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

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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

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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

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

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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

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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

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

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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

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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

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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

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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

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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]

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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

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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

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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

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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

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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

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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

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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

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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.

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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.

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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

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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.

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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,

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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

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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

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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,

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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.

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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.

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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).

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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.

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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.

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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

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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.

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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).

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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*).

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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).

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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

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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

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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.

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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 …

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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.

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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.

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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).

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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).

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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).

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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.

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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.

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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

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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

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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

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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:

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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).

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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

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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’.

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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

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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

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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’.

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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.

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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

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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

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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

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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

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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

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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.

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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.

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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

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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 [ 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.

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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

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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

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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

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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.

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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).

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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.,

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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.

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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).

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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.

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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

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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.

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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

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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

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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.

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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.

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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.

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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

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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).

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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

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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

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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

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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.

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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.

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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

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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.

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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.

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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.

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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