the clinic, was of critical importance in putting the treatment on the road to success. On this basis, primarily supporting work could be done with David in individual therapy. This theme had to be brought out into the open in the family therapy, but without apportioning blame. In this regard, a mixture of a resource-oriented and a confrontational approach seemed optimal, one that respected the family as a functional system but nevertheless recognized dysfunctional entanglements as such, thus providing access to opportunities for change. The psychotherapeutic treatment of children and adolescents with anorexic pathologies usually involves walking a tightrope between curbing and permitting autonomy. It alternates between restrictive control and the support of developing needs for independence. The treatment often takes on the form of a battle, one that cannot be won by the therapist with out the patient though it can be won by the patient without the therapist. This must be made very clear to the patient: the idea is to return control over his life and his decisions to him and to humiliate him as little as possible along the way. The case vignettes of Stefan and Michael should illustrate the way in which unrecognized or insufficiently treated eating disorders can turn into other disorder profiles. They should also illustrate the initially atypical contexts in which eating disorders can represent an expression of the psychological distress of a male adolescent.

References Blank, S., Zadik, Z., Katz, I., Mahazri, Y., Toker, I. and Barak, I. (2002) The emergence and treatment of anorexia and bulimia nervosa: A comprehensive and practical model. In: Int. J. Adolesc. Med. Health, 14, 257 – 260 Bruch, H. (1978) The golden cage. Cambrigde, MA: Harvard university Press Carlat, DJ, Camargo,CA., Herzog, DB. (1997) Eating disorders in males: a report on 135 patients. Am J Psychiatry, 154, 1127-1132

“I Couldn’t Find the Food I Liked” Anorexia in Boys. Three Case Reports

103

Chambry, J., Corcos, M., Guilbaud, O. and Jeammet, P. (2002) L' anorexie mentale masculine: réalités et perspctives. In: Ann. Med. Interne, 153, 1S61 – 1S67 Cierpka, M. and Reich, G. (1997) Die familientherapeutische Behandlung von Patientinnen mit Eßstörungen. In: Reich, G., Cierpka, M. (Hrsg. 127 - 150) Psychotherapie der Eßstörung. New York, Stuttgart: Thieme Dalem, I., Piccinin, B., Lerminiaux, D. and Ansseau, M. (2000) L' Anorexie Mentale Du Garcon. In: Rev. Med. Liege, 55, 1051-1057 Fosson, A., Knibbs, J., Bryant-Waugh, R. and Lask, B. (1987) Early onset anorexia. In: Arch Dis Childhood, 62, 114 – 118 Garfinkel, P. E. and Garner, D. M. (1982) Anorexia nervosa: A multidimensional perspective. New York: Brunner / Mazel Hoffmann-Müller, B. and Amstad, H. (1994) Körperbild, Gewicht und Eßverhalten bei Jugendlichen. In: Schweizerische Rundschau für Medizin, 83, 1337 - 1343 Jacobi, C., Thiel, A. and Paul T. (2000) Kognitive Verhaltenstherapie bei Anorexia nervosa und Bulimia nervosa. Weinheim: Beltz, PsychologieVerlagsUnion Jacobs, B., W.and Isaacs, S. (1986) Pre-pubertal anorexia nervosa: A retrospective controlled study. In: J. Child Psychol. Psychiatry, 27, 237 - 250 Kafka, Franz (1969) Sämtliche Erzählungen, Frankfurt a. Main, Fischer-Verlag Kjelsas, E., Bjornstrom, C. and Gotestam KG. (2004) Prevalence of eating disorders in female and male adolescents. In: Eat. Behav., 5, 13 – 25 Muise, A. M., Stein, D. G. and Abress, G. (2003) Eating disorders in Adolescent Boys: A Review of the Adolescent and Young Adult Literature. In: Journal of Adolescent Health, 33, 427 - 435 Ohzeki, T., Othara, H., Hanaki, K., Motozumi, H., and Shiraki, K. (1993) Eating Attitudes in Boys and Girls aged 6-18 years. In: Psychopathology, 26, 117 – 121 Olivry, E. and Corcos, M. (1999) L`anorexie mentale prépubertaire. In: La Presse Médicale, 28, 100- 102 Resch, F. et al. (1999) Entwicklungspsychopathologie des Kindes – und Jugendalters. Weinheim: Beltz, PsychologieVerlagsUnion Rief, W. (1995) Multiple somatoforme Symptome und Hypochondrie: empirische Beiträge zur Diagnostik und Behandlung. Bern, Göttingen: Huber Romeo, F. (1994) Adolescent boys and anorexia nervosa. In: Adolescence, 29, 643 – 647 Russell, CJ and Keel, P. (2002) Homosxuality as a specific risk facktor for eating disorders in men. In: Int. J Eat Disord. 31, 300-3006 Sack, M., Henniger, S. and Lamprecht, F. (2002) Veränderungen im Körperbild und Körpererleben bei essgestörten und nichtessgestörten Patienten im Verlauf einer stationären Psychotherapie. In: Psychotherapie, Psychosomatik, Medizinische Psychologie, 52, 64 – 69 Schepker, R. (1994) Die Bedeutung der Schulleistungen bei Jugendlichen mit anorektischen Störungen. In: Prax. Kinderpsychol. Kinderpsychiat. 42, 8-14 Schweiger, U., Peters, A. and Sipos, V. (2003) Essstörungen. Stuttgart, New York: Thieme Severien, C., Benden A., and Menken, U. (1992) Anorexia nervosa bei Knaben – ein Fallbericht. In: Fortschr. Med., 110, 559 - 561 Sreenivasan, U. (1978) Anorexia in boys. In: Can. Psychiatr. Assoc. J., 23, 159 - 162

104

B. Bräutigam and M. Herberhold

Toifl, K., Waldhauser, F., Lischka, A., and Frisch., H. (1998) Anorexia nervosa bei männlichen Jugendlichen. In: Klinische Pädiatrie 200, 316-320 Walitza, S., Schulze, U. and Warnke, A. (2001) Unterschiede zwischen jugendlichen Patientinnen mit Anorexia nervosa und Bulimia nervosa im Hinblick auf psychologische und psychosoziale Merkmale. In: Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie, 29, 117 – 125 Woodside, D. B. (2004) Assessing and Treating Men with Eating Disorders. In: Psychiatric Times 3, 86-88

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 105-143 © 2006 Nova Science Publishers, Inc.

Chapter VI

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake, Eating Patterns, Eating Attitudes and Body Image of Brazilian Bulimic Patients Marle dos Santos Alvarenga1, Fernanda Baeza Scagliusi2 and Sonia Tucunduva Philippi3 1

Eating Disorders Unit of Clinics Hospital, Department of Psychiatry, Institute of Psychiatry, University of São Paulo 2 School of Physical Education and Sport, University of São Paulo and Eating Disorders Unit of Clinics Hospital, Department of Psychiatry, Institute of Psychiatry, University of São Paulo 3 Department of Nutrition, School of Public Health, University of São Paulo

Abstract Eating disorders (ED) have been treated in Brazil since 1992 with the creation of the ED Unit of the University of São Paulo, a public service that has treated 1,794 patients, mainly white, reasonable educated and aged between 21 and 40 years. Food intake and eating patterns and behaviors are disturbed in bulimia nervosa (BN). Food intake is defined as the food and nutrients that compose the diet, while eating patterns are the meal frequency, regularity and schedules, and eating behaviors are the attitudes, beliefs and relationship with food. In Brazil, the effect of multiprofessional treatment in BN had never been examined. Even in developed nations, only the frequency of bulimic symptoms has been evaluated. The Eating Disorder Inventory, Three-Factor Eating Questionnaire, Dutch Eating Behavior Questionnaire and Restraint Scale were used to analyze eating behaviors, although these questionnaires focus especially in dietary restraint, leaving the other eating behaviors’ aspects uncovered.

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

106 Methods

Thirty-nine women with BN (according to DSM-IV criteria) were followed. Treatment was composed by 12 weeks of cognitive-behavior therapy, pharmacotherapy and nutrition counseling. Measurements were made before and after treatment, and after three months. Patients recorded their food intake and occurrence of compulsions and purges in a diary. They fulfilled the EAT, BITE and BSQ, and also an eating attitudes questionnaire, especially developed for this research. Non-parametric statistics were used to test for differences among the three moments.

Results We observed an improvement in clinical symptoms; at the end of following 97.5% of the patients did not fulfill criteria for BN anymore. Scores of EAT, BSQ and BITEsymptoms decreased after treatment and even more after the later following. Nutrients intake did not alter, even though energy content of the meals followed by vomit decreased. Number of meals increased and patients did more meals seated, with company and less anxious. The belief of automatically gaining weight after a meal, and guilty and worry after eating a “forbidden” food decreased. Nevertheless, most of them remained hating the hunger sensation, having difficulties with food choices and not believing that they could have a normal diet and a normal weight.

Conclusion Based on the questions used to assess eating attitudes, we are now developing an eating attitudes questionnaire, which will be psychometrically tested. This study supports the idea of the importance of food issues and behaviors in ED, because even the patients that had a clinical improvement remained with a complicated relationship with food, which can contribute to relapses.

Introduction Just as in other developing countries, Brazil is undergoing a nutritional transition. Nutritional transition represents the changes that take place for centuries regarding nutritional patterns that result from shifts in the structure of the diet followed by the population. These changes are related to economic, social, and demographic changes, and they result in health changes as well (Popkin, 1993). These transitions can be seen worldwide, given globalization of current habits and consumption patterns. However, studies show that the pace of change in countries undergoing less development has been markedly quicker, with a notable progression from malnutrition to obesity. Particularly in Brazil, where great economic and demographic changes took place in the last decades - from 1960 on (Monteiro et al., 2002; 2004) - we see the presence of malnutrition along with obesity. In many studies regarding nutritional transition obesity and other chronic diseases are the main focus, but as appointed by Nasser (1988) and Yager

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

107

(2000) the increasing prevalence of eating disorders (ED) is also a characteristic feature of nutrition transition. There are no specific data regarding prevalence of ED in Brazil. Case reports from developing countries are rare; thus, it gives the wrong impression that these disorders are rare in non-developed countries (Negrão and Cordás, 1996). It is estimated that the prevalence of ED in Brazil is similar to that observed in western countries for young women: 0.5% for anorexia nervosa; 1.0% for bulimia nervosa, and 2-5% if partial syndromes are considered (Hay, 2002). Anyhow, it is known that the incidence of ED has been increasing in less developed countries (Nasser et al., 2001). Vilela et al. (2004) used some screening questionnaires to evaluate the prevalence of possible eating disorders and inappropriate eating behaviors in Brazilian children and adolescents aged 7 to 19 years old. According to the Eating Attitudes Test, 13.3% of the sample had inappropriate eating behaviors. Being female implied in a greater risk of having inadequate eating behaviors (odds ratio = 1.54; 95% confidence interval = 1.16 – 2.05). According to the Bulimic Inventory Test Edinburgh, 1.1% of the sample had a possible diagnosis of bulimia nervosa. Another Brazilian study assessed the prevalence of abnormal eating behaviors among 513 young women (aged 12 to 29 years) randomly selected (Nunes et al., 2003). Combining scores obtained in the Eating Attitudes Test and in the Bulimic Inventory Test Edinburgh, it was observed that 10.9% of the sample presented abnormal eating behaviors, while 23.8% had unusual eating patterns. Other striking findings were found by Nappo et al. (2002). Investigating a sample of 2,370 Brazilian subjects about the methods used by them in order to lose weight, the authors observed that 72.4% of the sample had been submitted to some treatment to lose weight, and 79.2% of these had consumed amphetamine-like anorectic drugs. The most interesting fact was that among these consumers, 60% had a Body Mass Index below 29.9 kg/m2, which shows that they did not need these drugs and that probably they were consuming them motivated by physical appearance aspects. Taken together, this data shows that is necessary to study, prevent and treat eating disorders in Brazil. Eating disorders have been treated in Brazil since 1992 with the creation of the ED Unit of Clinics Hospital of the University of São Paulo, which is a public service (visit http://www.ambulim.org.br for more information about this service). Together with the unit of ED in children and adolescents and the binge eating disorder (accompanied by obesity) unit, these services has treated 1,794 patients, mainly females (88.3%), white, reasonable educated (36.4% completed junior high or high school and 27% had studied for more than high school) and aged between 21 and 40 years (58.1%). Nowadays some Brazilian groups work with ED, offering some public assistance (Fontenelle et al., 2003; Negrão and Cordás, 1996) and doing researches (Borges et al., 2002; Nunes et al, 2003; Vilela et al, 2004). It is important to remind that there are only ten of these centers in Brazil, which certainly is too little for such populous country (total population: 182 million people – for more information visit http://www.ibge.gov.br). The Brazilian studies that focused in nutritional aspects of ED started to be conducted in 1994 as graduate researches of the dietitians that belonged to the Nutrition in Eating Disorders Study Group (visit http://www.genta.com.br for more information about this group) (Alvarenga et al., 2003; Dunker and Philippi, 2003; Scagliusi et al., 2005a). Our current researches focus mainly in bulimia nervosa (BN).

108

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

The interest for this area of research came from the observation that the majority of patients who looked for treatment in our unit had BN and this is an eating disorder marked not only by binge eating and compensatory practices, but also by an extremely affected eating behavior (ADA, 2001; APA, 1994). Distorted cognitions about nutrition and feelings of repugnance, hate and incompetence in dealing with food are also features of this disease (Sunday et al., 1992). Nutritional rehabilitation has a key and primary role with regards to treatment objectives, which should be performed by a multiprofessional staff aiming to end bulimic behaviors and to alter the patient’s relationship towards food and weight (ADA, 2001; APA, 1994; Eiger et al., 1996). The first studies regarding nutritional aspects of BN were conducted between 1980 and 1990, essentially in developed countries (Hadigan et al., 1989; Kissileff et al., 1986; Mitchell and Laine, 1985; Walsh et al., 1989). Researches describes that a chaotic eating pattern is present in BN, oscillating between severe dietary restraint and episodes in which the energy intake is extremely high (Wallin et al., 1995). The “diet – binge – purge” cycle illustrates the eating pattern of bulimic patients. They constantly start a new diet, which makes them eat a very limited amount of food and avoid those foods considered by them caloric or “fattening” (the named “forbidden foods”). This restraint leads to a binge eating episode, where the energy consumption can be very high (Reiff, 1992). The items more consumed in these binge episodes are those most avoided by the patients due to their fear of gaining weight (for example, cookies, chocolates, candies, etc) (Alvarenga et al., 2003; Wallin et al., 1994; Walsh et al., 1989). Some authors argue that the disturbed eating pattern is a general feature of BN and not only a characteristic of their restrictive diets and binge episodes, which explain the difficulties faced in order to normalize their intake (Hetherington et al., 1993; Sunday and, Halmi, 1996). Besides their unhealthy food consumption, its is known that these patients have other disturbed eating behaviors, as difficulties regarding food choice, abnormal patterns of hungry and satiety, food aversion, fears, taboos and prejudices regarding food and weight control (Elmore and Castro, 1991; Hetherington et al., 1993; Sunday and Halmi, 1996). The studies conducted in laboratories, metabolic units or hospitals (with inpatients) observed in the binges episodes an energy intake varying from 1,436 to 8,585 kcal, which was generally followed by vomits. These episodes usually lasted 59 minutes and they were composed by 59% of carbohydrates, 43% of lipids and 8% of proteins. Without the binges patients had a wide range of energy consumption, varying from 69 to 10,620 kcal (Hadigan et al., 1989; Hetherington et al., 1994; Kissileff et al., 1986; Mitchell and Laine, 1985; Sunday and, Halmi, 1996; Walsh et al., 1989). The artificial settings and the low ecological validity of these studies may have limited their findings, but the ample difference between the minimal and maximal values shows that there is a great variability in food intake data of bulimic patients. This scenario shows that it is hard to study nutritional aspects of BN, especially if one considers that the term “nutritional aspects” embodies several different variables. In our studies we divided this term in the following components: food intake (foods that are eaten and their energy and nutrient content); eating pattern (general characteristics of the intake, as

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

109

number, types and schedules of the meals) and eating attitudes (relationship with food, feelings and beliefs related to food). Among these aspects, we are most interest in eating attitudes, not only because of the scarce number of studies concerning it but also because it seems that it is one of the most disturbed characteristics of BN. Due to our interest, we created a more specific definition of eating attitudes, based on the statements of Garcia (1999) and Johnson (1985): what, how, with what, with whom, where, and when we eat, why we eat that, in which situation we eat, what we think and feel towards food. It is also important to ask in what are food choices based on, and where there is difficulty, lack of control, aversion, and what are the feelings related to food. Although follow-up studies of bulimic patients are commonly carried out in developed countries (Collings and King, 1994; Fahy and Russell, 1993; Keel et al., 1999; Keel and Mitchell, 1997; Leung et al., 2000; Maddocks et al., 1992), outcome measurements and follow-up studies are not conducted systematically in Brazil. Studies to measure outcome are hard to be conducted because of methodological difficulties, which include the definition of a recovery criteria and follow-up methods. The definition of recovery varies in each study: some considered recovery as those patient that presented bulimic episodes and purging episodes once a month (Pyle et al., 1990) whereas others consider it as just those that did not present any episode (Herzog et al., 1996; Keller et al., 1992; Maddocks and Kaplan, 1991). To assess the effects of BN treatment, most studies compare the frequency of pre and post treatment bulimic behavior (vomiting episodes, for example) (Herzog et al., 1996). In addition to analyzing the frequency of binge eating and purging episodes, many follow-up studies utilized recovery predictors and indicated that the frequency of bulimic behavior at baseline was not associated to the outcome (Abraham et al., 1983; Fairburn et al., 1986; Hsu and Holder, 1986). Nevertheless, several factors are used as prognostic predictors: age at the beginning of the disorder, presence of comorbidities, psychosocial aspects, weight at the start of the treatment, eating behavior and methods used to lose weight (Herzog et al., 1996). Also, there are some standardized tests used to screen patients with eating disorders, such as Eating Attitudes Test - EAT-26 (Garner et al., 1982), Bulimic Inventory Test Edinburgh BITE (Henderson and Freeman, 1987), and Eating Disorder Inventory - EDI (Garner et al, 1983), among others. The results of some of these tests are analyzed in studies on recovery predictors, in which Olmested et al. (1994) found a high score in the subscale of bulimia of EAT-26 (Garner and Garfinkel, 1979) and high score in the interpersonal distrust subscale of the Eating Disorder Inventory-EDI (Garner et al., 1983) among the recurrence predictors. According to Steinhausen and Seidel (1993), self-applied scales should be used in prognostic studies. Although there are many studies using screening tests in several populations (Adami et al., 1997; Beals, 2002; Bhugra et al., 2003; Ghazal et al., 2001; Lee et al., 2002; Nobakht and Dezhkam, 2000), even to compare results of healthy individuals to those from ED patients (Behar et al., 2003; Nakazato et al., 2003), few studies assessed the scores of individuals with ED post-treatment (Brambilla et al., 1995; Fernandéz et al., 1998; Steinhausen and Seidel, 1993). The uncertainty remains as to whether the scores attained on these tests return to normal patterns after the remission of ED symptoms. Even in developed countries, few studies have assessed the nutritional progress of bulimic patients and no study has evaluated the effect of a multiprofessional intervention with

110

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

regards to important BN aspects: relationship and behavior towards food. Also, as far as we are concerned the food intake of bulimic patients was analyzed only in cross-sectional studies, so it is not know if the treatment improves the food consumption of these patients. Therefore, this issue requires further study (Whisenant and Smith, 1995). The few studies that have assessed the effect of treatment on eating behavior used tools such as food diaries and standardized tests such as the Eating Disorder Inventory (Garner et al., 1993). Although we presented above these tests as interesting measurement tools, one must remember that these instruments do not encompass the wide concept of food behavior and are frequently limited to the analysis of dietary restraint (Herman and Mack, 1975). Because of that, researchers with interest in nutritional aspects of BN have to use other instruments able to approach these aspects in a more comprehensive manner. Whisennat and Smith (1995) interviewed dietitians who worked with ED and stressed the importance of more objective evaluations of the nutritional treatment. This idea is supported by Eckstein-Harmon (1993) who attested the importance of the outcome measurements of nutritional education and rehabilitation in eating disordered outpatients and inpatients. So we conducted an follow-up study to assess the effect of multiprofessional intervention on bulimic symptoms, food intake, eating patterns, eating behavior and body image in bulimic patients treated at a center considered to be one of reference in Brazil: the ED Unit of Clinics Hospital of the University of São Paulo.

Methods Thirty-nine female patients with BN treated at the Eating Disorders Unit of the University of São Paulo (in Brazil) were followed-up. Subjects were evaluated by a psychiatrist, and BN was diagnosed by means of a semi-structured clinical interview, according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders - DSMIV (APA, 1994). The descriptive data of the patients were collected in this interview. Patients had their weights and heights measured, and this data was used to calculate Body Mass Index (BMI – weight in kg/height2 in meters). Patients gave informed consent before participation. They were also informed that the goal of the study was to evaluate the outcome of the treatment. The study was approved by the Committee of Ethics of the Clinics Hospital of the College of Medicine of the University of São Paulo. Measurements were performed at baseline (Phase 1), immediately after treatment (Phase 2) and three months after treatment (Phase 3). All measures were compared between these phases. Bulimia nervosa should be treated by a multiprofessional staff working to end bulimic behaviors and to change patients’ relationship towards food and weight (Gannon and Mitchell, 1986; ADA, 1988; APA, 1994). Cognitive Behavioral Therapy (CBT) is considered the best technique to treat BN (Agras et al., 2000; Leung et al., 2000). Because of that, treatment consisted of 12 weeks of cognitive behavioral therapy (CBT) – with one weekly consultation with the psychiatrist, the psychology and the nutrition education teams. At the end of treatment, the unit provided 3 more months of care, but in an unstructured form.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

111

The number of weeks of treatment was defined arbitrary, but its structure and content followed the models proposed by Fairburn (1981), Johnson et al. (1986), Lacey (1985), Nutzunger and Zwann (1990) and Vanderlinden et al. (1989), which described cognitivebehavioral techniques and provided guidelines for nutritional counseling, even suggesting some educative materials. The goals of the nutritional treatment were to: a) decrease the binge and purging episodes; b) minimize dietary restraint; c) establish a regular meal pattern; d) increase food variety; e) correct nutritional deficiencies and f) implant a healthy food intake and behavior (ADA, 1994; ADA, 2001; Latner and Wilson, 2001). The approach can be divided in some key points: a) education about the disease and its implications; b) education about food and nutrition; c) reduction of weight concerns; d) self-monitoring of the food intake by means of a food record and e) implementation of a healthy eating pattern (Story, 1986). Weekly nutritional treatment consisted of one hour of nutrition education and 30 minutes of individual counseling based on the food record. The topics addressed during the nutrition education program were: role of nutrients; energy and nutrient requirements; food pyramid; ineffectiveness of dietary restraint and of restrictive diets; definitions of hunger and satiety; healthy weight and build; guidance for buying food and how to eat at restaurants and social events. After the 12 weeks, the topics discussed were chosen by patients and/or the professional team such as issues from lay magazines about body and nutrition, the social and emotional meanings of foods and exchange of ideas about methods and tips to handle difficult situations regarding food. Patients received one hour and half of psychology consultation, in which the following issues were addressed, according to the models of Villapiano and Goodman (2001a; 2001b) and those described above: a) the kinds of hunger (physical, emotional and social); b) the beliefs involved in the diet-binge-purge cycle; c) the personal meaning of BN; d) body image dysfunctions; e) mechanisms used in order to copy with the emotions; and f) barriers for change. The dietitians instructed the patients to register all food consumed, the amount eaten, and the schedule and duration of their meals in a food diary (ADA, 1988; Story, 1986). They were also asked to mark if they considered the meal a binge eating episode and if any purging method had been used to compensate it. If the answer was yes, they had to specify which ones. Weekly frequencies of binges, vomits and use of laxatives, diuretics and diet pills were obtained through this diary. The food records were also used to obtain patients’ energy and nutrient intakes, number and type of meals consumed. To do so, diaries filled at weeks 2, 12 and 24 were analyzed. We chose to use the diary from the second week as a baseline measurement because the record from the first week was used by the dietitians to check if the patients were registering their intake and bulimic behaviors in a proper manner. If one patient did not fill her record in one of these weeks, the prior or the next week diary was utilized. Only the days that were completely recorded were analyzed. For example, if the patient did not describe correctly one meal, this day was excluded from analysis. The food intake was converted into energy and nutrient intake by means of the software Virtual Nutri (Version 1.0) (Philippi et al., 1996), which contains data regarding nutritional composition and serving sizes consumed in Brazil. When a patient registered that a meal was

112

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

followed by vomits, this meal was separated from the others. We calculated the energy and macronutrient intake from the meals not followed by vomits (named VET) and from those meals followed by vomits (named VOM). This differentiation (meals followed by vomiting or not) was made because it was impossible to take into account the energy of foods eaten in a meal followed by vomiting, insofar as the amount effectively absorbed is not known (Alvarenga et al., 2003; Gendall et al., 1997; Kaye et al., 1993) and would require a very complex physiological study. Energy consumption ranges for VOM and VET were defined, in which the values for energy were classified as hypoenergetic, normoenergetic, and hyperenergetic. Reference values used were: VOM: hypoenergetic < 600Kcal; normoenergetic 600–1,000 Kcal; and hyperenergetic > 1,001Kcal VET: hypoenergetic < 1,199 Kcal; normoenergetic 1,200–2,200 Kcal; and hyperenergetic > 2201 Kcal These VET values were defined according to the mean energy recommendation for young women (+/- 2,200Kcal) (NRC, 1989; Trumbo et al., 2002); and the VOM values were based on studies of the energy content of binges (Elmore and Castro, 1991; Woell et al., 1989). Also, the intake of the following minerals and vitamins were analyzed (using only the meals not followed by vomits): sodium, potassium, magnesium, calcium, iron and vitamins A, B1, B6, C, D and E. The values obtained were compared to the Dietary Reference Intakes – DRI’s (Institute of Medicine, 1997; 1998; 2000). Patients filled in a questionnaire about their eating attitudes and relationship with food specially developed for this population. The scale contained 24 questions about feelings and beliefs regarding food, behavior during meals, and others. These subjects were derived from our clinical experience (for example, based on the myths and misconceptions about nutrition that our patients usually declare) and from other questionnaires that in a certain manner approach eating behavior and EDs, such as Eating Disorder Inventory (Garner et al., 1983), Restraint Scale (Herman and Mack, 1975), Three-Factor Eating Questionnaire (Stunkard and Messick, 1975) and the Dutch Eating Behavior Questionnaire (van Strien et al., 1986). The instrument had been applied in a previous sample of patients in order to verify if it was clear and easily understandable. They also answered the Eating Attitudes Test - EAT-26 (Garner et al., 1982), translated to Portuguese by Nunes et al. (1994), which measures concern over diet, certain types of food consumed and body image; the Bulimic Inventory Test Edinburgh - BITE (Henderson and Freeman, 1987), translated to Portuguese by Cordás and Hochgraf (1993), which measures the symptoms and the severity of BN; and the Body Shape Questionnaire - BSQ (Cooper et al., 1987), translated to Portuguese by Cordás and Castilho (1994), which measures concern over body image, shape and size. Statistical analysis was performed using the Statistical Package for Social Sciences (SPSS) software for Windows v. 6.0. Data is presented by phase, as percent frequencies or as mean, standard deviation, median, and minimum and maximum values. Significance level adopted was p ≤ 0.05.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

113

Friedman´s test was used to compare the frequency of bulimic behaviors, the energy and nutrient intakes and the EAT, BITE and BSQ scores throughout the phases. When significant results were found, the Bonferroni test was used to assess which phase would differ from the other. The chi-square test was performed to see if there was any difference between the proportion of individuals in each classification of VET and VOM energy intakes (hypoenergetic, normoenergetic and hyperenergetic), among the phases. The Wilcoxon Matched-Pairs Signed-Ranks test was used to check if the macronutrient profile differed between meals not followed by vomits (VET intake) and meals followed by vomits (VOM intake). In order to analyze the evolution of eating behaviors and relationship toward food throughout the phases, the following approach was adopted. For the questions regarding eating attitudes and beliefs, the frequency of affirmative or negative responses was calculated. A chi-square test compared the ratio of affirmative responses for these questions between the phases. For the questions regarding the relation with food, the first three options of answers (always, very often, often) were grouped as “frequent thought or feeling”, and the last three (sometimes, rarely, and never) as “infrequent thought or feeling”. Chi-square test was also performed to compare the ratio of frequent and infrequent answers for the questions of relationship towards food between the phases. The Spearman correlation coefficient was used to determine the existence of correlations between these variables: frequencies of vomiting and binges, BMI and EAT, BITE and BSQ scores. Kruskal-Wallis ANOVA was used to determine if the frequency of bulimic behavior and EAT, BITE and BSQ scores varied according to the energy intake range (for VET and VOM consumption), and the Mann-Whitney test was used when the independent variable had only two categories.

Findings and Discussion Thirty-nine patients started the study (Phase 1); at the end of 3 months (Phase 2), 20 were still undergoing treatment; at the end of 6 months (Phase 3), there were only 15 patients – for a 48.7% dropout rate during treatment and 61.5% dropout rate during the entire follow-up. This high rate may have limited our results, but other outcomes studies also found an elevated dropout rate (Bacaltchuk and Hay, 1999; Elmore and Castro, 1991). For example, Agras et al. (2000) found that 26% of the patients abandoned the treatment after approximately five weeks. The diaries returned at each phase, the responses to the tests, and the n of each parameter varied. The data for the 19 patients that quit follow-up from Phase 1 to Phase 2 were not used for analysis, but merely to describe the group profile. Most patients belonged to the BN bulimic subtype (90%); the length of the disorder varied from 1 to 20 years; 3 patients (15%) had a previous history of anorexia nervosa; 70% did not have a partner; 65% had at least started college; 25% had professions or activities that demanded a lean body (dietitian, physical education teacher, nutrition student, dancer, and

114

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

actress); and 70% were taking antidepressants according to psychiatric evaluation. Table 1 shows other descriptive data. The patients presented a profile similar to those described in the literature as characteristic of bulimic patients: young women, unmarried, with a high level of education and with a greater prevalence of the purging subtype (Dolan et al., 1990; Fitcher et al., 1992; Gendall et al., 1997; Hetherington et al., 1994). Table 1- Patients descriptive data at the beginning of treatment (phase 1) Characteristics Age (years) Age when dieting started (years) Age when binges started (years) Age when vomiting started (years) Weight (pounds) Body Mass Index (kg/m2) Desirable weight (pounds) Weight variation throughout adulthood (pounds)

Mean ± Standard Deviation 27.7 ± 6.3 17.3 ± 4.6 18.7 ± 4.2 20.5 ± 6.1 135.9 ± 23.7 22.9 ± 3.9 120.0 ± 14.0 33.3 ± 17.5

Although the patients were still young (median age was 25 years), they were slightly older than the bulimic patients from developed countries – whose age varies between 16 and 20 years (Joergensen, 1992). This may be due to the long time of the disease and also to the long time that the patients took to seek treatment, probably because they felt ashamed of their behaviors or because the lack of awareness about the disorder (Becker et al., 1999). These findings are corroborated by other studies of bulimic patients, which also found a higher mean age and a long time of disease (Hadigan et al., 1989; Hetherington et al., 1993; Kissileff et al., 1986; Leung et al., 2000; Wallin et al., 1994; Woell et al., 1989). Nevertheless, this difference between Brazilian results and the literature may be due to our health care system. In this study the sample were patients of the Eating Disorder Unit, at Institute and Department of Psychiatry (a public institution), University of São Paulo. This was the first center in Brazil to treat eating disorders and it is still the most known and important center. People from all over the country come to be treated in this unit, which makes our sample very representative of eating disorders cases in Brazil. In the other hand, the vacancies are not much and the wait-list is long, which may explain the higher mean age of our sample. Finally, in Brazil there are no primary care services preventing and detecting eating disorders, so the diagnosis of the disorders happens too late, usually when the disease is very severe. Regarding the anthropometrical data, the initial BMI was normal as appointed by other authors (Gendall et al., 1997; Wallin et al., 1994). The mean desirable weight was 15.9 pounds lower than the mean current weight, evidencing the persistent desire to loose weight that is characteristic of BN. The mean weight’s oscillation in the adulthood was also high (33.3 pounds), which illustrated the weight cycling derived from the many times the patients tried to loose weight, following the restraint/binge/purge cycle of BN (Reiff, 1992). Kell et

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

115

al. found (1999) a mean weight’s oscillation of 35.2 pounds in the historic of bulimic patients, while Sunday and Halmi (1996) affirmed that the bulimic recruited in their study had been heavier in the past. Table 2 shows the progress of binge eating and purging behaviors in the 3 different phases. There was a significant statistical difference between Phases 1 and 3, and between 2 and 3, regarding the frequency of binge eating episodes per week. However up until Phase 2, the mean number of binge eating episodes per week met the DSM-IV criteria for bulimic frequency (minimum of twice a week for at least three months); in Phase 3, the mean number of binge eating episodes per week was below the minimum frequency established by the DSM-IV (APA, 1994). Table 2 - Measures of bulimic behaviors along the follow-up (data presented as mean ± standard deviation (median; minimal-maximal)) Phases

1 – Before treatment 2 – Immediately after treatment 3 – Three months after treatment

Weekly frequency of binges 9.5 ± 8.5* (7; 0-29) 4.2 ± 4.7* (3.5; 0-20) 1.6 ± 2.3 (0.5; 0-7)

Weekly Weekly use Weekly use Weekly use frequency of laxatives of diuretics of diet pills of vomits 4.2 ± 6.6 1 ± 1.6 1.4 ± 3.6 0.55 ± 2.5 (1.5; 0-28) (0; 0-6) (0; 0-13) (0; 0-11) 2.4 ± 3.4 0.9 ± 2.3 0.65 ± 1.9 0 (0; 0-11) (0; 0-9) (0; 0-8) 0.4 ± 0.9 0.08 ± 0.3 0.92 ± 3.2 0 (0; 0-3) (0; 0-1) (0; 0-11)

*: significantly different from results obtained three months after treatment

There was no significant statistical difference between the phases, regarding the number of vomiting episodes per week. Even though, the median of vomiting episodes was zero in Phase 2 and at Phase 3 the mean value was below the minimum frequency demanded by DSM-IV. There was no significant statistical difference between the phases regarding use of laxatives, diuretics and diet pills. This type of compensatory method was less utilized than vomiting, and the medians were zero in all phases. Regarding percentage of improvement in the bulimic behaviors assessed, there was clear improvement in the binge eating and purging symptoms at the end of the six-month followup: 75% of the patients had a frequency of binge eating bellow that one that fulfill diagnostic criteria, and 91.7% had this result in regard to vomiting episodes. Other purging behavior, such as the use of laxatives, diuretics, and appetite moderators, was shown in 100% of the responses below the diagnostic criteria. The frequency of other compensatory methods (fasting, dieting, physical activity) could not be estimated and compared to the DSM-IV criteria (APA, 1994). The percentages found are somewhat compatible with the data described in literature. Lacey (1983) observed that 80% of these patients completely ended their binge eating and vomiting episodes at the end of 10 sessions of CBT; actually, in this study, it took more than 12 sessions for patients to significantly cease these behavioral patterns. The major difference

116

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

was that in Lacey’s study patients spent half a day, once a week, being treated, whereas they stayed 3 hours per week at our center. Mitchell et al. (1988) found that 75% of patients had improved their eating behavior (without defining what kind of changes had taken place) and that 60% did not show bulimic behavior after treatment. Collings and King (1994) found that 52% of patients fully recovered, 39% experienced some symptoms, and 9% still suffered from this disease after treatment. Leung et al. (2000) found an over 50% decrease in bulimic symptoms after 12 CBT sessions. This data can be compared to the findings for this study: 60% did not meet the diagnostic criteria for BN according to the frequency of vomiting after 12 weeks, and 45% did not meet the diagnostic criteria for BN according to the frequency of binge eating episodes after 12 weeks. After six months, 8.3% vomited more than twice a week. This finding is very important. According to Olmested et al. (1994), the frequency of vomiting episodes, even if at low levels, seems to be a poor prognostic indicator and can be considered one of the best parameters for residual symptoms in these patients. It can be seen, as stated by Keel et al. (1999), that a longer period of treatment and follow-up (at least six months) yields better results. Nevertheless, the length of follow-up was short and patients may have had relapse episodes after this period of time. Regarding recovery after six months, based on the definition by Pyle et al. (1990), of maximum of two episodes of binge eating and purging episodes in the last two weeks of treatment, these patients should be considered already under recovery. According to the criteria adopted by Maddocks and Kaplan (1991) (less than one episode of binge eating or purging in the last 4 weeks), these patients presented a "moderate" response. One needs to consider that BN is known for being a disorder with poor prognostics because most patients remain with symptoms at the end of treatment (Garner, 1987). According to Becker et al. (1999), half of the patients attain full recovery, about 30% attain partial recovery, and 20% do not present significant symptom improvement. The criterion proposed by Keel et al. (1999) is much more severe: "absence of changed behavior for at least six months, and the weight and shape cannot influence how the subject felt." From this point, we cannot assess patients from this study, who would require a longer follow-up to verify a six-month abstinence. Perhaps it would be very difficult to consider them recovered based on the criteria of non-influence of weight and body shape. As stated by Herzog et al. (1996), in their review, a comparison of results between studies is very difficult because of the variability of how improvement, diagnostic criteria, duration of intervals and evaluation methods are defined. Table 3 presents the number of meals consumed in one week among the treatment phases. We observed that after six months the median number of lunches was 7 (significantly different from Phase 1), which means having lunch everyday. There were no significant differences regarding the number of the other meals. Even so, at the end of the following the median number of the breakfasts was 7, and the median number of the afternoon snacks, dinners and evening snacks were slightly higher than at baseline. Tables 4 and 5 show the energy and nutrient consumption along the treatment phases, in the VET intake (meals not followed by vomits) and in the VOM intake (meals followed by vomits), respectively.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

117

The results showed that the mean intake of energy in the meals not followed by vomits (VET intake) was much lower than the energy consumption recommendation to young women (+/- 2,200 kcal) (NRC, 1989; Trumbo et al., 2002). Wallin et al. (1994) and Gendall et al. (1997) found similar results and attested that these patients use the binges episodes to regularize their limited intake. It seems like that the patients usually eat less energy than necessary, which leads to a binge episode in order to compensate this deficit. The studies regarding eating pattern and nutrient intakes of bulimic patients are diverse. According to Gendall et al. (1997), empirical studies noticed a variation of 605-4,800 kcal in the energy intake, while the macronutrient consumption seems to follow the American diet pattern. Woell et al. (1989) found a mean energy intake of 3,100 kcal per day, including the binges episodes. On the other hand, Wallin et al. (1995) observed a mean intake of 762 ± 560 kcal/day. Sunday and Halmi (1996) observed that bulimic patients ate less energy than anorexic patients in a weight maintenance phase. These great variability among studies was expected, since it is known that bulimic patients tend to have an atypical and chaotic food intake which varies between the restrictive and the compensatory phases or between the “regular” meals and the binge episodes (Gayle, 1998; Gendall et al., 1997; Hetherington et al., 1994; Wallin et al., 1994; Wallin et al., 1995; Walsh et al., 1989). According to Gayle (1998), these extreme fluctuations in energy intake disconcert the appetite regulation and other physiological functions. The author affirms that the low energy intake leads to a loss of control, in spite of the great amount of energy consumed subsequently. Due to that it is recommended to include as one of goals of the treatment the regularization of the eating pattern, in order to prevent fluctuations of the bulimic behaviors. Regarding the energy consumed in the meals followed by vomits (VOM intake), we found a range of 460-2,690 kcal. This data shows that the energy intake of these meals was not so high, which is surprising considering that these meals were more likely to be binge episodes. Woell et al. (1989) found that one third of the bulimic patients declared as compulsive episodes with less than 500 kcal (Rosen et al., 1986, obtained a very similar finding) and that this judgment depends not only of the amount of food or energy consumed but also of the type of food and the psychological state of the patient. Other studies found a great variability in the energy content of the binges. Mitchell et al. (1981) observed a mean intake of 3,415 kcal (range: 1,200-11,500 kcal), while Mitchell and Laine (1985) obtained a mean consumption of 4,394 kcal (range: 1,436 – 8,585 kcal). Elmore and Castro (1991) affirmed that the greater binges are more likely to be purged and that patients with longer time of disease had even greater binges. Gendall et al. (1997) declared that the binges that happen more frequently have greater energy content and also that although compulsive meals have more energetic value than the non-compulsive ones they do not have different macronutrient composition. The median macronutrient profile of the VOM intake was similar to those observed by Woell et al. (1989) in binges (42% of carbohydrates, 12% of proteins and 43% of lipids). We also observed that the macronutrient profile of the VOM intake did not differ much from the macronutrient profile of the VET intake, except for the lipid consumption (in percent contribution to total energy intake), which was higher in the VOM intake, but only at baseline (VET intake = 32.1 ± 7%; VOM intake = 35.3 ± 4%, p = 0.03).

118

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

Table 3 – Weekly number of meals along the follow-up (data presented as mean ± standard deviation (median; minimal-maximal)) Phases

Total meals Breakfast

Morning snack

Lunch

Afternoon snack

Dinner

Evening snack

1 – Before treatment 2 – Immediately after treatment 3 – Three months after treatment

25.8 ± 10 (23; 5-50) 25.4 ± 7 (23; 18-40) 31 ± 13 (27; 11-65)

2.9 ± 2 (3; 0-6) 2.3 ± 2 (2; 0-7) 2.3 ± 2 (2; 0-7)

4.3 ± 2 (5; 0-7)* 5.2 ± 1 (6; 3-7)* 6.5 ± 2 (7; 1-8)

3.4 ± 2 (4; 0-6) 4.0 ± 2 (4; 1-6) 4.7 ± 3 (5; 0-9)

4.5 ± 1 (4; 2-7) 3.7 ± 1 (4; 1-7) 5.1 ± 2 (6; 0-9)

2.3 ± 2 (3; 0-6) 3.1 ± 2 (3; 0-7) 3.0 ± 2 (3; 0-6)

4.1 ± 2 (4; 0-6) 4.7 ± 2 (5; 0-7) 6.3 ± 2 (7; 3-8)

*: significantly different from Phase 3.

Table 4 – Energy and macronutrient content (as percentage contribution to total energy intake) of the meals not followed by vomits, along the follow-up (data presented as mean + standard deviation (median; minimal-maximal)) Phases

Energy intake (kcal) 1,529 ± 945 (1,197; 337- 4,094)

Protein intake (%) 14.6 ± 3 (14; 10-21)*

Carbohydrate intake (%) 53.5 ± 8 (51; 44-72)

Lipid intake (%) 32.1 ± 7 (32; 19-43)

2 – Immediately after treatment

1,475 ± 771 (1,277; 577-3,853)

15.8 ± 3 (15; 12-21)

50.8 ± 6 (49; 44-65)

32.6 ± 5 (32; 24-40)

3 – Three months after treatment

1,337 ± 519 (1,393; 641-2,131)

17.6 ± 3 (18; 13-21)

50.4 ± 6 (50; 40-60)

31.6 ± 6 (31; 22-42)

1 – Before treatment

*: significantly different from Phase 3.

Table 5 – Energy and macronutrient content (as percentage contribution to total energy intake) of the meals followed by vomits, along the follow-up (data presented as mean + standard deviation (median; minimal-maximal)) Phases

Energy intake (kcal) Protein intake (%) 1,310 ± 686 17.5 ± 7 (1,274; 460-2,689) (14; 7-32)

Carbohydrate intake (%) 47.4 ± 6 (49; 37-55)

Lipid intake (%) 35.3 ± 4 (36; 26-41)

2 – Immediately after treatment

1,402 ± 707 (1,320; 584-2,664)

17.2 ± 7 (16; 10-33)

45.9 ± 15 (44; 21-69)

34.2 ± 7 (35; 21-43)

3 – Three months after treatment

1,211 ± 226 (1,238; 927-1,440)

10.1 ± 5 (9; 6-17)

60.7 ± 3 (60; 57-65)

28.1 ± 3 (28; 24-31)

1 – Before treatment

In every phase, the percentage contribution of each macronutrient to the VET intake was similar to those recommended in Reference Dietary Allowances (NRC, 1989; Trumbo et al.,

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

119

2002). The values were also similar to those obtained in a prior cross-sectional study conducted with Brazilian bulimic patients (Alvarenga et al., 2003). In that study, the mean carbohydrate intake contributed with 50.8% of the total intake, while the mean lipid consumption contributed with 32.3% and the mean protein intake with 17.9%. In this chapter, we observed that along the phases, only protein intake significantly changed (the baseline intake was lower than the intake presented at Phase 3). Table 6 shows the distribution of patients in each energy intake range, considering the meals not followed by vomits (VET) and the meals followed by vomits (VOM). Table 6 - Proportion of subjects classified in each category of energy intake, within the phases of the follow-up Energy intake

Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec Hypoenergetic intaked Normoenergetic intakee Hyperenergetic intakef

Phase 1 – Before treatment

Phase 2 – Immediately after treatment Meals not followed by vomits 52.6% 47.0% 31.6% 41.2% 15.8% 11.8% Meals followed by vomits* 21.0% 11.8% 47.4% 70.6% 31.6% 17.6%

Phase 3 – Three months after treatment 50.0% 50.0% 0% 25.0% 75.0% 0%

*: χ2 (2) = 21.32; p < 0.005. Meals not followed by vomits: a : Hypoenergetic = Intake < 1,199 kcal. b : Normoenergetic = Intake between 1,200 e 2,200 kcal. c : Hyperenergetic = Intake > 2,201 kcal. Meals followed by vomits: d : Hypoenergetic = Intake < 600 kcal. e : Normoenergetic = Intake between 600 e 1,000 kcal. f : Hyperenergetic = Intake > 1,001 kcal.

The results indicated that there was no significant change in the number of patients in each category in regard to energy intake of meals not followed by vomiting (VET). Only a non-significant increase in normoenergetic intake, and a non-significant reduction in hypereneregetic intake were observed. In relation to the meals followed by vomiting (VOM), the number of patients that presented episodes with an intake less than or equal to 600 Kcal decreased by half after 12 weeks of treatment and then increased after six months. Regarding meals of 601-1,000 Kcal, the number of patients increased after 12 weeks and after six months, and meals with over 1,001 Kcal decreased after 12 weeks and fell to zero after six months. It was concluded that there was a trend of decrease for hyperenergetic meals followed by vomiting throughout the phases.

120

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

As for the nomenclature used to describe the energy intake of these patients, the terms hypo, normo, hyper for VET applied, respectively, to eating less energy than one should, eating the right amount of energy, and eating more energy than one should. The same terms were used for VOM, meaning meals with a low intake of energy, with an intermediate intake of energy and with high intake of energy; therefore, hypo VOM does not mean that the patient ate less energy than he should at that moment. These categories were based on the energy content of binges, supposing that meals followed by vomiting are more likely to be binge eating episodes. Even though, one must also consider that not only binges are followed by vomiting (since regular meals also can be followed by vomiting) and not all binge episodes are followed by vomiting. Elmore and Castro (1991) stated that greater binge eating episodes are more likely to be purged, and that, as the length of the disorder progresses, the size of these binge eating episodes also increases. This paper shows that throughout the follow-up stage patients decreased the size of their meals followed by vomits, however these are patients undergoing treatment. Most probably, patients without treatment will present binge eating episodes with higher energetic content. The intake of vitamins and minerals along the phases, as well their adequacies in relation to the recommended intakes, can be seen in Table 7. In a broad manner, intake of micronutrients was below the recommendations of the Dietary Reference Intakes (Institute of Medicine, 1997; 1998; 2000). Intake of vitamins A and C was closer to the recommendations, while the most inadequate intakes were found to sodium, calcium, magnesium, potassium and iron It is not possible to affirm that this unhealthy intake is characteristic of bulimic patients, because since we did not have a control group we could not know if the intake of healthy young women is so inadequate as the patients’ intake. The fact that the sodium and potassium intake was so low is very preoccupant because, when combined with compensatory behaviors as vomiting and use of laxatives and diuretics, this may cause a hydroeletrolitic disturbance (Greenfeld et al., 1995; Lasater and Mehler, 2001). This inappropriate pattern of intake did not change throughout the phases. This result suggests that the nutritional treatment was not able to correct this unhealthy eating pattern. It is necessary to evaluate why this happened and what could be done to improve the micronutrient intake of these patients. Chart 1 shows the results of frequency of affirmative responses for questions about eating behavior and beliefs. The reduction of guilt declarations when patients ate foods whose consumption they restricted demonstrates greater permissiveness towards these foods. There was a gradual reduction in statements regarding behavior change after eating sweets, fast food, and “different” foods; however, less than half of the patients changed. It is remarkable that, even with significant changes, most of them were still feeling guilty and having difficulties in eating the foods regarded as “dangerous”, behavior also described by Keller et al. (1992). More than half of the patients were still practicing some kind of restraint on their diet at the end of the following. This ratifies that diet restraint is a symptom much more common among BN patients and that it is difficult to eliminate (Keller et al., 1992).

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

121

Table 7 – Micronutrient intake and adequacy, obtained in the meals not followed by vomits, along the treatment phases Nutrient Vitamin A (mcg)

Vitamin C (mg)

Thiamin (mg)

Vitamin B6 (mg)

Vitamin D (mcg)

Vitamin E (mg)

Sodium (mg)

Calcium (mg)

Magnesium (mg)

Potassium (mg)

Iron (mg) a

Phase

Amount consumeda

1d 2e 3f 1d 2e 3f 1d 2e 3f 1d 2e 3f 1d 2e 3f 1d 2e 3f 1d 2e 3f 1d 2e 3f 1d 2e 3f 1d 2e 3f 1d 2e 3f

710 ± 377 (680; 27 – 1,632) 774 ± 337 (765; 219 – 1,612) 1117 ± 460 (990; 656 – 2,050) 88 ± 74 (69; 1 - 258) 84 ± 44 (85; 16 - 186) 217 ± 259 (124; 60 - 992) 1 ± 0.7 (0.7; 0.4 – 3.2) 1 ± 0.6 (0.8; 0.3 – 2.7) 0.9 ± 0.4 (0.7; 0.5 – 1.5) 0.8 ± 0.4 (0.7; 0.1 – 1.4) 0.9 ± 0.4 (0.8; 0.4 – 2.0) 0.9 ± 0.4 (0.8; 0.5 – 1.7) 18 ± 29 (0.8; 0 – 95) 10 ± 15 (1; 0 – 55) 8 ± 20 (0.6; 0 – 68) 7 ± 5 (6; 0 – 22) 9 ± 7 (7; 2 – 25) 7 + 5 (5; 3 – 16) 1,551 ± 1,156 (1,236; 68 – 4,406) 1,604 ± 1,125 (1,123; 598 – 4,917) 1,397 ± 669 (1,427; 483 – 2,652) 552 ± 289 (481; 99 – 1,081) 855 ± 960 (569; 196 – 4,178) 632 ± 288 (578; 344 – 1,414) 113 ± 54 (119; 19 – 241) 132 ± 79 (116; 43 – 356) 132 ± 39 (133; 73 – 199) 1,195 ± 539 (1,128; 211 – 2,433) 1,265 ± 513 (1,061; 508 – 2,625) 1,493 ± 382 (1,390; 1,015 – 2,150) 6 ± 4 (5; 0.4 – 15) 7 ± 3 (6; 2 – 15) 6 ± 3 (5; 3 – 12)

Recommende Adequacyc d intakeb (%) 89 800 97 140 118 75 112 289 95 1.1 91 81 58 1.3 68 72 351 5 199 166 49 15 57 49 65 2,400 67 58 55 1,000 86 63 37 310 43 42 34 3,500 36 43 34 18 37 35

: mean ± standard deviation (median; minimal-maximal). b: Recommended intake to young women, according to the Dietary Reference Intakes (Institute of Medicine, 1997; 1998; 2000). c: Percent adequacy of the mean intake, when compared to the recommended intake. d: Phase 1 – before treatment. e: Phase 2 – immediately after treatment. f: Phase 3 – three months after treatment.

122

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

Chart 1 - Frequency of affirmative answers to the questions regarding eating attitudes and beliefs towards food, between the treatment phases. Questions

Do you make any restrictions in your regular diet? Do you feel guilty whenever you eat one of the foods that you try to cut from your diet?* Do you feel pleasure when you eat? Do you like cooking? Do you usually eat the meals that you prepare? When you eat sweets, fast-foods, pizza, or when you go to aparty, do you eat in a different manner?** Does it bother you to eat in the presence of other people?a Do you believe that there is a combination of food that is dangerously “fattening”? Do you believe that there is a food or some thing that “melts” fat? a Do you believe that overeating in one meal or in special occasion automatically makes you put on weight?*** Do you believe that not eating for one day or eating a liquid diet can make you lose weight?

Phase 1 – Before treatment 94%

Phase 2 – Phase 3- Three Immediately months after after treatment treatment 75% 57%

70%

65%

60%

75% 70% 74%

71% 65% 76%

76% 59% 82%

95%

76%

53%

60%

29%

29%

74%

59%

59%

35%

29%

6%

90%

41%

29%

65%

41%

35%

*: p ≤ 0.05; **: p ≤ 0.01; ***: p ≤ 0.001; a: p = 0.09

Regarding the feeling of nuisance while eating in the presence of others, positive answers were less than half after 12 weeks of CBT and they maintained the same pattern along the following, almost reaching significance. It showed that the treatment provided a more adequate eating pattern for this issue, probably decreasing the episodes of “hidden eating” and making possible for the patients the opportunity of sharing the meals with other people. Even so, at the end of the following approximately one third of the patients still felt bothered while eating in the presence of the others, which was also observed by Keller et al. (1992). No important shifts were found in the statements regarding eating with pleasure. We believe that treatment does not alter feelings as much as behavior regarding food; and that it

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

123

is harder to change the relationship with food than to change behavior. Patients seem to associate food preparation with the possibility of loosing control and eventually dislike the activity, as indicated by the gradual reduction of affirmative answers with regards to the enjoyment of cooking. One question asked if they ate the food that they prepare. This question was based on the observation that anorexics usually cook for their relatives, but do not eat the food prepared (Reiff and Reiff, 1992). The high frequency of affirmative answers, even at baseline, showed that this disturbed behavior (not eating what they prepare) was not common among bulimics. Among the misconceptions about diet, significant reductions were observed just in the proportion of patients who thought they would gain weight immediately after eating and who believed that something could melt fat (here, p value was close to significance). Part of the sample still believed that some food combinations were especially “fattening” and that fasting for one day would make them thinner, which suggests that in spite of all the information provided, fear and suspicion in relation to food were not eliminated. Chart 2 shows the responses for questions about the relationship with food. At the end of follow-up, most of them no longer worried about food all the time. We think that the establishment of a regular diet pattern decreases obsessive thinking about food since the relationship between obsessive dieting and extreme concern in relation to food is a wellknown fact (Polivy, 1996). There was also a significant reduction in concern with body weight and in feeling fat regardless of what they ate, which could suggest that the treatment was able to address some body image issues, as extolled in the literature (Garfinkel et al., 1992). However, many patients remained with such perceptions and feelings, which is corroborated by the observation of Swift et al. (1987) that, regardless of the result of the treatment, weight fluctuations and body dissatisfaction remain. Even though, it is known that many healthy women, without EDs, feel fat and overestimate their body sizes, so these features are not exclusively of bulimic patients (Cash and Henry, 1995; Rodin et al., 1984; Strigel-Moore et al., 1986). Almost one third of patients declared that they dream of a pill that would replace food at the end of the following. Such an impossible and surreal desire clearly indicates an inadequate and pathological relationship toward food that could not be altered for some patients, which is very preoccupant. The results appointed that most of the patients started the treatment already believing that they could achieve a regular intake and a regular weight, which is very important since motivational aspects are considered predictors of improvement (Herzog et al., 1996; Rorty et al., 1993). Even though, the answers’ pattern to this question did not change along the following, suggesting that the treatment did not increase motivation of those patients who were not motivated at baseline. This feature should be carefully observed during treatment, and the professionals should try to have a better understanding of the reasons for such lack of motivation, in order to provide an adequate treatment for all patients.

124

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

Chart 2 - Frequency of ‘frequent’ or ‘not frequent’ answers to the questions regarding relationship towards food, between the treatment phases Questions

I worry all the time about what I am going to eat** I worry all the time with my weight** I feel fat despite what I eat** I hate feeling hungry It is hard for me to choose what to eat I wish I did not have the need to eat I dream of a pill that would replace food I don’t believe I’ll ever be able to follow a regular intake and achieve a regular weight In a situation in which there is much food, such as parties and buffets, I get nervous and/or lose control* Whenever I have a problem, I look for food My eating habits have a great interference in my life as a whole**

Phase 1 – Before treatment Freq. Infreq. 95% 5%

Phase 2 – Phase 3 – Immediately Three months after treatment after treatment Freq. Infreq. Freq. Infreq. 71% 29% 44% 56%

100%

0%

94%

6%

56%

44%

95% 50% 60%

5% 50% 40%

82% 59% 41%

18% 42% 59%

56% 38% 38%

44% 63% 63%

60% 42%

40% 58%

53% 35%

47% 65%

36% 31%

63% 69%

44%

56%

35%

65%

19%

81%

63%

37%

53%

47%

25%

75%

65%

35%

47%

53%

46%

56%

89%

11%

59%

41%

40%

60%

*: p ≤ 0.05; ** p ≤ 0.01

Regarding the question of feeling nervous or loosing control in situations with abundant food, the most important reduction took place only at the end of the six months, indicating that longer treatment is needed for patients to gain confidence and ease to eat in any situation. The analysis of the question about “the way you eat” interfering greatly in their lives as a whole demonstrated a significant change, although 40% of the patients were still answering positively after six months, indicating that to a subgroup, BN represented the complex role of food in human life. There were no significant shifts in the question related to looking for food whenever they have a problem. This suggests that food still performed many different roles in the lives of these patients, as an expression of feelings and impulses and “a means of external adaptation and an attempt at internal control” (Johnson and Maddi, 1988). Thus, faced with many possibilities, ED patients choose weight control and, therefore food control, as a way of life. Changing this behavior pattern seems to demand much more than 12 weeks of CBT and

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

125

nutritional education. No significant alterations were observed in the answers about “being angry when feeling hungry”, “having difficulty in choosing foods” and “I wish I did not have to eat”. These data reflect the inadequate relationship with food, with the denial of the physiological and emotional needs for food, probably due to their feeling of incompetence towards it (Keller et al., 1992). Figures 1 and 2 shows the percent distribution of affirmative answers regarding the way they behave during the meals and the feelings experienced while they ate outside home, along the phases. The number of patients who ate their meals sitting at a table increased significantly over the phase periods, just as those who had their meals with a companion. These changes were important, because eating quickly while standing, often in front of the refrigerator, may be associated with bulimic behavior. CBT seemed to be also effective in reducing the discomfort of eating in the presence of other people, as there was a falling trend in the frequency of answers to this question. One of the most difficult behaviors to change seems to be that of reading while eating, or eating in front of the TV. However, it is well known that today, many people eat alone and entertain themselves in this manner, and this is not a distinguishing feature of EDs. Patients started to feel more at ease and less anxious when eating out. The feeling of irritation was the one that showed the smallest reduction in affirmative answers, still indicating difficulty in the relationship with food. One should also note that the nutritional approach of the treatment was based on more elementary subjects of nutritional education and that there was no specific approach to address the relationship of patients with food. Some authors (Rosen et al., 1995; Wolff and Clark, 2001) say that traditional CBT is not enough to change body image issues in EDs, and that specific interventions are needed for that purpose. We can infer that the same is true for eating attitudes and relationship towards food. Table 8 shows the test scores throughout the follow-up. There was significant statistical difference for EAT from one phase to another, showing continuous improvement provided by treatment. However, diet behavior was still significant at the end of the 12 weeks of CBT. The symptoms started to disappear only six months after the beginning of the follow-up, showing that more time is necessary for the patients to stop presenting the symptoms, according to data from the EAT questionnaire. The scores from this study could not be compared to those found in literature, because most of the studies used EAT-40 and those which utilized EAT-26 had a study design very different from ours, not allowing a comparison. Significant statistical difference was observed in the BITE (symptom subscale) from Phase 1 to Phase 2. The initial mean value (23.6) found was similar to that observed in the study conducted by Fahy and Russell (1993) of 26.3, and lower than that found by Thiels et al. (2003) of 31.2 and by Hetherington et al. (1993) of 48.7. Thiels et al. (2003) did a reevaluation after 16 weeks of CBT, obtaining a score of 16.2, and another reevaluation after 6 months, with score of 17.2. Fahy and Russell (1993) reassessed the patients after 1 year, and observed a mean score of 16.9. The scores observed by Thiels et al. (2003) after 6 months, and by Fahy and Russel (1993) after 1 year were higher than the mean found after the 6-month follow-up of this study (15.8). Regarding the progress of BITE-symptom, data showed that a significant difference in bulimic symptoms occurred after 12 weeks of CBT. Actually, the guidelines for this approach aim at reducing bulimic symptoms, so this change

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

126

was expected. The scores of the BITE-symptom showed just a "sub-clinical" group after six months of follow-up, showing positive evolution of these patients.

Phase 1

Phase 2

uie t* Q

Re ad ing W atc hin gT W V ith att en tio n Ta lki ng

Al on e

Si ttin g* St an W din ith g so me bo dy *

100% 90% 80% 70% 60% 50% 40% 30% 20% 10% 0%

Phase 3

*: p < 0.05 Figure 1 – Percent distribution of the affirmative answers to the question “How do you usually eat your meals?”

90% 80% 70% 60% 50% 40% 30% 20% 10% 0% At ease*

Anxious* Phase 1

Irritated Phase 2

Fearful

Nervous

Phase 3

*: p < 0.05 Figure 2 – Percent distribution of the affirmative answers to the question “How do you feel when you go to a restaurant, coffee shop or a bar?”

There was no significant statistical difference between the phases in regard to the BITE severity scale. The mean score after six months showed a "clinically significant" group. This result is similar to that found in the Fahy and Russell (1993) follow-up in which the mean initial score was 14.1, and after one year, 6.1, showing a still "clinically significant" group.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

127

Table 8 - Scores obtained in the scales (EAT, BITE and BSQ), along the follow-up (data presented as mean + standard deviation (median; minimal-maximal)) Phases 1 – Before treatment 2 – Immediately after treatment 3 – Three months after treatment

EATa 38.6 ± 10 (40; 15-53)†* 25.5 ± 14 (28; 6-49)* 17.0 ± 11 (16.5; 2-42)

BITE symptomsb 23.6 ± 5 (25; 11-29)†* 19.8 ± 8 (23; 1-28) 15.8 ± 8 (17.5; 1-28)

BITE severityc

BSQd

15.3 ± 5 (14; 3-25) 10.1 ± 6 (8; 2-23) 7.6 ± 6 (5.5; 2-24)

145.2 ± 28 (142; 99-190)* 132.6 ± 40 (149; 48-189)* 109.2 ± 44 (103.5; 47-189)

† significantly different from the scores obtained immediately after treatment *: significantly different from results obtained three months after treatment.

BSQ showed significant statistical difference between Phases 1 and 3, and between 2 and 3, thereby indicating a continuous improvement. The BSQ initial mean score (145.2) was lower than the 156 described by Hetherington et al. (1993). No study showed the evolution of BSQ scores throughout follow-up. Results show that concern over body image takes more than 12 weeks of CBT to present significant changes. These results are consistent with those found by Swift et al. (1987), in which weight variations and body dissatisfaction remained present even among asymptomatic patients. Some authors (Ramirez and Rosen, 2001; Wolff and Clark, 2001) declare that traditional CBT is not enough to improve body image in EDs, and that specific intervention is required to this end, so the improvement found in the classification regarding concern over body image through BSQ was surprising. Although we found this improvement in body image issues at the end of the follow-up, one might argue that the BSQ along did not provide much information about what changes did occur in relation to body image. Using this scale, it is not possible to know if whether overestimation of body size or body dissatisfaction or body disparagement decreased. For this reason, nowadays it is recommend the use of tests more specifics to the body image aspect that is intended to be measured (Thompson, 2004). A series of studies used the Eating Disorders Inventory (EDI) to measure outcome (Brambilla et al., 1995; Fernandéz et al., 1998; Hedges et al., 2003; Steinhausen and Seidel, 1993), but the EDI test has not yet been translated to Portuguese. When this study was carried out, BITE, EAT, and BSQ were the only tests that had been translated to Portuguese and that were available to assess BN. Currently, there are other tests that have been translated, which measure the chronic practice of restrictive diets (Restraint Scale – Scagliusi et al., 2005-a), body attitudes (Body Attitudes Questionnaire – Scagliusi et al., 2005-c), perception and satisfaction with body size and shape (Stunkard’s Figure Rating Scale – Scagliusi et al., 2006), nutritional knowledge (Scagliusi et al., 2005-b), among others. Therefore, an analysis of the evolution of classification based on test scores showed good results, but not as good as the findings for binge eating and purging behavior. Notwithstanding, these tests do not diagnose ED, they just address some issues and suggest a classification.

128

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

Table 9 shows the correlations between BITE, EAT, BSQ, BMI, number of vomiting episodes per week and number of binge eating episodes per week, found in each phase. EAT and BSQ presented a positive correlation in the 3 phases of the program, showing that for these bulimic patients, the higher their EAT score, the greater their concern over body image, regardless of the timeframe. It is known that these two responses, greater dissatisfaction with body image after treatment and higher EAT scores, are related to a poor outcome or a complication of the disease during follow-up (Agras et al., 2000; Freeman et al., 1985; Olmested et al., 1994). The number of binge eating episodes and BITE-symptom presented a positive correlation just at the beginning of the treatment, showing that, at that point, the more severe the level of BN symptoms, the greater the number of binge eating episodes per week presented by the patient. The severity of BN symptoms at the beginning of treatment was considered a predictor of recurrence by Fahy and Russell (1993). This correlation was no longer true in the following phases, and it seemed that, after treatment and follow-up, the bulimic symptoms had somehow changed and no longer had any correlation to the frequency of binge eating episodes. It seemed that, despite the bulimic symptoms, the number of binge eating episodes had decreased. Positive correlations between BMI and BITE-symptom inventory test and between BMI and number of binge eating episodes per week were found just at the beginning of treatment. This shows that to patients not being treated, the higher the BMI, the more severe the levels of BN symptoms, and the greater the number of binge eating episodes. According to Maddocks and Kaplan (1991) patients who have been heavier in the past had more chances of presenting worse treatment outcome. After treatment, it was concluded that patients with a higher BMI no longer presented the more severe levels of BN symptoms nor presented higher frequency of binge eating episodes, that is, the symptoms originated from the psychopathology of the disorder and not from inadequate body weight. After 12 weeks of treatment, and also after six months of follow-up, EAT and BITEsymptom inventory test presented a positive correlation. Bite-severity inventory test and EAT presented a positive correlation only during Phase 2. These correlations were not present at the beginning. This result shows that after being treated, the stronger the concern of the patient over diet, foods eaten, and body image, the more severe the patient’s symptoms and BN itself. The study also suggests that the severity of BN was not related to the level of concern over food and body at the beginning and after 6 months of treatment. This data suggests that these patients (more concerned over food and their body, even after treatment) are highly prone to experiencing recurrence, as described by Freeman et al. (1985) and by Fahy and Russell (1993). It could be thought that the frequency of binge eating and the frequency of vomiting episodes would present a correlation during all phases, but this became true only after 12 weeks of treatment, suggesting that only at this moment did a greater number of binge eating episodes result in more vomiting episodes. In fact, the presence of binge eating and vomiting episodes did not present such a correlation at the beginning of treatment and after six months. This finding is supported by Olmested et al. (1994) who said that vomiting can be used to control weight, stress and affection, among others factors, and not only to compensate binge eating.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

129

BMI and BSQ presented a positive correlation after 12 weeks of treatment showing that, at this phase, the higher the BMI, the greater the concern over body image. This finding supports the fact that individuals with ED are overly concerned about body image regardless of their weight (Dowson and Henderson, 2001), insofar as it is the pathological condition that causes this concern. When patients are treated, their concern for the body is the same as what is presented by the overall population: the heavier they are, the more concerned they are (Hill and Williams, 1998; Scagliusi et al., 2006). This finding also shows that treatment can minimize weight-related concerns in individuals who are not overweight. Table 9 - Spearman correlation coefficients between scales scores, bulimic behaviors and body mass index, along the follow-up Scales and EAT measures BSQ EAT BITE severity BITE symptoms Frequency of binges

0.59* -

BSQ EAT BITE severity BITE symptoms Frequency of binges

0.80* -

BSQ EAT BITE severity BITE symptoms Frequency of binges

0.78* -

-

-

-

BITE BITE Frequency severity symptoms of binges Phase 1 – Before treatment 0.28 0.44 0.38 0.40 0.06 0.22 0.44 0.38 0.44* -

-

-

Phase 2 – Immediately after treatment 0.45 0.48 -0.01 0.63* 0.75* 0.13 0.61 0.22 0.40 -

-

-

Phase 3 – Three months after treatment -0.04 0.73 0.15 0.21 0.81* 0.30 0.28 0.62* 0.47 -

-

-

Frequency BodyMass of vomits Index -0.20 0.10 -0.13 -0.11

0.06 -0.13 0.19 0.45*

0.20

0.57*

-0.05 -0.19 0.21 0.36

0.50* 0.36* 0.02 0.39

0.48*

0.09

-0.08 0.03 0.68* 0.28

0.10 0.01 -0.40 0.13

0.49

-0.18

*: p ≤ 0.05; a: bulimic behaviors are expressed as weekly frequencies.

BITE-symptom inventory test and BSQ presented positive correlation only after the sixmonth follow-up, showing that the greater the number of symptoms of BN presented at the end of this period, the greater the concern of the patient over body image. This result was not observed at the beginning or after 12 weeks. It seems that BN symptoms are significantly

130

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

affected by body image only if the patient still remains highly concerned about his image after six months of treatment. As shown by Freeman et al. (1985), Fahy and Russell (1993) e Agras et al. (2000), patients with more BN symptoms and more concern about their bodies at the end of the treatment present a higher risk of recurrence. Only after six months of follow-up was any positive correlation found between BITEseverity scale and the number of vomiting episodes per week and between this scale and weekly frequency of binges, showing that the more vomiting and binge episodes after this length of treatment, the more severe the BN. It can be said that a patient that still presents a significant number of vomiting and binge episodes after six months of treatment has more severe and more treatment-resistant bulimia, supporting the presence of vomiting and binge episodes as an indicator of poor prognosis (Olmested et al., 1994; Herzog et al., 1996). Actually, severity measurement by BITE scale considers the frequency of binge eating and vomiting episodes, among others (use of drugs and fasting). Since the number of binge eating and vomiting episodes presented positive correlation with the BITE-severity score only after six months, it seems that the severity of bulimia at the beginning of treatment and after 12 weeks was related to other factors of this test, such as the use of drugs and the practice of fasting. Tables 10 and 11 show BITE-symptom and severity, BSQ, EAT scores, and the number of binge eating and vomiting episodes per week according to the energetic intake ranges for VOM and VET in each of the 3 phases. The goal was to assess these different response variables between patients that had hypoenergetic, normoenergetic or hyperenergetic intake. Table 10 – Mean ranks of the scores and bulimic behaviors, within each interval of energy intake in meals not followed by vomits, along the follow-up Energy intake in meals BSQ not followed by vomits

BITE severity

BITE EAT symptoms

Weekly frequency of vomits

Weekly frequency of binges

13.4* 6.8 5.0

11.2 6.0 14.0

11.6d 7.0 5.5

10.6 6.6 11.0

8.0* 5.0

8.4* 4.6

Phase 1 – Before treatment Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec

7.9 9.8 13.7

Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec

5.6 8.9 12.0

10.0 10.0 10.0

8.6* 8.7 17.3

10.8 8.8 6.3

Phase 2 – Immediately after treatment 6.6 5.5

6.5 5.6

e

e

5.2 8.5 9.0

Phase 3 – Three months after treatment a

Hypoenergetic intake Normoenergetic intakeb

5.7 7.2

9.3* 3.7

7.2 5.8

6.5 6.5

*: significantly different from the others energy categories, within the same phase. a : Hypoenergetic = Intake < 1,199 kcal. b : Normoenergetic = Intake between 1,200 e 2,200 kcal. c : Hyperenergetic = Intake > 2,201 kcal. d : p = 0.07 between the energy categories, within phase 2. e : missing value (no subject from this category filled this questionnaire).

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

131

Table 11 – Mean ranks of the scores and bulimic behaviors, within each interval of energy intake in meals followed by vomits, along the follow-up Energy intake in meals followed by vomits

BSQ

Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec

9.6 7.0 12.7

Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec

2.0d 7.0 13.0

BITE severity

BITE symptoms

EAT

Weekly Weekly frequency of frequency vomits of binges

Phase 1 – Before treatment 9.4 9.9 10.6

5.5* 8.6 15.1

11.5 8.8 9.0

11.0 10.1 9.2

8.9 9.3 11.8

5.5 9.6 9.0

10.0 7.8 13.0

6.8 6.4

6.7 6.4

Phase 2 – Immediately after treatment 4.0 6.2 6.0

3.0 6.1 8.0

4.5 6.4 11.0

Phase 3 – Three months after treatment a

Hypoenergetic intake Normoenergetic intakeb

7.3 6.2

8.8 5.7

8.0 6.0

9.0 5.7

*: significantly different from the others energy categories, within the same phase. a : Hypoenergetic = Intake < 600 kcal. b : Normoenergetic = Intake between 600 and 1,000 kcal. c : Hyperenergetic = Intake > 1,001 kcal. d : p = 0.06 between the energy categories, within phase 2.

Findings show that the scores of BITE-severity were significantly higher in patients with hypoenergetic VET in Phase 3. Therefore, the patient that ate less in Phase 3 presented a more severe case of BN; that is, the more restrictive a patient is, the more severe is her disorder. In regard to the BITE-symptom, Phase 1 results presented a mean rank very similar to the scores for hypo and normoenergetic VET, but very different from the hyperenergetic category, showing that patients with hyperenergetic intake presented more symptoms of BN. As for the number of vomiting episodes per week, it was significantly higher for those with hypoenergetic VET intake in Phases 1 and 2 (p = 0.07 in Phase 2). This shows that the greater the food restriction, the greater the vomiting episodes, even without more binge eating episodes. Again, this shows that vomiting is used for several reasons not related to the purging of excessive food intake (Olmested et al., 1994). Gendall et al. (1997) found the same result, and according to them, the less a patient eats, the more often the purgation occurs. In regard to the number of binge eating episodes per week, the result was significantly higher for patients with hypoenergetic VET intake in Phase 3, which proves, once again, that food restriction leads to binge eating episodes (Reiff, 1992). In regard to meals followed by vomiting and BITE-symptom, it was observed that: those with hypoenergetic intake presented a lower score, that is, patients with low energy consumption (in the VOM intake) presented less symptoms; however, this difference was

132

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

observed only in Phase 1, indicating that, after treatment, the level of energy intake of meals followed by vomiting did not determine BN symptoms. Phase 2 showed that BSQ scores were lower in patients with hypoenergetic VOM. It can be concluded that if the patient worried less about her body, she would eat less energy during her meals followed by vomiting. Gendall et al. (1997) also compared energy intake and clinical variables, and they also found that, the less the patient ate (apart from binge eating episodes), the more often he purged. They also found that patients that presented more binge eating episodes had a higher energy intake during these episodes, and that body dissatisfaction scores were higher among those consuming meals with less energy intake – indicating severe food restriction. This data was not followed up in this paper. However, the study by Gendall et al. was a cross-sectional, and not a follow-up study. Some considerations should be made about this study: firstly, the number of patients was relatively small, and it became smaller because of the high rate of treatment dropout. However, it is believed that the number of patients followed up until the end of the process was sufficient, considering that there are few studies on ED in Brazil, particularly follow-up studies of bulimic patients and nutritional issues. The number of patients that filled in the tests and food diaries in Phases 2 and 3 of the follow-up was also low because of dropouts, and eventually led to missing values, which may have affected the analysis. It is important to note that the method of dietary assessment – food record – has limitations and it is subject to bias. Even so, Gayle (1998) affirmed that this method is the only one able to assess energy intake and to identify binges in free-living bulimic subjects. We are aware that subjects who fill a food record may change their intake, motivated by feelings of guilty and shame. Besides that, one still has to consider that the process of coding the food consumption may have mistakes and that the software used to convert food intake into nutrient intake may not have values for all foods consumed, for example (Livingstone and Black, 2003). Few studies tested strategies to improve the self-report of food intake, especially by means of not changing the intake during the recording period. Goris and Westerterp (2000) observed that confronting subjects with implausible results from a prior diary decreases the errors. In Brazil, Scagliusi et al. (2003) verified that confronting the subjects and conducting an intensive training on how to record the intake attenuate the error, although it remains high. In the present research, some procedures were used in order to improve the record. Patients were told to register their intakes soon after them and instructed on how to describe the foods consumed and to estimate portion sizes. Every week, a dietitian reviewed the diaries when the patients returned them, probing the patients and instructing them one more time when necessary. Moreover, all the records were coded and analyzed by only one researcher, who was previously trained. We believe that these procedures should have decreased the errors associated to dietary assessment. As stated by Woell et al. (1989) even with this bias it is possible to analyze food intake by means of a food diary. Other authors used this method to assess food intake of bulimic patients and considered it a valid instrument (Elmore and Castro, 1991; Gendall et al., 1997; Woell et al., 1989). The instrument used to assess aspects of eating attitudes and relationship with food was developed for this research based on clinical practice. Many studies confuse the term eating

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

133

behavior with food intake, so that the questionnaires that claim to measure behavior, in fact only assess if some groups of foods are bought and eaten (Kubik et al., 2002; Townsend et al., 2003). In other researches, food behavior is cited but is not defined, as for example in the study of Mitchell et al. (1988) which showed that bulimics with poorer prognostic had more abnormal eating behaviors, without specification of what these behaviors would be. Some studies focus on behaviors that are important to EDs, but their interrogations only cover the classical symptoms of BN, like for example vomiting frequency (Martín et al., 1999). There are some widely used scales in ED research, like the Restraint Scale (Herman and Mack, 1975), which measures chronic dieting or the switch between periods of restraint and lapses, the Three-Factor Eating Questionnaire (Stunkard and Messick, 1985), a measure of disinhibition, restraint and subjective assessment of hunger, and the Dutch Eating Behavior Questionnaire (van Strien et al., 1986), which also measures restraint. Although these scales are useful and well developed psychometrically, they are limited in scope, and assess mainly dietary restraint. These factors are associated to BN, but they do not encompass the wide range of dysfunctional eating attitudes that this disease implies. In this manner, using only these questionnaires supplies a lot of relevant data, but also ignores other pieces of information, such as beliefs and perceptions about food, the pleasure of eating, hidden eating, difficulty in handling with hunger, social events, food choice, and feelings towards food. We believe it is relevant to research these aspects, as we could note, with the data of this study, that even the patients whose clinical status becomes normal may still have a complicated relationship with eating and their bodies. This may, in turn, cause psychological distress and lead to recurrence. In this manner, the questions utilized in this research served as a starting point for the development of a specific tool to measure eating attitudes in patients with EDs. Today, based on these results an instrument is being adapted and validated. Moreover, the results of specific nutritional interventions for the treatment of BN could not be separately tested in controlled studies, because they are a part of a total treatment program (Rock and Curran-Celentano, 1996). Using just the nutritional intervention, without the due clinical, psychiatric and therapeutic follow-ups would be unethical. Also, due to ethical considerations, control groups, to which only one of the treatment components is provided, are not recommended.

Conclusion In summary, some positive changes were observed after 12 weeks of CBT: a significant change in the EAT and the BITE-symptom scores, and zero median for laxative, diuretic and appetite moderator drug use. After six months follow-up, the positive changes found were: the patients did not meet the diagnostic criteria for BN, taking into consideration the means and medians of binge eating and vomiting episodes; EAT and BITE-symptom scores showed a non-symptomatic group; and there was significant difference in the BSQ score. Regarding eating behaviors and relationship toward foods the following improves were observed: guilty after eating ‘forbidden foods’ decreased (as well as the behavior while and after eating these foods improved), some misconceptions about food were reverted (as thinking that eating a little more automatically causes weight gain), some negative feelings

134

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

involving food were reduced (as anxiety, lack of control and nervousness) while the feeling of tranquility has increased. The obsession with food has also decreased, resulting in a smaller interference of food in patients’ life. Nevertheless, it is remarkable that many disturbed attitudes did not change, especially those related to feelings, reflected by the lack of pleasure with food and the difficulties in dealing with hunger. On the other hand, we did not find changes in food intake. This result is preoccupant and should be carefully monitored by dietitians while they treat bulimic patients. Treatment should encourage a regular meal pattern, composed by frequent meals rich in nutrient-dense foods. The assessment of these patients, based on standardized tests, showed positive progress, as shown by the progress of bulimic symptoms. The use of standardized score tests and data regarding bulimic behavior and energy intake allowed for a clearer understanding of the pattern of the disease and its prognosis. It was possible to confirm an important fact, namely that energy restriction is related to higher frequency of binge eating and purging. It is believed that standardized tests are an effective strategy to assess follow-up of bulimic patients, since measuring the treatment outcome just by verifying changes in the frequency of bulimic symptoms cannot cover the complexity of ED. Furthermore, it is relevant to include measurements of nutritional consumption, such as energy intake in eating episodes, whether followed by vomiting or not. Because it is known that BN is a chronic disorder, with a high chance of recurrence, it is necessary to think about recovery in a broader manner, aiming to improve the relation towards body, weight and food in addition to other positive psychological changes. The main objective of the traditional nutritional approach for BN is to establish a normal eating pattern and to cease the purging practices. Further nutritional treatment, based specially on counseling, should aim to help the patient to distinguish behavior related to food and weight from feelings and psychological issues, and to promote improvements in eating attitudes (ADA, 2001). New techniques and interventions are required to treat and to alter the relation established by the patient towards food. In-depth knowledge about eating attitudes is necessary to design a nutritional intervention able to improve the quality of the diet of these patients and also to promote behavioral changes (Hetherington et al., 1993; Sunday and Halmi, 1996). Researchers and practitioners need to understand and treat all the disordered eating aspects presented by patients with BN and not only the bulimic episodes that define this syndrome (Hetherington et al., 1993). Therefore, other measures – such as relationship and attitudes towards food – should be investigated and assessed after the intervention. We believe that this kind of comprehensive treatment is necessarily long and can be conducted only if the professionals involved have a broad understanding of all meanings that food (and also the disease) has. As stated by Levine (1994), “people with eating disorders are people struggling with fantasies, motives, anxieties, and coping mechanisms that are established and vigorously reinforced by our culture. They are not ‘ics’ – anorexics or bulimics”. So dietitians that work with ED should strive to better understand these topics and to seek training in counseling, cognitive techniques and motivational interviewing to improve the treatment of all features of the eating attitudes of these patients.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

135

Based on the results presented in this chapter, our program of nutritional treatment was improved. Its duration was increased to 18 weeks, and the individual counseling has been receiving more attention and time. We are also developing a new treatment program, whose aim will be the improvement of eating attitudes and relationship with the body and food. This new program will be provided to patients after completion of the 18-weeks program. We believe that the first treatment goal is to end bulimic behavior and establish a healthier intake, but if we do not provide a deeper understanding of all food and body issues that the patient presents it is very likely to have a relapse. Also, by providing a more comprehensive care we can be sure that we are treating a person and not a disease. It is also relevant to note that in order to meet this goal, tools for measuring eating attitudes, especially those focused on feelings, beliefs and attitudes towards food, should be developed and validated. Our research group is now working with the instrument tested in this study. Considering the findings of this research, this eating attitudes questionnaire is being adapted and will be psychometrically tested. Finally, our data showed that eating disorders are also a reason for concern in an undeveloped country as Brazil. Our health system needs to be more prepared to deal with this problem, since there are too few centers that treat these diseases in Brazil. Perhaps it is even more necessary to discuss prevention of eating disorders, especially because they afflict mainly young women. In Brazil, young women live in a difficult scenario, already marked by a poor health status, which could be more aggravate with the presence of an eating disorder. It is also relevant to attest that in order to prevent eating disorders specific interventions should be provided to a wide range of people, specially young girls and women, with focus in nutrition education, body image improvement, size acceptance and with strategies to improve relationship towards food. As a research group on nutrition and eating disorders, we believe that improvement of eating attitudes and relationship towards food is necessary not only for treatment of eating disorders, but also for its prevention.

Authors= Notes We thank Cynthia York, Dr. Rebecca Cohen, Natalie Demidenko, Deborah Evans, Katie Harkins and Amanda Scott for help with data input. Dr. Jo Wood provided statistical consultation. This project was supported by the Departments of Psychiatry and Psychology at the Ottawa Hospital.

References Abraham, SF; Mira, M; Llewellyn-Jones, D. Bulimia: a study of outcome. Int J Eat Disord, 1983, 2, 175-80. Adami, G; Bauer, B; Gandolfo, P; Scopinaro, N. Body image in early-onset obese patients. Eat Weight Disord, 1997, 2, 87-93.

136

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

Agras, WS; Crow, SJ; Halmi, KA; Mitchell, JE; Wilson, GT; Kraemer, HC. Outcome predictors for cognitive behavior treatment of bulimia nervosa: data from a multisite study. Am J Psychiatry, 2000, 157, 1302-08. Alvarenga, MS; Philippi, ST; Negrão, AB. Nutritional aspects of eating episodes followed by vomiting in Brazilian patients with bulimia nervosa. Eat Weight Disord, 2003, 8, 150-56. American Dietetic Association (ADA). Position of the American Dietetic Association: nutritional intervention in the treatment of anorexia nervosa and bulimia nervosa – technical support paper. J Am Diet Assoc, 1988, 88, 69-71. American Dietetic Association (ADA). Position of the American Dietetic Association: nutritional intervention in the treatment of anorexia nervosa, bulimia nervosa and binge eating. J Am Diet Assoc, 1994, 94, 902-7. American Dietetic Association (ADA). Position of the American Dietetic Association: nutritional intervention in the treatment of anorexia nervosa, bulimia nervosa, and eating disorders not otherwise specified (EDNOS). J Am Diet Assoc, 2001, 101, 810-19. American Psychiatric Association (APA). Diagnostic and Statistical Manual of Mental Disorders (4th ed.), Washington DC: American Psychiatric Association; 1994. Bacaltchuk, J; Hay, P. Treatment of bulimia nervosa: a synthesis of evidence. Rev Bras Psiq, 1999, 21, 1-8. Beals, KA. Eating behaviors, nutritional status, and menstrual function in elite female adolescent volleyball players. J Am Diet Assoc, 2002,102,1293-96. Becker, AE; Grinspoon, SK; Klibanski, A; Herzog, DB. Eating disorders – current concepts. New Engl J Med, 1999, 8, 1092-98. Behar, R; de la Barrera, M; Michelotti, J. Clinical characteristics and gender identity among eating disordered patients subtypes. Rev Med Chil, 2003, 131,748-58. Bhugra, D; Mastrogianni, A; Maharajh, H; Harvey, S. Prevalence of bulimic behaviours and eating attitudes in schoolgirls from Trinidad and Barbados. Transcult Psychiatry, 2003, 40, 409-28. Borges, MB; Jorge, MR; Morgan, CM; Da Silveira, DX; Custodio, O. Binge-eating disorder in Brazilian women on a weight-loss program. Obes Res, 2002, 10, 1127-34. Brambilla, F; Draisci, A; Peirone, A; Brunetta, M. Combined cognitive-behavioral, psychopharmacological and nutritional therapy in bulimia nervosa. Neuropsychobiology, 1995, 32, 68-71. Cash, TF; Henry, PE. Women’s body images. The results of a national survey in the USA. Sex Roles, 1995, 33, 19. Collings, S; King, M. Ten-year follow-up of 50 patients with bulimia nervosa. Br J Psych, 1994, 164, 80-7. Cooper, PJ; Taylor, M; Cooper, Z; Fairburn, CG. The development and validation of the Body Shape Questionnaire. Int J Eat Disord, 1987, 6, 485-94. Cordás, TA; Castilho, S. Body image in eating disorders - Assessment instrument: "Body Shape Questionnaire". Psiq Biol, 1994, 2, 17-21. Cordás, TA; Hochgraf, PB. The BITE: instrument for bulimia nervosa assessment. J Bras Psiq, 1993, 42, 141-4. Dolan, JB; Lacey, H; Evans, C. Eating behavior and attitudes to weight and shape in British women from three ethnic groups. Br J Psych, 1990, 157, 523-28.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

137

Dowson, J; Henderson, L. The validity of a short version of the Body Shape Questionnaire. Psychiatry Research, 2001, 102, 263-71. Dunker, KLL; Philippi, ST. Food habits and behavior in adolescents with symptoms of anorexia nervosa. Rev Nutrição Puccamp, 2003, 16, 51-60. Eckstein-Harman, M. Eating disorders: the changing role of nutrition intervention with anorexic and bulimic patients during psychiatric hospitalization. J Am Diet Assoc, 1993, 93, 1039-40. Eiger, MR; Christie, BW; Sucher, KP. Change in eating attitudes: An outcome measure of patients with eating disorders. J Am Diet Assoc, 1996, 96, 62-4. Elmore, DK; Castro, JM. Meal patterns of normal, untreated bulimia nervosa and recovered bulimic women. Psychol Behav, 1991, 49, 99-105. Fahy, TA; Russell, GFM. Outcome and prognostic variables in bulimia nervosa. Int J Eat Disord, 1993,14, 135-45. Fairburn, CG. A cognitive behavioral approach to the treatment of bulimia. Psychol Med, 1981, 11, 707-11. Fairburn, CG; Kirk, J; O´Connor, M; Cooper, PJ. A comparison of two psychological treatments for bulimia nervosa. Behav Res Therapy, 1986, 24, 629-43. Fernández, F; Sánchez, I; Turón, JV; Jiménez, S; Alonso, P; Vallejo, J. Psychoeducative ambulatory group in bulimia nervosa. Evaluation of a short-term approach. Actas Luso Esp Neurol Psiquiatr Cienc Afines, 1998, 26, 23-8. Fitcher, MM; Quadflieg, N; Rief, W. The German longitudinal bulimia nervosa study. In: Herzog, W; Deter, HC; Vanderycken, W. (Eds.), The course of eating disorders: long term follow-up studies of anorexia and bulimia nervosa. New York: Springer-Verlag; 1992; pp.133-49. Fontenelle, L; Mendlowicz, M; Menezes, GB; Papelbaum, M; Freitas, S; Godoymatos, A; Coutinho, W; Appolinario, JC. Psychiatric comorbidity in a Brazilian sample of patients with binge-eating disorder. Psychiatry Research, 2003, 119,189-94. Freeman, RJ; Beach, B; Davis, R; Solyom, L. The prediction of relapse in bulimia nervosa. J Psych Res, 1985, 9, 349-53. Gannon, MA; Mitchell, JE. Subjective evaluation of treatment methods by patients treated for bulimia. J Am Diet Assoc, 1986, 86, 520-21. Garcia, RWD. The food, the diet, the taste. Changes in the Urban Food Culture. [dissertation]. São Paulo (SP): University of São Paulo; 1999. Garfinkel, PE; Goldbloom, D; Davis, R; Olmested, MP; Garner, DK; Halmi KA. Body dissatisfaction in bulimia nervosa: relationship to weight and shape concerns and psychological functioning. Int J Eat Disord. 1992, 11, 151-61. Garner, DM. Psychotherapy outcome research with bulimia nervosa. Psychoth Psychos, 1987, 48, 129-40. Garner, DM; Garfinkel, PE. The eating attitudes test: an index of the symptom of anorexia nervosa. Psychol Med, 1979, 9, 273-9. Garner, DM; Olmested, MP; Bohr, Y; Garfinkel, PE. The eating attitude test: psychometric features and clinical correlates. Psychol Med, 1982, 12, 871-79.

138

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

Garner, DM; Olmested, MP; Polivy, J. Development and validation of a multidimensional eating disorder inventory for anorexia nervosa and bulimia. Int J Eat Disord, 1983, 2, 1534. Gayle, MT. Caloric intake patterns of nonpurge binge-eating women. West J Nurs Res, 1998, 20, 103-18. Gendall, KA; Sullivan, PE; Joyce, PR; Carter, FA; Bulik, CM. The nutrient intake of women with bulimia nervosa. Int J Eat Disord, 1997, 21, 115-27. Ghazal, N; Agoub, M; Moussaoui, D; Battas, O. Prevalence of bulimia among secondary school students in Casablanca. L´Encephale, 2001, 27, 338-42. Goris, AHC; Westerterp, KR. Improved reporting of habitual food intake after confrontation with earlier results on food reporting. Brit J Nutr, 2000, 83, 363-9. Greenfeld, D; Mickley, D; Quinlan, DM; Roloff, P. Hypocalemia in outpatients with eating disorders. Am J Psychiatry, 1995, 152, 60-3. Hadigan, CM; Kissileff, HR; Walsh, BT. Patterns of food selection during meals in women with bulimia. Am J Clin Nutr, 1989, 50, 759-66. Hay, PJ. Epidemiology of eating disorders: current status and future developments. Rev Bras Psiquiatr, 2002, 24, 13-7. Hedges, DW; Reimherr, FW; Hoopes, SP; Rosenthal, NR; Kamin, M; Karim, R; Capece, J. Treatment of bulimia nervosa with topiramate in a randomized, double-blind, placebocontrolled trial, part 2: improvement in psychiatric measures. J Clin Psychiatry, 2003, 64,1449-54. Henderson, M; Freeman, A. A self-rating scale for bulimia: the BITE. Brit J Psych, 1987, 150, 18-24. Herman, CP; Mack, D. Restrained and unrestrained eating. J Pers, 1975, 43, 647-60. Herzog, DB; Nussbaum, KM; Marmor, AK. Comorbidity and outcome in eating disorders. Psych Clin North Am,1996, 9, 843-59. Hetherington, MM; Altemus, M; Nelson, ML; Bernat, AS; Gold, PW. Eating behavior in bulimia nervosa: multiple meal analyses. Am J Clin Nutr, 1994, 60, 864-73. Hetherington, MM; Spalter, AR; Bernat, AS; Nelson, ML; Gold, PW. Eating pathology in bulimia nervosa. Int J Eat Disord, 1993, 13, 13-24. Hill, AJ; Williams, J. Psychological health in a non-clinical sample of obese women. Int J Obes, 1998, 22, 578-83. Hsu, LKG; Holder, D. Bulimia nervosa: treatment and short-term outcome. Psychol Med, 1986, 16, 65-70. Institute of Medicine. Dietary Reference Intakes: for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Food and Nutrition Board. Washington, D.C.: National Academy Press; 1997. Institute of Medicine. Dietary Reference Intakes: for Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Food and Nutrition Board. Washington, D.C.: National Academy Press; 1998. Institute of Medicine. Dietary Reference Intakes: for Vitamin C, Vitamin E, Selenium and Carotenoids. Food and Nutrition Board. Washington, D.C.: National Academy Press; 2000.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

139

Joergensen, J. The epidemiology of eating disorders in Fyn County, Denmark, 1977-1986. Acta Psych Scand, 1992, 85, 30-4. Johnson, C. Initial consultation for patients with bulimia and anorexia nervosa In: Garner, DM; Garfinkel PE. (Eds). Handbook of psychotherapy for anorexia nervosa and bulimia. New York: Guilford Press; 1985; 19-51. Johnson, C; Maddi, K. Etiologia de la bulimia: perspectivas biopsicosociales In: Feinstein, SC; Sorosky, AD. (Eds). Transtornos en la alimentación. Buenos Aires: Ediciones Nueva Vision; 1988; 53-80. Johnson, WG; Shlundt, DG; Jarrell, MP. Exposure with response prevention, training in energy balance and problem/solving therapy for bulimia nervosa. Int J Eat Disord, 1986, 5, 35-46. Kaye, WH; Weltzin, TE; Hsu, LKG; McConaha, CW; Bolton, B. Amount of calories retained after binge eating and vomiting. Am J Psychiatry, 1993,150, 969-71. Keel, PK; Mitchell, JE. Outcome in bulimia nervosa. Am J Psychiatry, 1997,154, 313-21. Keel, PK; MitchelI, JE; Miller, KB; Davis, TL; Crow, SJ. Long-term outcome of bulimia nervosa. Arch Gen Psych, 1999,56, 63-9. Keller, MB; Herzog, DB; Lavori, PW; Bradburn, IS; Mahoney, EM. The naturalistic history of bulimia nervosa: extraordinary high rates of chronicity, relapse, recurrence, and psychosocial morbidity. Int J Eat Disord, 1992, 12, 1-9. Kissileff, HR; Walsh, BT; Kral, JG; Cassidy, SM. Laboratory studies of eating behavior in women with bulimia. Physiol Behav, 1986, 38, 563-70. Kubik MY; Lytle, LA; Hannan, PJ; Story, M; Perry, CL. Food-related beliefs, eating behavior, and classroom food practices of middle school teachers. J Sch Health, 2002, 72, 339-345. Lacey, JH. Bulimia nervosa, binge eating, and psychogenic vomiting: a controlled treatment study and long term outcome. Brit Med J, 1983, 286, 1609-13. Lacey, JH. Time limited individual and group treatment for bulimia. In: Garner, M; Garfinkel, PE. (Eds). Handbook of Psychotherapy for anorexia nervosa and bulimia. New York: Guilford Press; 1985; p. 431-57. Lasater, LM; Mehler, PS. Medical complications of bulimia nervosa. Eat Behav, 2001, 2, 279-92. Latner, JD; Wilson, T. Cognitive-behavioral therapy and nutritional counseling in the treatment of bulimia nervosa and binge eating. Eat Behav, 2000, 1, 3-21. Lee, S; Kwok, K; Liau, C; Leung, T. Screening Chinese patients with eating disorders using the Eating Attitudes Test in Hong Kong. Int J Eat Disord, 2002, 32, 91-7. Leung, N; Waller, G; Thomas, G. Outcome of group cognitive-behavior therapy for bulimia nervosa: the role of score beliefs. Behav Res Ther, 2000, 38, 145-56. Levine, M. Some basic principles for understanding, referring, and preventing eating disorders. [Presented at the 13th National NEDO Conference, Columbus, Ohio, October 3, 1994.] Livingstone, MBE; Black, AE. Markers of the validity of reported energy intake. J Nutr, 2003, 133, 895S-920S. Maddocks, SE, Kaplan, AS. The prediction of treatment response in bulimia nervosa - A study of patient variables. Brit J Psych, 1991, 159, 846-9.

140

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

Maddocks, SE; Kaplan, AS; Woodside, DB; Langdon, L; Piran, N. Two year follow-up of bulimia nervosa: the importance of abstinence as the criterion of outcome. Int J Eat Disord, 1992, 12, 133-41. Martín, AR; Nieto, JMM; Jiménez, MAR; Ruiz, JPN; Vasquez, MCD; Fernández, YC; Gómez, MAR; Fernández, CC. Unhealthy eating behaviour in adolescents. Eur J Epidemiol. 1999, 15, 643-8. Mitchell, JE; Laine, DC. Monitored binge-eating behavior in patients with bulimia. Int J Eat Disord, 1985, 4, 177-83. Mitchell, JE; Pyle, RL; Eckert, ED. Frequency and duration of binge-eating episodes in patients with bulimia. Am J Psychiatry, 1981, 138, 835-6. Mitchell, JE; Pyle, RL; Hatsukami, D; Goff, G; Glotter, D; Harper, J. A 2-5 year follow-up study of patients treated for bulimia. Int J Eat Disord, 1988, 8, 157-65. Monteiro, CA; Conde, WL; Popkin, BM. Is obesity replacing or adding to undernutrition? Evidence from different social classes in Brazil. Public Health Nutr, 2002, 5, 105-12. Monteiro, CA; Conde, WL; Popkin, BM. The burden of disease from undernutrition and overnutrition in countries undergoing rapid nutrition transition: a view from Brazil. Am J Public Heath, 2004, 94, 433-4. Nakazato, M; Hashimoto, K; Shimizu, E; Kumakiri, C; Koizumi, H; Okamura, N; Mitsumori, M; Komatsu, N; Iyo, M. Decreased levels of serum brain-derived neurotrophic factor in female patients with eating disorders. Biol Psychiatry, 2003,54, 485-90. Nappo, SA; Tabach, R; Noto, AR; Galduróz, JCF; Carlini, EA. Use of anoretic amphetaminelike drugs by Brazilian women. Eat Behav, 2002, 3, 153-65. Nasser, M. Culture and weight consciousness. J Psychosom Res, 1988, 32, 573-7. Nasser, M; Katzman, MA; Gordon, RA. Eating disorders and cultures in transition. New York: Taylor and Francis; 2001. National Research Council (NRC). Recommended Dietary Allowances (RDA). 10.ed. Washington, D.C.: National Academy Press; 1989. Negrão, AB; Cordás, TA. Clinical characteristics and course of anorexia nervosa in Latin America, a Brazilian sample. Psychiatry Res, 1996, 62,17-21. Nobakht, M; Dezhkam, M. An epidemiological study of eating disorders in Iran. Int J Eat Disord , 2000, 28, 265-71. Nunes, MA; Bagatini, LF; Abuchaim, AL; Kunz, A; Ramos, D; Silva, A; Somenzi, L; Pinheiro, A. Eating disorders: considerations about The Eating Attitudes Test (EAT). R ABP-APAL, 1994, 16, 7-10. Nunes, MA; Barros, FC; Anselmo Olinto, MT; Camey, S; Mari, JDJ. Prevalence of abnormal eating behaviours and inappropriate methods of weight control in Young women from Brazil: a population-based study. Eat Weight Disord, 2003, 8, 100-06. Nutzinger, DO; Zwann, M. Behavioral treatment of bulimia nervosa. In: Fitcher, MF. (Ed.). Bulimia nervosa: basic research, diagnosis and therapy. Chischester: John Willey and Sons; 1990; p.292 Olmested, MP; Kaplan, AS; Rockert, W. Rate and prediction of relapse in bulimia nervosa. Am J Psychiatry, 1994, 151, 738-43.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

141

Philippi, ST; Szarfarc, SC; Latterza, AR. Virtual Nutri (Version 1.0 for Windows). [Computer software]. São Paulo, SP: Department of Nutrition, School of Public Health, University of São Paulo; 1996. Polivy, J. Psychological consequences of food restriction. J Am Diet Assoc, 1996, 96, 589-92. Popkin, BM. Nutritional patterns and transitions. Pop Devel Res, 1993, 19, 138-57. Pyle, RL; Mitchell, JE; Eckert ED; Hatsukami, D; Pomeroy, C; Zimmerman, R. Maintenance treatment and 6 month outcome for bulimic patients who respond to initial treatment. Am J Psychiatry, 1990, 147, 871-75. Ramirez, EM; Rosen, JC. A comparison of weight control and weight control plus body image therapy for obese men and women. J Consult Clin Psychol, 2001, 69, 440-46. Reiff, DW. Behavior change: bulimia nervosa. In: Reiff, DW; Reiff, KKL. (Eds.). Eating disorders – Nutrition therapy in the recovery process. Maryland: Aspen Publishers; 1992; p.360-4. Reiff, DW; Reiff, KKL. Eating disorders – Nutrition therapy in the recovery process. Maryland: Aspen Publishers; 1992. Rock, CL; Curran-Celentano, J. Nutritional management of eating disorders. Psych Clin North Am, 1996, 19, 701-13. Rodin, J; Silberstein, L; Striegel-Moore, R. Women and weigh: a normative discontent. In: Sonderegger, TB. (Ed.) Nebraska symposium on motivation: psychology and gender. Lincoln: University of Nebraska Press; 1984; p.267. Rorty, M; Yager, J; Rossoto, E. Why and how do women recover from bulimia nervosa? The subjective appraisals of forty women recovered for a year or more. Int J Eat Disord, 1993, 14, 249. Rosen, JC; Leitenberg, H; Fisher, C; Khazam, C. Binge-eating episodes in bulimia nervosa: the amount and type of food consumed. Int J Eat Disord, 1986, 5, 255-67. Rosen, JC; Reiter, J; Orosan, P. Cognitive-behavioral body image therapy for body dysmorphic disorder. J Consult Clin Psychol, 1995, 63, 263-9. [Erratum in: J Consult Clin Psychol, 1995, 63, 437.] Scagliusi, FB; Polacow, VO; Artioli, GG; Benatti, FB; Lancha Jr, AH. Selective underreporting of energy intake in women: magnitude, determinants, and effect of training. J Am Diet Assoc, 2003, 103, 1306-13. Scagliusi, FB; Polacow, VO; Cordás, TA; Coelho, D; Alvarenga, MS; Philippi, ST; Lancha Jr, AH. Test-Retest Reliability and Discriminant Validity Of the Restraint Scale Translated into Portuguese. Eat Behav, 2005a, 6, 85-93. Scagliusi, FB; Polacow, VO; Cordás, TA; Coelho, D; Alvarenga, MS; Philippi, ST; Lancha Jr AH. Translation, adaptation and psychometric evaluation of a nutrition knowledge scale. Brazilian Journal of Nutrition, 2005-b. (in press) Scagliusi, FB; Polacow, VO; Cordás, TA; Coelho, D; Alvarenga, MS; Philippi, ST; Lancha Jr AH. Translation into Portuguese and validation of the Body Attitudes Questionnaire. Percept Mot Skills. 2005-c, 100, 25-41. Scagliusi, FB; Alvarenga, MS; Polacow, VO; Cordás, TA; Queiróz GKO; Coelho, D; Philippi, ST; Lancha Jr AH. Concurrent and discriminant validity of the Stunkard’s Figure Rating Scale adapted into Portuguese. Apettite, 2006. (in press)

142

M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi

Steinhausen, HC; Seidel, R. Correspondence between the clinical assessment of eatingdisordered patients and findings derived from questionnaires at follow-up. Int J Eat Disord, 1993, 14, 367-74. Story, M. Nutrition management and dietary treatment of bulimia. J Am Diet Assoc, 1986, 86, 517-19. Stunkard, AJ; Messick, S. The three-factor eating questionnaire to measure dietary restraint, disinhibition and hunger. J Psychosom Res. 1985, 29, 71-83. Sunday, SR; Einhorn, A; Halmi, KA. Relashionship of perceived macronutrient and caloric content to affective cognitions about food in eating-disordered, restrained, and unrestrained subjects. Am J Clin Nutr, 1992, 55, 362-71. Sunday, SR; Halmi, KA. Micro-and macroanalyses of patterns within a meal in anorexia and bulimia nervosa. Appettite, 1996, 26, 21-36. Strigel-Moore, RH; Silberstein, LR; Rodin, J. Toward an understanding of risk factors for bulimia. Am Psychologist, 1986, 41, 246-63. Swift, WJ; Ritholz, M; Kalin, NH; Kaslow, N. A follow-up study of thirty hospitalized bulimics. Psychosom Med, 1987, 49, 45-55. Thiels, C; Schmidt, U; Treasure, J; Garthe, R. Four-year follow-up of guided self-change for bulimia nervosa. Eat Weight Disord, 2003, 8, 212-17. Thompson, JK. The (mis)measurement of body image: ten strategies to improve assessment for applied and research purposes. Body Image, 2004, 1, 7-14. Townsend, MS; Kaiser, LL; Allen, LH; Joy, AB; Murphy, SP. Selecting items for a food behavior checklist for a limited-resource audience. J Nutr Educ Behav, 2003, 35, 69-82. Trumbo, P; Schlicker, S; Yates, AA; Poos, M. Dietary Reference Intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein and amino acids. J Am Diet Assoc, 2002, 102, 1621-30. Vanderlinden, J; Norre, J; Vanderycken, W. A practical guide to the treatment of bulimia nervosa. New York: Brunner/Mazel; 1989. Van Strien, T; Frijters, JE; van Staveren, WA; Defares, PB; Deurenberg, P. The predictive validity of the Dutch Restrained Eating Scale. Int J Eat Disord, 1986, 5, 747-55. Villapiano, M; Goodman, LJ. Eating Disorders: Time for Change. Philadelphia: Taylor and Francis; 2001a. Villapiano, M; Goodman, LJ. Eating Disorders: The Journey to Recovery Workbook. Philadelphia: Taylor and Francis; 2001b.

Vilela, JE; Lamounier, JA; Dellaretti Filho, MA; Barros Neto, JR; Horta, GM. Eating disorders in school children. J Pediatr, 2004, 80, 49-54. Wallin, G.van der Ster, Noring, C; Holmgren, S. Binge eating versus nonpurged eating in bulimics: is there a carbohydrate craving after all? Acta Psych Scand, 1994, 89, 376-81. Wallin, G van der Ster; Noring, C; Lennernas, MAC; Holmgren, S. Food selection in anorectics and bulimics: food items, nutrient content and nutrient density. J Am Coll Nutr, 1995, 4, 271-2. Walsh, BT; Kissileff, HR; Cassidy, SM; Dantzic, S. Eating behavior of women with bulimia. Arch Gen Psych, 1989, 46, 54-8. Whisenant, SL; Smith, BA. Eating disorders: current nutrition therapy and perceived needs in dietetics education and research. J Am Diet Assoc, 1995, 95,1109-12.

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

143

Woell, C; Ficther, MM; Pirke, KM; Wolfram, G. Eating behavior of patients with bulimia nervosa. Int J Eat Disord, 1989, 8, 557-68. Wolff, GE; Clark, MM. Changes in eating self-efficacy and body image following cognitivebehavioral group therapy for binge eating disorder: a clinical study. Eat Behav, 2001, 2, 97-104. Yager, J. Weighty perspectives: contemporary challenges in obesity and eating disorders. Am J Psychiatry, 2000, 157, 851-3.

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 145-158 © 2006 Nova Science Publishers, Inc.

Chapter VII

Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept in Women with Bulimia Nervosa and Binge Eating Disorder Giorgio A. Tasca1,2,3, Louise Balfour1,2, Kanchan Kurichh2, Monique Potvin-Kent2 and Hany Bissada1,2 1

Ottawa Hospital, 2University of Ottawa, 3Carleton University

Abstract It was hypothesized that higher levels of actual-desired BMI discrepency (ADBD) would be associated with higher binge eating symptoms, lower self concept, and higher body dissatisfaction for a clinical sample of women with Bulimia Nervosa (BN) and Binge Eating Disorder (BED). A theoretical frame for ADBD was put forward based on self discrepancy theory. Also hypothesized was that women with BN would have greater eating and self related pathology than those with BED. Fifty-one participants diagnosed with BN and 41 with BED drawn from a clinical sample completed questionnaires assessing eating disorder and general psychopathology. Greater ADBD was related to greater body dissatisfaction for the BN and BED groups, and lower self concept for the BN group. Those with BN had more self-related pathology. ADBD can be easily assessed by clinicians and may be used as an index of body dissatisfaction and overall self concept. ADBD may be a vulnerability factor for developing an eating disorder for women.

Researchers have identified actual-desired body weight discrepancy (ADBD) among those with eating disorders as an important variable in the clinical assessment of eating disorder symptoms (Crowther and Sherwood, 1997), and ADBD has been implicated in the clinical literature in the etiology of Bulimia Nervosa (BN; Casper, 1983). Similarly, Thompson (1996) argued that discrepancies between actual body size and desired body size is an index of body dissatisfaction (Thompson, 1996). Within these clinical

146

Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh et al.

conceptualizations of ADBD, there is little theoretical formulation for why this particular discrepancy may have an impact on psychological functioning, well being, and/or eating disorder symptoms. A notable exception is McKinley (1998) who suggested that the negative impact of ADBD on the body esteem of college women is a result of internalized cultural standards encouraging negative body experiences. In general however, the impact of ADBD on eating disorder symptomatology has received little empirical attention. Tiggeman, Winefield, Winefield and Goldney (1994) looked at the relationship between ADBD and psychological well being among young adults. They found that greater ADBD, defined as Aperceived overweight@, was related to low self evaluation and to lower levels of psychological well being. In a sample of undergraduate women, McKinley (1998) found that ADBD was related to body esteem and high body shame. She also reported higher ADBD among women than among men. Snyder (1997) found a significant correlation between perceived overweight and the Body Dissatisfaction, Drive for Thinness and Interoceptive Awareness scales of the Eating Disorders Inventory –2 (EDI-2; Garner, 1991). These studies of general population college women were all suggestive of the role of ADBD for a clinical sample of women with eating disorders. Some studies have looked at ADBD among an eating disordered population. A recent study by Doll and Fairburn (1998) found that women with BN had a greater ADBD than normal controls. Similarly, studies have found that adolescent girls with BN and severe binge eating reported greater ADBD than those with mild binge eating and normal controls (Crowther and Chernyk, 1986; Post and Crowther, 1985). Few studies have looked at the relationship between ADBD and severity of eating disorder symptoms and psychological variables. Heffernen (1996), studied a sample of lesbians with BN, and found a significant correlation between ADBD and body dissatisfaction. Heffernen’s (1996) study looked at ADBD as a variable of secondary interest, and did not conceptualize ADBD within a broaden psychological context in order to increase our understanding of ADBD’s role in eating disorder pathology. The current study looked at the importance of assessing for ADBD in a clinical context and developed a conceptual understanding of this variable as a potential risk factor for eating disorders (Casper, 1973). ADBD was seen as important in women with eating disorder symptoms when desired body weight was lower than actual body weight. ADBD was defined as a different but related construct to body dissatisfaction. Body dissatisfaction is specifically related to body shape and size but not necessarily to a self discrepancy. Because ADBD was defined in terms of a discrepancy between one=s weight and one=s personal ideal or what is proscribed as an ideal, then ADBD likely taps into core issues of ideal self image based on personal or cultural standards, and self evaluation (Tiggeman et al., 1994). In this study, ADBD’s relationship with eating disorder symptoms and psychological sequelae of eating disorders in a clinical sample of women diagnosed with BN or with BED was studied. First, a theoretical formulation of how ADBD may be an important predictor of eating disorder symptoms and psychological problems in women with BN or BED is proposed. To do so Higgins= (1987) self discrepancy theory is used as a framework.

Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept …

147

Self Discrepancy Theory There is an increasing consensus in the literature that Western sociocultural values emphasize thinness and appearance for young women (Heffernan, 1996). Striegel-Moore (1993) argued that the internalization of these values as ideals among women constitute a risk factor for the development of an eating disorder. This may be due to the discrepancy between cultural standards of unrealistic thinness that may be internalized, and actual BMI and body shape that generally do not meet these standards. This discrepancy likely leads to a sense of not living up to a social standard among some women, resulting in further attempts to attain this ideal. With repeated failures at reaching this goal, some women may experience a sense of personal failure, low self esteem, and dissatisfaction with their self and body. Higgins (1987) proposed similar notions of discrepancy with regard to the self in his self discrepancy theory. Higgins (1987) suggested that there are several domains of self including the actual self, ideal self and ought self. Actual self refers to aspects and attributes of the self that one actually possesses. Ideal self refers to aspect or attributes that one would like to possess. Ought self refers to aspects or attributes that one believes one should possess. Ideal self and ought self are self guides that are personal standards that people set up. These standards may be those established as important by others, or may be internally held standards, or both. For the purposes of this study, a culturally sanctioned ideal of thinness is seen as a self guide (i.e. ought self), especially if it has been internalized by women (i.e. ideal self). Moretti and Higgins (1990) found that discrepancies between self guides and actual self can lead to emotional distress and potential emotional problems; the greater the discrepancy, the greater the distress and problems. In a study looking at self discrepancy among college women, Strauman, Vookles, Berenstein, Chaiken, and Higgins (1991) found that self discrepencies were related to body dissatisfaction and maladaptive eating in female college students. Snyder (1997) found significant correlations between actual - ideal self discrepancies and body dissatisfaction even after actual BMI was controlled. Body weight and weight related self perceptions are integral parts of the experience of the self for women with eating disorders. The emphasis and importance placed on actual weight is a pivotal part of the disorder. Just as the discrepancy between actual self and self guides is related to psychological distress, problems with self concept, and eating disorder related psychopathology (Snyder, 1997; Strauman et al, 1991), we hypothesized that the discrepancy between actual and desired BMI for women with BN and BED will be related to eating disorder symptoms, body dissatisfaction, and low self concept. ADBD represents a tangible parallel to actual-desired self discrepancies that is particularly salient to women who are vulnerable to eating disorders. Because of the parallel, ADBD could represent a core self related construct for those with eating disorders. Although one could argue that body dissatisfaction may imply some discrepancy from an ideal or standard, ADBD is a more direct measure of such a discrepancy.

Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh et al.

148

Bulimia Nervosa and Binge Eating Disorder BED has recently been included as a diagnosis requiring further research in the Diagnostic and Statistical Manual for Mental Disorders (DSM-IV; APA, 1994). Research has indicated that in a community sample (Hay and Fairburn, 1998) and in a clinical sample (Tasca, Wood, Demidenko, Bissada, 2002) those with BED had lower levels of psychopathology than those with BN. Other researchers have found those with BED to be distinct from obese controls, and to be a homogeneous group on a number of variables. For example, obese people who binge eat compared to obese people who do not binge eat show greater psychopathology (Marcus, Wing, Ewing, Kern, Gooding and McDermott, 1990), greater eating pathology (Yanovski, Nelson, Dubbert, and Spitzer, 1993), lower self esteem and greater discrepancy between their current and ideal body size (Striegel-Moore, Wilson, Wilfley, Elder, and Brownell, 1998). Although Striegel-Moore et al, (1998) found greater body dissatisfaction among binge eaters than controls, other studies have not found the same result (de Zwaan et al, 1994; Antoniou, Tasca, Bissada, and Balfour, 2002). Binge eating is a symptom held in common between BN and BED and often the criteria for evaluating binge eating is similar for both disorders (Walsh and Garner, 1997). Problems with self esteem and self concept are also shared among these disorders (Striegel-Moore, et al., 1998). Body image disturbance and dissatisfaction is a hallmark symptom of BN (Kearney-Cook and StriegelMoore, 1997).

Hypotheses The first hypothesis for this study was that a greater ADBD, where actual body weight is greater than desired body weight, will be associated with greater binge eating symptoms, lower self concept, and greater body dissatisfaction for women in the BN and BED groups. Second, women with BN will exhibit more eating disorder and self related problems than women with BED on the measures used in this study. We predict that those with BN will have greater ADBD, more binge eating symptoms, lower self concept and greater body dissatisfaction than women with BED.

Method Participants A total of 92 women were assessed as part of this study. These were patients referred by family physicians to a consultation service of a center for the treatment of eating disorders in a medium sized urban setting. Of the 92, 51 patients met diagnostic criteria for BN and 41 met diagnostic criteria for BED. Table 1 presents diagnostic and demographic data of these patients. Results of univariate comparisons of these variables will be discussed below.

Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept …

149

Table 1 Demographic and Clinical Data for Women With Bulimia Nervosa (BN) and Binge Eating Disorder (BED), With Univariate Comparisons and Effect Size (d).

Age Actual BMI Desired BMI ADBD Binge Episodes in 28 days Binge Days in 28 days Body Dissatisfaction

BN (n=51) M 30.81 28.59 22.76 17.69 16.96 14.95 21.02

Self Concept Factor High Self Esteem (Man-G) Low Self Efficacy (DEP-C) Identity Instability (BOR-I)

2.86 45.51 73.79 70.89

sd 8.85 7.28 3.21 13.02 15.94 9.52 6.90

BED (n=41) M 40.88 41.74 27.20 33.15 16.98 14.37 22.57

sd 9.92 9.41 5.37 12.07 20.31 9.64 5.40

F 27.33 58.84 31.63 35.47 .00 .07 1.41

p <.001 <.001 <.001 <.001 .997 .786 .238

d .95 1.24 .91 1.04 .00 .06 - .25

.93 11.02 17.24 11.75

3.34 46.58 65.93 61.81

1.01 12.09 16.91 13.50

5.69 0.18 4.96 12.26

.019 .714 .028 .001

.48 - .09 .45 .68

Note: Effect sizes (d) are small (>.20), medium (>.50) or large (>.80) effects (Cohen, 1988).

Procedure Patients were assessed by a psychiatrist or a psychologist. Just prior to the consultation, patients completed a battery of tests including the Eating Disorders Inventory-2 (EDI-2; Garner, 1991), the Personality Assessment Inventory (PAI; Morey, 1991), and the Diagnostic Survey of Eating Disorders (DSED; adapted from Johnson and Connors, 1987). They were then given a DSM-IV multiaxial diagnosis by the psychiatrist or psychologist (APA, 1994). A referral to one of several treatment options offered by the Center or in the community was often suggested. As a validation check on the diagnosis, 10% of all initial consultations (N = 210) referred to the Center were randomly selected and re-evaluated by an independent clinician blind to the diagnosis. Identifying information and diagnostic conclusions were removed from the re-evaluated reports. Agreement between the independent clinician and the original diagnosis was 86% suggesting a high level of agreement.

Measures Actual-Desired BMI Discrepancy (ADBD). Actual height and body weight were measured at the time of assessment and Body Mass Index (BMI; k/m2) was calculated from these. As part of the DSED, patients were asked what their desired weight was. Based on this and their actual height, a desired BMI was calculated, and then desired BMI was subtracted from actual BMI. To control for the effect of actual body weight, the difference between actual and desired BMI was divided by actual BMI. The

150

Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh et al.

result was multiplied by 100 so that ADBD was expressed as a percent deviation from actual BMI ([actual BMI - desired BMI / actual BMI] x 100).

Binge Eating Symptoms Objective binges were assessed using the criteria outlined in the Eating Disorder Examination (EDE; Fairburn and Cooper, 1993). Consistent with DSM-IV (APA, 1994), frequency of binges were used for the BN group and days binged was used for the BED group. The number of symptoms over the past 28 days were counted using a calendar recall method.

Body Dissatisfaction The Body Dissatisfaction Scale of the EDI-2 (Garner, 1991) is a 9-item scale that measures dissatisfaction with overall shape and size. Internal consistency was reported at alpha = .92 (Garner, 1991).

Self Concept Morey (1996) described self concept to encompass domains of self esteem, stability of identity, and self efficacy. Self Concept was measured by using three scales from the Personality Assessment Inventory (PAI; Morey, 1991). The Mania - Grandiosity (MAN-G) scale was used to assess self esteem, as an evaluative component of self perception. The Depression - Cognitive (DEP-C) scale measured personal competence and perceived control, and is considered a measure of self efficacy (Morey, 1991). Stability of identity was measured by the Borderline - Identity Problems (BOR-I) scale and represents vulnerability to environmental stressors. Morey (1996) looked at the configuration of scores on these three scales to assess self concept. High self concept is suggested by high scores on MAN-G and low scores on DEP-C and BOR-I. Low self concept is suggested by low scores on MAN-G, and high scores on DEP-C and BOR-I. Tasca, et al. (2002) report adequate psychometric properties of PAI scales and subscales for eating disordered populations.

Results Initial Inspection of the Data There were no univariate or multivariate outliers in the data, all variables had acceptable distributions, and there was no multicolinearity among dependent variables. Table 2 shows the zero order Pearson Product Moment correlations among the variables for each diagnostic group.

Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept …

151

Table 2 Correlations among variables for women with Bulimia Nervosa (BN) and Binge Eating Disorder (BED) groups.

Binge Symptoms1 Body Dissatisfaction Self Concept

ADBD BN (n=51) -.093 .465* * -.284*

BED (n=41) .261 .427** -.298

Binge Symptoms1 BN BED

Body Dissatisfaction BN BED

.175 -.100

-.263

-.062 -.223

-.309*

1

Binge symptoms for BN are binge episodes in 28 days, and for BED are binge days in 28 days. *p<.05, **p<.01The SPSS General Linear Model (GLM) program was used to perform an overall multivariate analysis among ADBD and all the other variables for each diagnotic group. Individual Pearson correlations were calculated to assess for the relationship between ADBD and the number of binge episodes in the past 28 days (for the BN group), days binged in the past 28 days (for the BED group), the EDI-2 Body Dissatisfaction Scale, and the PAI Self Concept Factor for the BN and BED groups separately.

Self Concept Factor As stated, Morey (1996) suggested an analysis of the configuration of three PAI scales in order to assess self concept. However, this approach does not easily lend itself to using self concept as a continuous variable in a data analysis. Therefore, a self concept factor was created by conducting a principal components factor analysis with no rotation of the MAN-G, DEP-C and BOR-I scales of the PAI (Morey, 1991) for both the BN group and the BED group. As expected, and consistent with Morey=s (1996) conceptualization, one factor emerged for the BN and BED groups separately accounting for 59.15% and 65.26% of the variance respectively. Also as expected, the component matrix had the MAN-G load negatively (-.65 and -.60 respectively), the DEP-C scale load positively (.93 and .94 respectively), and the BOR-I scale load positively, (.70 and .84 respectively). These findings are consistent with Morey=s (1996) configural approach but allows for a single score representing self concept for each participant. Scores on the self concept factor were reversed so that low scores on this factor represents low self concept and high scores represent high self concept.

Actual-Desired BMI Difference Bulimia Nervosa Group Using the Wilks= criterion, the combined variables (binge episodes, body dissatisfaction and self concept) were significantly related to the parameter ADBD for the BN group, approximate F(3, 47) = 5.395, p < .003. There was a strong association between ADBD and the combined dependent variables (02 = .26) (Cohen, 1988). Table 2 shows the correlations

152

Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh et al.

between ADBD and individual variables for the BN group. Higher ADBD was significantly related to higher scores on the Body Dissatisfaction Scale and lower scores on the Self Concept Factor. ADBD was not significantly associated with binge episodes for the BN group.

Binge Eating Disorder Group The Wilks= criterion suggested that the combined variables (binge days, body dissatisfaction, and self concept) were significantly related to ADBD for the BED group, approximate F(3, 37) = 3.791, p < .018. There was a strong association between ADBD and the combined variables (02 = .24) (Cohen, 1988). Table 2 shows the individual bivariate correlations between ADBD and each of the other variables. Higher ADBD was significantly associated with higher scores on the Body Dissatisfaction Scale. The correlation approached significance for the relationship between ADBD and the Self Concept Factor. ADBD was not significantly associated with days binged for the BED group.

Comparing Bulimia Nervosa to Binge Eating Disorder As indicated in Table 1, those with BN were significantly younger, had a lower actual BMI and lower desired BMI than those with BED. Because older patients may weigh more, age was covaried when the groups were compared on actual BMI. The difference in actual BMI remained significant even when age was covaried in an ANCOVA (F(3,88) = 55.50, p < .001). Those with BED had a significantly higher ADBD than those with BN (Table 1). In this study, ADBD was calculated as the percent discrepancy from actual BMI, so it is possible that the higher BMI of those with BED may account for this difference. To test this, an ANCOVA covarying actual BMI was conducted. When the variance accounted for by actual BMI was covaried, there was no significant difference on ADBD between those with BN and those with BED (F(3,88) = .083, p > .05). That is, any difference in ADBD is likely due to those with BED weighing significantly more than those with BN, and so the percent discrepancy can be accounted for by the initial difference in weight between the two groups. There were no differences between the BN and BED groups on measures of binge episodes or binge days. There was also no significant difference between the two groups on the Body Dissatisfaction scale. On the overall Self Concept Factor derived from the PAI, those with BN had significantly lower self concept than the BED group. When the individual scales making up that factor were considered (Table 1), it was apparent that the BN group had lower self efficacy (DEP-C), and greater identity instability (BOR-I). There were no differences in level of self esteem (MAN-G) between the two groups.

Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept …

153

Discussion This study looked at ADBD among women with BN and BED, and conceptualized the impact of ADBD on eating disordered women within the framework of self discrepancy theory (Higgins, 1987). Despite clinical references to the importance of ADBD (Crowther and Sherwood, 1997), this is the first known attempt to look directly at the relationship between ADBD and eating disorder related psychopathology in a clinical sample. The hypothesis that ADBD would be related to higher eating disorder symptoms, higher body dissatisfaction and lower self concept in women with BN and BED was partially supported. It was clear that for the BN group, greater ADBD was significantly related to body dissatisfaction and low self concept. For the BED group, greater ADBD was associated with greater body dissatisfaction, and there was a trend toward a correlation with low self concept. In self discrepancy theory (Higgins, 1987) greater actual self vs ideal self dicrepancies predict more emotional discomfort and distress (Moretti and Higgins, 1990). This appears to be paralleled in the ADBD of our eating disordered samples. ADBD likely results in a number of vulnerabilities such as a sense of personal shortcomings and personal dissatisfaction, especially for eating disordered women for whom body weight and shape are so crucial to self evaluation. In light of internalized social ideals of thinness for women with eating disorders (Striegel-Moore, 1993), and given the results of this study, ADBD may be viewed as a potential vulnerability factor for women in developing BN and BED. Prospective studies among adolescent girls using ADBD would provide a stronger test of this hypothesis. ADBD was not related to binge eating symptoms for either the BN or BED groups, and so no support was found for this hypothesis. It is possible that while ADBD is related to self related experiences, such as body dissatisfaction and self concept, it may not be directly related to symptoms of binge eating.

Comparing Bulimia Nervosa and Binge Eating Disorder The clearest difference between the two diagnostic groups in this study was on self concept, with women with BN having lower self concept as measured by the PAI (Morey, 1991; Morey, 1996). Specifically, those with BN had greater identity instability (BOR-I) and lower self efficacy (DEP-C). This suggested greater self related problems and pathology among those with BN as compared to women with BED. This is consistent with reports in the literature indicating that BN is a more severe disorder than BED (Hay and Fairburn, 1998; Tasca, et al., 2002), and that there is a high comorbid diagnosis of self related pathology, such as borderline personality disorder, among those with BN (Dennis and Sansone, 1991; Rossiter, Agras, Telch and Schneider, 1993). Had this study focused on self esteem (e.g. MAN-G) only, differences between groups would not have emerged. This is consistent with a study finding no differences between eating disorder diagnostic groups on two measures of self esteem (Griffiths, et al., 1999). The Self Concept Factor, allowed for differences to emerge among the diagnostic groups by defining self related problems in broader terms that

154

Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh et al.

includes self esteem, identity stability and self efficacy. This broader self construct may be more meaningful to the understanding of an eating disordered population than self esteem alone. There were no differences between the BN and BED groups on the number of binge episodes or days binged over the previous 28-day period. This is consistent with previous research that found no difference in the number of objective binges between BN and BED samples (Hay and Fairburn, 1998). The means for these two groups in this study were almost identical (Table 1). This result does not support the notion that BED is a less severe than BN when it comes to objective binge eating symptoms. Our study did not find differences in body dissatisfaction between those with BED and BN. In addition, both diagnostic groups had mean Body Dissatisfaction Scale scores above the clinical cutoff for the EDI-2 (Garner, 1991), suggesting severe problems in this area for the majority of women in both groups. This result is consistent with the work of StriegelMoore, et al (1998) who found greater body dissatisfaction among obese binge eaters than controls. The results of this study also indicated that body dissatisfaction among these eating disordered samples were related to ADBD and their associated self discrepancies.

Self Concept Factor To our knowledge this is the first report in the literature using self concept as defined by the PAI (Morey, 1991) with an eating disordered population. As stated, our results suggested that this broader construct may be more meaningful to the study of an eating disordered population that self esteem alone. Furthermore, this is the first report to create a self concept factor based on the configural analysis of self concept from the PAI as suggested by Morey (1996). The prinicpal components analysis produced a factor with loadings from the component scales (MAN-G, DEP-C, and BOR-I) that parallel Morey=s (1996) configural interpretation of those scales. The advantage of using this approach is that it allows for the creation of a single continuous variable measuring self concept that lends itself to multifactorial analysis. The disadvantage is that unique information provided by the individual component scales gets diluted within the overall factor score.

Clinical Implications of ADBD Using 95% confidence intervals, cutoffs for the percent deviation from individuals= actual BMI were calculated. In our sample, if an individual with BN had a desired BMI that was less than 21% of their actual BMI, then it would be considered clinically significant. For example, the mean actual BMI in our sample of women with BN was 28.59. A clinical cutoff could be established so that a patient with BN who had a BMI of 28.59 and a desired BMI of 22.59 (21% below actual BMI for the BN group) or less would have a 95% probability of having problems with body dissatisfaction and low self concept. Interestingly, in our BN sample, the mean desired BMI was 22.76, which is almost exactly 21% below the mean BMI for the BN group. Clinicians could easily calculate the percent deviation from actual BMI,

Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept …

155

use the clinical cutoffs suggested by our sample, and have an index of how problematic body dissatisfaction and self concept are for those with BN. Similar calculations could be made for the BED group for whom a desired BMI of less than 37% of actual BMI would be considered clinically significant.

Limitations and Future Research The small sample size of the BED group may have reduced the power of some of the analyses. This is particularly apparent in Table 2 where correlations between binge symptoms for the BN group is significantly correlated with Self Concept (r = -.284), but a slightly higher correlation within the BED groups for the same variables(r = -.298) was not statistically significant. Given that ADBD was related to eating disorder related variables in these clinical samples, it would be interesting to see if this discrepancy predicted problems with self concept, body dissatisfaction, mood, and other psychological variables in a female sample in the general population. One would expect a similar pattern of results in a general population as well. However, the relationship between ADBD likely will be more salient within the clinical and subclinical range of that population. Longitudinal research starting with an adolescent sample and then following that sample could be done to see if ADBD is a risk factor for developing an eating disorder. We do not expect ADBD to be as important an issue for men since cultural standards of unrealistic thinness is more likely to occur with women (Striegel-Moore, 1993), and McKinley (1998) found higher ADBD among women. If, as our theory suggests, ADBD is a core self discrepancy that leads to negative mood and eating disorder symptoms, then we would expect ADBD to be a risk factor for developing an eating disorder for young women but not necessarily for men. For men, issues related to ideal body shape (e.g. muscle and low body fat percentage) and not body weight per se may be a more important variable predicting self concept and eating disorder related symptoms.

Conclusion A theory of ADBD as a self discrepancy is presented that may represent a risk factor for eating disorders among women. Self discrepancy theory suggests that a greater discrepancy between actual self and ideal self leads to greater distress and emotional problems (Moretti and Higgins, 1990). Similarly, the results of this study indicated that ADBD is associated with lower self concept and greater body dissatisfaction. ADBD could be an issue targeted in the assessment and treatment of women with BN, and also for those with BED. Its assessment is relatively straight forward, and the 95% confidence intervals presented here could be used as cutoffs for clinical samples. Targeting ADBD in treatment by focusing on its relevance to eating disordered individuals, its impact on feelings about their body, and its impact on self concept may allow women with eating disorders to begin to moderate the effects of these discrepancies. The impact of ADBD found in this study continue to lend importance to the

156

Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh et al.

notion that the internalization of culturally sanctioned ideals of thinness (Striegel-Moore, et al., 1998) are corrosive to women=s body and self esteem (McKinley, 1998).

References American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th ed.). Washington, DC: Author. Antoniou, M., Tasca, G.A., Wood, J., Bissada, H. (2003). Binge Eating Disorder versus overeating: A failure to replicate and common factors in severely obese treatment seeking women. Eating and Weight Disorders, 8, 145-149. Brownell, K.D., and Rodin, J. (1994). The dieting maelstrom. American Psychologist, 49, 781-791. Casper, R.A. (1983). On the emergence of Bulmia Nervosa as a syndrome: A historical view. International Journal of Eating Disorders, 2, 3-16. Cohen, J. (1988). Statistical power analysis for the behavioral sciences. (2nd ed.). Hillsdale, NJ: Earlbaum. Crowther, J.H. and Chernyk, B. (1986). Bulimia and binge eating in adolescent females: A comparison. Addictive Behaviors, 11, 415-424. Crowther, J.H and Sherwood, N.E. (1997). Assessment. In D.M. Garner and P.E. Garfinkel (Eds.) Handbook of treatment for eating disorders. New York: Guilford. Dennis, A.B. and Sansone, R.A. (1991). The clinical stages of treatment for the eating disorder patient with borderline personality disorder. In C. Johnson (Ed.) Psychodynamic treatment of anorexia nervosa and bulimia. New York: Guilford. de Zwaan, M., Mitchell, J.E., Seim, H.C., Specker, S.M.., Pyle, R.L., Raymond, N.C. and Crosby, R.B. (1994). Eating related and general psychopathology in obese women with binge eating disorder. International Journal of Eating Disorders, 15, 43-52. Doll, H.A. and Fairburn, C.G. (1998). Heightened accuracy of self-reported weight in bulimia nervosa: A useful cognitive Adistortion@. International Journal of Eating Disorders, 24, 267-273. Fairburn, C.G. and Cooper, Z. (1993). The Eating Disorder Examination (12th Ed.). In C.G. Fairburn, and G.T. Wilson (Eds.) Binge eating: Nature, assessment, and treatment. New York: Guilford. Garner, D. (1991). Eating Disorders Inventory-2 Professional Manual. Odessa, FL: Psychological Assessment Resources. Griffiths, R.A., Beumont, P.J., Giannakopoulos, E., Russell, J., Schotte, D., Thornton, C., Touyz, S.W., Varano, P. (1999). Measuring self-esteem in dieting disordered patients: The validity of the Rosenberg and Coopersmith contrasted. International Journal of Eating Disorders, 25, 227-231. Hay, P. and Fairburn, C.G. (1998). The validity of the DSM-IV scheme for classifying bulimic eating disorders. International Journal of Eating Disorders, 23, 7-15. Heffernen, K. (1996). Eating disorders and weight concern among lesbians. International Journal of Eating Disorders, 19, 127-138.

Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept …

157

Higgins, E.T. (1987). Self-discrepancy: A theory relating self and affect. Psychological Review, 94, 319-340. Johnson, C. and Connors, M.E. (1987). The etiology and treatment of bulimia nervosa: A biopsychosocial approach. New York: Basic. Kearney-Cook, A., and Striegel-Moore, R. (1997). The etiology and treatment of body image disturbance. In D.M. Garner and P.E. Garfinkel (Eds.) Handbook of treatment for eating disorders. New York: Guilford. McKinley, N.M. (1998). Gender differences in undergraduates= body esteem: The mediating effect of objectified body consciousness and actual/ideal weight discrepancy. Sex Roles, 39, 113-123. Marcus, M.D., Wing, R.R., Ewing, L., Kern, E., Gooding, W., and McDermott, M. (1990). Psychiatric disorders among obese binge eaters and non-binge eaters. International Journal of Eating Disorders, 9, 69-77. Moretti, M.M., and Higgins, E.T. (1990). Relating self-discrepancy to self-esteem: The contribution of discrepancy beyond actual-self ratings. Journal of Experimental Social Psychology, 26, 108-123. Morey, L.C. (1991). Personality assessment inventory. Odessa, FL: Psychological Assessment Resources. Morey, L.C. (1996). An interpretive guide to the personality assessment inventory (PAI). Odessa, FL: Psychological Assessment Resources. Post, G., and Crowther, J.H. (1985). Variables that discriminate bulimic from nonbulimic adolescent females. Journal of Youth and Adolescence, 14, 85-98. Rossiter, E.M., Agras, W.S., Telch, C.F., and Schneider, J.A. (1993). Cluster B personality disorder characteristics predict outcome in treatment of bulimia nervosa. International Journal of Eating Disorders, 13, 267-274. Snyder, R. (1997). Self discrepancy theory, standards for body evaluation, and eating disorder symptomatology among college women. Women and Health, 26, 69-84. Strauman, T.J., Vookles, J., Berenstein, V., Chaiken, S., and Higgins, E.T. (1991). Selfdiscrepancies and vulnerability to body dissatisfaction and disordered eating. Journal of Personality and Social Psychology, 61, 946-956. Striegel-Moore, R.H. (1993). Etiology of binge eating disorder: A developmental perspective. In C.G. Fairburn and G.T. Wilson (Eds.) Binge eating: Nature, assessment, and treatment. New York: Guilford. Striegel-Moore, R.H., Wilson, G.T., Wilfley, D.E., Elder, K.A., and Brownell, K.D. (1998). Binge eating in an obese community sample. International Journal of Eating Disorders, 23, 27-37. Tasca, G.A., Wood, J., Demidenko, N., and Bissada, H. (2002). Using the PAI in an eating disordered population: Scale characteristics and differences among diagnostic groups. Journal of Personality Assessment, 79, 337-356. Thompson, J.K. (1996). Assessing body image disturbance: Measures, methodology and implementation. In J.K. Thompson (Ed.) Body image, eating disorders and obesity: An integrative guide for assessment and treatment. Washington, DC: American Psychological Association.

158

Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh et al.

Tiggeman, M.., Winefield, H.R., Winefield, A.H., and Goldney, R.D. (1994). Gender differences in the psychological correlates of body-weight in young adults. Psychology and Health, 9, 345-351. Walsh, B.T., and Garner, D.M. (1997). Diagnostic issues. In D.M. Garner and P.E. Garfinkel (Eds.) Handbook of treatment for eating disorders. New York: Guilford. Yanovski, S.Z., Nelson, J.E., Dubbert, B.K., and Spitzer, R.L. (1993). Association of binge eating disorder and psychiatric comorbidity in obese subjects. American Journal of Psychiatry, 150, 1472-1479.

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 159-184 © 2006 Nova Science Publishers, Inc.

Chapter VIII

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa Sarah Fischer, Gregory T. Smith and Melissa A. Cyders University of Kentucky

Abstract Heritability studies provide a general framework for understanding risk for bulimia nervosa (BN): liability is a function of both genetic and environmental factors. The authors propose a specific model that integrates identified heritable and environmental risk factors for BN. Trait urgency, the tendency to act rashly in response to distress, is a heritable risk factor that increases the likelihood that one will engage in some form of rash, maladaptive behavior pattern (such as BN). The specific form of one’s maladaptive behavior is a function of learned experiences from one’s environment. Individuals who learn to expect alleviation of negative mood from eating, and overgeneralized life improvement from thinness, are more likely to engage in bulimic behaviors. Thus, the general, heritable risk from high levels of urgency is likely to become expressed as BN when one learns to expect benefits from eating when distressed and extreme benefits from thinness. The proposed process is empirically supported and consistent with findings from heritability research.

Introduction An important recent advance in understanding bulimia nervosa (BN) has been the recognition that both genetic and environmental factors appear to play roles in the emergence of BN. That perspective, of course, is very general: there are many ways in which genes and environment might combine in the risk process. Our intent in this chapter is to propose a specific theory of this process, by describing key heritable causes of BN, key environmental

160

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

causes of BN, and mechanisms by which they combine. We propose that the heritable trait of urgency, which is the tendency to act rashly when distressed, is a general risk factor for addictive/risky behaviors. The combination of trait urgency and certain kinds of psychosocial learning (indexed as expectancies for the consequences of eating and of dieting), lead to substantially increased risk for BN. We argue here that urgency reflects an important part of the heritable component of risk, and that psychosocial learning reflects an important part of the impact of environmental risk. To make this argument, we will briefly review general evidence for the heritability of BN and for environmental causes of BN. We will then describe our specific model, illustrate how it fits within a gene-environment framework, and review the empirical evidence supporting it.

Heritability of BN and Binge Eating The concept of heritability refers to the proportion of population variance on an attribute that overlaps with genetic variance (Keel and Klump, 2003). Typical heritability studies compare monozygotic twins reared together to those reared apart, and monozygotic twins to dyzygotic twins. Adoption studies are also employed. Behavioral genetic methods allow researchers to partition the population variance on an attribute three ways: that due to genetic influences; that due to environmental influences shared among study participants; and that due to environmental events unique to individuals. Recent studies of the heritability of BN seem to converge on the finding that risk for the disorder has large genetic influences, large non-shared environmental influences, and very few to no shared environmental influences (Bulik, Sullivan, and Wade, 2000). Thus, causes of BN appear to include a genetic preparedness along with unique aspects of an individual’s learning history, but not environmental events which one shares with one’s siblings. According to a meta analysis of these findings, estimates of genetic effects for the disorder range from .28 to .83 (Bulik et al., 2000). In their study using the Virginia Twin Registry, Kendler, MacLean, Neale, et al. (1991) concluded that approximately 50% of the variability in BN diagnosis is due to additive genetic effects. Specific evidence to that effect is (a) concordance of diagnosis in monozygotic twins was significantly greater than that in dizygotic twins, and (b) if a member of a monozygotic twin pair was diagnosed with BN, the co-twin was eight times as likely as a member of the general population to also be diagnosed with BN (Kendler et al., 1991). These effects were not explained by shared environmental features or current contact with the co-twin. Various other studies using the Virginia Twin Registry have found similar results for partial syndrome BN, for diagnoses of BN that adhere to strict diagnostic criteria, and for binge eating behavior (Bulik, Sullivan, and Kendler, 2003; Bulik et al., 2000). Findings from two other twin registries are consistent with those from the Virginia Twin Registry. Work with the Minnesota Twin Registry found that a large portion of variability in BN is heritable (Klump, McGue, and Iacono, 2000, 2002), and findings from the Australian Twin Registry showed moderate heritability for BN (Wade, Neale, Lake, and Martin, 1999). Interestingly, Wade et al. (1999) differed from the other reports in also finding moderate effects of common environmental influences.

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

161

In sum, several studies conducted using twin samples in the last fifteen years have converging results: a moderate to large portion of the variance in BN is genetically influenced, and a moderate to large portion of the variance is influenced by unique or nonshared environmental effects. Very little of the disorder’s variance, and perhaps none, is influenced by shared environmental factors. A comprehensive model of risk for BN must incorporate genetic risk for the disorder. It is also true that the rates of BN appear to have risen in Western cultures in recent decades (Keel and Klump, 2003). To understand why varying rates of BN can exist, even though risk for BN is heritable, it is important to understand that there are different possible mechanisms of genetic risk. One mechanism is that there is a genetic/biological cause of some specific behavior or dysfunction. When the cause is present, the disorder inevitably occurs. Under such a circumstance, there is no reason to expect the rate of the disorder to vary across time and across contexts. A different possible mechanism is that there is a genetic risk for a more general behavioral disposition, and the general disposition can take varying forms, depending on environmental and cultural factors. In the case of BN, the heritable risk appears likely to be of this second form, because although there is heritable risk, the rates of the disorder vary across time and across cultures. One obvious implication is that environmental factors are also important influences on the liability for BN.

Evidence for the Role of Environment in the Development of BN The causal role of environmental and cultural factors in BN has, in fact, been much more widely emphasized in the literature. Among the classic indicators of those factors are the ideal female images presented in the media. Anyone with access to a television or magazines in Western society may plausibly assume that we live in a high risk media environment for disordered eating. Images of women in the media are much thinner than the average Western woman, and these images are pervasive. The British Medical Association (BMA) recently released a statement saying that the media play a large role in the development of both anorexia nervosa (AN) and BN (BMA, 1999). This assumption is due, at least in part, to the fact that Western media images of women seem to be getting thinner and thinner, while average individuals in industrialized nations get bigger and bigger (Wadden, Brownell, and Foster, 2002). The Western cultural ideal of attractiveness—the thin ideal--is quite different from the physical reality of most adults. This appears to increase women’s body dissatisfaction (Rodin, Silberstein, and Striegel-Moore, 1985). In fact, some researchers suggest that dissatisfaction with one’s body is now normative among Western women (Rodin et al., 1985). These factors, the thin ideal for women and body dissatisfaction, appear to promote bulimic behaviors (Stice, 2002). Stice summarized a theoretical model for cultural effects on risk for BN (Stice,1994). In this model, pressure from society on women falls into three categories: the thin-ideal body image for women, the importance of appearance in the female gender role, and the reinforcement of attractiveness. He reviews evidence that the shrinking body size of women in the media is correlated with increases in dieting articles in women’s magazines (Stice,

162

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

1994). Therefore, it is hypothesized that the ideal image of women in Western society is very thin. This ideal seems to be associated with gender roles for women. Thin body shapes are rated as more feminine, endorsing traditional female gender roles is associated with endorsement of the thin ideal, and women who eat less food are rated as more feminine (Stice, 1994). So, thinness is associated with attractiveness and femininity. In addition, there is evidence that attractive people are perceived more positively and receive more reinforcement than do unattractive people. Attractive people are rated as more intelligent, socially skilled, honest, and better qualified for jobs than unattractive people (Feingold, 1992). If being thin is considered attractive for women, and level of attractiveness has real consequences in social and work settings, then it seems there is extreme pressure for women to try to be thin in our society (Stice, 1994). The internalization of this pressure has come to be described as thin-ideal internalization (Stice, 2002; Thompson, van den Berg, Roehrig, Guarda, and Heinberg, 2004). Internalization is defined as “the incorporation of specific values to the point that they become guiding principles” (Thompson et al., 2004). Thin-ideal internalization is considered a risk factor for body dissatisfaction, dieting, and bulimic symptoms themselves. The evidence for the relationship of dieting, body dissatisfaction, and thin-ideal internalization to bulimic symptoms can be construed as evidence that environmental factors influence the development of the disorder. Polivy and Herman (2002) stated in a recent review that “the influence of sociocultural factors in the context of eating disorders can be summarized succinctly as the idealization of thinness.” A recent meta-analysis by Stice (2002) summarizes findings of prospective longitudinal studies and experimental studies of risk factors for BN, including thin-ideal internalization. He found that thin-ideal internalization led to increases in bulimic symptoms, with a significant effect size of .08 (Stice, 2002). A subscription to a teen magazine featuring thin models led to increased bulimic symptoms among girls with low social support (Stice, Spangler, and Agras, 2001). Additionally, bulimic women endorse the thin ideal more than women without bulimia (Thompson et al., 2004). There is also evidence that thin-ideal internalization is present in girls as young as age nine (Sands and Wardle, 2003). Body dissatisfaction may mediate the influence of thin-ideal internalization on bulimic symptoms (Stice, 1994). Body dissatisfaction is defined as negative subjective evaluation of physical attributes (Stice and Shaw, 2002). This risk factor for bulimia (Stice, 2002) is thought to be primarily transmitted through media influences. Body dissatisfaction likely results from social comparison, in which women look at media images and compare themselves unfavorably to those images. This relationship has been confirmed in the laboratory many times. The basic paradigm is that women are asked to rate their body dissatisfaction and negative affect both before and after viewing images of thin models. The majority of studies find that after viewing thin models, women experience an increase in negative affect and body dissatisfaction. Halliwell and Ditmar (2004) expanded on this model by assessing level of internalization of the thin ideal and how this affected body dissatisfaction in the experimental paradigm. Women with higher internalization reported greater anxiety after viewing thin model slides.

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

163

Body dissatisfaction is an important risk factor for BN because it is hypothesized to lead to the disorder in at least two ways. The theoretical consequences of body dissatisfaction are that (1) it results in increased dieting, which then leads to increase in eating disorder symptoms, and (2) it leads to increased negative affect, which could lead to increased binge eating (Stice and Shaw, 2002). Meta analytic findings were that body dissatisfaction had a marginally significant effect size of .26 on dieting, and a marginally significant effect size of .14 on negative affect (Stice, 2002). Additionally, the effect of body dissatisfaction on increased eating disorder symptoms was marginally significant and had an effect size of .13 (Stice, 2002). Not surprisingly, there is evidence that attempts to diet or concern with dieting may serve as a risk factor for bulimic symptoms (Fairburn, 1997; Heatherton and Polivy, 1992). Attempts to diet are thought to result from internalization of the thin ideal and body dissatisfaction, and are thought to lead to increases in symptoms because the attempts make one vulnerable to disinhibited eating. When attempting to diet, one exerts cognitive control over one’s eating instead of physiological control. Failure to eat in response to physiological need may result in binge eating (Polivy and Herman, 1985). Prospective studies show that measures of dietary restraint efforts predict the onset of binge eating (Stice and Agras, 1998, Stice, Killen, Hayward, and Taylor, 1998, Stice, Presnell, and Spangler, 2002). It should be noted, though, that commonly used measures of dietary restraint are not associated with unobtrusive measures of actual caloric intake (Stice, Fisher, and Lowe, 2004). They appear to measure concern with dieting or, perhaps, attempts to diet, but not reduced food consumption. Correlations between these risk factors (the thin ideal, body dissatisfaction, and dietary restraint) and bulimic symptoms reflect the association of individual differences in risk with individual differences in symptom levels. It is perhaps important to recognize that, in modern Western culture, these individual difference factors operate in a context that is new to human history. Today, Western people tend to have an abundance of food. As a result, providers of food compete to make their food products more desirable, by increasing fat and sugar content, and by offering pre-prepared food (fast food). They also advertise their food products, typically with an emphasis on fun and taste. There is, therefore, a relatively new phenomenon in which (a) it is possible to binge on food, and (b) food is advertised providing pleasures beyond hunger reduction. On this point, American children view an average of 40,000 television commercials per year, and at least 50% of them are for food (Strasburger, 2001). The food portrayed is often easy-access sugared cereals, junk food, candy, and fast food. Television watching has been shown to be related to overweight and obesity in both descriptive and experimental studies (Anderson, Crespo, Bartlett, Cheskin, and Pratt, 1998; Robinson, 1999. Experimental studies have shown that children eat more food and choose junk food more often when watching television with food ads than when watching television without food ads (Halford, Gillespie, Brown, Pontin, and Dovey, 2004). In short, the combination of enticing media messages about food and the easy access to large quantities of food in Western society may create an environment that is conducive to binge eating (Battle and Brownell, 1997; Wadden, et al., 2002). Thus, women are simultaneously exposed to encouragement to eat for non-hunger reasons and given ready access to food, and exposed to messages emphasizing the importance of thinness. This convergence of cultural phenomena

164

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

may help explain the rise in BN rates in the West: if all Western women are exposed to this combination of influences, more of the highest risk women are likely to develop BN. To summarize, our current society’s emphasis on thinness and the view that slimness is attractive is thought to contribute to risk for BN through four main mechanisms. First, Western culture is thought to promote internalization of the thin ideal. This internalization leads to both dieting attempts and body dissatisfaction, and it also is thought to lead directly to bulimic symptoms. Second, body dissatisfaction, which is thought to stem from social comparisons based on the thin ideal, is a risk factor for bulimic symptoms. Third, concern with dieting or attempts to diet, which follow from thin-ideal internalization and body dissatisfaction, appear to predict the development of disordered eating. Fourth, these factors operate in a cultural context in which large amounts of food are readily available, food is prepared to entice consumers beyond their hunger, and food is portrayed as having benefits beyond hunger alleviation. Two conclusions seems relevant from this literature. First, there is considerable evidence that environmental factors increase risk for BN. Second, the effect sizes of environmental causes are modest, suggesting the need to (a) integrate environmental causal models with genetic ones and (b) explore additional environmental factors.

General Integration of Heritability and Environmental Perspectives From the foregoing, we know there is an inherited risk for BN, and we know that environmental risk factors increase risk for the disorder. Bulik et al. (2000) provide a general integration of the two types of causes in their liability threshold risk model. The notion is that liability for BN reflects the combination of several genetic and environmental effects, each of which likely has a small individual effect. This liability has a normal distribution in the population and is only expressed as the disorder if one’s liability is greater than a particular critical threshold. In the case of BN, there may be several genetic and environmental effects that contribute to the expression of the disorder, but BN appears only in that small percentage of individuals with enough of the factors to cross the critical threshold. Thus, the incidence rate of BN is roughly 2.5% (APA, 1994; Bulik et al., 2000). Bulik et al. (2000) go on to argue that a genotype by environment interaction is an important mechanism in increasing risk beyond the threshold. Thus, individuals who are genetically liable for the disorder will be the ones to develop the disorder, but will do so only in a high risk environment. Therefore, the effect of the environment on an individual depends on the genotype of that person (Klump, Wonderlich, Lehoux, Lilenfeld, and Bulik, 2002). Several authors note that this genotype by environment interaction may be an important direction of study for risk for BN (Bulik et al., 2000; Kaye et al., 2004; Keel and Klump, 2003; Klump et al., 2002). An interaction of this type would reconcile the perception that the Western environment is high risk with the awareness that only a small percentage of women develop BN: the environment may be high-risk for a BN diagnosis only among women with high liability, even if it is high-risk for subclinical eating and dieting problems for women in general.

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

165

This framework of risk is very general. We propose one specific inherited risk factor (trait urgency) and a set of specific psychosocial learning risk factors (measured as expectancies for reinforcement from eating and from dieting) that, we believe, operate as risk factors in the way that Bulik et al.’s (2000) model describes. We make the argument as follows. First, we present a theoretical rationale for the consideration of urgency as a risk factor. We then demonstrate that urgency is distinct from other impulsivity-related constructs and heritable, and we review evidence for its role in relation to BN and binge eating. Next, we present a theoretical rationale for focusing on learned expectancies to capture individual differences in environmental risk. We follow that with empirical evidence for eating and dieting expectancy theory. Finally, we present a theoretical integration of urgency and learned expectancies (which includes interaction effects), and we summarize empirical evidence for that integration.

Urgency as a Risk Factor for BN One of the most common ways researchers have tried to explain rash, maladaptive action, such as binge eating and purging, is through use of the broad construct of impulsivity. A number of studies have attempted to relate impulsivity to BN and binge eating, but the findings have been inconclusive and the effect sizes small (Stice, 2002). There is growing evidence that these inconsistent findings occur because the broad construct of impulsivity actually includes several more specific constructs, which themselves are only moderately related to each other and which account for different phenomena (Evendon, 1999; Petry, 1999; Whiteside and Lynam, 2001). Impulsivity has often, but not always, been described as acting without thinking. Descriptions of impulsivity in the DSM-IV include acting without thinking, the inability to concentrate, and the tendency to become easily distracted. In addition, specific acts, such as binge eating and substance abuse, are described as impulsive (APA, 1994). Whiteside and Lynam (2001) conducted a factor analysis of several different major selfreport measures of impulsivity and found four factors or impulsivity-related constructs. Sensation seeking is the tendency to seek out novel and thrilling experiences. A lack of deliberation is the tendency to act without thinking. A lack of persistence is the inability to remain focused on a task. Urgency is the tendency to act rashly when faced with distress. They developed a self-report inventory to assess these four impulsivity- related constructs (UPPS-R: Whiteside and Lynam, 2001). The measure was designed to assess each trait uncontaminated by items measuring similar constructs. For example, the sensation seeking scale was designed without items measuring a lack of planning. They found that the four scales were only modestly intercorrelated. Prior to their work, impulsivity measures tended to include items reflecting some, or all, of the four constructs, and the proportional representation of different constructs varied from scale to scale. Since scales included four different constructs, to varying degrees, there was built-in inconsistency in measurement (Smith, Fischer, and Fister, 2003). Among those four impulsivity-like constructs, we believe trait urgency--the tendency to act rashly when distressed—is the construct that best captures the nature of binge eating and

166

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

bulimic behavior. Binge behavior does not reflect lack of persistence, nor does it primarily reflect pursuit of new and novel sensations. Although there may be a lack of planning component to some binge eating, we contend that the propensity to act rashly or maladaptively, in response to distress, best reflects what clinicians mean when they refer to the impulsivity of binge eating and BN clients. We also favor trait urgency because of its specificity: rather than referring to general impulsive tendencies, the idea is that if one has a propensity to act rashly when distressed, then one is at increased risk for binge eating and BN problems. There is considerable evidence that stress, distress, and negative mood often precede binge eating episodes. Experimental studies indicate that binge eating provides immediate, if fleeting, relief of negative affect (Deaver, Miltenberger, Smyth, Meidinger, and Crosby, 2003; Kaye, Gwirtzman, George, Weiss, and Jimerson, 1986; Sanftner and Crowther, 1998; Steinberg, Tobin, and Johnson, 1989; but see Davis, Freeman, and Solyom, 1985), perhaps by facilitating escape from self-awareness (Heatherton and Baumeister, 1991). Laboratory induced negative affect leads to increases in eating (Stice, 2002). Motives for eating include comforting oneself and distracting oneself from negative emotion (Jackson, Cooper, Mintz, and Albino, 2003). Binge eating has been tied to the avoidance of emotions and the use of distraction (Freeman and Gil, 2004). Stress is associated with binge eating on the day that the stress occurred (Crowther, Sanftner, Bonifazi, and Shephard, 2001; Freeman and Gil, 2004). As we have noted elsewhere, negative affectivity is an obvious precursor to urgency: among those experiencing negative affect, those women high in urgency are most likely to act rashly to relieve their distress (Fischer, Smith, Spillane, and Cyders, in press). It therefore seems quite possible that urgency may be the impulsivity-like construct most relevant to binge eating and BN.

The Distinctiveness and Heritability of Urgency Urgency is actually represented as distinct from the other three impulsivity-related constructs in the predominant, integrative personality trait model: the five factor model of personality. The five factors include neuroticism, extraversion, agreeableness, conscientiousness, and openness to experience. In Costa and McCrae’s (1992) self-report measure of the five factor model, the NEO-PI-R, urgency is represented as the impulsivity facet of the broader domain of neuroticism. They have described this facet as a “craving” factor, indicating a dyscontrolled impulse to eat, drink, etc. in response to distress (Costa and McCrae, 1992). This facet of the neuroticism domain of the NEO-PI-R loaded highly onto the urgency factor in Whiteside and Lynam’s (2001) factor analysis of impulsivity measures. The other impulsivity-related constructs are represented elsewhere among the five factors (sensation seeking is a facet of extraversion, lack of deliberation is a facet of conscientiousness, and lack of persistence is also a facet of conscientiousness). There are several studies documenting the heritability, stability, and correlates of this facet (Costa and McCrae, 1992; McCrae et al., 2000; Paunonen and Ashton, 2001). In a multi-national twin study of the domains and facets of the NEO-PI-R, urgency correlated higher among monozygotic twins than among dizygotic twins (Jang et al., 1998). Jang and

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

167

colleagues examined the heritability of the specific variance unique to urgency (i.e., that variance not shared by the other facets of neuroticism). They found that, controlling for error variance, the heritability estimate for the impulsivity/urgency facet in their two samples was .49 (Jang et al., 1998). McCrae and Costa (1994) found long-term stability of the facet. Correlates of the urgency/impulsivity facet include, for example, greater tobacco consumption, greater alcohol consumption, more obesity, and less religiosity (Paunonen and Ashton, 2001). Castellani and Rugle (1995) found that cocaine and alcohol abusers scored higher on the urgency/impulsivity facet than a control sample. Miller, Flory, Lynam, and Leukefeld (2003) found that the urgency/impulsivity facet was positively related to risky sexual behavior, problems with alcohol use, and a composite measure of eating disorders symptoms. In short, there is consistent evidence that the urgency/impulsivity facet of the NEO-PI-R correlates with negative mood (Costa and McCrae, 1992) and with rash, maladaptive actions, including excessive eating and drinking. We have also recently examined Whiteside and Lynam’s (2001) measure of urgency. We first sought to replicate the four-factor structure for impulsivity-related constructs that has been operationalized in their UPPS-R (Whiteside and Lynam, 2001). The structure replicated successfully in three different undergraduate samples (with sample sizes ranging from 156 to 1,200). Evidence for the discriminant validity of urgency from sensation seeking, lack of planning, and lack of perseverance was also present. For example, in the sample of 1,200, urgency’s correlations with the other constructs were .39 with lack of planning, .30 with lack of persistence, and .11 with sensation seeking (Fischer, Smith, Cyders, and McCarthy, 2004a). We also conducted a multitrait, multimethod (MTMM) study of urgency and the other three impulsivity-related constructs. We developed a semi-structured interview based on the UPPS-R, in order to examine the potential role of method variance in the assessment of urgency and in its relations with other constructs (Campbell and Fiske, 1959). A total of 156 undergraduates completed the semi-structured interview of the UPPS-R, the self-report version of the UPPS-R, and self-report measures of various criterion variables, such as problem drinking, binge eating, gambling, and school performance (Fischer et al., 2004a). Results of that study supported the convergent and discriminant validity of each construct, including urgency. Correlations between the same construct measured in the two different ways were much higher than were correlations of different constructs measured in the same way. For example, interview-assessed urgency correlated with self-report urgency at r = .75, p <.001, while the correlations between interview-assessed urgency and the other constructs, also assessed by interview, were .21 for lack of persistence, .29 for lack of deliberation, and .03 for sensation seeking (Fischer et al., 2004a). Additionally, both interview and self-report assessed urgency had similar relationships to criterion variables. For example, self-report assessed urgency was positively correlated with a self-report measure of pathological gambling behavior (r = .27, p <.01). No other self-report assessed impulsivity construct was associated with pathological gambling. And, interview assessed urgency was correlated with self-report pathological gambling (r = .25, p <.01). No other interview assessed impulsivity-related constructs were associated with pathological gambling (Fischer et al., 2004a). Different means of measuring urgency agree, urgency is

168

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

distinct from other impulsivity-related constructs regardless of method of assessment, and urgency predicts outcome variables consistently, regardless of means of measurement. One possibility is that urgency may be an interaction of neuroticism and lack of planning impulsivity, or a combination of these two traits, instead of a personality construct in its own right. In a recent sample (n =130 women), we found that although urgency related to the combination of neuroticism and lack of planning, there was considerable systematic variance in urgency unexplained by those constructs. In addition, urgency accounted for an additional 6.5% of the variance in bulimic symptoms, beyond that explained by the other constructs. The beta weight of urgency was .34 (p <.05), the largest beta weight of all predictors in the model. The trait of urgency does not seem to be reducible to a combination of neuroticism and lack of planning. Cross-cultural evidence also supports the validity of the construct of urgency. As noted above, urgency/impulsivity as measured by the NEO-PI-R appears to be comparably heritable in different cultures. There is also evidence that both broad personality traits and specific facets such as impulsivity tend to have the same external correlates in different cultures (Church, 2000; Saucier and Ostendorf, 1999). While cross cultural studies have been conducted using the facets of the NEO-PI-R, they have not yet been done with the UPPS-R. However, Spillane and Smith (2003) conducted a study of individual difference variables that affect Native American drinking on a reservation where high rates of alcohol abuse are observed. While environmental factors appeared to affect drinking levels to a large extent, they also found that urgency was positively associated with alcohol use and problem drinking, just as it is in Caucasian samples. To summarize, there is evidence that the unique variance associated with urgency is heritable, that urgency can be measured with either self-report or interview methods, that urgency correlates with various measure of negative affectivity and maladaptive behavior, that urgency is not simply the sum or product of neuroticism and lack of planning, and that urgency appears to operate similarly across cultures. This body of evidence is crucial for the claim we make that urgency reflects an important part of the heritable liability for BN.

Urgency’s Relation to Binge Eating and BN We have begun to examine urgency’s relation to binge eating and BN, and we have compared its role to that of the other impulsivity-like constructs. In each of four samples of college women, urgency correlated highly with binge eating behavior (Fischer, Anderson, and Smith, 2004b; Fischer and Smith, 2004a; Fischer, Smith, and Anderson, 2003; Fischer, Smith, and Lander, 2004). None of the other four impulsivity-related constructs correlated meaningfully with binge eating. Most recently, a meta-analysis of impulsivity-related constructs found the following magnitudes of relation to bulimic symptoms: urgency (r = .43), sensation seeking (r = .18), lack of perseverance (r = .02), and lack of planning (r = .18) (Fischer and Smith, 2004b). One limitation of the meta analysis was that many studies did not use measures designed specifically to differentiate among the four constructs. Therefore, for instance, lack of planning measures may have included some urgency content, and vice versa. In other words, the effect size comparisons likely underestimate the true differences in

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

169

effects. Nonetheless, the findings clearly point to the primary importance of urgency, among impulsivity-like constructs, in accounting for binge eating behavior. It is important to note that these findings come from cross-sectional research. Therefore, although they clarify the likelihood that urgency is the one impulsivity-like construct relevant to BN, they do not show a prospective or causal relation between the trait and the disorder. For the promise of this perspective to be realized, prospective and experimental designs that clarify urgency’s possible causal role are essential. Of course, the trait of urgency does not directly produce binge eating behavior and BN. Rather, urgency reflects a general tendency to act rashly in response to distress. We believe that urgency is best considered a general, distal risk factor for a variety of “acting out” behaviors. We suggest that the particular form of “acting out” behavior that results from high urgency is a function of psychosocial learning. Some individuals may learn that drinking alleviates distress, others may learn that gambling does so, and some may learn that bulimic symptoms can play that role. Therefore, to understand when urgency is likely to lead to bulimic symptoms, it is necessary to consider psychosocial learning. We have adopted expectancy theory for this purpose.

Expectancy Theory: Psychosocial Learning In the early part of the 20th century, psychology was captivated by the power of learning models in explaining behavior. Contingencies of reinforcement and punishment clearly exert a powerful influence on behavior (Skinner, 1953; Watson, 1930), and so to explain behavior, researchers focused on the learning of behavioral contingencies. During this time, Tolman (1932) advanced learning theory by demonstrating that the content of learning may be more cognitive than strictly behavioral in nature. After teaching rats to run mazes, he found that rats could just as successfully swim or ride a trolley car through the maze. He concluded that rats, instead of just learning a series of motor behaviors in response to reinforcement, actually developed cognitive maps of the maze itself. Essentially, as a result of learning, they knew how the maze was laid out so that they could get to the end by any number of motoric acts. In a nutshell, Tolman (1932) argued that rats form expectancies about the maze, based on their experiences with it. This finding of the cognitive nature of learning helped pave the way for future cognitive and social learning theories. Tolman, along with many other researchers to follow (Bolles, 1972; MacCorquodale and Meehl, 1952; Rotter, 1954), described two basic kinds of expectancies: Stimulus-stimulus expectancies and response-outcome expectancies. Stimulus-stimulus expectancies are described as expectations that a given circumstance will be followed by some other specific circumstance. Response-outcome expectancies are expectancies that a given behavior will result in a given outcome. Thus, the mechanism of learning is that, as a result of one’s learning history, one forms response-outcome and stimulus-stimulus expectancies, and those expectancies then influence one’s future behavioral choices. In other words, one’s expectancies summarize one’s learning history, and so are the cognitive mechanism by which prior learning leads to subsequent behavior.

170

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

Expectancy theory has become an important construct in many areas of psychology, including the examination of psychopathology (Alloy and Tabachnick, 1984), interpersonal processes (Jones, 1986), affect (Carver and Scheier, 1990), gambling behavior (Walters and Contri, 1998), and risk for alcohol abuse (Goldman, Brown, Christiansen, and Smith, 1991; Smith Goldman, Greenbaum, and Christiansen, 1995). Alcohol expectancy theory is one of the most developed expectancy theories and demonstrates applied support for the idea that expectancies are one mechanism by which learning shapes subsequent behavior. Alcohol expectancy theory rests on the idea that alcohol expectancies, which are useful in predicting early onset problem drinking, appear to be formed prior to drinking onset, presumably by modeling (Miller, Smith and Goldman, 1990; Smith et al., 1995). Researchers have also shown that reducing alcohol expectancies can lead to reduced drinking in males (Darkes and Goldman, 1993, 1998). In both basic science expectancy studies, such as those initiated by Tolman, and applied clinical studies, such as those on alcohol, there is substantial support for the notion that learned expectancies are one mechanism by which learning shapes subsequent behavior. Expectancy Theory Applied to Eating Disorders. Recently, researchers have shown that expectancy theory can also be applied usefully to eating disorders. The central idea is that individuals are exposed to different learning experiences concerning eating, dieting, and thinness, and that, as a result, they form different expectancies for the consequences of those behaviors and states. Hohlstein, Smith, and Atlas (1998) proposed that learned expectancies for reinforcement from eating may be a mechanism by which one’s learning history leads to overeating and binge eating. To the degree that some women have come to associate eating with powerful reinforcers, they hold unusually strong expectancies for reinforcement from eating, and so pursue food with greater vigor. Likewise, they argued that learned expectancies for reinforcement from dieting and thinness may be a mechanism by which one’s learning history leads to an emphasis on thinness. To the degree that some women have come to associate thinness with powerful and overly general reinforcers, they hold strong expectancies for reinforcement from thinness, and hence pursue thinness more strongly than do others. Eating and dieting expectancy theory holds that a woman’s learned expectations are the cognitive summaries of her learning history, and they operate to shape her subsequent behavioral choices. The identification of specific eating and dieting expectancies grew out of expectancy statements voiced by both clinical and non-clinical women. Examples of such statements are the following: “When I am feeling depressed or upset, eating can help me take my mind off my problems.” “When I have nothing to do, eating helps relieve the boredom.” “Eating seems to decrease my level of anxiety if I am feeling tense or stressed.” I would feel more capable and confident if I were thin.” “I would be more attractive if I were thin.” I would feel like I could do whatever I wanted to if I were thin” (Hohlstein et al., 1998). In sum, the individually different learning histories women have regarding eating, dieting, and thinness result in individual differences in expectancies for the consequences of those behaviors. Extreme eating and dieting behaviors, then, result from extreme expectancies, which, in turn, result from extreme learning histories.

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

171

Understanding Current Measures of Sociocultural nfluence from the Standpoint of Expectancy Theory Many existing measures of sociocultural influences on dieting, thinness, and eating can be though of from the perspective of expectancy theory and thus can be incorporated into this theoretical framework. We offer a representative, though not comprehensive, list of models to demonstrate this fact: the Perceived Sociocultural Pressure Scale (PSPS; Stice, 2001), the Sociocultural Attitudes Toward Appearance Questionnaire (SATAQ; Heinberg, Thompson, and Stormer, 1995), and the body dissatisfaction and drive for thinness subscales from the Eating Disorder Inventory-2 (Garner, 1991). We chose these measures because each has proved a reliable, valid predictor of eating disorder symptom endorsement, many of them in longitudinal designs (Stice, 2002). Items from the PSPS include: “I’ve noticed a strong message from my friends to have a thin body” and “I’ve felt pressure from people I’ve dated to lose weight.” From a learning theory perspective, these items appear to ask women to record a learning experience, or summarize a set of learning experiences. If one has felt pressure to lose weight, or to be thin, one has had a learning experience that will contribute to the expectancies one forms about the benefits of dieting and thinness. Thus, in a sense, the PSPS appears to measure precursors to thinness and dieting expectancies. In other words, the scale measures individual differences in one of the causes of expectancy formation. From an expectancy theory perspective, that is why scores on the PSPS predict subsequent onset of symptomatology: they contribute to the formation of expectancies, which then influence subsequent behavior. In a practical way, they serve as markers of likely expectancy endorsement. The social pressure awareness subscale of the SATAQ can also be thought of under the expectancy theory rubric. Items such as “People think that the thinner you are, the better you look,” and “Attractiveness is very important if you want to get ahead in our culture,” seems to reflect exposure to social learning about the benefits of thinness and attractiveness. The items measure the individual’s recognition and endorsement of the social learning message. The more women recognize that message, the more likely they will form expectancies for reinforcement from thinness. These expectancies are then likely to influence their behavior. Thus, SATAQ Awareness scale items also seem to reflect precursors to expectancy formation. Consider next items reflecting internalization of the thin ideal. Examples include Stice’s (2001) “Slender women are more attractive” and the SATAQ Internalization scale’s “Photographs of thin women make me wish that I were thin.” These items are different from the preceding ones, in the sense that they appear to reflect conclusions on the part of the respondent, not simply exposure to learning situations. Women who endorse these items strongly apparently feel more strongly about the value of thinness. The Stice item refers to one specific expectancy for thinness: thinness is more attractive. The SATAQ item’s reference to a wish to be thinner may reflect the same expectancy (thinness is attractive), but may also or instead reflect a more global expectancy for the benefits of thinness. Conclusions

172

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

of this kind are, essentially, endorsements of expectancies that should play a role in influencing subsequent behavior. Items on the Drive for Thinness scale of the EDI-2 are indicative of motivations to be thin. Example items include “I am preoccupied with the desire to be thinner,” and “I exaggerate or magnify the importance of my weight.” From an expectancy theory standpoint, expectancies for reinforcement from dieting and thinness could lead to this kind of preoccupation with one’s weight. Thus, the Drive for Thinness subscale appears to reflect consequences of expectancy formation and endorsement of these items may serve as markers of one’s expectancies. The Body Dissatisfaction subscale of the EDI-2, which includes items such as “I think that my thighs are too large” and “I think my hips are too big,” are conclusions one might draw, and they may reflect the influence of dieting/thinness expectancies. If one endorses expectancies for reinforcement from dieting and from thinness more strongly than the average woman, one would likewise be more inclined to value a thinner body, and hence be dissatisfied with one’s own body. In this sense, body dissatisfaction can be understood as a consequence of one’s learning history, as crystallized in one’s expectancies for dieting and thinness. In sum, the above examples represent different stages in the psychosocial learning process concerning eating, dieting, and thinness. We believe these constructs should be organized from a learning theory perspective, because psychosocial learning has been shown to be a very powerful and important tool in explaining behavior. By organizing them in this way, they can be seen to be parts of a coherent whole, rather than as individual instruments, each proceeding from a slightly different stage in the psychosocial learning process. Understanding the place of each of these constructs within expectancy learning theory both clarifies their connections with each other and produces an integrated theory of symptom acquisition that can be readily understood with the same theoretical tools used for many other psychological phenomena.

The Direct Measurement of Expectancies for Reinforcement from Eating and from Dieting/Thinness Hohlstein et al. (1998) developed measures of expectancies for reinforcement from eating and from dieting/thinness within the framework of the expectancy theory. To do this, they interviewed both clinical and non-clinical women about their expectancies. After a series of test development steps, they identified five scales to the 34-item Eating Expectancy Inventory (EEI) and one, global scale to the 44-item Thinness and Restricting Expectancy Inventory (TREI). The five-factor structure of the EEI and the one-factor structure of the TREI have been replicated in nine samples (four early adolescent female samples: MacBrayer, Smith, McCarthy, Demos, and Simmons, 2001; Simmons, Smith, and Hill, 2002; one late adolescent sample: Simmons et al., 2002; one college female Caucasian sample and one college female African American sample: Atlas, Smith, Hohlstein, McCarthy, and Kroll,

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

173

2002; and two more college samples, one female and one male: Boerner, Spillane, Anderson, and Smith, 2004). The five-factor structure of the EEI is made up of two positive reinforcement scales (“Eating is pleasurable and useful as a reward” and “Eating enhances cognitive competence”), two negative reinforcement scales (“Eating helps manage negative affect” and “Eating alleviates boredom”), and one scale assessing the expectancy that “Eating leads to feeling out of control.” The five-factor structure provided the best goodness-of-fit as compared to alternative factor structures (CFI=.95, rmsea=.04) The TREI’s one factor solution fit the data well (CFI = .99, rmsea = .01), and, although multifactor solutions also fit well, intercorrelations among putative subscales were all greater than .80, suggesting the merit of describing one, overall factor (“Thinness and restricting food intake lead to overgeneralized self-improvement”). Important content domains included in the TREI are reflected in these sample items: “I feel like I could conquer things more easily if I were thin,” “I would feel more capable and confident if I were thin,” “I would cope better with failures at work or school if I were thin,” and “I would be more attractive if I were thin.” There is considerable evidence for the validity of these measures of eating and dieting/thinness expectancies. In early adolescent, late adolescent, and college samples (the latter including men, women, Caucasians, and African Americans), expectancies that eating helps manage negative affect, alleviate boredom, and leads to feeling out of control, along with the expectancy that thinness/dieting leads to overgeneralized self-improvement, consistently account for substantial variance in Bulimia Test scores, Restraint Scale scores, and Three Factor Eating Questionnaire scores. In these analyses, correlations generally ranged from r = .40 to r = .62 (Atlas et al., 2002; Boerner et al., 2004; Hohlstein et al., 1998; MacBrayer et al., 2001; Simmons et al., 2002). Eating and Thinness expectancy profiles discriminated among anorexic patients, bulimic patients, psychiatric controls, and normal controls. There were no differences between psychiatric and normal controls, and classification accuracy among the three groups of anorexics, bulimics, and controls was 96% (94% if one does not use the expectancy that eating leads to feeling out of control, which is almost identical to a bulimia nervosa symptom). Bulimic patients simultaneously held expectancies that eating helps alleviate negative affect and boredom, and that thinness leads to overgeneralized self-improvement. Anorexic patients held strong expectancies for the benefits of thinness, and unusually low expectancies for the benefits of eating. Simmons et al. (2002) found that expectancies accounted for different symptom variance from that explained by EDI-2 personality risk factors (perfectionism, interpersonal distrust, and ineffectiveness). MacBrayer et al. (2001) found cross-sectional evidence consistent with the hypothesis that various expectancy scales mediate the influences of (a) negative maternal modeling regarding eating, and (b) family teasing about weight, on bulimic symptoms. The next step in testing eating and dieting expectancy theory was to conduct a longitudinal study of expectancy and symptom endorsement. We focused on early adolescence, by following a sample of U.S. middle school children from grade 7 through grade 9 (Smith et al., in press). We examined three expectancy scales (eating helps manage

174

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

negative affect, eating alleviates boredom, and thinness/dieting leads to overgeneralized selfimprovement) and one symptom measure, the Bulimia Test-Revised (BULIT-R). First, we examined the cross-sectional, multiple regression correlations between the three expectancy scales and the BULIT-R scores, which ranged from .60 to .69 across three years. The uncontrolled, time-lagged analyses indicated that expectancies correlated with subsequent BUILT-R scores in the .40 to .50 range. However, because these correlations did not control for prior BULIT-R scores, they could be a product of the high cross-sectional relationships and stable variable scores. In order to control for prior BULIT-R scores, we utilized structural equation modeling to examine a series of models. The model that best fit the data was one that specified reciprocal influences: expectancies at time 1 influenced symptom level at time 2, and symptom level at each time influenced expectancy scores at the subsequent time. The overall fit of the model was quite good (Comparative Fit Index = .96). Reciprocal influences between expectancies and symptom level are consistent with expectancy theory. Learned expectancies should predict subsequent changes in symptoms, and symptom level itself brings learning experience, and so should predict subsequent changes in expectancies. It is interesting to note that the nature of the predictions was of the positive feedback loop variety. Greater endorsement of expectancies for reinforcement from both dieting and thinness predicted greater bulimic behavior, which in turn predicted yet greater expectancies for reinforcement from both eating and dieting/thinness (Smith et al., in press). The mechanism by which this progression operates is not yet known, but it is worth noting that the same kind of positive feedback, reciprocal influence phenomenon was observed with early adolescent drinking behavior (Smith et al., 1995). Thus, these longitudinal data provide evidence supporting the application of expectancy theory to eating disorder symptomatology. Taken together, the early empirical work testing eating disorder expectancy theory clearly suggests that eating and dieting expectancies operate in accord with basic expectancy learning theory and very similarly to how expectancies operate in other applied areas. These findings speak to the value of integrating the many measures of sociocultural influence under an expectancy learning theory umbrella. When one considers the documented, successful prospective, predictive role of expectancy-related constructs (perceived sociocultural pressure, thin-ideal internalization, and so on: Stice, 2002), there currently exists evidence that precursors to expectancy formation, global expectancies, specific expectancies, and consequences of expectancies all predict the subsequent onset of bulimic symptomatology. More specifically, bulimic women appear to simultaneously hold unrealistic expectancies for reinforcement from both eating and from dieting/thinness (Hohlstein et al., 1998). Analogous to that which has been documented in other areas of psychology, unusually strong learned expectations for reinforcement from eating and from dieting/thinness predict bulimic symptom endorsement.

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

175

A Heritable Trait Combines with Psychosocial Learning: Integration of Urgency and Expectancy Risk Models As we noted at the beginning of the chapter, one general advance in understanding risk for BN is the recognition that both heritable and environmental factors contribute to liability. Our aim is to make this general advance more specific, by identifying one specific heritable risk factor and one specific set of environmental risk factors. We have argued that urgency (the tendency to act rashly or maladaptively when distressed) is one important heritable trait that increases liability for BN. We have also argued that individual differences in environmental risk can be captured using the expectancy construct. Expectancies for reinforcement from eating and from dieting/thinness are thought to summarize one’s relevant learning history, and so reflect a wide range of learned inputs into one’s eating and dieting predilections. In this section, we attempt to integrate these two risk factors. Doing so has two advantages. First, it provides substance to the general argument that genetic and environmental factors are both involved. Second, it suggests a more general integration of dispositional and learning risk factors that may have value beyond the eating disorder field. We emphasize two key dimensions to the urgency-expectancy integration. First, trait urgency is a general risk factor, in the sense that it increases one’s likelihood of developing some form of rash/maladaptive action in response to one’s distress. Examples of rash action patterns one might develop include binge eating, BN, alcohol use, and gambling behavior. Which of those action patterns a highly urgent person engages in is a function of the person’s learning history. Through modeling and experience, some individuals form expectancies for distress relief from drinking, others from gambling, and others from binge eating. They share the general, heritable liability of trait urgency, but their different learning histories cause them to form different expectancies, resulting in different characteristic forms of rash action (there are, no doubt, other forms of rash action beyond those listed, perhaps including risky sex or dyscontrolled shopping). This notion of a general, heritable liability that can be instantiated in various ways is consistent with what we know about risk for BN. Since BN rates vary across time and culture, the heritable risk for BN cannot be specific to BN symptomatology: it must involve more general dispositions that can lead to BN under the right environmental circumstances. If this model is accurate, one should be able to show that urgency correlates with each of those action patterns, and that what distinguishes among people with the different action patterns is their different expectancies. We have demonstrated this process in two recent, cross-sectional studies. Fischer et al. (2004b) showed that urgency correlated with both alcohol use and binge eating, that alcohol expectancies correlated with drinking levels but not with binge eating, and that eating expectancies correlated with binge eating but not with drinking. Fischer and Smith (2004a) extended the earlier findings by including gambling behavior. Here, too, urgency correlated with problem drinking, binge eating, and problem gambling, but the three types of expectancies (for alcohol, for eating, and for gambling) were behavior-specific. For instance, problem gamblers shared trait urgency with binge eaters, but problem gamblers had strong

176

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

gambling expectancies and weak eating expectancies, whereas binge eaters had strong eating expectancies and weak gambling expectancies. Although there are limitations to these findings (their cross-sectional nature and the failure to include identified clinical cases), their potential implications are clear. It seems possible that high levels of trait urgency place one at risk for some form of “acting out” behavior, and that one’s learning history, represented as expectancies, shapes the direction and nature of one’s “acting out.” Moreover, the notion of dispositional tendencies being shaped into specific behavioral predilections as a result of one’s particular learning experience may well have importance beyond the field of eating disorders. A second dimension to the urgency-expectancy integration is that, in the case of binge eating, disposition and learning interact. In a series of studies, we have shown that among individuals high in trait urgency, those who expect eating to alleviate negative affect are much more likely to binge eat than are others (Fischer, Smith, Anderson, and Flory, 2003; Fischer et al., 2004b; in press). Among individuals low in trait urgency, there is virtually no relation between the eating expectancy and binge eating. The presence of this interaction is quite consistent with the nature of each construct: eating to alleviate negative affect should be much more likely among urgent individuals than among others, and it is. What we are describing is not a comprehensive model of risk for BN, but it is one integrated component of such a model. We have offered a specific theory of the integration of genetic and learned risk, and we have provided empirical support for the theory. Evidence is consistent with the possibility that trait urgency is an important part of the heritable liability for BN. We have also shown that individual differences in learning can be understood using the expectancy concept, and we have demonstrated that expectancies differentiate BN patients from others and that expectancies predict the onset of BN symptomatology prospectively among adolescents. We have shown that urgency is a general risk factor for maladaptive behavior patterns, and that learned expectancies influence the particular form of rash action one chooses. There are, no doubt, other aspects to the heritable risk for BN. One likely possibility is negative affectivity. For urgency (rash action in response to subjective distress) to be active, there must be negative affect (Fischer et al., in press). Negative affectivity appears to be a necessary precursor to high levels of urgency, and so heritable dispositions toward negative affectivity are another part of the heritable liability for BN. Of course, the role of negative affectivity is different, because it likely influences many more syndromes than does urgency. Individuals experiencing negative affect, but who are not urgent, likely tend toward internalizing disorders, such as depression and anxiety. Other individuals experiencing negative affect tend toward externalizing disorders or rash, maladaptive actions (Krueger et al., 2002; Krueger, McGue, and Iacono, 2001): they are likely the ones high in urgency (Fischer et al., in press). So, negative affectivity may be one part of the risk process, but the risk for BN is increased when urgency is present as well. In sum, important advances in risk for BN are being made. Evidence from heritability studies indicating the presence of both genetic and environmental risk factors dovetails nicely with empirical demonstrations of the roles of heritable urgency and learned expectancies. Several avenues of investigation may build on this knowledge. What is the precise role of negative affectivity in this process? What other risk factors are also relevant? For instance, is

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

177

it possible that individuals vary in the extent to which endorphins are released via food consumption, and hence form different expectancies for the mood effects of eating for biological (rather than environmental) reasons? If the urgency-expectancy integration is valid, how should one then approach prevention and intervention? Can expectancies be modified successfully, as appears to be the case with respect to drinking (Darkes and Goldman, 1993)? Should individuals high in urgency be targeted early for multi-component prevention programs? On another plane, are any of the same risk factors relevant for anorexia nervosa (AN), or is AN actually a straightforward genetic disorder not caused by learning (as suggested by Keel and Klump, 2003)? Are learning factors, such as expectancies, causal for BN but artifacts of a genetic process for AN? Despite the progress in understanding risk for BN, there are, clearly, many unanswered questions that require further investigation. The prospect of addressing them is exciting.

References Alloy, L.B., and Tabachnik, N. (1984). Assessment of covariation by humans and animals: The joint influence of prior expectations and current situational information. Psychological Review, 91, 112-149. American Psychiatric Association (1994). Diagnostic and Statistical Manual of Mental Disorders (4th ed.). Washington, DC : APA. Anderson, R. E., Crespo, C. J., Bartlett, S. J., Cheskin, L. J., and Pratt, M. (1998). elationship of physical activity and television watching with body weight and level of fatness mong children: Results from the third national health and nutrition examination survey. ournal of the American Medical Association, 279, 938-942. Anderson, K.G., and Smith, G. T. (2001, August). Personality, expectancy, and eating behavior in college women. Paper presented at the annual meeting of the American Psychological Association, San Francisco, California. Anderson, K. G., Smith, G. T., and Fischer, S. (2003). Women and acquired preparedness: Personality and learning implications for alcohol use. Journal of Studies on Alcohol, 64, 384-392. Agras, W. S., and Telch, C. F. (1998). The effects of caloric deprivation and negative affect on binge eating in obese binge eating disordered women. Behavior Therapy, 29, 491503. Atlas, J. G., Smith, G. T., Hohlstein, L. A., McCarthy, D. M., and Kroll, L. (2002). Similarities and differences between Caucasian and African American women on eating disorder risk factors and symptoms. The International Journal of Eating Disorders, 32(3), 326-334. Bandura, A. (1969). Principles of behavior modification. New York: Holt, Rinehart, and Winston. Battle, E. K., and Brownell, K. D. (1997). Confronting a rising tide of eating disorders and obesity: Treatment vs. prevention and policy. Addictive Behaviors, 21, 755-765. Bolles, R.C. (1972). Reinforcement, expectancy, and learning. Psychological Review, 79(5), 394-409.

178

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

Boerner, L. M., Spillane, N. S., Anderson, K. G., and Smith, G. T. (2004). Similaritiesand differences between women and men on eating disorder risk factors and symptom measures. Eating Behaviors, 5, 209-222. British Medical Association (BMA). (2000). BMA takes part in body image summit. (Online). Available at web.bma.org.uk/pressrel.nsf. Brown, S. A., Goldman, M. S., Inn, A. M., and Anderson, L. (1980). Expectancies of reinforcement form alcohol: Their domain and relation to drinking patterns. Journal of Consulting and Clinical Psychology, 48, 419-426. Bulik, C. M., Sullivan, P. F., and Kendler, K. S. (2003). Genetic and environmental contributions to obesity and binge eating. International Journal of Eating Disorders, 33, 293-298. Bulik, C. M., Sullivan, P. F., Wade, T. D., and Kendler, K. S. (2000). Twin studies ofeating disorders: A review. International Journal of Eating Disorders, 27, 1-20. Campbell, D. T., and Fiske, D. W. (1959). Convergent and discriminant validation by the multitrait-multimethod matrix. Psychological Bulletin, 56(2), 81-105. Carver, C. S., and Scheier, M. F. (1990). Origins and functions of positive and negative affect: A control process view. Psychological Review, 97, 19-35. Castellani, B. and Rugle, L. (1995). A comparison of pathological gamblers to alcoholics and cocaine misusers on impulsivity, sensation seeking, and craving. The International Journal of the Addictions, 30, 275-289. Church, A. T. (2000). Culture and personality: Toward an integrated cultural trait psychology. Journal of Personality, 68, 651-703. Costa, P. T., Jr., and McCrae, R. R. (1992). NEO-PI-R: Revised NEO personality inventory. Odessa, FL: Psychological Assessment Resources. Crowther, J. H., Snaftner, J., Bonifazi, D. Z., and Shepherd, K. L. (2001). The role of daily hassles in binge eating. International Journal of Eating Disorders, 29, 449-454. Darkes, J., and Goldman, M.S. (1993). Expectancy challenge and drinking reduction: Experimental evidence for a mediational process. Journal of Consulting and Clinical Psychology, 61, 344-353. Darkes, J. and Goldman, M.S. (1998). Expectancy challenge and drinking reduction: Process and structure in the alcohol expectancy network. Experimental and Clinical Psychopharmacology, 6, 64-76. Davis, R., Freeman, R., and Solyom, L. (1985). Mood and food: An analysis of bulimic episodes. Journal of Psychiatric Research, 19, 331-335. Deaver, C. M., Miltenberger, R. G., Smyth, J., Meidinger, A., and Crosby, R. (2003). An evaluation of affect and binge eating. Behavior Modification, 27, 578-599. Evendon, J. (1999). Impulsivity: A discussion of clinical and experimental findings. Journal of Psychopharmacology, 13, 180-192. Fairburn, C. G. (1997). Eating Disorders. In D. M. Clark and C. G. Fairburn (Eds.), Science and practice of cognitive behavior therapy (pp. 209-241). Oxford, England: Oxford University Press. Feingold, A. (1992). Good-looking people are not what we think. Psychological Bulletin, 111, 304-341.

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

179

Fischer, S., Anderson, K. G., and Smith, G. T. (2004b). Coping with distress by eating or drinking: The role of trait urgency and expectancies. Psychology of Addictive Behaviors, 18, 269-274. Fischer, S., and Smith, G. T. (2004a). Binge eating, problem drinking, and problem gambling: Linked by a common pathway to impulsive behavior. Manuscript submitted for publication. Fischer, S., and Smith, G. T. (2004b). Another look at impulsivity: A meta-analytic review of types of impulsivity and bulimic symptoms. Manuscript submitted for publication. Fischer, S., Smith, G. T., and Anderson, K. G. (2003a). Clarifying the role of impulsivity in bulimia nervosa. The International Journal of Eating Disorders, 33, 406-411. Fischer, S., Smith, G. T., Anderson, K. G., and Flory, K. H. (2003b). Expectancy influences the operation of personality on behavior. Psychology of Addictive Behaviors, 17, 108-14. Fischer, S., Smith, G. T., Cyders, M.A., and McCarthy, D. M. (2004a). On the convergent and discriminant validity of four impulsivity-related constructs. Manuscript submitted for publication. Fischer, S., Smith, G. T., Spillane, N. S., and Cyders, M. A. (in press). Urgency: Individual differences in reactions to negative mood and implications for addiction. In Colombus, F. (Ed.) The Psychology of Mood. New York: Novascience Press. Freeman, L. M. Y., and Gil, K. M. (2004). Daily stress, coping, and dietary restraint in binge eating. International Journal of Eating Disorders, 36, 204-212. Garner, D. M. (1991). Eating Disorder Inventory-2 Professional Manual. Odessa, FL: Psychological Assessment Resources, Inc. Goldman, M.S., Brown, S.A., Christiansen, B.A., and Smith, G.T. (1991). Alcoholism and memory: Broadening the scope of alcohol expectancy research. Psychological Bulletin, 110, 137-146. Halford, J. C. G., Gillespie, J., Brown, V., Pontin, E. E., Dovey, T. M. (2004). Effect of television advertisements for foods and food consumption in children. Appetite, 42, 221225. Halliwell, E., and Ditmar, H. (2004). Does size matter? The impact of model’s body size on women’s body focused anxiety and advertising effectiveness. Journal of Social and Clinical Psychology, 23, 104-122. Heinberg, L. J., Thompson, K. L., and Stormer, S. (1995). Development and validation of the Sociocultural Attitudes Towards Appearance Questionnaire. International Journal of Eating Disorders, 17, 81-89. Hermes, S. F., and Keel, P. K. (2003). The influence of puberty and ethnicity on awareness and internalization of the thin ideal. International Journal of Eating Disorders, 33, 465467. Heatherton, T.F. and Baumeister, R.F. (1991). Binge eating as escape from self-awareness. Psychological Bulletin, 110(1), 86-108. Heatherton, T. F. and Polivy, J. (1992). Chronic dieting and eating disorders: A spiral model. In J. H. Crowther, D. L. Tennenbaum, S. E. Hobfold, and M. A. Parris (Eds.), The etiology of bulimia nervosa: The individual and family context (pp. 133-155).

180

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

Hohlstein, L.A., Smith, G.T., and Atlas, J.G.(1998). An application of expectancy theory to eating disorders: Development and validation of measures of eating and dieting expectancies. Psychological Assessment, 10(1), 49-58. Jackson, B., Cooper, M. L., Mintz, L., and Albino, A. (2003). Motivations to eat: Scale development and validation. Journal of Research in Personality, 37, 297-318. Jang, K. L., McCrae, R. R., Angleitner, A., Riemann, R., and Livesley, W. J. (1998). Heritability of facet level traits in a cross cultural twin sample: Support for a hierarchical model of personality. Journal of Personality and Social Psychology, 74, 1556-1565. Jones, E.E. (1986). Interpreting interpersonal behavior: The effects of expectancies. Science, 234, 41-46. Kaye, W. H., Gwirtzman, H. E., George, D. T., Weiss, S. R., and Jimerson, D. C. (1986). Relation of mood alterations to bingeing behavior in bulimia. British Journal of Psychiatry, 149, 479-485. Kaye, W. H., Devlin, B., Barbarich, N., Bulik, C. M., Thornton, L., Bacanu, S. A., Fichter, M. M., Halmi, K. A., Kaplan, A. S., Strober, M., Woodside, D. B., Bergen, A. W., Crow, S., Mitchell, J., Rotondo, A., Mauri, M., Cassano, G., Keel, P., Plotnicov, K., Pollice, C., Klump, K. L., Lilenfeld, L. R., Ganjei, J. K., Quadflieg, N., and Berrettini, W. H. (2004). Genetic Analysis of bulimia nervosa: Methods and sample description. International Journal of Eating Disorders, 556-570. Keel, P. K. and Klump, K. L. (2003). Are eating disorders culture bound syndromes? Implications for conceptualizing their etiology. Psychological Bulletin, 129, 747-769. Kendler, K. S., MacLean, C. , Neale, M., Kessler, R., Heath, A., and Eaves, L. (1991). The genetic epidemiology of bulimia nervosa. American Journal of Psychiatry, 12, 16271637. Klump, K. L., McGue, M., Iacono, W. G. (2000). Age differences in genetic and environmental influences on eating attitudes and behaviors in preadolescent and adolescent female twins. Journal of Abnormal Psychology, 109, 239-251. Klump, K. L., McGue, M., and Iacono, W. G. (2002). Genetic relationships between personality and eating attitudes and behaviors. Journal of Abnormal Psychology, 111, 380-389. Klump, K. L., Wonderlich, S., Lehoux, P., Lilenfeld, L. R. R., and Bulik, C. M. (2002). Does environment matter? A review of nonshared environment and eating disorders. International Journal of Eating Disorders, 31, 118-135. Krueger, R. F., Hicks, B. M., Patrick, C. J., Carlson, S. R., Iacono, W. G., and McGue, M.(1998). Etiologic connections among substance dependence, antisocial behavior, and personality: Modeling the externalizing spectrum. Journal of Abnormal Psychology, 111, 411-424. Krueger, R. F., McGue, M., and Iacono, W. G. (2001). The higher-order structure of common DSM mental disorders: internalization, externalization, and their connections to personality. Personality and Individual Differences, 30, 1245-1259. MacBrayer, E.K., Smith, G.T., McCarthy, D.M., Demos, S., Simmons, J. (2001). The Role of Family of Origin Food-Related Experiences in Bulimic Symptomatology. The International Journal of Eating Disorders, 30, 149-160.

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

181

MacCorquodale, K. and Meehl, P. E. (1953). Preliminary suggestions as to the formulation of expectancy theory. Psychological Review, 60(1), 55-63. McCrae, R. R., and Costa, P. T., Jr. (1994). The stability of personality: Observations and evaluations. Current Directions in Psychological Science, 3, 173-175. McCrae, R. R., Costa, P. T., Ostendorf, F., Angleitner, A., Hrebickova, M., Avia, M. D., Sanz, J., Sanchez-Bernardos, M. L., Kusdil, M. E., Woodfield, R., Saunders, P. R., and Smith, P. B. (2000). Nature over nurture: Temperament, personality, and life span development. Journal of Personality and Social Psychology, 78, 173-186. Miller, J. D., Flory, K., Lynam, D., and Leukefeld, C. (2003). A test of the four factor model of impulsivity related traits. Personality and Individual Differences, 34, 1403-1418. Miller, P. M., Smith, G. T., and Goldman, M. S. (1990). Emergence of alcohol expectancies in childhood: A possible critical period. Journal of Studies on Alcohol, 51(4), 343-349. Paunonen, S. V., and Ashton, M. C. (2001). Big five factors and facets and the prediction of behavior. Journal of Personality and Social Psychology, 81, 524-539. Petry, N. M. (2001). Substance abuse, pathological gambling, and impulsiveness. Drug and Alcohol Dependence, 63, 29-38. Peveler, R. and Fairburn, C., 1990. Eating disorders in women who abuse alcohol. British Journal of Addiction, 85, 1633-1638. Polivy, J., and Herman, P. C. (1985). Dieting and binging: A causal analysis. American Psychologist, 40, 193-204. Polivy, J., and Herman, P. C. (2002). Causes of eating disorders. Annual Review of Psychology, 53, 187-213. Robinson, T. N. (1999). Reducing children’s television viewing to prevent obesity: A randomized controlled trial. Journal of the American Medical Association, 282, 15611567. Robinson, J. L., Kagan, J., Reznick, J. S., and Corley, R. (1992). The heritability of inhibited and unihibited behavior: A twin study. Developmental Psychology, 28, 1030-1037. Rodin, J., Silberstein, L. R., and Striegel-Moore, R. H. (1985). Women and weight: A normative discontent. In T. B. Sonderegger (Ed.), Nebraska symposium on motivation: Vol. 32. Psychology and gender (pp. 267-307). Rotter, J. B. (1954). Social Learning and Clinical Psychology. Englewood Cliffs, N. J.Prentice-Hall. Sands, E. R., and Wardle, J. (2003). Internalization of body shapes in 9-12 year old girls. International Journal of Eating Disorders, 33, 193-204. Sanftner, J. L., and Crowther, J. H. (1998). Variability in self-esteem, moods, shame, and guilt in women who binge. International Journal of Eating Disorders, 23, 391- 397. Saucier, G., and Ostendorf, F. (1999). Hierarchical subcomponents of the Big Five personality factors: A cross-language replication. Journal of Personality and Social Psychology, 76(4), 613-627. Saudino, K. J. (1997). Moving beyond the heritability question: New directions in behavioral genetic studies of personality. Current Directions in Psychological Science, 6, 86-90. Sher, K.J. and Trull, T.J. (1994). Personality and disinhibitory psychopathology: Alcoholism and antisocial personality disorder. Journal of Abnormal Psychology,103, 92102.

182

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

Skinner, B. F. (1953) Science and Human Behavior. New York: Free Press. Simmons, J. R., Smith, G. T., Hill, K. K. (2002). Validation of Eating and Dieting Expectancy Measures in Two Adolescent Samples. The International Journal of Eating Disorders, 31, 461-473. Smith, G. T., and Anderson, K. G. (2001). Adolescent risk for alcohol problems as acquired preparedness: A model and suggestions for intervention. In P. M. Monti, S. M. Colby, and T. A. O’Leary (Eds.), Adolescents, Alcohol, and Substance Abuse: Reaching Teens Through Brief Interventions, pp. 109-144. New York: Guilford Press. Smith, G. T., Cyders, M., Fischer, S., and Simmons, J. (in press). Integrating dispositional and psychosocial learning risk factors for bulimia nervosa. Revista de Psicología Conductual: Revista Internacional de Psicología Clínica y de la Salud (Journal of Behavioral Psychology: International Journal of Clinical and Health Psychology). Smith, G.T., Fischer, S., and Fister, S. M. (2003). Incremental validity principles of test construction. Psychological Assessment, 15, 467-477. Smith, G. T., Fischer, S., Spillane, N. S., and Cyders, M. (2004). On the relations among negative affectivity, lack of planning, and urgency. Unpublished data. Smith, G. T., Goldman, M. S., Greenbaum, P. E., and Christiansen, B. A. (1995). The divergent paths of high-expectancy and low-expectancy adolescents. Journal of Abnormal Psychology, 104, 32-40. Smith, G.T., Williams, S. Fister, Cyders, M., and Kelley, S. (2004). Individual differences in behavioral inhibition and behavioral activation cause differential learning to the same event. Manuscript submitted for publication. Spillane, N., and Smith, G. T. (2003, June). Application of psychological theory to problem drinking among Native Americans. Paper presented at the annual meeting of the Research Society on Alcoholism, Fort Lauderdale, FL. Steinberg, S., Tobin, D., and Johnson, C. (1989). The role of bulimic behaviors in affect regulation: different functions for different patient subgroups? International Journal of Eating Disorders, 9, 51-55. Stice, E. (1994). Review of the evidence for a sociocultural model of bulimia nervosa and an exploration of the mechanisms of action. Clinical Psychology Review, 14, 633-661. Stice, E. (2001). A prospective test of the dual-pathway model of bulimic pathology: Mediating effects of dieting and negative affect. Journal of Abnormal Psychology, 110, 124135. Stice, E. (2002). Risk and maintenance factors for eating pathology: A meta-analytic review. Psychological Bulletin, 128, 825-848. Stice, E., and Agras, W. S. (1998). Predicting onset and cessation of bulimic behaviors during adolescence: A longitudinal group analysis. Behavior Therapy, 29, 257-276. Stice, E., Fisher, M., and Lowe, M. R. (2004). Are dietary restraint scales valid measures of acute dietary restriction? Unobtrusive observational data suggest not. Psychological Assessment, 16, 51-59. Stice, E., Killen, J. D., Hayward, C., and Taylor, C. B. (1998). Age of onset for binge eating and purging during adolescence: A four year survival analysis. Journal of Abnormal Psychology, 107, 671-675.

Integrating Personality and Environmental Risk Factors for Bulimia Nervosa

183

Stice, E., Presnell, K., and Spangler, D. (2002). Risk factors for binge eating disorder onset: A prospective investigation. Health Psychology, 21, 131-138. Stice, E., and Shaw, H. E. (2002). Role of body dissatisfaction in the onset and maintenance of eating pathology: A synthesis of research findings. Journal of Psychosomatic Research, 53, 985-993. Stice, E., Spangler, D., and Agras, W. S. (2001). Exposure to media portrayed thin ideal images adversely affect vulnerable girls: A longitudinal experiment. Journal of Social and Clinical Psychology, 20, 270-288. Stice, E., Trost, A., and Chase, A. (2002). Healthy weight control and dissonance based eating disorder prevention programs: Results from a controlled trial. International Journal of Eating Disorders, 33, 10-21. Strasburger, V. C. (2001). Children and tv advertising: Nowhere to run, nowhere to hide. Developmental and Behavioral Pediatrics, 22, 185-187. Striegel-Moore, R. H., Morrison, J. A., Schreiber, G., Schumann, B. C., Crawford, P. B., and Obarzanek, E. (1999). Emotion induced eating and sucrose intake in children: The NHLBI growth and health study. International Journal of Eating Disorders, 25, 389-398. Sullivan, P. F., Bulik, C. M., Kendler, K. S. (1998). Genetic epidemiology of binge eating and vomiting. British Journal of Psychiatry, 173, 75-79. Swendson, J. D., Tennen, H., Carney, M. A., Affleck, G., Willard, A., and Hromi, A. (2000). Mood and alcohol consumption: An experience sampling test of the self-medication hypothesis. Journal of Abnormal Psychology, 109, 198-204. Tellegen, A. (1982). Multidimensional Personality Questionnaire Manual. Minneapolis, MN: University of Minnesota Press. Thompson, J. K., van den Berg, P., Roehrig, M., Guarda, A. S., and Heinberg, L. J. (2004). The sociocultural attitudes towards appearance scale-r (SATAQ-3): Development and validation. International Journal of Eating Disorders, 35, 293-304. Tiggemann, M. and McGill, B. (2004). The role of social comparison in the effect of magazine advertisements on women’s mood and body dissatisfaction. Journal of Social and Clinical Psychology, 23, 23-44. Tolman, E.C. (1932). Purposive behavior in animals and men. New York: Century Company. Wadden, T. A., Brownell, K. D., and Foster, G. D. (2002). Obesity: Responding to the global epidemic. Journal of Consulting and Clinical Psychology, 70, 510-525. Wade, T., Neale, M. C., Lake, R. I. E., and Martin, N. G. (1999). A genetic analysis of the eating and attitudes associated with bulimia nervosa: Dealing with the problem of ascertainment. Behavior Genetics, 29, 1-10. Walters, G. D., and Contri, D. (1998). Outcome expectancies for gambling: Empirical modeling of a memory network in federal prison inmates. Journal of Gambling Studies, 14, 173-191. Watson, J. B. (1930). Behaviorism (Rev. Ed.). Chicago: University of Chicago Press. Whiteside, S. P., and Lynam, D. R. (2001). The five factor model and impulsivity: Using a structural model of personality to understand impulsivity. Personality and Individual Differences, 30, 669-689.

184

Sarah Fischer, Gregory T. Smith and Melissa A. Cyders

Wildes, J. E., Emery, R. E., and Simons, A. D. (2001). The roles of ethnicity and culture in the development of eating disturbance and body dissatisfaction: A meta- analytic review. Clinical Psychology Review, 21, 521-551. Wilson, G. T. (2002). The controversy over dieting. In C. G. Fairburn and K. D. Brownell (Eds.) Eating disorders and obesity: A comprehensive handbook, (2nd ed., pp. 93-97). London: Guilford Press.

In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain, pp. 185-204 © 2006 Nova Science Publishers, Inc.

Chapter IX

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health Alex Milosevic Liverpool University Dental Hospital Liverpool L3 5PS UK

Abstract The dental and oral health of individuals with an eating disorder has been largely underinvestigated and ignored as health care professionals focus on the general medical, dietary and psychiatric/psychological needs of patients. Disordered eating and chaotic lifestyle may affect patterns of caries (decay) and gum disease. Oral microbial flora, either in dental plaque or saliva, could theoretically differ to normal flora as a consequence of repeatedly low intra-oral pH secondary to self-induced vomiting (SIV). Parotid salivary gland enlargement and altered salivary composition have been described. The presence of gastric acid in the mouth can result in acid erosion, with disfiguring consequences to the dentition. The impact of anomalous behaviours such as chaotic eating and self-induced vomiting upon the dental health of eating disordered subjects may not be apparent to the subjects themselves or their carers, be they physicians, psychiatrists, psychologists, nurses or relatives. Nonetheless, the effects upon the teeth can be significant such that it has been postulated that the dentist may be the first health care professional to suspect an eating disorder in an otherwise healthy individual. The mouth is the first part of the digestive system and commonly exhibits signs of disease occurring elsewhere. This chapter reviews the literature and illustrates the clinical problems faced by real cases. Prevention will also be discussed.

Alex Milosevic

186

Oro-Dental Effects of the Eating Disorders Soft Tissues Nutritional deficiencies can give rise to a range of health problems but few have specific effects on the oral soft tissues. Fewer still are the reports in the literature describing oral lesions related to anorexic or bulimic behaviour. Vitamin B2 (Riboflavin) deficiency is associated with inflammatory and degenerative changes in the mucous membranes of the lips and tongue. Angular stomatitis also termed cheilosis, consisting of red, sore fissures at the angles of the mouth and shiny reddened mucous membranes are characteristic. The inflamed and sore tongue is termed glossitis [Cawson, 1991]. There are no recorded cases of this in the eating disorders. The well described swollen bleeding gums present in Vitamin C deficiency or scurvy are a very late stage of the disease and have not been described in the eating disorders. Glossitis and stomatitis are sometimes early changes in nicotinamide deficiency (pellagra). The tongue tip and lateral borders become reddened, swollen and occasionally deeply fissured as can the gum margins [Cawson, 1991]. No reports of this in the eating disorders have been made. A tongue abscess was described in a 30-year-old female with anorexia who presented with submandibular tenderness and difficulty swallowing (dysphagia). This was associated with angular stomatitis, minor apthous ulceration of the lips and tongue depapillation. Cervical lymphadenopathy was not present but proteinuria was. Blood chemistry revealed a severe anaemia with a Haemoglobin concentration of 7.0g/dL (normal range 11.5-16.5 g/dL) and a decreased total plasma protein concentration of 55 g/L (normal range 62-80g/L) [Keith and Flint, 1989]. Although the abscess was of dental origin, it was an unusual presentation and the authors believed secondary immuno-deficiency was a predisposing factor. Treatment included an extraction, intravenous antibiotics and a 5-day course of oral penicillin with antifungal cream for the lip commisures [Keith and Flint, 1989]. Contrary to an anecdotal report, the potential chronic irritation to the oral mucosa from long term vomiting has not resulted in any reported case of malignant change [Brady, 1980].

Saliva Saliva has several important functions in the maintenance of oral health. Its proteins have protective antibacterial, digestive and lubricative actions and, with respect to the mineral content of teeth, saliva can be supersaturated with calcium and phosphate and thus promote remineralisation. Furthermore, all the soft tissue membranes such as cheeks and tongue are covered by protective mucous and the teeth themselves are coated by the acquired salivary pellicle. The pellicle has a significant role in protecting the tooth from caries and erosion. The salivary functions of lubrication and neutralization of intra-oral acids also termed buffering capacity are probably most important during bouts of self-induced vomiting (SIV).

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

187

Initial case reports described salivary parotid gland enlargement in cases of bulimia [Levin et.al., 1980; Hasler, 1982; Burke, 1986; Taylor and Sneddon, 1987]. Most studies have investigated function (see below) rather than structure, probably because needle aspiration biopsy and sialography are invasive procedures. The parotid gland sialogram on an 18-year-old female showed a hypertrophic “leafless tree” pattern and the aspiration biopsy demonstrated packed acini with few ducts [Hasler, 1982]. Other sialograms performed on a 19-year-old female student [Levin et.al., 1980], the 20-year-old female reported by Burke (1986) and on the 26-year-old female reported by Taylor and Sneddon (1987) found no structural abnormality of the gland. It seems that parotid gland enlargement is not a consistent feature, is usually asymptomatic, although some have noted discomfort and can resolve spontaneously and is thus episodic in nature. The histological appearance of parotids in malnourished South Africans was of cellular hypertrophy with accumulation of secretory granules, nuclear displacement and cellular distention [du Plessis, 1956]. Nutritional mumps was used to describe the parotid swelling seen in starvation and malnutrition [Batsakis and McWhirter, 1972]. The mechanism for gland enlargement remains unclear although humoral transmission between the pancreas and parotid was postulated with changes in serum amylase [Kakizaki et.al, 1978]. Salivary amylase accounts for 55% of the total serum amylase and the rest is of pancreatic origin [Gillard et.al., 1983]. Raised salivary amylase in anorexia and bulimia has been reported [Humphries et.al.,1987; Kronval and Theander 1987; Hempen et al., 1989]. The severity of abnormal eating behaviours, measured as binge frequency and SIV, was not correlated with salivary amylase concentration although significant reductions in amylase levels were found in patients with good treatment outcome but not in those with poor treatment outcome [Kronvall et.at., 1992]. Stimulated and unstimulated salivary concentrations of potassium, chloride, calcium, urea nitrogen and albumin were reported to be within normal values although unstimulated salivary values were measured in only one subject [Tylenda et.al., 1991]. Although resting salivary flow rates were originally investigated, stimulated salivary flow is more relevant as salivary flow increases dramatically before vomiting because the medullary centre that controls vomiting is connected to salivary nuclei [Edgar, 1992]. Any nausea caused by esophageal and stomach distention after a binge eating episode will further stimulate salivation. Little is known about the influence of general metabolic disturbance in eating disordered subjects upon salivary function. Chronic malnutrition in Indian children reduced stimulated salivary secretion and buffering capacity and the authors speculated that the low protein diet coupled with low fat favoured reduced salivary buffering capacity [Johansson et.al., 1992].Others assessed the influence of personality traits on salivary flow but concluded that psychological factors appeared to have no predictive power on salivation despite the evidence to show that depression and anxiety can affect salivation [Millar et.al., 1993]. Flow rate, buffering capacity and pH were assessed in both resting and paraffinstimulated saliva in anorexia nervosa [Hellstrom, 1977]. Although a very low resting saliva rate was reported, this was not statistically significant nor would it be clinically significant as stimulated saliva is of greater interest. Stimulated flow rates between anorexics, bulimics and controls were not statistically different, but the mean salivary pH in both eating disorder

188

Alex Milosevic

groups was significantly lower than the control subjects [Liew et.al., 1991;Touyz et.al., 1993]. Bulimics with and without pathological dental erosion had significantly lower (p<0.01) mean stimulated saliva flow rates compared to the control group [Milosevic and Dawson, 1996]. Salivary pH was within the normal range whereas the mean bicarbonate concentration was significantly lower (p<0.01) in the two bulimic groups compared to the control group. Bulimics with pathological or unacceptable dental erosion had significantly more viscous saliva compared to bulimics without pathological erosion and the controls see Table 1. Table 1. Mean whole salivary viscosity measured in Centipoise (cP) according to the presence or absence of pathological erosion Group Bulimics with pathological erosion (N=9) Bulimics without pathological erosion (N=8) Controls (N=10)

Salivary viscosity, cP 7.39 (3.56) 4.46 (0.43) 4.12 (0.54)

Reduced parotid gland function in bulimia could result in a less watery or serous output and reduced bicarbonate contribution to whole saliva. Furthermore, a significant reduction in parotid secretion could result in an increased salivary viscosity because of a proportional increase in submandibular and sublingual salivary gland secretion which are more viscous [Milosevic and Dawson, 1996]. A subjective feeling of dry mouth or xerostomia was more frequent among the bulimic group (34%) than controls (10%) despite there being no difference in stimulated flow rates [Rytőmaa et.al., 1998]. Overall, salivary function is altered in the eating disorders. There are, however, few reported cases of significant difficulties associated with this. It seems likely that parotid gland hypertrophy is episodic but the clinical picture is very varied with some cases of altered salivary output which is not associated with parotid enlargement.

Periodontal Disease The supporting structures of the teeth include the bony socket, the cementum layer of the root and the intervening ligament which, with the overlying gum, are collectively termed the periodontium. The first stage of periodontal disease is inflammation of the superficial tissues, the gums or gingivae, manifest as swollen, bleeding gums and called gingivitis. This is caused by ineffective oral hygiene or plaque control. Chronic gingivitis can be followed by progress of the inflammatory response to deeper tissues such that bone resorption (loss of attachment) takes place but in certain resistant individuals gingivitis does not lead to periodontitis. The inflammation and subsequent loss of attachment is in response to the microbial flora or dental plaque which may be characterised by specific species or particular virulence factors such that its chronic progressive nature results in tooth loosening and eventual tooth loss. Smoking is a co-factor. Hence the importance of correct and effective

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

189

oral hygiene procedures which includes tooth brushing ideally with fluoridated toothpaste, flossing and use of mouth rinses. The evidence that periodontitis is worse in the eating disorders is conflicting. The initial studies found unremarkable levels of plaque, gingivitis and periodontitis. Inflammation was significantly more common in the non-vomiting group than in the vomiting or regurgitating anorexics [Hurst et.al., 1977]. The presence of plaque and gingivitis was similar in the vomiters and non-vomiters although periodontal bone loss was not assessed [Hellstrom, 1977; Roberts and Li, 1987]. The approximal plaque index and sulcus bleeding index were significantly higher in the healthy controls compared to the anorexia and bulimia study groups but calibration and the degree of reproducibility of the examiners was not stated although the authors did state that “patients had no loss of attachment” [Philipp et.al., 1991]. One study found that controls had more surfaces with a plaque score of 0 but the anorexics had significantly more lingual/facial sites with plaque scores of 1 and scores of 2 were similar between the two groups [Liew et.al., 1991]. The clinical significance of differences in plaque score and gingivitis around the dental arch is not apparent and probably not important. More recent results consistently failed to find any difference between plaque, gingivitis and periodontal disease between eating disordered subjects and controls [Milosevic and Slade, 1989; Altshuler et.al., 1990].

Dental Erosion Dental erosion is the acid dissolution of tooth substance. It differs to dental caries (decay) in that it does not involve bacterial or plaque acids but does involve dietary or gastric acids having a direct effect upon enamel and dentine. Carbonated beverages such as cola drinks, fresh fruit juices, herbal teas and white wines have been associated with erosion as have fresh fruit and pickled foods. The increased consumption of these food stuffs increases the risk of erosion although the epidemiological evidence for this is limited. Gastric acid enters the mouth secondary to gastro-oesophageal reflux disease (GORD) or during vomiting. Selfinduced vomiting (SIV) is a common purging behaviour in the eating disorders and may produce a similar pattern of erosion as in subjects with GORD or excessive dietary intake of acids. The impact of eating disorders upon oral health was initially reported by Hellstrom (1977) and Hurst et al. (1977). In of a sample of 39 anorexics, severe lingual-occlusal erosion was reported in 27 subjects (Hellstrom, 1977) although no attempt was made to correlate vomiting variables with the outcome of erosion. Furthermore, buccal erosion due to a high consumption of acid fruits and drinks to relieve thirst was more frequent in vomiting than non-vomiting subjects. Fresh fruit was eaten in order to induce diarrhoea. The presence or absence of erosion was related to the duration of vomiting [Simmons et.al., 1986]. Of the 66 females in study sample, 25 (38%) had significant erosion. Eroded teeth occurred in a third of cases sampled by Roberts and Li (1987) despite the observation that only 65% of the anorexics vomited compared to all the bulimics. The strength of association between vomiting variables and the outcome of dental erosion has been investigated more recently. In 58 subjects with an eating disorder, compared

Alex Milosevic

190

to 50 age-matched controls, significant differences were found between the observed frequencies in the absence or presence of pathological tooth wear within the various groups, see Table 2 [Milosevic and Slade, 1989]. Table 2. Number of cases within groups showing presence or absence of pathological tooth wear

Pathological erosion/tooth wear present Pathological erosion/tooth wear absent Column Totals

Group 1 Bulimics with SIV 14 (42%)

Group 2 Bulimics without SIV 2 (28%)

Group 3 Anorexics 6 (33%)

Group 4 Controls 3 (6%)

Row Totals 25

19 (58%)

5 (72%)

12 (67%)

47(94%)

83

33

7

18

50

108

It is clear from Table 2 that far more erosion/tooth wear is present in the eating disorder groups compared to the control group. The within group proportion with erosion was highest in the vomiting bulimics (group 1) which was also reported in a South African case-control study published in the same year [Jones and Cleaton-Jones, 1989]. Bulimic patients were also found to have more severe erosion compared to anorexics although neither the method used to measure erosion nor the comparison test were stated [Philipp et.al., 1991]. In the study by Milosevic and Slade, the frequency of SIV, its duration and the product of these two variables, the total number of vomiting episodes, were not linearly associated (Pearson correlation coefficient) with dental erosion. Similarly, the severity of erosion was no different between those who vomited more frequently compared to those that vomited less frequently [Robb et.at., 1995]. This result was counter intuitive as it would be expected that more vomiting episodes would lead to increased severity or presence of eroded teeth. Other factors, therefore, must be involved in determining whether or not erosion occurs. Table 3. Presence or absence of dental erosion/tooth wear in vomiting bulimics according to total number of vomiting episodes

Pathological tooth wear present Pathological tooth wear absent Column total

Total number of vomiting episodes <1100 >1100 3 11 14 15 4 19 18 15 33

Chi square = 8.56, p= 0.003; Relative Risk 3.73

Further analysis of the 14 cases in Group 1 found that 11 had 1100 or more vomiting episodes which forms the basis for Table 3. From the data in Table 3, the Relative Risk is 3.73 (95% CI 1.5, 9.3) for the occurrence of dental erosion if subjects have vomited more than 1100 times. Similar results were reported by Altshuler et al. [1990]. Vomiting duration was only moderately associated with the number of eroded teeth (r=0.46, p=0.01) but the frequency of SIV was not significantly related to dental erosion (r=0.11, ns). The authors did

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

191

comment that after six months of SIV most bulimics exhibited one or more eroded tooth surfaces and that after five years all subjects exhibited some erosion. The greater severity of erosion in bulimics compared to anorexics was confirmed in a sample of Australian cases who had six-fold the number of eroded surfaces [Touyz et.al., 1993]. Both the prevalence and severity of dental erosion were greater in Finnish bulimic subjects compared to controls [Rytőmaa et al., 1998]. Interestingly, over half the bulimics had discovered erosion themselves (12 out of 22) and in a quarter of cases the erosion was diagnosed for the first time by the examiners.

The Distribution of Acid Eroded Teeth In any one mouth, all the teeth are at risk of erosion, although most workers have assessed its surface or site distribution and compared it to controls groups [Jones and Cleaton-Jones, 1989; Milosevic and Slade, 1989; Robb et.al., 1995; Rytőmaa et al., 1998]. The most commonly eroded teeth are the upper incisors. The commonest surfaces to be severely affected by erosion in subjects with an eating disorder are the palatal (upper inner sites) and occlusal (the biting top surfaces of bicuspids and molars). These sites are also eroded in subjects who drink excessive amounts of fruit juice or carbonated beverages and therefore it can be difficult to determine the relative contributions from intrinsic gastric acid and extrinsic dietary acid. Mean palatal and labial (front facing sites) exhibited significantly greater erosion in vomiting anorexics and bulimics compared to abstaining anorexics and controls [Robb et.al., 1995]. The authors also reported that abstaining and vomiting anorexics exhibited more lower posterior erosion on buccal (cheek facing surfaces) and occlusal surfaces than controls. The reason why non-vomiting anorexics had buccal and occlusal erosion is not clear although Scheutzel [1996] believed that extrinsic acids affected the buccal and labial surfaces whereas gastric acid from SIV attacked the palatal and occlusal surfaces. This hypothesis has not been proven and others reported that the etiology of the erosion could not be ascertained from its location or distribution [Jarvinen et.al., 1992].

Dentine Hypersensitivity Severe enamel erosion may result in exposed dentine. This can be sensitive to temperature change and normal activities like tooth brushing and drinking become painful. Dentine sensitivity may be presenting feature. Its management is discussed later. Dental Caries (Decay) and Its Difference to Dental Erosion Dental decay or caries is caused by the bacterial breakdown of fermentable carbohydrates, most notably sucrose, resulting in acidic metabolic by-products which attack a susceptible site on a tooth surface. Bacterial plaque acids mainly implicated in the carious process are lactic, acetic and propionic acids. This is a different process to acid erosion as the

192

Alex Milosevic

teeth become cavitated and require fillings. Erosion by contrast occurs when dietary acids “bathe” the whole tooth with resultant thinning of the surface rather than a small area of demineralisation beneath the plaque. Enamel is the initial dental tissue to be involved as it forms the “cap” or covering of the tooth. A further distinguishing feature of dental decay is that enamel caries is a sub-surface phenomenon with the body of the lesion having greater porosity (5-25%) than the surface zone (approximately 1%). Erosion, by contrast, is a surface development with loss of the original surface tooth substance and porosity or softening of the remaining surface see Figures 2 and 5. This new surface is more readily worn away by tooth grinding habits (bruxism), tooth brushing (abrasive processes) and chewing hard foods. The evidence that dental caries is worse in eating disordered individuals than the normal population is slightly conflicting. Although caries experience was not different in the 27 vomiters compared to the twelve non-vomiters [Hellstrom, 1977)], others reported nonvomiters to have less caries experience [Hurst et al., 1977]. The latter authors discussed diet and recognised that the abnormal eating pattern including bouts of high carbohydrate consumption would increase the risk of caries. Neither study benefited with a control group and measures for caries and erosion were not validated. The standard measures for decay, DMFT (Decayed, Missing and Filled Teeth) and DMFS (Decayed, Missing and Filled Surfaces) were used by Roberts and Li (1987) who concluded that caries experience between anorexics and bulimics was no different and believed neither group were more or less susceptible to dental caries than healthy people. “Clinically detectable” caries occurred in only two cases out of 66 bulimics examined by Simmons et.al., 1986. The mean DMFS scores for a bulimic group and age and sex-matched controls were 27.9 and 19.1 respectively, which was not statistically significant (Jones and Cleaton-Jones, 1989). No difference in DMFS between eating disorder groups and controls was reported by Milosevic and Slade (1989), Altshuler et. al. (1990) and Rytömaa et.al. (1998) and for DMFT by Touyz et.al. (1993). Bulimic individuals had significantly greater DMF-“value” compared to anorexics and controls, although whether the index related to surfaces or teeth is unclear (Philipp et.al, 1991). Overall, the literature indicates that dental decay is no worse in eating disordered subjects compared to controls. This is despite the greater theoretical risk associated with haphazard eating habits and increased intake of carbohydrates. Perfectionist tendencies or obsessive-compulsive traits are common in the eating disorders which may manifest as good oral hygiene practices so reducing the risk of caries.

Microbiology As discussed in the previous section, dental caries involves microbial plaque acids attacking the tooth surface. Repeatedly low intra-oral pH from SIV could in theory manifest as an altered oral microbial flora to more aciduric species [Bretz et.al., 1989]. Streptococcus mutans and Lactobacilli are cariogenic because they are able to produce acid rapidly from fermentable carbohydrates. They thrive under acid conditions and adhere tenaciously to tooth surfaces because not only do they produce acids but very sticky extracellular polysacchharides [Kidd and Joyston-Bechal, 1987].

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

193

The selective serotonin re-uptake inhibitor, fluoxetine or Prozac, has been used to reduce binge-eating and vomiting. In a double-blind placebo-controlled trial, fluoxetine was effective in reducing the frequency of bingeing and purging and salivary levels of Streptococcus sobrinus [Bretz et.al., 1993]. The authors demonstrated that Streptococcus sobrinus was capable of producing acid at low pH values, whereas other streptococci ceased acid production. It was believed that Streptococcus sobrinus could be a marker of emetic activity and therefore instruct carers on compliance with treatment. Neither Streptococcus mutans nor Lactobacillus counts were any different between anorexics, bulimics and controls although the authors failed to state whether they cultured dental plaque or saliva [Touyz et.al., 1993]. Salivary bacterial counts of Streptococcus sobrinus were statistically higher in the eating disorder group than in the healthy controls [Bretz et.al., 1989]. Furthermore, salivary levels of Streptococcus mutans, Lactobacilli and yeast were increased but this was not reflected in greater decay as the DMFS (see above) in the eating disorder group was actually lower than a high risk caries comparison group [Bretz et.al., 1989]. These authors offered several explanations for this contradictory result, including an alteration of microbial virulence secondary to vomiting, reduced risk of decay because of the older age of onset of bulimia and a protective effect from greater consumption of dietary fat which protects for decay. None of these possible reasons have been investigated.

Temporo-Mandibular Joint Function and Tooth Grinding (Bruxism) Mouth opening, closing and lateral movements are enabled by the jaw joint, termed the temporo-mandibular joint (TMJ). The TMJ is principally between the articular inferior surface of the squamous temporal bone and the mandibular condyle. Between the cranially convex glenoid fossa and the condylar head is an intra-articular collagenous fibrous disc of variable thickness that completely divides the jaw joint into upper and lower joint compartments [McKay et.al., 1992]. Detailed description of the TMJ is beyond the scope of this chapter, but joint dysfunction is a common and well-recognised problem. It is associated with parafunctional tooth clenching and grinding known by dentists as bruxism. Bruxism is believed to be a stress relieving mechanism that occurs during sleep in the early hours of the morning. The extremely high loads imposed across the teeth and the jaw joint result in tooth wear (attrition) and a clicking joint. If muscle spasm is present, pain can also co-exist with limited mouth opening. Masseter muscle hypertrophy is a feature of long standing bruxism. None of the studies on the oral and dental sequelae to the eating disorders have described TMJ dysfunction as a finding despite the hypothetical risk to the joint from frequent wide opening of the mouth during bouts of SIV and stress related bruxism. Perhaps acid erosion of teeth has overshadowed any assessment of dental attrition, which would be difficult to see if erosion was present.

194

Alex Milosevic

Table 4. The facial, oral and dental problems possibly associated with eating disorders Non-specific Dental caries Gingivitis Chronic Periodontitis Temporo-mandibular joint dysfunction Bruxism

Specific Erosion (secondary to SIV) Altered oral microbial flora Altered salivary function including parotid hypertrophy

The Inter-Relationship of Psychological Wellbeing and Body Image Distortion with Facial, CircumOral and Dental Appearance Facial appearance has universal importance, especially so in dentistry, yet few studies have assessed the influence of distorted body image on satisfaction with facial and oral features [Cunningham, 1999]. Dental and facial aesthetics were reported to have a very important role in self-esteem and self-image [McLain and Proffit, 1985] whilst body dysmorphic disorder (previously known as dysmorphophobia) has a classic pattern with individuals presenting with a minor or imagined defect and a level of concern that is out of all proporton [Cunningham, 1999]. Patients with an eating disorder attending dental clinics have a range of problems which may be exacerbated if a dental fixation is present. The presence of an anterior open bite or other dental abnormality was not associated with patient reports of SIV [O’Reilly et.al., 1991]. Digital depression of the tongue and increased intra-oral pressure to induce vomiting was not therefore the cause of the open bite. In children requesting orthodontic treatment, body image satisfaction did not differ to the control group, although girls scored significantly lower than boys and the few subjects with prognathic teeth had lower scores than the other malocclusion groups [Klima et.al., 1979]. The influence of poor dental appearance on mental well being has been investigated and the results are contradictory although recent reports concluded that satisfaction with dental appearance was an important factor for psychological health and patients’ expectations of treatment [Albino et.al., 1989; Birkeland et.al., 2000; Bos et.al., 2003; Shaw et.al., 1985]. Certain dental traits in a 15-year follow up study of Danish subjects were found to adversely affect body image and self concept, not only in adolescence but also into adulthood [Helm et.al., 1985]. In an attempt to understand the influence of facial and dental appearance on body image distortion (BID), a recent study measured BID, both perceived and desired, and related it to the Body Satisfaction Scale and the Eastman Esthetic Index [Milosevic et.al., 2003]. Although only a small convenience sample of 15 eating disordered subjects were assessed, the results indicated that teeth were not associated with body image but the face was associated with an over estimate of body image (rho= +0.52, p<0.05). Overall, the group over estimated their body image by a mean of 28% and desired to be a mean 25% thinner [Milosevic et.al., 2003]. It was concluded that dental treatment in anorexia and bulimia may not lead to better perception of body image. Whether a general disturbance in body image

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

195

perception and possible dissociation in symptomatology exists such that body image is specific to the body and excludes the teeth and mouth is unclear. This was an area recommended for further research.

Management of the Dental Aspects of Eating Disorders The bulk of the dental literature regarding anorexia and bulimia focuses on issues of management whereas few papers discuss the added difficulty of history taking in these cases.

History Taking and Ethical Considerations Knowledge of eating disorders by dentists was thought to be important as they may be the first to health care professional to suspect an eating disorder because of the characteristic oral presentation [Burke et.al., 1996]. Unfortunately in a survey of 100 dentists working in the county of Kent, England, the general level of knowledge regarding the oral signs of bulimia was very low [Harwood and Newton, 1995]. This was despite 29% having provided dental treatment for a sufferer. Moreover, patients diagnosed in dental clinics are often younger than those seen in eating disorder clinics and hence have a better prognosis for treatment [Brown and Bonifazi, 1993]. The dental management of patients with anorexia and bulimia can be broadly divided into intervention and non-intervention. Whichever approach is adopted it must be sympathetic and non-judgmental [Kidd and Smith, 1993]. A further and potentially more difficult problem to solve concerns issues of confidentiality and consent [Crossley et.al., 2001]. Should the dentist suspect an eating disorder and question the patient regarding this, is it ethical to refer to a medical practitioner? If the patient is an adolescent is it ethical to inform the child’s parents or guardians that he/she has admitted to an eating disorder? In the latter situation, if the child is deemed competent a breach of confidentiality would be unethical, despite the morbidity and mortality associated with the disorder. Referral to another health care professional would be less of a breach of confidentiality as there is an understanding of implied consent for any information disclosed during examination which can be passed on to professional colleagues in order to benefit the patient. Many eating disorder patients are highly secretive or are too embarrassed to admit they have a problem and thus disclosure is not forthcoming [Milosevic, 1999]. However, direct communication with the patient and involvement in all aspects of decision making and treatment planning is very important otherwise feelings of lack of control may become exacerbated [Crossley et.al., 2001]. Treatment is unlikely to succeed in a non-compliant and poorly motivated patient. Another contentious issue for the eating disordered patient is the provision of care in relation to their disorder. Some have advocated that treatment is withheld or at least the advanced “comprehensive” procedures are not undertaken until the individual is cured or significant improvement in vomiting behaviour has been achieved [Faine, 2003]. The ethics of a dentist withholding treatment for a dental problem are uncertain. Finally, taking a relevant medical

196

Alex Milosevic

history is mandatory and this may identify other medical conditions unassociated with the eating disorder.

The Examination Extra-orally, the parotid glands, facial muscles and jaw joint function are checked. The oral and dental examination should follow a standard protocol for all patients irrespective of the eating disorder. Soft tissues and gums (gingivae) should be examined prior to the teeth, lest problems with teeth disrupt a thorough examination of all the mouth. Plaque and gingivitis should be measured with recognised indices and examiners should be calibrated for diagnostic accuracy of scoring criteria. Dental erosion and caries are assessed with the aid of good lighting and dry teeth. Radiographs are usually also required, certainly at the initial presentation. Once the dentist has gained all the information, the patient is informed about the oral condition and discussion can ensue as how best to proceed with treatment.

Non-Interventionist Dental Management The dentist can make several recommendations to minimise the effect of dietary acid and vomitus harming the mouth, see Table 5. If erosion is present, the patient needs to be informed about the causes and given appropriate advice as to how to reduce its effects. Unless the eroded surfaces are visible, patients do not usually complain about them. Therefore, once explanation of the causes of dental erosion are made, its progress can be monitored by way of study casts which require an impression, photographs or a putty index. A review one year after initial presentation and comparison with the previously mentioned techniques will help determine if the erosion has progressed. Dental decay can be controlled by correct oral hygiene techniques and dietary advice. Naturally occurring sugars in milk and fruit are virtually non-cariogenic, whereas sucrose, glucose, fructose and maltose have all been associated with dental decay. Both the frequency and quantity of sugar intake should be reduced to lessen the risk of decay [Rugg-Gunn, 1996]. The mean intake of diet soda was more than three litres per day in a group of bulimics resident in an inpatient unit [Hetherington et .al., 1994]. Such drinking patterns and chaotic eating habits will only serve to increase risk of decay and possibly erosion. Hygienist phase therapy to professionally remove deposits and instruct on effective plaque control will help lessen the risk of both periodontal health and caries. Diet sheets are helpful in identifying the time and pattern of food consumption, but it is unlikely that eating disordered patients would comply with a request percieved to be too intrusive.

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

197

Table 5 Advice to minimise dental problems in eating disorders Raise awareness of the role of plaque and diet in dental caries: • • •

The importance of effective plaque control Reduction in frequency of intake of sweet foods, snacks etc but balance this with any programme to improve weight Maintain close liaison with dietitician/nutritionist

Raise awareness of acidic sources in the diet: • • • • • •

Reduce intake of acidic drinks, such as carbonated colas and fresh fruit juice (low calorie drinks are still potentially erosive) Increase consumption of water (carbonated or fizzy water has low erosive potential) Use of a straw will reduce fluid contact with tooth surfaces Monitor intake of fresh fruit and especially acidic fruits such as citrus, sour apples Alcohol eg white wine, cider, mixers (tonic and colas) Vinegar dressing, pickled foods

Post-vomiting methods to increase pH and improve oral milieu: • •

After self-induced vomiting (SIV), chew gum, rinse mouth with water or milk Gentle tooth brushing with a small amount of desensitising or bicarbonate tooth paste after SIV may be safe

Check that medication does not provoke dry mouth or nausea For salivary hypofunction/dry mouth •

Prescribe neutral artificial saliva or sialogogue pastilles

Toothbrushing after vomiting is generally regarded as inadvisable as the softened, demineralised dentine is more susceptible to tooth brush abrasion. Two research groups independently assessed post-vomiting oral hygiene practices with the degree of erosive wear and reported that that the erosion was no worse in the eating disordered subjects who brushed immediately after SIV [Robb et.al., 1995; Milosevic et.al., 1997]. Eroded palatal sites are probably not easily brushed but buccal sites (facing the cheeks) are more readily abraded.

Interventionist Treatment Application of desensitising pastes on exposed hypersensitive dentine is a short term solution whereas greater durability will be achieved by sealing and impregnating the dentine

Alex Milosevic

198

surface with a commercially available un-filled resin. This can only be done in the dental office.

Placement of Dental Composite Filled Resin One of the most effective methods of replacing worn/eroded surfaces is by way of bonding composite resin. Dental composite is a tooth coloured filling material, made in different shades, comprising quartz filler particles embedded in resin. This allows it to be closely matched to patient’s teeth. The major advantages are its reversibility and ease of use because bonding to the tooth surface precludes the need to cut the tooth. Paradoxically the surface needs to be acid etched, usually with ortho-phosphoric acid, in order to key or roughen the surface so that the bonding resin can penetrate and retain the overlying composite resin which has the same polymeric structure as the bonding resin. Thus the cross linkage of resins produces a strong and hard wearing restoration and the resin penetration into dentine and/or enamel gives good to excellent micro-mechanical adhesion. Furthermore, composite resin is not acid soluble and thus will not dissolve in subjects who continue to engage in SIV. Composite provides reduction in sensitivity, improvement in aesthetics and protection from further erosion.

Resin Bonded Ceramic Crowns These are an extension of the above method as porcelain or ceramic crowns are attached to eroded teeth using bonding technology. Also known as dentine bonded crowns, they require minimal preparation of the teeth and are additionally regarded as reversible. They are indicated where there is greater loss of tooth substance requiring bulk coronal build-up. The fitting surface of the crown has to be etched in the laboratory in order for the bonding resin to impregnate the porcelain and thus retain the crown on the tooth [Milosevic and Jones, 1996].

Conventional Ceramo-Metal Crowns These crowns need sufficient tooth structure in order to retain the crown and allow adequate preparation to be made. Given that eroded teeth may have lost significant tooth substance, conventional crowns can be difficult.

Dento-Alveolar Compensation A further problem is dento-alveolar compensation secondary to acid erosion. Despite the teeth getting thinner and shorter, a gap between the upper and lower teeth does not automatically occur as there is a tendency for teeth to re-establish contact and physically erupt to maintain contact with opposing teeth. It appears that in some cases the rate of wear

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

199

and eruption are equal, although in some individuals it may not occur. This dento-alveolar compensation causes difficulty when patients wish to regain longer teeth as there is no space to do so. Space can be gained by the interim use of a Dahl appliance or an anterior bite platform, which intrudes the anterior teeth and allows eruption of the posterior teeth. This may take several months and depends on the skeletal and incisal relationships and degree of space needed for build up of the eroded front teeth.

Case 1 This male, aged 28 years at initial presentation in 1990, was referred to the dental hospital as he complained of pain and having lost fillings. He was diagnosed with gingivitis, caries (decay) and erosion although the latter was attributed to acidic drinks. His treatment included an extraction, both amalgam and tooth coloured restorations as well as hygienist phase therapy and palatal veneers to the upper four incisors. It was only after this treatment had been completed that he volunteered he had “psychiatric” problems and had taken an overdose resulting in hospitalisation. Furthermore, the patient stated he had “regurgitated” for the previous six years although he had only received treatment for this for six months. His then medication was Amitryptilline 10mg daily. He attended for review over several years and at one stage presented with bilaterally enlarged parotid salivary glands which was worse on the right. During this time the dental erosion progressed, other teeth became carious and at least one bicuspid became abscessed requiring root canal therapy. By 1996, his medication changed to Fluoxetine, Chlorpromazine Hydrochloride and Propranolol with cessation of the Amitryptilline. Unfortunately, he continued to engage in occasional SIV, his oral hygiene was not well maintained and his dietary intake of sugary food continued. Consequently, teeth became carious around the existing restorations resulting in larger restorations and the erosion progressed. The parotid enlargement is illustrated in figure 1 and the appearance of his teeth is shown in figure 2.

Fig 1. Facial view of bilateral enlarged parotid glands in the male described in Case 1.

200

Alex Milosevic

Fig 2. Intra-oral view of eroded upper teeth in Case 1. Note the proud amalgam restoration indicating that tooth substance has dissolved from around the amalgam.

Fig 3. The palate appears to have a hematoma probably caused by the fingers traumatising the soft tissues during bouts of SIV. Female aged 26 years.

Case 2 This patient, a female nurse, was aged 26 years when first seen by the specialist. She was not taking any medication although she admitted to SIV over a ten year period. Her main complaint was of the poor dental appearance and inability to incise food because of the significant erosion to the front teeth, which is shown in figures 4 and 5. She was worried that the teeth would disappear. On examination, she had good plaque control and a generally

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

201

caries free dentition. The upper teeth were very eroded whereas the lower teeth less so. Indeed, the upper teeth exhibited deeper dentine and the pulps were visible on several teeth, see figure 5. Despite the significant erosion, dento-alveolar compensation had not occurred, and it can be seen from figure 4 that space is available to lengthen the short upper incisors.

Fig 4. Front view of Case 2 showing the severely eroded front teeth and the inability of the incisors to meet.

Fig 5. Case 2, palatal view of the upper teeth, showing the pulpal area of the teeth. Sensitivity is likely once most of the dentine has been eroded away.

It was decided to restore the upper teeth with resin bonded crowns and use a commercially available kit. This was carried out in stages, with restoration of the upper six anterior teeth followed by the posterior teeth. Space was not available on three teeth and so these were left untouched. The patient was delighted with the result and the crowns, although somewhat experimental at the time of placement, have proven a valuable method of restoring severely eroded teeth. Follow up several years later revealed the crowns had functioned well, although the margins had stained as the early bonding resin was permeable to food dyes eg tea, coffee, red wine etc.

202

Alex Milosevic

References Albino JE, Curet JJ, Fox RN. Variables discriminating individuals who seek orthodontic treatment. Journal of Dental Research, 1989; 60, 1661-1667. Altshuler BD, Dechow PC, Waller DA, Hardy BW. An investigation of the oral pathologies occurring in bulimia nervosa. International Journal of Eating Disorders, 1990; 9, 191199. Batsakis JG, McWhirter JD. Non-neoplastic diseases of the salivary glands. American Journal of Gastroenterology, 1972, 57; 226-247. Birkeland K, Boe OE, Wisth PJ. Relationship between occlusion and satisfaction with dental appearance in orthodontically treated and untreated groups. A longitudinal study. Europen Journal of Orthodontics, 2000; 22, 509-518. Bos A, Hoogstraten J, Prahl-Andersen B. Expectations of treatment and satisfaction with dentofacial appearance in orthodontic patients. Journal of Orthodontics and Dentofacial Orthopedics, 2003; 123, 127-132. Bretz WA, Krahn DD, Drewnowski A, Loesche WJ. Salivary levels of putative cariogenic organisms in patients with eating disorders. Oral Microbiology and Immunology, 1989; 4, 230-232. Bretz WA, Krahn DD, Drury M, Schork N, Loesche WJ. Effects of fluoxetine on the oral environment of bulimics. Oral Microbiology and Immunology, 1993; 8, 62-64. Brown S, Bonifazi DZ. An overview of anorexia and bulimia nervosa and the impact of eating disorders on the oral cavity. Compendium of Continuing Education in Dentistry, 1993; 14, 1594-1608. Burke FJT, Bell TJ, Ismail N, Hartley P. Bulimia: implications for the practising dentist. British Dental Journal, 1996; 180, 421-426. Burke RC. Bulimia and parotid enlargement – case report and treatment. The Journal of Otolaryngology, 1986; 15, 49-51. Crossley ML, Shearer AC, Mellor AC, Bridgeman AM. Treatment planning for the problem patient: Restorative, ethical, legal and psychological perspectives. Dental Update, 2001; 28, 241-246. Cawson RA. Essentials of Dental Surgery and Pathology. Fifth Edition. London: Churchill Livingstone; 1991. Cunningham SJ. The psychology of facial appearance. Dental Update, 1999; 26, 438-442. Du Plessis DJ. Parotid enlargement in malnutrition. South African Medical Journal, 1956; 30, 700-703. Faine MP. Recognition and management of eating disorders in the dental office. Dental Clinics of North America, 2003; 47, 395-410. Gillard BK, Simbala JA, Goodlick L. Reference intervals for amylase isoenzymes in serum of infants and children. Clinical chemistry, 1983; 29, 1119-1123. Harwood P, Newton T. Dental aspects of bulimia nervosa: Implications for the health care team. European Eating Disorders Review, 1995; 3, 93-102. Hasler JF. Parotid enlargement: A presenting sign in anorexia nervosa. Oral Surgery Oral Medicine Oral Pathology, 1982; 53, 567-573.

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health

203

Hellström I. Oral complications in anorexia nervosa. Scandinavian Journal of Dental Research, 1977; 85, 71-86. Hempen I, Lehnert P, Fichter M, Teufel J. Hyperamylasaemia in anorexia and bulimia: A clue to pancreatic disease? Deutsche Mediczinal Wochenschrift, 1989; 114, 1913-1916. Helm S, Krieborg S, Solow B. Psychological implications of malocclusion. American Journal of Orthodontics, 1985; 87, 110-118. Hetherington MM, Altemus M, Nelson ML, Eating behaviour in bulimia nervosa: multiple meal analysis. American Journal of Clinical Nutrition, 1994; 60, 864-873. Humphries LL, Adams LJ, Eckfeldt JH, Levitt MD, McLain CJ. Hyperamylasemia in patients with eating disorders. Annals of Internal Medicine, 1987; 106, 50-52. Hurst PS, Lacey JH, Crisp AH. Teeth, vomiting and diet: a study of the dental characteristics of seventeen anorexia nervosa patients. Postgraduate Medical Journal, 1977; 53, 298305. Johansson I, Saellström A-K, Rajan BP, Parameswaran A. Salivary flow and dental caries in Indian children suffering from chronic malnutrition. Caries Research, 192; 26, 38-43. Jones RRH, Cleaton-Jones P. Depth and area of dental erosions and dental caries in bulimic women. Journal of Dental Research, 1989; 68, 1275-1278. Kakizaki G, Sasahara M, Soeno T, Shoji S, Ishidate T, Senoo A. Mechanism of the pancreasparotid gland interaction. American Journal of Gastroenterology, 1978; 70, 635-644. Keith O, Flint S. Lingual abscess in a patient with anorexia nervosa. British Dental Journal, 1989; 167, 71-72. Kidd EAM, Joyston-Bechal S. Essentials of dental caries: The disease and its management. First edition. Bristol: Wright, 1987. Klima RJ, Wittemann JK, McIver JE. Body image, self-concept and the orthodontic patient. American Journal of Orthodontics, 1979; 75, 507-516. Kronvall P, Theander S. Elevation of serum salivary amylase in bulimia. In Hardoff D, Chigier E, editors, Eating Disorders in Adolescents and Young Adults. London: Freund; 1989. Kronvall P, Fahy TA, Isaksson A, Theander S, Russell GFM. The clinical relevance of salivary amylase monitoring in bulimia nervosa. Biological Psychiatry, 1992; 32, 156163. Levin PA, Falko JM, Dixon K, Gallup EM, Saunders W. Benign parotid enlargement in bulimia, 1980; 93, 827-829. Liew VP, Frisken KW, Touyz SW, Beumont PJV, Williams H. Clinical and microbiological investigations of anorexia nervosa. Australian Dental Journal, 1991; 36, 435-441. McKay GS, Yemm R, Cadden SW. The structure and function of the temporomandibular joint. British Dental Journal, 1992; 173, 127-132. McLain JB, Proffit WR. Oral health status in the US: Prevalence of malocclusion. Journal of Dental Education, 1985; 49, 386-396. Millar K, Geddes DAM, Hammersley RH, Boddy JM, Kelly J. Is salivary flow related to personality? British Dental Journal, 1993; 175, 13-19. Milosevic A. Eating disorders and the dentist. British Dental Journal, 1999; 186, 109-113. Milosevic A, Brodie DA, Slade PD. Dental erosion, oral hygiene and nutrition in the eating disorders. International Journal of Eating Disorders, 1997; 21, 195-199.

204

Alex Milosevic

Milosevic A, Dawson LJ. Salivary factors in vomiting bulimics with and without pathological tooth wear. Caries Research, 1996; 30, 361-366. Milosevic A, Jones C. Use of resin-bonded ceramic crowns in a bulimic patient with severe tooth erosion. Quintessence International, 1996; 27, 123-127. Milosevic A, Slade PD. The orodental status of anorexics and bulimics. British Dental Journal, 1989; 167, 66-70. Milosevic A, Thomas J, Mitzman S. Satisfaction with dento-facial appearance in the eating disorders. European Journal of Prosthodontics and Restorative Dentistry, 2004;11, 125128. O’Reilly RL, O’Riordan JW, Greenwood A. Orthodontic abnormalities in patients with eating disorders. International Dental Journal, 1991; 41, 212-216. Philipp E, Willershausen-Zönnchen B, Hamm G, Pirke K-M. Oral and dental characteristics in bulimic and anorectic patients. International Journal of Eating Disorders, 1991; 10, 423-431. Robb ND, Smith BGN, Geidrys-Leeper E. The distribution of erosion in the dentitions of patients with eating disorders. British Dental Journal, 1995; 178, 171-175. Roberts MW, Li S-H. Oral findings in anorexia nervosa and bulimia nervosa: a study of 47 cases. . Journal of the American Dental Association, 1987; 115, 407-410. Rugg-Gunn AJ. 2. Diet and dental caries. In: Murray JJ, editor. The Prevention of Oral Disease.3rd Edition. Oxford: Oxford University Press; 1996; 3-31. Rytőmaa I, Järvinen V, Kanerva R, Heinonen OP. Bulimia and tooth erosion. Acta Odontologica Scandinavica, 1998; 56, 36-40. Shaw WC, Rees O, Dawe M, Charles CR. The influence of dento-facial appearance on the social attractiveness of young adults. American Journal of Orthopedics, 1985; 87, 21-26. Simmons MS, Grayden SK, Mitchell JE. The need for psychiatric-dental liaison in the treatment of bulimia. American Journal of Psychiatry, 1986; 143, 783-784. Taylor VE, Sneddon J. Bilateral facial swelling in bulimia. British Dental Journal, 1987; 163, 115-117. Touyz SW, Liew VP, Tseng P, Frisken K, Williams H, Beumont PJV. Oral and dental complications in dieting disorders. International Journal of Eating Disorders, 1993; 14, 341-348. Tylenda CA, Roberts MW, Elin RJ, Li S-H, Altemus M. Bulimia nervosa: its effect on salivary chemistry. Journal of the American Dental Association, 1991; 122, 37-41.

Index

A acceptance, 8, 12, 45, 48, 49, 52, 54, 55, 56, 135 access, 51, 53, 102, 161, 163 accommodation, 54 accountability, 58 accounting, 46, 151, 169 acculturation, 50 accumulation, 187 accuracy, 156, 173, 196 achievement, 15 acid, xi, 73, 78, 79, 83, 85, 185, 189, 191, 192, 193, 196, 198 activation, 65, 73, 76, 79, 182 adaptation, 12, 26, 31, 124, 141 adenosine, 78, 89 adhesion, 198 adipose, 75 adiposity, 69 adjustment, 12, 15 adolescence, 9, 12, 15, 21, 22, 92, 173, 182, 194 adolescent drinking, 174 adolescent female, 156, 157, 172, 180 adolescents, 5, 7, 8, 12, 13, 14, 18, 20, 22, 23, 24, 26, 92, 93, 94, 95, 96, 100, 102, 103, 107, 137, 140, 176, 182 adulthood, 12, 22, 114, 194 adults, 2, 13, 85, 89, 146, 158, 161, 204 advertisements, 183 advertising, 179, 183 aesthetics, 194, 198 affect, xi, 6, 24, 50, 87, 93, 94, 95, 157, 162, 163, 166, 168, 170, 173, 174, 176, 177, 178, 182, 183, 185, 187, 194 affective disorder, 3, 26

African American women, 177 African Americans, 173 age, 6, 9, 10, 14, 28, 42, 45, 46, 53, 92, 93, 98, 99, 101, 109, 114, 152, 162, 190, 192, 193 aggression, 97, 98, 100 aggressive behavior, 9, 95, 96, 100 aging, 72, 85 agonist, 76 albumin, 79, 187 alcohol, 5, 6, 7, 10, 11, 13, 14, 96, 100, 101, 167, 168, 170, 175, 177, 178, 179, 181, 182, 183 alcohol abuse, 7, 10, 11, 14, 101, 167, 168, 170 alcohol consumption, 96, 167, 183 alcohol problems, 182 alcohol use, 167, 168, 175, 177 alcoholics, 178 alienation, 5 alternative, 32, 48, 49, 173 amalgam, 199, 200 ambivalence, 99 ambivalent, 14 amenorrhea, 92 American Psychiatric Association, 136, 156, 177 American Psychological Association, 157, 177 amino acids, 79, 83, 89, 142 amylase, 187, 202, 203 anemia, 83 anger, 11, 16, 98 animals, 74, 76, 177, 183 annihilation, 2 anorexia, vii, viii, ix, 1, 3, 4, 5, 6, 7, 8, 9, 10, 13, 15, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 31, 32, 33, 34, 37, 38, 39, 41, 42, 43, 44, 45, 46, 47, 50, 51, 52, 53, 54, 55, 57, 58, 59, 61, 63, 64, 65, 66, 67, 68, 69, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 82, 83, 85, 86, 87, 89, 90, 91, 92, 93, 94,

Index

206

96, 101, 102, 103, 107, 113, 136, 137, 138, 139, 140, 142, 156, 161, 177, 186, 187, 189, 194, 195, 202, 203, 204 ANOVA, 113 antagonism, 76 antidepressant, 3, 17, 24 antisocial behavior, 8, 180 antisocial personality, 8, 181 anxiety, 3, 6, 16, 18, 34, 35, 101, 134, 162, 170, 176, 179, 187 anxiety disorder, 6, 18 apoptosis, 78, 88 appetite, 31, 32, 64, 66, 67, 68, 69, 72, 78, 81, 82, 83, 84, 88, 89, 92, 93, 97, 115, 117, 133 appraisals, 141 argument, 160, 165, 175 arson, 100 Asia, 42 aspiration, 187 assessment, 33, 34, 36, 37, 66, 68, 84, 132, 133, 134, 136, 142, 149, 155, 156, 157, 167, 168, 193 association, 7, 15, 151, 152, 163, 189 asthenia, 89 asymptomatic, 127 ATP, 78, 89 attachment, 95, 102, 188, 189 attacks, 94 attention, 52, 56, 68, 71, 73, 77, 100, 135, 146 attitudes, viii, ix, 5, 8, 23, 41, 54, 56, 105, 106, 109, 112, 113, 122, 125, 127, 132, 134, 135, 136, 137, 180, 183 attractiveness, 161, 162, 171, 204 Australia, 41, 47, 58 authority, viii, 41, 49, 53, 56, 57, 58 autonomy, 12, 15, 99, 102 autopsy, 20 availability, 57, 65, 71, 76, 79, 86 avoidance, 92, 101, 166 awareness, 12, 42, 97, 114, 164, 171, 179, 197

B Barbados, 136 bargaining, 44, 47, 60, 61 barriers, 111 barter, 44 basic research, 140 Beck Depression Inventory, 30, 32, 38 behavior, vii, x, 1, 2, 3, 5, 6, 8, 9, 10, 11, 12, 13, 14, 15, 18, 19, 20, 21, 22, 24, 25, 35, 37, 92, 93, 94,

95, 96, 97, 98, 100, 106, 108, 109, 110, 111, 112, 113, 115, 116, 120, 122, 123, 124, 125, 127, 133, 134, 135, 136, 137, 138, 139, 140, 142, 143, 159, 160, 161, 166, 167, 168, 169, 170, 171, 172, 174, 175, 176, 177, 178, 179, 180, 181, 183 behavior modification, 177 behavior therapy, x, 95, 106, 139, 178 behavioral aspects, 37 behavioral change, 134 behavioral sciences, 156 beneficial effect, 65 benign, 67 beverages, 189, 191 bias, 37, 132 bicarbonate, 188, 197 bicuspid, 199 binding, 79, 84 bingeing, 180, 193 biological responses, 75 biopsy, 187 blame, 102 bleeding, 186, 188, 189 blocks, 97 blood, 71, 79 blood-brain barrier, 79 BMA, 161, 178 BMI, vi, vii, x, 1, 92, 101, 110, 113, 114, 128, 129, 145, 147, 149, 151, 152, 154 body, vii, viii, ix, x, 1, 3, 4, 7, 9, 11, 12, 15, 17, 23, 25, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 41, 42, 50, 56, 57, 70, 75, 77, 78, 80, 85, 91, 92, 93, 94, 97, 98, 99, 110, 111, 112, 113, 116, 123, 125, 127, 128, 129, 132, 134, 135, 136, 141, 142, 143, 145, 146, 147, 148, 149, 151, 152, 153, 154, 155, 157, 158, 161, 162, 163, 164, 168, 171, 172, 177, 178, 179, 181, 183, 184, 192, 194 body dissatisfaction, x, 123, 127, 132, 145, 146, 147, 148, 151, 152, 153, 154, 155, 157, 161, 162, 163, 164, 171, 172, 183, 184 body fat, 70, 80, 155 body image, vii, viii, ix, 5, 9, 25, 27, 28, 29, 30, 31, 32, 33, 35, 36, 37, 42, 91, 92, 93, 110, 111, 112, 123, 125, 127, 128, 129, 135, 136, 141, 142, 143, 157, 161, 178, 194 body mass index, vii, 1, 7, 129 body shape, 4, 28, 34, 116, 146, 147, 155, 162, 181 body size, 123, 127, 145, 148, 161, 179 body weight, 28, 35, 75, 77, 78, 85, 92, 123, 128, 145, 146, 148, 149, 153, 155, 177 bonding, 23, 198, 201

Index bonds, 93, 99 borderline personality disorder, 4, 5, 8, 10, 19, 23, 25, 153, 156 boredom, 170, 173, 174 bowel, 82 boys, ix, 14, 15, 91, 92, 93, 94, 99, 101, 103, 194 bradycardia, 92 brain, 64, 70, 71, 73, 75, 76, 79, 80, 86, 87, 90, 140 Brazil, ix, 105, 106, 107, 114 breakdown, 191 breathlessness, 67 bulimia, vii, viii, ix, x, 1, 3, 4, 7, 9, 10, 11, 13, 15, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 31, 32, 33, 34, 37, 38, 39, 61, 91, 93, 94, 95, 102, 105, 107, 109, 130, 136, 137, 138, 139, 140, 141, 142, 143, 156, 157, 159, 162, 173, 179, 180, 182, 183, 187, 188, 189, 193, 194, 195, 202, 203, 204

C cachexia, 68, 72, 74, 78, 80, 87, 88, 89, 90 calcium, 112, 120, 186, 187 calibration, 189 caloric intake, 72, 79, 89, 163 calorie, 65, 72, 79, 92, 197 Canada, 11, 60, 88 cancer, viii, 63, 64, 65, 66, 67, 68, 69, 71, 72, 74, 75, 76, 77, 78, 79, 81, 82, 83, 84, 86, 87, 88, 89 cancer cells, 82 candidates, 79 cannabinoids, 77 carbohydrate, 72, 119, 142, 192 case study, 45 cell, 82, 89, 90 central nervous system, 66, 82 ceramic, 198, 204 CFI, 173 chemotherapy, 83 childhood, 7, 93, 101 children, 12, 13, 14, 23, 24, 26, 93, 96, 98, 99, 101, 102, 107, 142, 163, 173, 177, 179, 183, 187, 194, 202, 203 cholesterol, 142 chronic irritation, 186 chronic obstructive pulmonary disease, 64 chronic renal failure, 71, 75, 76 chronic stress situations, 93 cirrhosis, 64, 83 civil liberties, 56 classification, 36, 101, 113, 127, 173

207

classroom, 139 cleavage, 72 clients, 166 clinical assessment, 142, 145 clinical disorders, 102 clinical judgment, 22 clinical presentation, 39 clinical psychology, 25 clinical trials, 17, 68, 77, 81 cluster, 3, 7 cluster analysis, 4 cocaine, 70, 74, 167, 178 coding, 132 coenzyme, 73, 85 coercion, 44, 45, 46, 50, 57 cognitive biases, 24 cognitive map, 169 cohort, 6, 67, 89 collaboration, 13, 97 combination therapy, 88 commercials, 163 common symptoms, 66 communication, 12, 13, 16, 47, 85, 195 community, 2, 14, 21, 38, 44, 48, 49, 51, 52, 54, 59, 148, 149, 157 comorbidity, 3, 10, 18, 21, 22, 23, 25, 39, 94, 137, 158 Comparative Fit Index, 174 compatibility, 36 compensation, 198, 201 competitive sport, ix, 91 complexity, 69, 73, 134 compliance, 22, 44, 49, 56, 60, 193 complications, 6, 46, 139, 203, 204 components, 13, 37, 79, 108, 133, 151, 154 composition, xi, 72, 111, 117, 185 comprehension, 3 compulsion, 35, 97 compulsive behavior, 37, 98 concentration, 4, 80, 84, 186, 187, 188 conceptual model, 60 conceptualization, 151 concordance, 160 conduct, 4, 6, 8, 9, 16, 50, 173 conduct disorder, 8 confidence, 17, 107, 124, 154, 155 confidence interval, 107, 154, 155 confidentiality, 195 configuration, 150, 151 conflict, 93, 94, 98, 99, 101, 102

Index

208

conflict avoidance, 93, 94 conformity, 60 confrontation, 138 consciousness, 157 consensus, 36, 147 consent, viii, 41, 46, 47, 48, 57, 195 conspiracy, 54 consumers, 50, 107, 164 consumption, 106, 108, 110, 112, 113, 116, 117, 119, 120, 132, 134, 163, 167, 177, 179, 189, 192, 193, 196, 197 consumption patterns, 106 context, 35, 36, 42, 49, 53, 146, 162, 163, 164, 179 continuity, 14 control, vii, viii, 1, 4, 5, 6, 16, 18, 20, 22, 32, 33, 34, 38, 41, 43, 49, 50, 51, 52, 53, 56, 57, 58, 66, 73, 76, 80, 84, 99, 102, 117, 120, 123, 124, 128, 133, 141, 149, 150, 163, 167, 173, 174, 178, 188, 190, 192, 194, 196, 197, 200 control group, 120, 188, 192 controlled trials, 17, 81 convergence, 54, 163 conversion, 60 conviction, 31, 36, 37 COPD, 65, 67 coping, viii, 2, 12, 94, 134, 179 correlation, 113, 128, 129, 146, 152, 153, 155, 190 correlation coefficient, 113 corticosteroids, 77, 78 corticotropin, 74 costs, 94 counseling, 111, 135, 139 covering, 192 crisis management, viii, 2 critical period, 181 criticism, 94 cross-sectional study, 119 CSF, 76, 86, 87 culture, 134, 163, 164, 171, 175, 180, 184 currency, 51 cycling, 96, 114 cytokines, ix, 63, 75, 76, 77, 78, 84

D data analysis, 151 death, vii, viii, 1, 2, 4, 5, 9, 10, 13, 14, 15, 16, 19, 25, 41, 42, 64, 67, 69, 80, 84, 88, 99 death rate, viii, 41 decay, xi, 185, 189, 191, 192, 193, 196, 199

decision making, viii, 2, 195 decisions, 43, 46, 54, 94, 102 defense, 82, 97 deficit, 117 definition, 2, 42, 65, 109, 116 delusion, 35, 36 delusions, 28, 36, 39 demographic change, 106 demographic data, 148 denial, ix, 12, 28, 51, 55, 91, 93, 125 Denmark, 8, 19, 139 density, 99, 142 dental caries, 189, 192, 203 dental plaque, xi, 185, 188, 193 dentist, xi, 185, 195, 196 Department of Health and Human Services, 23 dependent variable, 150, 151 depolarization, 76 depression, 3, 8, 9, 10, 12, 15, 22, 24, 37, 46, 66, 93, 94, 95, 176, 187, 194 depressive symptoms, 4, 9, 18 deprivation, 101, 177 derivatives, 78 desire, 54, 65, 114, 123, 172 detention, 50 developed countries, vii, 13, 107, 108, 109, 114 developed nations, ix, 105 deviation, 150, 154 diabetes, 71 diabetic patients, 82 Diagnostic and Statistical Manual of Mental Disorders, viii, 27, 28, 110, 136, 177 diagnostic criteria, viii, 6, 27, 28, 93, 116, 133, 148 dialysis, 71, 84, 86 diet, ix, 34, 35, 79, 105, 106, 108, 111, 112, 115, 117, 120, 122, 123, 125, 128, 134, 137, 163, 164, 187, 192, 196, 197, 203 dietary fat, 193 dietary habits, ix, 64 dietary intake, 189, 199 dieting, 39, 114, 115, 123, 133, 156, 160, 161, 162, 163, 164, 165, 170, 171, 172, 173, 174, 175, 179, 180, 182, 184, 204 differentiation, 61, 112 digestion, 65, 68, 71 direct measure, 147 disabilities, 101 disability, 101 disaster, 19 discipline, 96

Index disclosure, 195 discomfort, 35, 125, 153, 187 disorder, ix, x, xi, 3, 6, 7, 8, 9, 10, 14, 16, 17, 18, 20, 21, 22, 23, 25, 26, 29, 37, 38, 39, 45, 51, 53, 57, 86, 91, 92, 93, 94, 96, 97, 99, 100, 101, 102, 107, 108, 109, 113, 114, 116, 120, 128, 131, 134, 135, 136, 137, 138, 141, 143, 145, 146, 147, 148, 153, 155, 156, 157, 158, 160, 161, 162, 163, 164, 169, 171, 174, 175, 177, 178, 181, 183, 185, 187, 189, 190, 191, 192, 193, 194, 195, 196 displacement, 187 disposition, 161, 176 dissatisfaction, x, 4, 12, 28, 127, 128, 137, 145, 146, 147, 148, 150, 153, 154, 155, 161, 162, 163, 164 dissociation, 74, 195 distress, x, 2, 3, 7, 32, 33, 58, 102, 133, 147, 153, 155, 159, 165, 166, 169, 175, 176, 179 distribution, 31, 119, 125, 126, 191, 204 diuretic, 133 diversity, 44 divorce, 9, 47, 60 dizygotic, 160, 166 dizygotic twins, 160, 166 DMF, 192 docosahexaenoic acid, 78 doctors, 45, 53, 54 domain, 166, 178 domestic violence, 100 dopamine, ix, 63, 81, 87 dosage, 6, 81 down-regulation, 78 dream, 123, 124 drinking pattern, 178, 196 drinking patterns, 178, 196 drug abuse, 6 drug therapy, ix, 64, 69 drugs, 3, 6, 14, 80, 81, 107, 130, 140 DSM, viii, x, 7, 20, 23, 25, 26, 27, 28, 29, 42, 92, 93, 106, 110, 115, 148, 149, 150, 156, 165, 180 DSM-II, 7, 20, 23, 25, 26, 29 DSM-III, 7, 20, 23, 25, 26, 29 DSM-IV, viii, x, 25, 27, 28, 29, 93, 106, 110, 115, 148, 149, 150, 156, 165 duodenum, 71 durability, 197 duration, 7, 45, 53, 80, 111, 116, 135, 140, 189, 190 dysphagia, 66

209

E eating, vii, viii, ix, x, xi, 1, 2, 3, 6, 7, 8, 9, 10, 11, 14, 15, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 32, 34, 39, 41, 42, 45, 51, 53, 56, 57, 65, 67, 68, 69, 71, 91, 92, 93, 94, 95, 97, 100, 101, 102, 103, 105, 106, 107, 108, 109, 110, 111, 112, 113, 114, 115, 116, 117, 120, 122, 123, 124, 125, 127, 128, 130, 131, 132, 133, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 145, 146, 147, 148, 150, 153, 154, 155, 156, 157, 158, 159, 160, 161, 162, 163, 164, 165, 166, 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179, 180, 181, 182, 183, 184, 185, 186, 187, 188, 189, 190, 191, 192, 193, 194, 195, 196, 197, 202, 203, 204 eating disorders, vii, viii, ix, 1, 2, 3, 7, 8, 10, 11, 14, 15, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 39, 42, 91, 92, 93, 94, 95, 97, 101, 102, 103, 107, 109, 114, 134, 135, 136, 137, 138, 139, 140, 141, 143, 145, 146, 147, 148, 153, 155, 156, 157, 158, 162, 167, 170, 176, 177, 179, 180, 181, 186, 188, 189, 192, 193, 194, 195, 197, 202, 203, 204 ego, 94 eicosapentaenoic acid, 78, 88 elderly, 79, 83 electrolyte, 92 emergence, 53, 102, 156, 159 emotion, 2, 166 emotional disorder, 100 emotional distress, 147 emotional state, 4, 93 emotions, ix, 2, 91, 97, 111, 166 empathy, 16 employment, 11 encouragement, 163 endocrine, 89, 92 endorphins, 177 endorsements, 172 energy consumption, 108, 117, 131 England, 22, 60, 178, 195 enlargement, xi, 185, 187, 188, 199, 202, 203 entanglements, 102 enthusiasm, 99 environment, x, 14, 16, 45, 49, 56, 57, 77, 95, 99, 159, 161, 163, 164, 180, 202 environmental effects, 161, 164 environmental factors, x, 2, 159, 161, 162, 164, 168, 175 environmental impact, 16

Index

210

environmental influences, 160, 180 enzymes, 71 epidemic, vii epidemiology, 139, 180, 183 erosion, xi, 185, 186, 188, 189, 190, 191, 192, 193, 196, 197, 198, 199, 200, 203, 204 ethics, 57, 195 ethnicity, 179, 184 etiology, 145, 157, 179, 180, 191 Euro, 202 Europe, 2, 24, 42, 65 everyday life, 56 evidence, viii, 5, 9, 15, 17, 34, 36, 60, 63, 71, 73, 74, 75, 81, 82, 85, 136, 160, 161, 162, 163, 164, 165, 166, 167, 168, 173, 174, 178, 182, 187, 189, 192 evolution, 67, 113, 126, 127 examinations, 93 excitation, 87 exclusion, 37, 80 exercise, 42, 49, 50, 92 experimental design, 169 experts, 50 exposure, 13, 15, 171 expression, ix, 12, 35, 43, 49, 50, 51, 56, 64, 74, 98, 100, 102, 124, 164 externalization, 180 externalizing disorders, 176 extraction, 186, 199 extraversion, 166

F facial expression, 97 facial muscles, 196 factor analysis, 151, 165, 166 failure, viii, 6, 15, 32, 52, 63, 64, 65, 68, 74, 76, 79, 81, 83, 84, 86, 87, 147, 156, 176 family, 2, 9, 12, 13, 16, 23, 24, 34, 36, 42, 43, 44, 48, 49, 53, 54, 55, 83, 93, 94, 96, 97, 98, 99, 100, 101, 102, 148, 173, 179 family conflict, 93 family environment, 12 family members, 36, 48, 49, 83, 99 family therapy, 96, 97, 98, 99, 102 fast food, 120, 163 fasting, 28, 30, 34, 35, 37, 42, 92, 115, 123, 130 fat, 4, 30, 32, 33, 35, 36, 72, 73, 77, 85, 93, 98, 122, 123, 124, 142, 163, 187 fatty acids, 142 fear, 4, 16, 30, 36, 92, 94, 97, 98, 99, 108, 123

feedback, 71, 75 feelings, 4, 5, 12, 16, 55, 94, 99, 101, 108, 109, 112, 122, 123, 124, 125, 132, 133, 134, 135, 155, 195 females, 5, 6, 31, 107, 189 femininity, 162 fermentable carbohydrates, 191, 192 fibers, 71 filler particles, 198 Finland, 7 fish, 88 fish oil, 88 fixation, 194 flora, xi, 185, 188, 192, 194 fluctuations, 117, 123 fluid, 76, 78, 197 fluoxetine, 17, 20, 24, 193, 202 focusing, 155, 165 food, vii, viii, ix, 30, 52, 53, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 80, 81, 84, 85, 86, 87, 88, 92, 93, 95, 98, 101, 105, 106, 108, 110, 111, 112, 113, 117, 122, 123, 124, 125, 128, 131, 132, 133, 134, 135, 137, 138, 139, 141, 142, 162, 163, 164, 170, 173, 177, 178, 179, 189, 196, 199, 200, 201 food intake, viii, x, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 80, 81, 84, 85, 86, 87, 106, 108, 110, 111, 117, 131, 132, 133, 134, 138, 173 food products, 163 freedom, 50 friends, 44, 48, 49, 55, 100, 171 friendship, 68 fructose, 196 fuel, 85 fulfillment, 99

G gambling, 167, 169, 170, 175, 179, 181, 183 gastrointestinal tract, 72, 75 GATT, 61 gender, vii, 1, 92, 94, 102, 136, 141, 161, 162, 181 gender identity, 136 gene, 72, 160 genes, 159 genotype, 164 Germany, 8 gestures, 2, 8 gingivitis, 188, 189, 196

Index girls, ix, 3, 14, 15, 58, 64, 91, 92, 94, 101, 135, 146, 153, 162, 181, 183, 194 gland, xi, 185, 187, 188 globalization, 106 glossitis, 186 glucose, 82 goals, 111, 117 governance, viii, 42, 50, 57 grades, 15 granules, 187 group therapy, 97, 143 groups, viii, x, 4, 5, 6, 28, 29, 30, 31, 32, 33, 34, 36, 37, 49, 50, 56, 75, 80, 90, 107, 133, 136, 145, 148, 151, 152, 153, 154, 155, 157, 173, 188, 189, 190, 191, 192, 194, 197, 202 growth, 82, 89, 93, 183 growth hormone, 89 guidance, 111 guidelines, 111, 125 guiding principles, 162 guilt, 3, 15, 94, 99, 101, 120, 181 guilty, x, 95, 99, 106, 120, 122, 132, 133 gut, 73, 85

H hands, 95 harm, 4, 6, 13, 97 hate, 5, 108, 124 HE, 86, 88 healing, 15 health, xi, 2, 12, 13, 14, 18, 26, 43, 44, 45, 46, 49, 50, 51, 54, 59, 60, 68, 80, 106, 114, 135, 138, 177, 183, 185, 186, 189, 195, 196, 202, 203 health care, xi, 2, 26, 44, 50, 68, 114, 185, 195, 202 health care professionals, xi, 50, 68, 185 health problems, 186 health psychology, 60 health services, 14 health status, 135, 203 heat, 65 heat loss, 65 height, 149 hematoma, 200 hemodialysis, 67, 68, 79, 83, 85, 87 heritability, xi, 159, 160, 166, 176, 181 high fat, 72 high school, 107 hip, 16 homeostasis, 12, 73

211

Hong Kong, 139 hopelessness, 15 hormone, 69, 72, 74, 81, 89 hospice, 69, 84 hospitalization, 68, 101 host, 65, 82 human subjects, 83 hyperglycemia, 82, 89 hypertrophy, 187, 188, 193 hypothalamus, ix, 64, 69, 70, 71, 72, 74, 75, 76, 81, 86, 87 hypothesis, 10, 69, 70, 72, 79, 81, 86, 148, 153, 173, 183, 191

I iatrogenic, 16 ICD-, 92, 93, 100 idealization, 162 ideas, 35, 36, 39, 111 identification, 7, 51, 55, 170 identity, viii, ix, 11, 42, 43, 49, 54, 55, 56, 57, 59, 91, 94, 102, 150, 152, 153 idiosyncratic, 36 IL-6, ix, 63 imagery, 53 immune response, 78 immune system, 65 immunomodulatory, 78 implementation, 111, 157 impulsive, 10, 18, 20, 165, 166, 179 impulsiveness, 10, 181 impulsivity, 6, 10, 11, 23, 26, 165, 166, 167, 168, 179, 181 in vitro, 79, 88 incidence, 9, 10, 89, 94, 95, 107, 164 independence, 12, 101, 102 independent variable, 113 indication, 45, 94 indicators, 8, 11, 15, 161 indices, 80, 196 individual differences, 163, 165, 170, 171, 175, 176 induction, 13 infants, 202 inflammation, 71, 83, 84, 88, 188 influence, 15, 28, 47, 52, 68, 69, 71, 73, 75, 76, 79, 82, 84, 85, 116, 162, 169, 171, 172, 174, 176, 177, 179, 187, 194, 204 informed consent, 56, 110 ingestion, 72

Index

212 inhibition, 4, 70, 73, 75, 77, 78, 182 inhibitor, 22, 74, 90, 193 initiation, 15 injury, 11 input, 75, 135 insecurity, 93 insight, 31, 35, 36, 43, 46, 49, 52, 53, 65 instability, 4, 152, 153 institutions, 57 instruments, 29, 30, 43, 110, 172 insulation, 54 insulin, 71, 82, 84, 85, 89 integration, 37, 164, 165, 175, 176, 177 intensity, 97 intent, 10, 159 intentions, 94 interaction, 2, 34, 49, 55, 100, 164, 165, 168, 176, 203 interaction effect, 165 interaction effects, 165 interactions, viii, 41, 51, 56, 57, 75 interdependence, 65 interest, 12, 13, 65, 72, 81, 92, 108, 109, 110, 146, 187 interface, 28 internalised, 54, 56 internalization, 147, 156, 162, 163, 164, 171, 174, 179, 180 internalizing, 176 interpersonal processes, 170 interpersonal relations, 16 interpretation, viii, 41, 57, 58, 154 interval, 130, 131 intervention, viii, 6, 17, 24, 41, 51, 56, 57, 96, 109, 110, 127, 133, 134, 136, 137, 177, 182, 195 interview, 29, 52, 110, 167, 168 intimacy, 102 intravenous antibiotics, 186 invading organisms, 65 Iran, 140 Ireland, 20 iron, 112, 120 isolation, 2 Israel, 18, 58 Italy, 1, 9, 11

J Japan, 7, 23 jobs, 162

judgment, 14, 117 jurisdiction, 45 justification, 59

K kindergarten, 93, 96 knowledge, 17, 127, 134, 141, 154, 176, 195

L lack of control, 5, 28, 109, 134, 195 language, 55, 56, 57, 181 Latin America, 140 laws, 43, 45 lawyers, 48, 56 laxatives, 9, 120 lead, 12, 54, 56, 68, 69, 78, 81, 133, 147, 160, 163, 164, 169, 170, 172, 173, 175, 188, 190, 194 lean body mass, 80, 84 learning, viii, 14, 41, 56, 101, 160, 165, 169, 170, 171, 172, 174, 175, 176, 177, 182 learning process, 172 legislation, 43, 57 lens, 55, 59 leptin, ix, 63, 69, 70, 71, 73, 84, 85, 86 lesions, 186 liability, x, 159, 161, 164, 168, 175, 176 libido, 101 life course, 52 life span, 19, 181 lifestyle, xi, 53, 54, 185 lifetime, ix, 4, 6, 9, 10, 13, 29, 39, 91 ligament, 188 likelihood, x, 159, 169, 175 limitation, 80, 168 linkage, 198 links, 23 lipids, 88, 108, 117 liquids, 95 listening, 16 liver, viii, 63, 64, 65, 67, 71, 76, 79, 80, 85, 87, 88 liver cirrhosis, 64, 65, 67, 76, 79, 87 liver damage, 88 liver disease, 71, 85 liver failure, 67 liver function tests, 80 location, 191 loneliness, 15 longitudinal study, 173, 202

Index loss of appetite, 64 loyalty, 100 lumen, 71 lung cancer, 67, 83, 85, 89 lung disease, 67 lying, 9, 50 lymph, 186 lymphadenopathy, 186

M magazines, 111, 161 magnesium, 112, 120 major depression, vii, 1, 4, 18 malaise, 2 males, 2, 102, 170 malnutrition, viii, 36, 63, 64, 67, 68, 106, 187, 202, 203 malocclusion, 194 maltose, 196 management, viii, 16, 26, 41, 43, 44, 45, 47, 48, 49, 50, 51, 52, 54, 56, 59, 63, 65, 68, 88, 89, 141, 142, 191, 195, 202, 203 manipulation, 44 mapping, 45 marijuana, 78 mass, 15, 73 mass media, 15 matrix, 151, 178 meals, x, 77, 93, 101, 106, 109, 111, 112, 113, 116, 117, 118, 119, 120, 121, 122, 125, 126, 130, 131, 132, 134, 138 meanings, 36, 111, 134 measurement, 110, 111, 130, 142, 165, 168 measures, 43, 44, 45, 56, 57, 84, 110, 112, 129, 133, 134, 138, 148, 150, 152, 153, 163, 165, 166, 167, 168, 171, 172, 173, 174, 178, 180, 182, 192 meat, 66 media, 15, 24, 161, 162, 163, 183 media messages, 163 median, 112, 114, 115, 116, 117, 118, 121, 127, 133 medical expertise, viii, 41, 57 medication, 17, 98, 183, 197, 199, 200 melanocyte stimulating hormone, 74 melt, 123 melts, 122 membranes, 186 memory, 179, 183 men, ix, 7, 85, 91, 92, 93, 94, 101, 103, 141, 146, 155, 173, 178, 183

213

menstruation, 42 mental disorder, 8, 20, 21, 22, 37, 156, 180 mental health, 5, 43, 44, 45, 46, 53, 57, 58, 59 mental health professionals, 5 messenger RNA, 86 meta analysis, 160, 168 metabolism, 68, 73, 82, 85, 89 methodology, 31, 157 microinjection, 75 Middle East, 42 milk, 100, 196, 197 minority, 65 misconceptions, 112, 123, 133 modeling, 56, 170, 173, 175, 183 models, 20, 73, 74, 75, 76, 90, 111, 162, 164, 169, 171, 174 moderators, 115 mold, 50 molecules, 17, 78 monitoring, 13, 18, 203 monozygotic twins, 160, 166 mood, 3, 6, 17, 18, 98, 155, 177, 180, 183 mood disorder, 3, 6, 17 morale, 16 morbidity, viii, 42, 63, 68, 69, 82, 139, 195 mortality, viii, 5, 19, 23, 42, 63, 65, 68, 69, 82, 89, 195 mortality rate, 65 motivation, 13, 82, 123, 141, 181 motor behavior, 169 moulding, 55 movement, 2, 101 movement disorders, 101 mRNA, 74, 75 MTMM, 167 mucosa, 186 mucous membrane, 186 mucous membranes, 186 multidimensional, 2, 103, 138 multiple regression, 174 multiple sclerosis, 96 mumps, 187 mutual respect, 55

N narcissistic personality disorder, 22 National Research Council, 140 nausea, 68, 81, 100, 187

Index

214 needs, xi, 15, 68, 71, 74, 83, 93, 94, 102, 116, 125, 135, 142, 185, 196, 198 negative affectivity, 166, 168, 176, 182 negative consequences, 44 negative mood, x, 155, 159, 166, 167, 179 negative reinforcement, 173 negotiation, 47 nerve, 72 nervous system, 71, 72, 84 nervousness, 134 network, 55, 75, 178, 183 neurons, 71, 73, 74, 76, 87 neuropeptides, ix, 63, 75, 87 neuroticism, 166, 167, 168 neurotransmitter, 71, 75 neurotransmitters, ix, 63, 75 New South Wales, 45, 47 New Zealand, 18, 58, 59, 61 newspapers, 64 nicotinamide, 186 nicotine, 101 nitric oxide, 75, 82, 90 nitric oxide synthase, 82, 90 nitrogen, 187 norepinephrine, 87 normal distribution, 164 North America, 202 novelty, 4 nuclei, 75, 86, 187 nucleus, 69, 70, 73, 74, 76, 82, 86, 87 nurses, xi, 50, 69, 96, 185 nursing, 16, 50, 54, 59 nutrients, ix, 65, 68, 71, 75, 105, 111 nutrition, x, 83, 106, 107, 108, 110, 111, 112, 113, 135, 137, 140, 141, 142, 177, 203 nutritional deficiencies, 111

O obesity, 4, 18, 23, 25, 36, 71, 76, 94, 106, 107, 140, 143, 157, 163, 167, 177, 178, 181, 184 observations, 79, 87 obsessive-compulsive disorder, 29 occlusion, 202 OCD, 29, 35 olanzapine, 17 openness, 166 organ, 3, 89 organism, 65 organization, ix, 64

orientation, 12, 93, 94, 101 oscillation, 114 outliers, 150 output, 188 overweight, 129, 146, 163 oxidation, 73, 85

P Pacific, 25 pain, 2, 15, 193, 199 palliative, 65, 82, 83, 84 pancreas, 72, 187, 203 parameter, 113, 151 parental authority, 12 parental involvement, 20 parenting, 13, 18 parents, ix, 13, 15, 24, 26, 42, 91, 95, 96, 97, 98, 99, 100, 101, 102, 195 parotid, 187, 188, 194, 196, 199, 202, 203 parotid gland, 187, 188, 203 partition, 160 passive, 71 pathogenesis, 69, 71, 73, 74, 76, 80, 82 pathology, x, 4, 25, 93, 98, 99, 102, 138, 145, 146, 148, 153, 182, 183 pathways, ix, 55, 64, 69, 71, 72, 73, 74, 76, 82, 87 patient rights, 57 Pearson correlations, 151 peers, 12, 56 pellicle, 186 penicillin, 186 peptides, 71, 72, 75 perceptions, 54, 123, 133, 147 perfectionism, 173 periodontal, 188, 189, 196 periodontal disease, 188, 189 periodontitis, 189 peripheral blood, 71, 88 peripheral blood mononuclear cell, 71, 88 perseverance, 167, 168 personal identity, 56 personality, vii, 1, 3, 7, 10, 11, 16, 18, 20, 21, 22, 23, 25, 26, 35, 36, 101, 157, 166, 168, 173, 178, 179, 180, 181, 183, 187, 203 personality characteristics, 10 personality dimensions, 4, 21 personality disorder, 4, 7, 10, 22, 157 personality factors, 181 personality traits, 11, 18, 101, 168, 187

Index perspective, 18, 19, 42, 43, 50, 56, 59, 60, 66, 103, 157, 159, 169, 171, 172 persuasion, 44 pH, xi, 185, 187, 188, 192, 193, 197 pharmacological treatment, viii, 2, 17 pharmacotherapy, x, 15, 17, 106 phenomenology, 36 photographs, 196 physical abuse, 7 physical activity, ix, 91, 115, 177 physical education, 113 physical health, 12 placebo, 17, 20, 21, 22, 24, 26, 79, 81, 88, 89, 138, 193 planning, 165, 166, 167, 168, 182, 195, 202 plasma, 72, 76, 79, 82, 85, 86, 186 plasma levels, 79, 86 pleasure, 4, 12, 122, 133, 134 PM, 22 polyunsaturated fatty acids, 78 poor, 3, 6, 9, 14, 15, 68, 79, 80, 96, 116, 128, 130, 135, 187, 194, 200 population, vii, 1, 6, 7, 13, 79, 106, 107, 112, 129, 140, 146, 154, 155, 157, 160, 164, 192 porosity, 192 positive correlation, 128, 129, 130 positive feedback, 174 positive reinforcement, 173 potassium, 112, 120, 187 power, 15, 42, 43, 45, 47, 49, 50, 51, 52, 56, 57, 58, 69, 155, 156, 169, 187 power relations, 50 prediction, 137, 139, 140, 181 predictive validity, 142 predictors, 23, 109, 123, 136, 168 preference, 43, 85 pregnancy, 96, 101 premature death, 6, 13 preparation, 123, 198 preparedness, 160, 177, 182 pressure, 13, 93, 97, 161, 162, 171, 174, 194 prevention, vii, 2, 14, 15, 17, 80, 81, 135, 139, 177, 183 primary school, 93 principle, 72 probability, 4, 14, 34, 154 problem behavior, 13 problem drinking, 167, 168, 170, 175, 179, 182 production, 71, 75, 78, 81, 82, 88, 193 professions, 113

215

prognosis, viii, 25, 63, 64, 65, 130, 134, 195 program, 45, 97, 111, 128, 133, 135, 136, 151 projective test, 97 prostate, 75, 86 protective role, 20 proteins, 117, 186 proteinuria, 186 protocol, 196 Prozac, 193 psychiatric disorders, vii, 1, 3, 7, 20 psychiatric illness, 3 psychiatric patients, 8 psychiatrist, 30, 31, 43, 55, 110, 149 psychological health, 194 psychological pain, 16 psychological phenomena, 172 psychological problems, 146 psychological value, 69 psychological variables, 146, 155 psychologist, 149 psychology, 93, 97, 110, 111, 141, 169, 170, 174, 178, 202 psychometric properties, 150 psychopathology, vii, x, 2, 3, 4, 5, 9, 16, 23, 37, 38, 128, 145, 147, 148, 153, 156, 170, 181 psychoses, 38 psychosis, 29 psychosocial stress, 101 psychotherapy, viii, 2, 13, 15, 20, 97, 139 psychotic symptomatology, 29 psychotic symptoms, 29 pubertal development, 92 puberty, 42, 93, 100, 179 public health, 2 punishment, 11, 169

Q quality of life, 65, 69, 77, 78, 80, 81, 84 quartz, 198 questioning, 71

R range, ix, 6, 44, 91, 92, 94, 108, 113, 117, 119, 133, 135, 155, 160, 174, 175, 186, 188, 194 rash, x, 159, 165, 167, 175, 176 rating scale, 138 reading, 4, 125 reality, 11, 36, 37, 161

216

Index

reasoning, 44 recall, 150 receptors, 71, 74, 80, 81, 86, 87 recognition, 3, 10, 14, 159, 171, 175 reconcile, vii, 2, 164 reconstruction, 54 recovery, 23, 53, 55, 56, 65, 109, 116, 134, 141 recurrence, 109, 128, 130, 133, 134, 139 reduction, 66, 74, 79, 111, 119, 120, 123, 124, 125, 163, 178, 188, 198 reflexes, 72 regression, 12 regulators, 49 rehabilitation, 108, 110 reinforcement, 161, 162, 165, 169, 170, 171, 172, 174, 175, 178 reinforcers, 170 relapses, x, 17, 106 relationship, ix, 5, 12, 16, 20, 29, 39, 45, 50, 51, 53, 55, 86, 96, 97, 98, 100, 101, 102, 105, 106, 108, 109, 110, 112, 113, 123, 124, 125, 132, 133, 134, 135, 137, 146, 151, 152, 153, 155, 162 relationships, 12, 22, 49, 51, 54, 55, 93, 167, 174, 180, 199 relatives, 26, 44, 69 relevance, 65, 68, 79, 155, 203 reliability, 38, 66, 69, 83 religiosity, 167 religious beliefs, 38 remission, 3, 109 replacement, 12 repression, 12 reputation, 55 resins, 198 resistance, 33, 35, 36, 42, 50, 54, 56, 72, 97 resolution, 52, 94 resources, 2 respiratory, 83 responsibility, 44, 101 rhythm, 92 right to life, 57 risk, vii, x, 1, 3, 6, 7, 8, 9, 10, 11, 12, 13, 14, 16, 17, 18, 19, 22, 24, 26, 34, 35, 42, 53, 82, 92, 93, 101, 103, 107, 130, 142, 146, 147, 155, 159, 160, 161, 162, 163, 164, 165, 166, 169, 170, 173, 175, 176, 177, 178, 182, 189, 191, 192, 193, 196 risk factors, x, 8, 16, 26, 34, 93, 142, 159, 162, 163, 164, 165, 173, 175, 176, 177, 178, 182 risk-taking, 9, 13, 14 routines, viii, 41, 56

S sacrifice, 42, 94 safety, 46 saliva, xi, 185, 186, 187, 188, 193, 197 salivary glands, 199 sample, x, 4, 5, 6, 7, 8, 9, 10, 11, 18, 24, 31, 45, 46, 107, 112, 114, 123, 137, 138, 140, 145, 146, 148, 153, 154, 155, 157, 167, 168, 172, 173, 180, 189, 191, 194 sampling, 183 satisfaction, 4, 13, 127, 194, 202 schizophrenia, 6, 29, 38 school, viii, 2, 5, 14, 26, 44, 53, 93, 96, 100, 101, 107, 139, 142, 167, 173 school performance, 167 schooling, 31 scientific knowledge, 15 scores, viii, 6, 13, 28, 30, 36, 38, 107, 109, 113, 125, 127, 128, 129, 130, 131, 132, 133, 150, 151, 152, 154, 171, 173, 174, 189, 192, 194 scurvy, 186 search, 65 secondary school students, 138 secretion, 70, 71, 89, 93, 187, 188 security, 50, 100 selective serotonin reuptake inhibitor, 21 selectivity, 81 self, viii, x, xi, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 19, 20, 21, 22, 25, 28, 30, 31, 41, 42, 49, 50, 53, 54, 55, 56, 57, 58, 64, 68, 92, 99, 100, 109, 111, 132, 138, 142, 143, 145, 146, 147, 148, 150, 151, 152, 153, 154, 155, 156, 157, 165, 166, 167, 168, 173, 174, 179, 181, 183, 185, 186, 194, 197, 203 self esteem, 42, 147, 148, 150, 152, 153, 154, 156 self-awareness, 166 self-concept, 203 self-consciousness, 8 self-destruction, 4, 19 self-destructive behavior, 5, 11, 12, 14, 100 self-discrepancy, 157 self-efficacy, 143 self-esteem, viii, 2, 3, 8, 9, 20, 93, 156, 157, 181, 194 self-image, viii, 5, 41, 50, 54, 56, 194 self-monitoring, 111 self-mutilation, 2, 6, 10, 11, 19 self-regulation, 50 semantics, 58

Index sensation, x, 5, 71, 106, 165, 166, 167, 168, 178 sensation seeking, 165, 166, 167, 168, 178 sensations, 166 sensing, 73, 97 sensitivity, 191, 198 separation, 9, 93, 94, 95, 99, 100, 102 sepsis, 65 series, 42, 69, 75, 127, 169, 172, 174, 176 serotonin, ix, 63, 71, 75, 76, 79, 80, 81, 82, 86, 87, 88, 90, 193 sertraline, 17 serum, 71, 84, 85, 140, 187, 202, 203 services, 15, 44, 49, 107, 114 severity, 4, 11, 19, 37, 68, 112, 126, 128, 129, 130, 131, 146, 187, 190, 191 sexual behavior, 167 sexual contact, 93 sexual orientation, 101 sexuality, 102 shame, ix, 3, 15, 91, 95, 132, 146, 181 shape, 4, 11, 28, 57, 64, 112, 116, 127, 136, 137, 150, 153, 170 shaping, 42, 57 shares, 35, 160 sharing, 68, 122 shyness, 8 sialogram, 187 sialography, 187 sibling, 98 siblings, 160 side effects, 78 sign, 66, 67, 202 signalling, ix, 63, 69, 71, 73, 75 signalling pathways, ix, 63, 69, 73 signals, ix, 64, 69, 70, 71, 72, 73, 74, 85, 97, 98 significance level, 31 sites, 49, 84, 189, 191, 197 skeletal muscle, 68 skills, viii, 2, 12, 14 small intestine, 72 smoking, 12 social behavior, 100 social class, 140 social comparison, 162, 164, 183 social context, 52 social control, 43, 44, 56, 58 social environment, 43, 52 social events, 111, 133 social learning, 169, 171 social support, 162

217

sodium, 112, 120 software, 111, 112, 132, 141 solid tumors, 90 somatization, 97 species, 188, 192 specificity, 166 spectrum, 13, 14, 93, 95, 102, 180 speech, 96, 97, 100, 101 SPSS, 151 stability, 150, 154, 166, 181 stages, 54, 68, 92, 156, 172, 201 standard deviation, 112, 115, 118, 121, 127 standards, 146, 147, 155, 157 starvation, 7, 38, 58, 69, 187 statistics, x, 2, 6, 106 stigma, 13, 49, 56 stimulus, 71, 169 stomach, 89, 93, 100, 187 stomatitis, 186 strategies, vii, 2, 11, 56, 77, 89, 132, 135, 142 strength, 31, 78, 102, 189 streptococci, 193 stress, 3, 5, 12, 93, 94, 128, 166, 179, 193 stressors, 150 striae, 31 structural equation modeling, 174 students, 147 subjective experience, 54 substance abuse, 22, 165 substance use, 9, 10, 12 sucrose, 183, 191, 196 sugar, 163, 196 suicidal behavior, vii, 1, 2, 3, 5, 6, 7, 10, 11, 12, 15, 16, 18, 23 suicidal ideation, 2, 7, 9, 13, 15, 17, 23 suicidal wishes, 14 suicide, vii, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 96, 97, 98, 99 suicide attempters, 7, 13 suicide attempts, 4, 6, 7, 8, 9, 10, 11, 13, 15, 18, 19, 22, 25, 26 suicide rate, 17 summaries, 170 Sun, 89 supervision, 48 suppression, 12, 65, 75, 84 surveillance, viii, 41, 56 survival, 68, 69, 84, 90, 182 swelling, 187, 204

Index

218

symptom, viii, 11, 27, 28, 32, 33, 35, 36, 37, 65, 67, 83, 116, 120, 125, 128, 129, 130, 133, 137, 148, 163, 171, 172, 173, 174, 178 symptoms, vii, ix, x, 1, 8, 11, 17, 19, 29, 30, 31, 33, 37, 42, 64, 65, 66, 67, 68, 69, 77, 88, 91, 92, 93, 102, 105, 106, 109, 110, 112, 115, 116, 125, 128, 129, 130, 131, 133, 134, 137, 145, 146, 147, 148, 150, 151, 153, 154, 155, 162, 163, 164, 167, 168, 169, 173, 174, 177, 179 syndrome, 64, 65, 82, 87, 88, 89, 134, 156, 160 synthesis, 70, 71, 73, 76, 77, 78, 79, 136, 183 systems, ix, 64, 75, 83, 87

T target organs, 72 targets, viii, 41, 81 taxonomy, 13, 36 teachers, 96, 139 teaching, 45, 169 technology, 198 teenagers, 2, 12 teeth, xi, 185, 186, 188, 189, 190, 191, 192, 193, 194, 196, 198, 199, 200, 201 television, 100, 161, 163, 177, 179, 181 television advertisements, 179 television viewing, 181 temperature, 77, 191 tension, 2, 11, 52, 55 terminally ill, 67, 68, 83, 84 test scores, 125, 127 testosterone, 93 theory, 19, 146, 153, 155, 157, 159, 169, 170, 171, 172, 173, 174, 176, 180, 182, 192 therapeutic approaches, ix, 16, 91 therapeutic encounter, 16 therapeutic goal, 68 therapeutic interventions, 50 therapeutic relationship, 98, 99 therapists, 16, 55, 57 therapy, 16, 19, 22, 50, 60, 65, 77, 80, 85, 95, 96, 97, 98, 102, 110, 136, 139, 140, 141, 142, 196, 199 thinking, 16, 30, 123, 133, 165 threat, viii, 4, 41, 56, 57, 97 threats, 44, 46, 49 threshold, 164 time, viii, 10, 12, 13, 15, 16, 18, 29, 35, 41, 48, 49, 53, 55, 56, 57, 58, 65, 95, 96, 98, 114, 116, 117, 123, 124, 125, 132, 135, 149, 161, 169, 174, 175, 191, 196, 199, 201

tissue, 75, 186, 192 TNF, ix, 63, 77, 86, 87, 88 TNF-alpha, 86 tobacco, 167 tonic, 197 total energy, 117, 118 toxicity, 66, 78 tracking, 47, 83 training, 66, 100, 132, 134, 139, 141 traits, 8, 168, 180, 181, 192, 194 trajectory, 54 transactions, 43, 47 transduction, 69 transference, 16, 97 transformation, 36, 43 transition, 12, 54, 55, 99, 106, 140 transition to adulthood, 12 transitions, 16, 43, 54, 106, 141 transmission, 187 transport, 35, 79 trauma, 55 traumatic experiences, 7 treatment methods, 95, 137 trend, 4, 119, 125, 153 trial, 18, 19, 20, 21, 22, 24, 25, 47, 60, 79, 83, 89, 138, 181, 183, 193 tricyclic antidepressant, 87 triggers, ix, 32, 71, 91, 94 trust, 13 tryptophan, 76, 79, 83, 86, 87 tumor, 81, 83, 86, 87, 90, 100 tumor cells, 86 tumor growth, 90 tumour growth, 72, 73, 74, 82 twins, 160, 180

U UK, 8, 45, 59, 185 umbilical cord, 101 UN, 86 uncertainty, 56, 109 undernutrition, 140 uniform, 97 United Kingdom, 89 United States, 2, 13 university students, 24 urea, 187

Index

V vacancies, 114 vagus, 71 validation, 38, 83, 136, 138, 141, 149, 178, 179, 180, 183 validity, 38, 83, 108, 137, 139, 141, 156, 167, 168, 173, 179, 182 values, 36, 54, 79, 108, 112, 119, 132, 147, 162, 187, 193 variability, 108, 116, 117, 160 variable, 53, 145, 146, 151, 154, 155, 174, 193 variables, 10, 16, 31, 108, 113, 130, 132, 137, 139, 148, 150, 151, 152, 155, 167, 168, 189, 190 variance, 151, 152, 160, 161, 167, 168, 173 variation, 114, 117 violence, 7, 18 viscosity, 188 vitamins, 112, 120 voice, 97 voicing, 55 vomiting, xi, 4, 31, 100, 109, 112, 113, 114, 115, 116, 119, 120, 128, 130, 131, 133, 134, 136, 185, 186, 187, 189, 190, 191, 194, 195, 197, 203, 204 vulnerability, x, 20, 23, 145, 150, 153, 157

W walking, 102 water, 88, 197 wear, 190, 193, 197, 198, 204 web, 49, 53, 178

219

weight control, 24, 36, 108, 124, 140, 141, 183 weight gain, 101, 133 weight loss, 17, 35, 36, 76, 81, 83, 92, 95, 101 weight management, 51 Western countries, 7 wild type, 74 withdrawal, 45, 48, 57 withdrawals, 48 women, vii, viii, ix, x, 1, 4, 7, 9, 11, 19, 21, 22, 26, 27, 37, 42, 85, 91, 92, 106, 107, 123, 135, 136, 137, 138, 139, 140, 141, 142, 145, 146, 147, 148, 151, 153, 154, 155, 156, 157, 161, 162, 163, 164, 166, 168, 170, 171, 172, 173, 174, 177, 178, 181, 203 words, 168, 169, 171 work, 2, 15, 16, 43, 53, 54, 55, 56, 57, 95, 98, 102, 107, 134, 154, 162, 165, 173, 174 workers, 26, 191 World Health Organization, vii, 2, 6, 14, 26 worry, x, 106, 124 WTO, 61

X xerostomia, 188

Y yeast, 193 young men, 22, 92 young women, 8, 22, 26, 47, 61, 107, 112, 114, 117, 120, 121, 135, 147, 155