ANOREXIA NERVOSA AND BULIMIA NERVOSA: NEW RESEARCH
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ANOREXIA NERVOSA AND BULIMIA NERVOSA: NEW RESEARCH PAMELA I. SWAIN EDITOR Nova Science Publishers. New York . Inc.

or exemplary damages resulting.E18A55 2005 362. WM 175 A615 2005] I. Anorexia nervosa. 2. tape. cm. Swain. Fax 631-231-8175 Web Site: http://www. Library of Congress Cataloging-in-Publication Data Anorexia nervosa and bulimia nervosa : new research / Pamela I. Includes bibliographical references and index. FROM A DECLARATION OF PARTICIPANTS JOINTLY ADOPTED BY A COMMITTEE OF THE AMERICAN BAR ASSOCIATION AND A COMMITTEE OF PUBLISHERS.novapublishers. this material. Anorexia Nervosa. This publication is designed to provide accurate and authoritative information with regard to the subject matter covered herein. or reliance upon. RC552. [DNLM: 1. All rights reserved. the services of a competent person should be sought. in whole or in part. consequential. If legal or any other expert assistance is required. p. Swain (editor). Bulimia. New York . but makes no expressed or implied warranty of any kind and assumes no responsibility for any errors or omissions. 3. recording or otherwise without the written permission of the Publisher. Inc. For permission to use material from this book please contact us: Telephone 631-231-7269. No liability is assumed for incidental or consequential damages in connection with or arising out of information contained in this book.2'5--dc22 2005005548 Published by Nova Science Publishers. . stored in a retrieval system or transmitted in any form or by any means: electronic. mechanical photocopying. Bulimia. Inc. Pamela I. magnetic. The Publisher shall not be liable for any special.com NOTICE TO THE READER The Publisher has taken reasonable care in the preparation of this book. electrostatic. Eating disorders. 2. ISBN 978-1-61668-120-3 (E-Book) 1. It is sold with the clear understanding that the Publisher is not engaged in rendering legal or any other professional services. from the readers’ use of. No part of this book may be reproduced.Copyright © 2006 by Nova Science Publishers.

Bräutigam and M. Food Intake. Paolo Girardi. Herberhold Effects of Multiprofessional Treatment on Clinical Symptoms. Meguid. Michael M. Shadow of Law. Fernanda Baeza Scagliusi and Sonia Tucunduva Philippi vii 1 Chapter II 27 Chapter III 41 Chapter IV 63 Chapter V 91 Chapter VI 105 . or Disseminated Power and Control? Terry Carney. Eating Attitudes and Body Image of Brazilian Bulimic Patients Marle dos Santos Alvarenga. Antonia Cascino and Filippo Rossi-Fanelli "I Couldn´t Find the Food I Liked" Anorexia in Boys. Three Case Reports B.Contents Preface Chapter I Suicide in Anorexia Nervosa and Bulimia Nervosa Maurizio Pompili. Mim Ingvarson and David Tait Secondary Anorexia: A Neglected Issue in the Optimal Management of Patients Suffering from Acute and Chronic Diseases Alessandro Laviano. Amedeo Ruberto and Roberto Tatarelli Psychopathological Aspects of Body Image Disturbance on Anorexia and Bulimia Nervosa Simone Mancini Castilho Experiences of ‘Control’ in Anorexia Nervosa Treatment: Delayed Coercion. Eating Patterns.

Tasca. Gregory T. Smith and Melissa A. Louise Balfour.Desired BMI Discrepancy.vi Chapter VII Pamela I. Cyders The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health Alex Milosevic 145 Chapter VIII 159 Chapter IX 185 205 Index . Kanchan Kurichh. Swain Actual . Monique Potvin-Kent and Hany Bissada Integrating Personality and Environmental Risk Factors for Bulimia Nervosa Sarah Fischer. Body Dissatisfaction and Self Concept in Women with Bulimia Nervosa and Binge Eating Disorder Giorgio A.

which constitutes a risk factor for completed suicide. Risk factors for suicide and attempted suicide (which in many cases results in successful suicide) in anorexia nervosa and bulimia nervosa include: purging type. 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. 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. According to World Health Organization estimates. The percentage of suicide among patients with eating disorders (not differentiated) ranges from 1. lack of impulse control. Preventive strategies of suicide among these patients should include pharmacological . obsessive symptoms. A few studies have suggested that suicide is the major cause of death among patients with anorexia nervosa. therefore suicidal behavior is gender-related.8% to 7.3%. refuting the assumption that inanition generally threatens the life of these patients. suicidal behavior and eating disorders are alarming phenomenon among young people. chronic disease. drug abuse. Suicide in anorexia nervosa and bulimia nervosa is a major cause of death as reported in chapter I. 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. Suicide attempts are easily found among cohorts of patients with bulimia nervosa. on the other hand. Young women are heavily represented among these patients. 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.Preface The abundance of food in the developed countries of the world has seemingly spawned an epidemic of disorders connected to the food. Data concerning suicide in bulimia nervosa. and low body mass index (BMI) at presentation (for anorexia nervosa). 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. No doubt suicidal behavior is underestimated amongst patients with anorexia nervosa and bulimia 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. major depression. are still scarce.

at least formally (though the strategic possibilities of orders confers internal authority within the clinical setting). that of the ‘recovering’ patient. as one of the diagnostic criteria for these pathologies. Variables were analyzed with the Fisher’s Exact Test and Mann-Whitney non-parametric test (U). Rather. interactions with staff. based on an interpretation of Foucault. regular surveillance and measuring. to accept the ‘empowerment’ regime that is made even more convincing by the threat of legal intervention. visits and activities. through disciplinary practices embedded in everyday clinic life. in a sense. ‘control’ (or management) is exercised diffusely. since effective treatment of the underlying disease rapidly ameliorates food intake. Chapter II explores the presence of obsessive-compulsive and delusional features of the ‘Body Image Disturbance’ in anorexia and bulimia nervosa. including sepsis. fourth Edition (DSM-IV). Instead. chronic renal failure. 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. The patient learns to provide consent ‘freely’. is ‘the law’. or the success of less restrictive options which explains why law is so infrequently engaged. Chapter III argues that it is not the clumsiness of the law. Anorexia nervosa is often chronic. and attitudes to the body) and what Goffman called the ‘moral career’ of the patient (eg learning to play the ‘patient role’. or translate medical expertise into medical authority. since it contributes to the development of malnutrition. Body image disturbance is an important clinical feature on eating disorders and was characterized by the Diagnostic and Statistical Manual of Mental Disorders. Although the presence and importance of body image disturbance in eating disorders are well established. etc. thereby increasing morbidity and mortality. The analysis of the psychopathological differences of ‘Body Image Disturbance’ in anorexia and bulimia nervosa has diagnostic implications. The ‘fiction’ of acting ‘responsibly’. Accumulating evidence indicate that anorexia associated to different diseases . ‘carers’ and patients are mediated through conventions and rules. with one of the highest death rates for psychological conditions. anorexia does not represent a primary therapeutic target. The patient has become an active participant in the governance of self. 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. psychotherapy and school-based interventions involving crisis management. chronic liver failure. the psychopathological nature of this symptom is not yet defined. Anorexia and reduced food intake are relevant issues in the management of patients suffering from acute and chronic diseases. the authors conclude that the regulatory regime that shapes treatment of anorexia nervosa. such as daily routines of eating and washing. Swain treatments. The regime of governmentality within the clinic is shaped by practices which operationalise ‘duty of care’. becomes part of the new identity.viii Pamela I. cancer. and impinges on quality of life. to make the ‘correct’ choices. selfesteem enhancement and the development of coping skills and healthy decision making. behavioural ‘contracts’. but is rarely invoked. In time the constraints learned in this way become part of the new role. The regulatory regime not only touches on such ‘practices’ but also targets ‘identities’ (including self-image. or which conscript ‘empowerment’ as control. Law can compel treatment. employed so hesitantly at first. to ‘be’ an ‘anorexic’). or show how interactions between ‘experts’. In acute diseases. anorexia impacts on patients’ prognosis. In chronic diseases.

leptin].g. achieved via nutritional counselling. the optimal therapeutic approach to anorectic patients should be based on both changes in dietary habits. one that is more focused on masculine muscular form. In Brazil.. a fragile sexual identity. This situation is exacerbated by the fact that bulimia is perceived by the public as a disease that only affects girls.794 patients. and drug therapy. muscle building. the different therapeutic approaches. Eating disorders (ED) have been treated in Brazil since 1992 with the creation of the ED Unit of the University of São Paulo. IL-6. The lifetime prevalence of any eating disorder has been reported as 17. Discussion of the results encompasses psychodynamic and systemic issues. These include excessive physical activity. For example.g. The authors focus on the patients’ personal histories and the psychological conditions in the parents. 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. Although adolescent girls are still the group primarily affected by eating disorders. Food intake is defined as the food and nutrients that compose the diet. Their modes of action do not appear to be separate and distinct. neuropeptides [e. and eating behaviors are the attitudes. only the frequency of bulimic symptoms has been evaluated. Three-Factor Eating Questionnaire. Even in developed nations. the effect of multiprofessional treatment in BN had never been examined. while eating patterns are the meal frequency. although . and kinds of treatment.g. They also show less shame concerning binge eating. Chapter IV reports a number of factors are considered mediators of anorexia. 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. and ideals of physical perfection. cytokines [e.5% among men. The fact that the numbers for eating disorders among boys are so low is probably due in part to underdiagnosis. beliefs and relationship with food. However. convincing evidence suggest that a hierarchical organization exists in which cytokines play a key role. including hormones [e. reasonable educated and aged between 21 and 40 years. aimed at interfering with cytokine expression or hypothalamic monoaminergic neurotransmission. Thus. boys often exhibit a different form of body image distortion.Preface ix is multifactorial in its pathogenesis. nearly every tenth person suffering from an eating disorder is male. the Eating Disorder Inventory. In chapter VI. There are triggers for the disorders among boys that are different from those that have been identified among girls. rather they are closely inter-related.. There are also differences in the pathologies. Hypothalamic monoaminergic neurotransmission may significantly contribute to these effects. The number of boys affected by eating disorders is increasing. a public service that has treated 1. mainly white.. with the result that affected boys often have to struggle with emotions of shame and denial. TNF] and neurotransmitters [e.g. IL-1. by persistently activating anorexigenic systems and/or inhibiting prophagic pathways. Dutch Eating Behavior Questionnaire and Restraint Scale were used to analyze eating behaviors. Cytokine increased expression during disease inhibits the hypothalamus to appropriately respond to peripheral signals. regularity and schedules. NPY].9% among women and 6. serotonin and dopamine]. and suggest that most of the hypothalamic neuronal signalling pathways modulating energy intake are involved.. triggering the complex neurochemical cascade which leads to the onset of anorexia. Food intake and eating patterns and behaviors are disturbed in bulimia nervosa (BN). demanding requirements or expectations in the areas of competitive sports.

pharmacotherapy and nutrition counseling. Scores of EAT. Nevertheless. Chapter VIII proposes a specific model that integrates identified heritable and environmental risk factors for BN. They fulfilled the EAT. having difficulties with food choices and not believing that they could have a normal diet and a normal weight. and after three months. Treatment was composed by 12 weeks of cognitive-behavior therapy. most of them remained hating the hunger sensation. BITE and BSQ. Heritability studies provide a general framework for understanding risk for bulimia nervosa (BN): liability is a function of both genetic and environmental factors. and lower self concept for the BN group. they are now developing an eating attitudes questionnaire.x Pamela I. Individuals who learn to expect alleviation of negative mood from eating. with company and less anxious. Patients recorded their food intake and occurrence of compulsions and purges in a diary. ADBD can be easily assessed by clinicians and may be used as an index of body dissatisfaction and overall self concept. is a heritable risk factor that increases the likelihood that one will engage in some form of rash. Measurements were made before and after treatment. The specific form of one’s maladaptive behavior is a function of learned experiences from one’s environment. Thirty-nine women with BN (according to DSM-IV criteria) were followed. heritable risk from high levels of urgency is likely to become expressed as BN when one learns to expect benefits from eating . at the end of following 97. are more likely to engage in bulimic behaviors. Greater ADBD was related to greater body dissatisfaction for the BN and BED groups. BSQ and BITE-symptoms decreased after treatment and even more after the later following. which will be psychometrically tested. Thus. even though energy content of the meals followed by vomit decreased. Also hypothesized was that women with BN would have greater eating and self related pathology than those with BED. the general. Trait urgency. This study supports the idea of the importance of food issues and behaviors in ED. leaving the other eating behaviors’ aspects uncovered. and overgeneralized life improvement from thinness. and also an eating attitudes questionnaire. Fifty-one participants diagnosed with BN and 41 with BED drawn from a clinical sample completed questionnaires assessing eating disorder and general psychopathology. Swain these questionnaires focus especially in dietary restraint. which can contribute to relapses. and higher body dissatisfaction for a clinical sample of women with Bulimia Nervosa (BN) and Binge Eating Disorder (BED). the tendency to act rashly in response to distress. The belief of automatically gaining weight after a meal. lower self concept. Nutrients intake did not alter. Based on the questions used to assess eating attitudes. and guilty and worry after eating a “forbidden” food decreased. Non-parametric statistics were used to test for differences among the three moments. A theoretical frame for ADBD was put forward based on self discrepancy theory. The authors observed an improvement in clinical symptoms. because even the patients that had a clinical improvement remained with a complicated relationship with food. As described in chapter VII. maladaptive behavior pattern (such as BN). Those with BN had more self-related pathology. Number of meals increased and patients did more meals seated.5% of the patients did not fulfill criteria for BN anymore. ADBD may be a vulnerability factor for developing an eating disorder for women. especially developed for this research. it was hypothesized that higher levels of actual-desired BMI discrepency (ADBD) would be associated with higher binge eating symptoms.

with disfiguring consequences to the dentition. 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. psychologists. Parotid salivary gland enlargement and altered salivary composition have been described. be they physicians. dietary and psychiatric/psychological needs of patients. . Nonetheless. Disordered eating and chaotic lifestyle may affect patterns of caries (decay) and gum disease. Chapter IX reviews the literature and illustrates the clinical problems faced by real cases. 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. psychiatrists.Preface xi when distressed and extreme benefits from thinness. Prevention will also be discussed. 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. Oral microbial flora. The mouth is the first part of the digestive system and commonly exhibits signs of disease occurring elsewhere. The proposed process is empirically supported and consistent with findings from heritability research. could theoretically differ to normal flora as a consequence of repeatedly low intraoral pH secondary to self-induced vomiting (SIV). The presence of gastric acid in the mouth can result in acid erosion. either in dental plaque or saliva. nurses or relatives.

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1-26 © 2006 Nova Science Publishers. Data concerning suicide in bulimia nervosa. An effort to reconcile 1 Maurizio Pompili. 00189 Roma – Italy.Via di Grottarossa.3%. Chapter I Suicide in Anorexia Nervosa and Bulimia Nervosa Maurizio Pompili1.Sant’Andrea Hospital – Dep. 1035-1039. on the other hand. M. Amedeo Ruberto and Roberto Tatarelli Department of Psychiatry – Sant’Andrea Hospital University of Rome “La Sapienza” . maurizio. are still scarce. A few studies have suggested that suicide is the major cause of death among patients with anorexia nervosa. 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. Swain.Italy Abstract Suicide in anorexia nervosa and bulimia nervosa is a major cause of death. Suicide attempts are easily found among cohorts of patients with bulimia nervosa. refuting the assumption that inanition generally threatens the life of these patients. Young women are heavily represented among these patients.University of Rome “La Sapienza”. and low body mass index (BMI) at presentation (for anorexia nervosa).8% to 7. major depression. drug abuse. of Psychiatry. chronic disease. pp. Inc. Risk factors for suicide and attempted suicide (which in many cases results in successful suicide) in anorexia nervosa and bulimia nervosa include: purging type. 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. as in the case of affective disorders and personality disorders.it . therefore suicidal behavior is gender-related.pompili@uniroma1. Comorbidity between anorexia nervosa or bulimia nervosa and other psychiatric disorders is a frequent event.In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I.D. Paolo Girardi. The percentage of suicide among patients with eating disorders (not differentiated) ranges from 1. lack of impulse control. which constitutes a risk factor for completed suicide. obsessive symptoms. No doubt suicidal behavior is underestimated amongst patients with anorexia nervosa and bulimia nervosa.

who is considered the father of suicidology. Shneidman (1985). A major reason for this has been the very large increase in suicide in young people. Approximately 40. or unacceptable anguish. 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. suicide is a conscious act of selfinduced annihilation. 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. and 10 to 20 times as many attempted suicide worldwide in the year 2000 (WHO. The best way to prevent suicide is to learn what is causing the distress. suicidal behavior and eating disorders are alarming phenomenon among young people. genetic. gestures and attempts. social. 2000a). suicidal behavior among young people has increased over the past thirty years and statistics match with those of the U. the third leading cause of death among teenagers and young adults. Youth suicide. Preventive strategies of suicide among these patients should include pharmacological treatments.000 to 50. Among teenagers and young adults. approximately 1 million people died from suicide. may become a way of attempting to cope with this pain and the marked social isolation that results from eating disorders (Manley and Leichner. cultural and environmental factors. This averages out to one death every 40 seconds and one attempt every three seconds. Each suicide has a serious impact on at least six other people and the psychological. Reduce the level of suffering and the individual will choose to live”. Retrospective studies indicate that the absolute majority (81-100%) of suicides occurs in subjects with a psychiatric . no single reason. The World Health Organization (2000b) recognizes suicide as a complex problem for which there is no single cause. has proposed the following definition of suicide: “Currently in the Western world. It results from a complex interaction of biological. According to World Health Organization estimates. suicidal ideation. according to the WHO Databank. including self-mutilation. the tension and anguish – and the work to treat these emotions within the suicidal person. self-esteem enhancement and the development of coping skills and healthy decision making. it is the third most frequent cause of death. In Europe. psychological. Profound psychic pain is a major part of the clinical picture. Suicide is the ninth leading cause of death in the United States for all ages. Paolo Girardi. so much so that self-harming thoughts and behaviors. accounts for more deaths in the United States than natural causes combined for 15 to 24-years-olds. unendurable pain. seen in many countries.000 Americans die every year by their own hand. 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.S. According to World Health Organization estimates. Several governments around the world have established suicide prevention programs. 2003).2 Maurizio Pompili. especially males. social and financial impact of suicide on the family and community is immeasurable. best understood as a multidimensional malaise in a needful individual who defines an issue for which the suicide is perceived as the best solution”. according to the National Center for Health Statistics (2000). psychotherapy and school-based interventions involving crisis management.

Wonderlich et al. 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. 1985). Frequent hospitalizations and. and there is no doubt that suicidal behavior is an underestimated phenomenon. 1988. Skodol et al.. Hsu et al. in particular. Bruch.. Santonastaso. an important risk factor is a later onset of illness (Patton.. 1995. only subscale B of the Eating Disorder Inventory was associated with the presence of cluster B disorders. 1991). 1985.. 1988). 2000). 1990.. 1995). Some scholars believe that eating disorders represent a form of affective disorder (Cantwell et al. Winokur et al. It has been stressed that another cause of depression secondary to anorexia nervosa is reactive distress related to disturbed eating behavior. a lower weight at the first consultation are two predictive factors of suicidal behavior (Morgan and Russell.. et al. 2000). 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... avoidant. 1984.. also. 1995). most common were personality disorders of cluster C. analyzed suicidal behavior in-depth among patients with eating disorders. Milos et al. Halmi. aiming at destroying the body slowly rather than through a suicidal act. 1990. People with eating disorders usually evoke the idea of self-wounding features.Suicide in Anorexia Nervosa and Bulimia Nervosa 3 illness. concerns about body-image.. It has been suggested that depressive disorders in anorexia nervosa are.. Braun et al. which have been shown to have high prevalence in anorexia nervosa patients (Gartner et al. 1989. Braun et al. anxiety and substance-related disorders.. in fact. Halmi et al. 1999).. suicide occurs not only in the late phases of the illness but above all in periods of symptomatic remission (Jeammet et al. Depression disorders in patients with anorexia nervosa may be related to personality disorders. Kennedy et al.. 1979. 1985. 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. secondary to eating disorders (Ivarsson et al. in the case of the anorexic patients. patients with eating disorders may be responding to the anti-panic nature of the drugs rather than to their antidepressant characteristics. for Axis II. 1993. shame and guilt (Halmi et al. Gillberg et al.. 1994. (2004a) investigated comorbidity of psychiatric disorders with eating disorders. 1988). 1980. in particular in patients with anorexia nervosa and bulimia nervosa. a feature identifiable in histories of suicidal individuals (Russell. poor self-esteem.. Cooper. 1988). According to these authors the symptomatology of cluster . Viesselman and Roig (1985) suggested that response to an antidepressant does not necessarily mean that the disorder being treated is depression. 1992. borderline and obsessive compulsive personality disorders (Piran et al.. This misconception often leads to ignoring the risk of suicide. Patton. Few studies.. Herzog et al. 1977. 1991. According to various authors. There has been recent recognition of a very definite increased risk for suicide in girls with eating disorders (Apter et al. A few studies suggested that suicide is the major cause of death among patients with anorexia nervosa (Toltrup et al. 1975. Eating disorders are often comorbid with depression. They found that the most common Axis I disorders were affective. depression being the most common diagnosis (Lonnqvist. Hudson et al. 1995). in general. 1983) and antidepressant medications have been employed. 1994. Patton. 1979). refuting the assumption that inanition generally threatens the life of these patients.

among patients of this sample. requiring concentration. Russell (1979) reported that 87% of patients with eating disorders also had depressive symptoms and 37% of them had attempted suicide. while bodily dissatisfaction . binge eating and obesity. 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. Also. or disgust. The body is experienced with intense fear because it may gain weight or become fat or. History of suicide attempts was also linked to inpatient experience. and hysterical diagnosis. Both anorexia nervosa and bulimia nervosa share the disturbance in the way in which one’s body or shape is experienced. suicide attempts were significantly more common in subjects with a lifetime diagnosis of major depression. self-harm and behavioral inhibition in response to threat. They observed that personality disorder difficulties are particularly represented in patients who binge eat. The authors concluded that depression may be a contributing factor to suicide attempts in bulimia. shame. women with anorexia nervosa. affective instability. self-directedness. (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. Patients had planned and carefully thought out their suicide attempts and they told no one of their plans. reading items carefully. self-evaluation is unduly influenced by body shape and weight. on the other hand. Karwautz et al. Bruce et al. Bulik et al. regardless of the presence of lifetime major depression. especially cluster B disorders and to a lesser degree depressive/negative personality disorders. was associated with a history of inpatient treatment. Spindler and Milos (2004) found that among bulimic subjects. but not to a history of underweight. (2003) reported results of an investigation among patients with eating disorders. or it may be a clinical consequence of the possible increase of bipolar and secondary depression in this group. there was a higher frequency of conduct. secret. (1999) found that in the bulimia nervosa group of their sample. This assumption may explain why these patients are not represented in studies employing questionnaires. A history of suicide attempts is frequent in women with diagnosis of anorexia nervosa or bulimia nervosa and major depression. They found that there was a continuum of severity in borderline personality disorder pathology between the groups of patients with bulimia nervosa. Paolo Girardi. 45% of these attempts were serious suicidal gestures. (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. and deciding the most appropriate answer. were equally likely to attempt suicide. but previous suicide attempts in the sample of women with anorexia nervosa presented in the study appear independent of affective disorders. as in the case of bulimia nervosa. Orbach et al. and cooperativeness and high levels of harm avoidance. axes II comorbidity. which may in turn decrease the probability that they will endorse items describing psychopathology. Women suffering from bulimia nervosa also showed a statistical trend to report a less severe intention to die. Van Hanswijck de Jonge et al. (2004) found that women with bulimia nervosa and comorbid avoidant personality disorder may be characterized by interpersonal submissiveness and avoidance.4 Maurizio Pompili. Amedeo Ruberto and Roberto Tatarelli B patients often impairs patients’ ability to perceive and recognize their own emotional states and processes. Similar percentages have been reported by Vasselman and Roig (1985). antisocial.

indicating that inability or unwillingness to protect the body and dissociative bodily tendencies (body aberration) are strongly associated with suicidal tendencies. (2001) investigated a sample of adolescents to examine the relationship between cognitive and affective attitudes toward the body. lack of body protection. 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. Mazza and Reynolds (2001) investigated self-reported psychopathology in a school-based sample of 456 suicidal and non-suicidal adolescents. They found that attitudes and feelings toward the body. an interrelationship between attraction to death. body experiences and suicide.. can result in great alteration in perception. 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. feelings. 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. Extreme negative life events. Such changes may facilitate self-destructive behavior when under stress. attitudes. Individuals with anorexia nervosa and bulimia nervosa show a very peculiar attitude toward their bodies. they fear their body and struggle with it as an ominous enemy that has to be killed. 1986). 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. the sense of lack of control over the body also distinguished the suicidal group from the normal group. insensivity and indifference to sensation. These self-destructive tendencies are highly associated with a pervasive sense of disturbance of body image and experience. Orbach et al. Sullivan (1995) derived a crude rate of mortality due to all causes of death of 5.9 % for individuals with . bodily detachment. Among this sample. in another. body hate. 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. and loss of bodily boundaries. In one way. which deserves a suicidal gesture. such as physical and mental traumas. Also. typically performed with drug overdose and alcohol. they believe that their body is the most precious and important thing that surrounds them. and experiences of the body in the form of body rejection. and body aberration were the three factors that differentiated the suicidal group and the two nonsuicidal groups. They found that females who engaged in suicidal behavior reported experiencing significant levels of symptomatology associated with anorexia nervosa. sense of lack of control. 2003).Suicide in Anorexia Nervosa and Bulimia Nervosa 5 may increase suffering and intensify self-destructive attitudes. 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. The authors interpreted this result. Suicide and Attempted Suicide in Anorexia Nervosa According to Patton (1988) suicide is the main cause of death among individuals with anorexia nervosa. protection of the body. and body aberration emerged.

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. which is four times higher . This author analyzed 42 studies (178 deaths in 3066 individuals). (2004a) also performed a meta-analytic investigation of cohorts of patients with anorexia nervosa. excessive dosage of drugs. 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. Paolo Girardi. 1983). They found that the suicide risk was 23 times that expected for the combined group. George’s cohort). 89 (54%) of the deaths could be attributed to the complications of an eating disorder. 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.. Suicide attempts are also a prerogative of patients with anorexia nervosa. in which the individual deliberately initiates a non-habitual behavior that. Herzog et al. 1983.. and other events of this ilk – are. The overall risk of suicide range from 1. In the 38 studies in which the cause of death was specified (N=164). The WHO/EURO (Platt et al.. Also. Apter et al.6 Maurizio Pompili. and 31 (19%) to unknown or other causes. The meta-analysis showed that suicide in anorexia nervosa was. Patients with binge eating and purgative behavior usually have a weak control over impulsivity associated with the eating disorder.. Garner et al. (2000) found that anorexia nervosa carries a substantial risk of premature death. Milos 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. 1992) multicenter study defines suicide attempts as “an act with non fatal outcome. 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.8% (Patton. without intervention from others.000 individuals. They calculated expected suicides in a year in 100. properly speaking. and suicide in their sample was significantly higher than expected. Pompili et al.3% (Ratnasuriya et al. “quasi-suicidal attempts” or probably. 1993).000 individuals if they all suffered from anorexia nervosa. “non-suicidal attempts”. Among these individuals alcohol and drug abuse is also widespread. 1991). more accurately. These authors selected 10 studies (see table I) and identified suicides which occurred in the follow-up period of each cohort. or deliberately ingests a substance in excess of the prescribed or generally recognized therapeutic dosage. In literature. Amedeo Ruberto and Roberto Tatarelli anorexia nervosa. mood disorders seem to affect those who manifest such behavior more than they do restrictive anorexics (Vandereychen and Pierloot. a more frequent phenomenon than their counterparts in the general population. The suicide risk for anorexia nervosa increased 23 times. ranging between zero and 100 times. 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. and which is aimed at realizing changes which the subject derived via actual or expressed physical consequences”. 44 (27%) to suicide. Great differences exist among sub-groups of anorexics. All others – selfmutilations. Harris and Barraclough (1997) selected thirteen studies which described cohorts of anorexic and bulimic patients and performed a meta-analysis. will cause self-harm. 1992 – St. 1988) to 7. (2004b) found a lifetime prevalence of suicide attempts of 26%. except in one study (Crisp et al.

1996. Comorbidity of personality disorder with other psychiatric disorders contributes to suicidality. such as sexual and physical abuse. Marttunen and colleagues (1994) estimated that 17% of the adolescents aged 13 to 19 years who died by . 2000). Cheng et. Engström et al.. 1997. even though the strongest association was found with sexual abuse.. Foster et al. 1994. anorexia nervosa and bulimia nervosa were considered together in patients who had both. The personality of anorexic patients has been described as obsessive-compulsive. moreover it has been reported that patients with anorexia nervosa have typical personality clusters. 1997.. 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). 1994. cluster B and cluster C were both represented. 1999) and up to 77% of suicide attempters (Suominen et al. 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. Bulik et al. Virtually all kinds of childhood traumatic experiences were found to be associated with a history of suicide attempts. These patients seemed to have a more serious form of anorexia.. at least one-third (31-62%) of people who have committed suicide (Henriksson et al.. 1999. only rarely were such associations found in men. Lesage et al. (1998) found that if anorexia nervosa alone was taken into account.. 1997.. which might contribute to higher levels of suicidal ideation in this group. suicide attempts included. if. In fact. Comorbidity between personality disorders and eating disorders is frequent and it is a major issue. DSM-III-R cluster C was more prevalent. Viesselman and Roig. with lower body mass index. Matsunaga et al. and may markedly elevate suicide risk (Suominen et al. (1997) reported that in their sample of patients with personality disorders. The same study outlined the fact that anorexia nervosa participants were more likely to engage in suicidal ideation than bulimia nervosa participants. physical abuse and the witnessing of violence were found to be associated with self-destructive and suicidal behavior of different kinds. 1993. Ferreira de Castro et al. 1985). Nimeus et al. The results of this study confirm these findings in women. 1994) and is comparable to rates previously reported for eating disorder samples (Corcos et al. 6%) (Weissman et al. Self-destructive behavior. this points to the role of bulimia nervosa in the identification of individuals belonging to cluster B.. In the comprehensive Psychological Autopsy Study in Finland.. starvation is a form of chronic self-harming behavior and continuously maintaining underweight generates considerable distress. Suicide attempters with personality disorders have the highest level of repetition. In a study performed in Japan. higher levels of obsessionality and more frequent drug and/or alcohol abuse than non-attempters. Modestin et al... 1998) have suffered from personality disorders.Suicide in Anorexia Nervosa and Bulimia Nervosa 7 than the lifetime prevalence found in the general female population in Western countries (ca. those patients who had attempted suicide were older than non-attempters. instead. The authors suggested that in anorexia nervosa.. including suicide attempts. has often been associated with traumatic experiences in childhood. since the two conditions seem to increase the risk of suicide dramatically. 2002. socially insecure and dependent. sexual abuse. 1999. had a longer duration of illness and a greater number of previous failed treatments. 2003).. Foster et al. Brent et al. Choquet. introverted. The rates of personality disorders among adolescents who died by suicide have been studied (Links et al. In Favaro and Santonastaso’s study (1997). 1997. which is also consistent with the result of the study by Favaro and Santonastaso (1997).

whereas low self-esteem was associated with depression. These authors reported that self-esteem has a different role among the various types of mental disorders.. (USA) Herzog et al. “psychopathic deviate”. 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 . 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. 1998. 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. (UK) Emborg. 1997 (Denmark) Kreipe et al. Marttunen et al. (USA) Toltrup et al. (2003) investigated self-esteem in a sample of adolescent psychiatric patients.. 1988. especially the young one. to a greater risk of suicide. Psychotic disorders were associated with a relatively intact self-esteem when they were characterized by positive symptoms. (1994) examined adolescents with nonfatal suicidal behavior.1992. (UK) Eckert et al. (2004) investigated a sample of young women through the MMPI-2 and observed that some scales were risk indicators for suicide. and “low self-esteem”. or the degree to which one holds attitudes of acceptance or rejection of oneself. (USA) Crisp et al. and found that approximately 45% of male adolescents and 33% of female adolescents were characterized by antisocial behavior. “antisocial practices”. (Denmark) Deter and Herzog. 1985. Table I – Suicides among various cohorts of patients with anorexia nervosa. 2003 – modified) Study Patton. 1994. Milos et al. (Pompili et al. In this study adolescents with a history of suicide attempts showed significantly lower self-esteem. “obsessiveness”. “shyness/self-consciousness”. Guillon et al. 2000. Amedeo Ruberto and Roberto Tatarelli suicide met criteria for conduct disorder or antisocial personality disorder.1992 (St George's) Crisp et al. Wonderlich and Swift (1990) reported an association between borderline personality disorder (which belongs to cluster B) and suicide gestures in eating disorders. They found that anorexic patients with antisocial practices are at serious risk for suicide. They pointed out that self-esteem can be defined as an individual’s opinion of him/or herself... The same authors reported that in the case of anorexia nervosa purging type. Paolo Girardi... Given the fact that patients with eating disorders usually present low self-esteem we can hypothesize that rejection of oneself exposes the individual.1995. (Germany) Corem and Hewitt. (Aberdee). they found the following traits as risk factors for suicide: “hysteria”. (2004b) in their sample of patients with eating disorders found that cluster B disorders showed a strong association with a history of suicide attempts.8 Maurizio Pompili.. Youssef et al.

2000).. (Kotila and Lönnqvist.) 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. Corcos et al. In bulimic patients with a history of suicide attempts. 1997. In a study which investigated 205 bulimic patients. Patients with a history of suicidal attempts used laxatives and diuretics more frequently. Lewinsohn et al. These patients have an extraordinarily high rate of suicide (Favaro and Santonastaso. 1997). 68 with BN nonpurging type and 25 with anorexia nervosa binge eating purging type). which is a characteristic feature of bulimia nervosa occurring independently of depression and associated with poor body image. 1999 (USA) Wiederman and Pryor. 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). They found that more than twothirds had suicidal ideation during adolescence and their age at onset of the first eating disorder had been. (1997) suggested that low self-esteem. . 2003 – modified) Study Viesselman and Roig. on average. 1986). Bulik et al.. 1999. 1987). 1996 (Italy) Bulik et al. the body of evidence suggests that depressive symptoms reported by patients with bulimia nervosa are secondary.. 1996 (USA) Kreipe et al. pathological lying. running away. which is a major risk factor for completed suicide. stealing. 1997 (Italy) Favaro and Santonastaso. Kent et al. 1989 (USA) Sample 13 167 164 70 59 6 49 Follow-up 6 3 6 A. risk-taking behavior. one and a half years younger than for subjects with no history of suicide attempts. 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. the onset of psychopathology seemed to have been particularly precocious.S.1985 (USA) Favaro and Santonastaso.S 3 15 13 19 2 Suicide and Attempted Suicide in Bulimia Nervosa Suicide is one of the main causes of death among individuals with bulimia nervosa (Keel and Mitchell... 1999). Also. is the factor associated with increased levels of internally directed irritability. 25% of those that attempted suicide also had at least one past suicide attempt (1997). had more lifetime depressive disorders. As stated for anorexia nervosa. rather than primary phenomena (Cooper and Fairburn. Several studies have reported a lifetime frequency of suicide attempts in bulimics between 15% and 40% (Favaro and Santonastaso.Suicide in Anorexia Nervosa and Bulimia Nervosa 9 Table II Attempted suicides (A. or hetero-aggressive behavior. (2002) presented a sample of 295 women with bulimia nervosa (202 with BN purging type. and more lifetime frequencies of substance use and disorders of conduct (self-injurious behavior.

Viesselman and Roig (1985) found that 20% of the bulimic patients analyzed who had attempted suicide. 80% of the patients with this features had a history of suicide attempts or self-mutilation prior to the onset of bulimia nervosa. Paolo Girardi. such as late onset. 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. affective disorders. Borderline personality disorder is no doubt extremely frequent in patients suffering from bulimia nervosa. Amedeo Ruberto and Roberto Tatarelli Data concerning suicide in bulimia nervosa are still scarce. in fact. Also. In two long term follow-up studies of borderline patients treated in residential settings. . substance and alcohol abuse and borderline personality characteristics including impulsiveness.. 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. Comorbidity of personality disorder and major depressive episode was associated with an increased number of suicide attempts. comorbidity between personality disorders and eating disorders is frequently found among cohorts of patients. 1993) of the following behaviors: alcohol or drug abuse. Among bulimic patients a number of clinical variables have been linked to a greater risk of suicide. 1992. In this study. Fichter et al. (1988) found that suicide attempts were more serious in those patients who had a borderline personality disorder comorbid with the eating disorder. 1989). no significant difference in age at the first suicide attempt was found in patients with borderline personality disorder and patients with comorbid disorders. is associated with the number of suicide attempts independent of comorbid depression or substance use disorder.. 1993. among patients with borderline personality disorder. 1985. Fichter et al. 11% of these individuals were drug and alcohol abusers. 1988. 1994). repeated self-mutilation. 1994) or at least one (Fahy and Eisler. in their sample only 27% of the multi-impulsive bulimics met the borderline personality disorder criterion. sexual disinhibition. such as “multi-impulsive bulimia” or “multi-impulsive personality disorder” (Lacey. 1993. consistent with the natural history of the disorder. and a higher lifetime number of attempts.. The authors questioned the hypothesis that impulsivity in bulimia nervosa is not necessarily part of a comorbid borderline personality disorder. Shearer et al. respectively. impulsivity. (2000) found that patients with borderline personality disorder or comorbid disorders attempted suicide for the first time earlier in life than the depressed patients. the patients with borderline personality disorder differed from the depressed patients in having an earlier onset of suicidal behavior. Soloff et al.. McGlashan (1986) and Stone (1987) found that 3% and 9%. Some authors call for the recognition of a distinct diagnostic subgroup of bulimia nervosa.. also had a diagnosis of major depressive disorder.10 Maurizio Pompili. Vandereychen and Pieters. purging behavior. of borderline go on to complete suicide. This subgroup is usually defined by the existence of at least three (Lacey. Sheares et al. Mitchell. Nagata et al. 1992). assessed as a diagnostic criterion. shoplifting. 1988). As stated above. 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. (2000) investigated a sample of patients with eating disorders and found that 18% of the 114 bulimic patients showed multi-impulsivity. The incidence of completed suicide in borderline personality disorder has been unknown until recently (Paris et al. Yet in some studies suicide seems to be the main cause of death (Mitchell et al. suicide attempts.

1992. 1996 (Italy) Bulik et al. 1996). 1992). 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.S. weight and shape of body preoccupations and have a history of suicide attempts. Favazza et al. 1985. 1989. Table III Attempted suicides (A.. (Favaro and Santonastaso. drug and alcohol abuse and self-injurious behavior. Bulimia nervosa is without doubt linked to self-injury (Dulit et al. 1995).Suicide in Anorexia Nervosa and Bulimia Nervosa 11 Youssef et al.. (2004) found among women with bulimia nervosa purging type a number of personality traits associated with suicide risk. 1980 (Canada) Favaro and Santonastaso. 1995).1998 (Italy) Favaro and Santonastaso. Suicidality among these patients seems to be increased by the number of compensatory behaviors that the patients engage in. Nevertheless. They observed through the employment of the MMPI-2 that in bulimic women with suicidal attempts the following scales were risk indicators: “psychasthenia”. Da Costa and Halmi. 1998)... Suicide attempts were associated with more serious psychiatric symptoms and with higher levels of obsessionality. impulsivity does predict suicidal behavior (Favaro and Santonastaso.. Mitchell. 2003 – modified) Study Viesselman and Roig 1985 (USA) Garfinkel et al. 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). 1996 (USA) Favaro and antonastaso. in fact. Herpertz. as they more frequently experience depressive symptoms.. the greater the risk of suicide (Favaro and Santonastaso. this behavior has also been linked to a number of dissociative symptoms (Everill et al.1997 (Italy) Favaro and Santonastaso.. However. 1999 (USA) Wiederman and Pryor. 1983 (USA) sample 36 155 210 161 152 58 125 175 15 follow-up 8 6 3 2 A. 1994. (Pompili et al. Van der Kolk et al. “anger” and “fear”.S. (1991) have considered eating disorders a form of self-destructive behavior similar to suicide attempts and selfcutting. Patients with purging behavior have a more serious course of illness. the more strategies utilized. 1999 (Italy) Raynes et al. Patients. 1997.. but rather to the presence of purging behavior. 1994. 1991). Dulit et al.) among cohorts of patients with bulimia nervosa. A typical symptom of bulimia nervosa is self-injuring and self-mutilation. Viesselman and Roig. describe this behavior as an invincible impulse to self-inflict punishment. Self-mutilation should not be considered a feature of suicide behavior but a way to reduce tension and induce relief (Root and Fallon. in order to reduce weight. patients have the chance to experience their body and look for a sense of reality and their own identity. 36 38 28 47 18 23 29 6 . purgative behavior might be considered a sort of self-wounding action.

nevertheless. many children and adolescents not only try to lose weight and are concerned about what they should and should not eat. The effect of the behaviors is long-term. some kind of adaptation is achieved which may or may not be in the best interest of that person and his fellows (Farberow. thus persisting for a long time and impairing intrafamily relationships. 2) need to gratify the present and to overcome feelings of inadequacy. 8) superficial and casual relationship. illicit substance use and risky driving are methods to gain acceptance and respect among peers. if problems were not adequately worked through. As Litman (1980) put it. 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. 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. i. Paolo Girardi. 4) no immediate action taken towards stress. mastery. When repetitive and habitual. regression. 5) need of stimulating actions and games.. and the need for repression is also chronic. Caplan (1964) states: “A crisis is an upset in a steady state or disturbance of homeostasis”. behavior such as smoking. Unfortunately. Dysfunctional behavior in the family environment may undermine development during adolescence and lead to indirect self-destructive behavior. enhance competence and develop initiatives. drinking. but when conflicts are solved. narcissism). behavior patterns adopted during this period may constitute dysfunctional behavior in adulthood. the symbolic replacement or symbolic partial expression of the problem in its own turn becomes chronic and fixed. especially depression.12 Maurizio Pompili. . They distinguish developmentally constructive risk taking (adaptive experimentation to build confidence. necessitating longterm adjustment. establishing independence from parental authority. 7) lack of messages and communication with others. 1967). and skills essential for transition to adulthood) from pathogenic. According to Jessor (1991). such behavior is given up. which underline their inner struggle with the body. deviant. Individuals in crisis often resort to indirect self destructive behavior as a coping mechanism. To give up the indirect self-destructive behavior is not an easy task. indirect self-destructive behavior endangers life. Some investigators argued that risk taking is a part of normal adolescence (Baumrind. Eventually. suppression. but also engage in high risk behaviors. and the person is usually unaware of or does not care about the effect of the behavior”.e. In this section we analyze high risk behavior among teenagers and point out its role as a consistent part of suicidal behavior. it is a chronic process. 3) lack of future orientation and little maturity. 1987). life-threatening risk taking that potentially jeopardizes health and life. 6) various coping mechanisms (denial. are chronic rather than transitory. we recognize this as a time-limited condition. In the case of adolescent “crisis”. since it means the loss of pleasure and reactivation of painful depression”. Many forms of indirect selfdestructive behavior that developed as coping mechanisms have often also been a source of temporary pleasure. “When painful psychological states. High risk behavior is strictly linked to indirect self-destructive behavior. Farberow (1980) persuasively presented the following features of such behaviors: 1) undermining physical health. behavior promoting autonomy.

Another open issue is those deaths called subintentioned deaths. is supposed to reduce perceived stigma in children and adolescents. metatherapy. 2002). an unintentioned death is any death in which the decedent plays no effective role in effecting his own demise. and its risk. Hence. Self-destructive and risk-taking behavior. should not be disregarded. Even minimal manifestations of this continuum. techniques aiming at correction of pathogenic beliefs may prove useful for adolescents and adults (Weiss and Sampson.. 1994). 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. A recent paper (Borawski et al. This study clearly stressed the importance of parents in induction of health risk behavior. 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. a holistic family technique focuses on children and their parents and aims at increasing appropriateness of child-parent communication (Pfeffer. these data point at a healthy. such as alcohol or illicit drug abuse. In particular. Furthermore. as assessed through the Adverse Childhood Experiences (ACE) scores. and plateaus thereafter (Reynolds and Rob. such as drug or alcohol exposure. unprotected sex. . 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.Suicide in Anorexia Nervosa and Bulimia Nervosa 13 Suicide is a leading cause of death in developed countries. namely a death in which the decedent plays some partial.. traditional-style family. an intentioned death is any death in which the decedent plays a direct. a psychotherapy based on the collaboration of the parental couple. conscious role in affecting his own demise. although they cannot be classified as suicide sensu strictu. 1983). Finally. Compliance with prescription. which is linked to suicide attempts. and risky driving. care should be taken to involve and educate parents. The role of parents is a critical one in this respect. Various approaches were suggested to treat suicidal children and adolescents. either pharmacological or behavioral. These scores also correlate with risk-related behavior. 1986). 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. displayed to comply with peer pressure. In this discussion it is paramount to define a subintentioned death. from part of a broad suicide continuum that may increase premature death in individuals conforming to this spectrum.. 2001). which may be represented in individuals with anorexia nervosa and bulimia nervosa. increases with increasing ACE scores (Dube et al. 1982). rises to peak until 15 years. as the major determinant of protection from risk-related behavior. Taken together. as they could give rise to successful suicide attempts or impair the organism’s defenses and render the individual more vulnerable to various noxae. Onset of problem behavior is at 12 years. 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. 1989). in managing youths exhibiting such behavior. lifetime prevalence of attempted suicide is about 4% in a United States population attending a primary care clinic. Coordinated efforts are needed when dealing with children or adolescents with suicidal ideation. modifying the youth’s perception of his own parents may be critical in reducing both suicidal thoughts and deliberate self-harm (Martin and Waite. as well as to increase satisfaction with parental role in parents (Vaz-Leal.

Subintentioned deaths are often identifiable in individuals who manifest poor judgment. Amedeo Ruberto and Roberto Tatarelli covert. Paolo Girardi. driving after alcohol abuse. foster the development of personal skills. self-destructive style of life. These difficult-to-treat disorders also demonstrate a continuity between adolescent onset and adult risk for the presence of an eating disorder (Kotler. bearing in mind that individuals who die after an accident may actually have had a role in the occurrence of that accident. Eating disorders are becoming more prevalent and observable across cultures. a conscious act may be lacking or may not be recognized. Given the fact that in many countries and regions most people in this age group attend school. 2001). Shneidman (1991. 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. bringing about his own death) in the immediate future (today. we should emphasize the need to improve recognition of all manifestations of the suicide spectrum. or their unconscious wish to be dead may play a role in all those deaths that belong to the subintentional category. as if they preferred a slow lethal action rather than a sudden death (Pompili et al. create supportive environment. this appears to be an excellent place to develop appropriate prevention action. learning and working. tomorrow. However. unprotected sex.. 2004c). The World Health Organization (2000a. One may wonder how to identify deaths from accidents and from suicide. Individuals with eating disorders may in some cases interchange their suicidal wishes with high risk-behaviors. the next day. the next month). People who engage in high risk behaviors may paradoxically be protected from suicide per se. 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. or unconscious role in hastening his own demise. Given the fact that patients with eating disorders manifest a number of behaviors that do reflect lethality towards themselves and high risk behaviors. 2004b).e. especially when the individual is ambivalent in his decision. acting more like a suicidal person than a victim of adverse circumstances. excessive risk-taking.14 Maurizio Pompili. in the case of undetermined death. defined as the probability of a specific individual’s killing himself (i. 2000c) defines a “Health-Promoting School” as a school that is constantly strengthening its capacity to be a healthy setting for living. Deaths from suicide are underreported because of the tendency to group them as accidental deaths or deaths from undetermined causes. abuse of alcohol. The promotion of children’s health through school is recognized at the international level as an important means of influencing health behavior. disregard of prescribed lifesaving medical regimen. This leads to a distinction between suicide and subintentional deaths even if they share various elements. strengthen community action. 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. Specifically. these programs aim to build healthy public policies. and reorient health services to embrace . misuse of drugs..

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. Psychotherapy with Suicidal Anorexic and Bulimic Patients Psychotherapy with suicidal patients is a real challenge for any clinician. The media can play a powerful role in educating the public about suicide prevention as well as in eduating youth about eating disorders. stem from frustrated or thwarted psychological needs. Adolescence is not an easy time psychologically. parents and community members work together to set priorities and plan actions. hopelessness. Psychotherapy may offer a key opportunity to reduce pain. 2001a. If the function of suicide is to put a stop to an unbearable flow of painful consciusness. mass media do not help in either the prevention of suicide or eating disorders. for exhibition. for understanding. These psychological needs include the need for achievement.Suicide in Anorexia Nervosa and Bulimia Nervosa 15 health promotion in addition to clinical and curative services (WHO. 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. such as risk taking behavior in individuals with eating disorders and suicidality among them. the rate of failure to respond is typically high and not readily explained by current scientific knowledge (Hsu. particularly for the treatment of anorexia nervosa. During adolescence. Psychotherapy has also been employed in the treatment of anorexia nervosa and bulimia nervosa especially in conjuction with pharmacotherapy. 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?”. 2) a particular death is reported at length or in many stories. Research finds an increase in suicide by readers or viewers when 1) the number of stories about individual suicide increases. numerous studies have considered the association between media reporting and portrayal of suicide and actual suicidal behavior and ideation (Pirkis and Blood.b). especially in suicide prevention. and adjustment indicators are important. for order. In fact. rage. for counteraction. 2000). and so forth. kills himself over poor grades”). There are relatively few evidence-based findings. international literature does not provide definitive results on the efficacy of psychotherapy in the treatment of such diseases. The power of mass media has been investigated in connection with suicidal behavior. such as shame. for nurturance. Shneidman (1993) described what he called “psychache”. In the few studies that have shown the statistical effectiveness of a certain approach. 3) the story of an individual death by suicide is placed on the front page or at the beginning of a broadcast. girls have a much higher prevalence of depression and eating disorders and engage more in suicidal ideation and suicide attempts than boys. 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. Unfortunately. for affiliation. guilt. 10. for autonomy. loneliness. 2004). HealthPromoting Schools also help pupils. They use information about the determinants of health and wellbeing. 4) the headlines about specific suicide death are dramatic (a recent example: “Boy. Shneidman (1993) also pointed out that the main sources of psychological pain. The healing effects . then it follows that the therapist’s main task is to mollify that pain. Nevertheless.

cannot be over-emphasized in this respect. various therapeutic approaches have been employed. and concerned more with the patient’s present and future than with the past. A lesson may be learned from the studies devoted to suicide among inpatients. The main goal of a psychotherapy with anorexic patients is to help the patient get in touch with inner feelings and experiences. the suicidal patienta are particularly prone to provoking countertransference reactions. . Due to their ability to cause strong emotional feelings. 2003). but cognitive behavioral therapy seems the most effective strategy for these patients. teacher. or working alliance. Therapists may fear the death of the patient but at the same time may enhance the risk of a suicidal death. 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. Crammer (1974) pointed to the potentially disruptive effects of transitions – for example. Hospitalization may carry an extra risk for suicide and staff should always keep an open mind throughout the entire stay of the patients. change in staff. Not evey therapist may be an appropriate therapist for suicidal patients.16 Maurizio Pompili. also therapy should change dysfunctional thinking which plays an important role in the psychopathology of this disorder. 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. Psychotherapy with bulimic patients is also a key element of the therapeutic armamentarium. and ward layout have been suggested as risk factors. 1973). they believe that the therapist should be active and should function in the therapeutic encounter as a parent. guide and coach. Poor communications about risk between medical and nursing staff. such as low morale or the absence of key personnel. initial acclimation toward life or plans for discharge or rehabilitation. Yet. Paolo Girardi. Amedeo Ruberto and Roberto Tatarelli of careful listening to the patient’s story and the development of empathy. 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. Despite different approaches. problem-oriented. Doctors usually treat patients who desperately want to live. The personality of the therapist is a major therapeutic element in the treatment of patients with anorexia nervosa (Hsu. most probably add to the suicide risk for a schizophrenic patient. Suicidal patients generate more anxiety and more feelings of anger. 2004). 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. countertransference reactions play an important role in the management of suicidal patients. According to Crammer (1974) an anti-suicidal ward is one with calm routine. to identify and verbalize them. Many authors have written about psychotherapy for patients with anorexia nervosa. Also. Anorexic and bulimic patients may be hospitalized especially in the case of severe medical complications. A sound therapeutic relationship. so that the patient feels truly understood. semistructured. suicidal patients. He also emphasized the environmental impact of staff variables. in contrast. Treatment is active. as well as the need for effective communication among relevant staff about patients judged as having an increased risk of suicide. 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. Insufficient control over counter-transference problems may increase suicide risk in the patient and suicide may result from an iatrogenic event (Andriola.

ondansetron (Faris et al. that is why prevention of relapses and amelioration of symptoms through proper pharmachotherapy is a key feature. Recent evidence points to the role of topiramate. 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. 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. especially those employing antidepressant medications.. trazodone (Pope et al.. 1986). 2001). Powers et al. 1991. FBNC.. fluoxetine. and treatment of the main disorder should be a second target of the therapeutic intervention. 1986)... 1998). bupropion (Horne et al.. brofaromine (Kennedy et al. 2001). Blouin et al.. Despite the fact that these medications do reduce overall suicide rates. . 1986... fluoxetine (Fichter et al.. chlorpromazine and amisulpride (Ruggiero et al. 2005. Over the past twenty years a considerably controlled trials have been devoted to bulimia nervosa compared with those devoted to anorexia nervosa. 2003). Antidepressant medications can reduce binge eating and purging independent of the presence of a mood disorder. Treating suicidal patients with eating disorders without any question a clinical challenge that requires great confidence in one’s own body of knowledge. As stated above. Suicidal patients need to be sedated. Nevertheless. Romano et al. 1989). 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. 2005). 2002).Suicide in Anorexia Nervosa and Bulimia Nervosa 17 carried out daily by staff who are themselves unworried and confident of the immediate future. 1988). A continous balance of the medication employed might be necessary in certain periods. cyroheptidine (Halmi et al. which has been found to have both antibinge and weight loss properties (McElroy et al. 2005. desimipramine (Hughes et al. 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. 1992. isocaboxazide (Kennedy et al.. and fluoxetine (Kaye et al. phenelzine (Walsh et al. Molecules showing more efficacy than placebo were amitriptyline (Halmi et al. Goldstein et al. Yet. 2005). Suicide risk is strongly linked to the persistence of severe symptomatology. infectious. several recent studies have examined the use of olanzapine (Mehler et al. sertraline (Santonastaso et al. haloperidol (Cassano et al.. 1995. Pompili et al. Their calm is. this is of great benefit since compensatory behaviors are associated with increased risk of suicide. Pompili et al. pharmacological treatments.. should be used very carefully in suicidal patients. 2000)..... 1988).. so to speak.. 1983).. The first-line medication is probably fluoxetine at high dose (20-80 mg). 1993). 2002)... 2003)... antidepressant medications such as fluoxetine and imipramine should be used very carefully in case of suicidal ideation (Baldessarini et al. However. 1988). 1988). 2001. pharmacological studies have not yet identified any medication resulting in definitive improvement of the core symptoms of anorexia nervosa..

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19:131-9. Preventing suicide. Eur Psychiatry 2004. Multi-impulsivity among women with bulimia nervosa.9:629-628. Geneva. Int J Eat Disord 1990. Goodman S.26 Maurizio Pompili.. Gladis M. 182-197. Preventing suicide. 2000c.. In: Herzog et al. Swift WJ.20:359-365. Roig M. Winokur A. p. Figure and facts about suicide (adaptation of the 1999 document). New York: Guilfor Press. Psychother Psychosom 1989. The significance of subclassification in anorexia nervosa: a comparative study of clinical features in 141 patients. 1986. A large-scale longitudinal follow-up study of patients with eating disorders. Pieters G. Viesselman JO. Am J Psychiatry 1980. WHO. Mendels J.137:695-8. and Empirical Research. Weissman MM. Phenelzine vs placebo in 50 patients with bulimia. World Health Oorganization.13:543-549. Swift WJ. Laget J.9:607-616. Geneva. WHO. Wonderlich SA. .45:471-5. Flament MF. Paolo Girardi. Int J Eat Disord 1996.29:9-17.52:125-132. Primary affective disorder in relatives of patients with anorexia nervosa. Plancherel B. Vandereycken W. Wiederman MW. Clinical Observation. 2000b. The Psychoanalytic Process: Theory. Stewart JW. A resource for primary health care workers. Canino GJ. (Ed. Psychol Med 1999. Roose SP. Stetner F. Sampson H. Amedeo Ruberto and Roberto Tatarelli Vandereychen W.). World Health Organization. Int J Eat Disord 1990. Youssef G. Slotnick HB. Corcos M.46:118-124 Walsh BT. March V. Glassman AH. 1992. Prevalence of suicide ideation and suicide attempts in nine countries. Depression and suicidality in eating disorders. Psychotherapeutic management of suicide attempts in children and early adolescents: working with parents. Psychol Med 1983. Pryor T. Personality trait risk factors for attempted suicide among young women with eating disorders. Halfon O. Borderline versus other personality disorders in the eating disorders: a clinical description. Vaz-Leal FJ. Pierloot R. A resource for teacher and other school staff. Berlin: Springer-Verlag. et al. J Clin Psychiatry 1985. Bland RC. Wonderlich SA. WHO. The course of eating disorders. 2000 World Health Organization. Arch Gen Psychiatry 1988. DSM-III-R personality disorders in eating-disorder subtypes. Geneva. Weiss J.

São Paulo. .In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. São Paulo. Universidade São Judas Tadeu. Chapter II Psychopathological Aspects of Body Image Disturbance on Anorexia and Bulimia Nervosa Simone Mancini Castilho Instituto de Psiquiatria. as one of the diagnostic criteria for these pathologies. fourth Edition (DSM-IV). 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. Although the presence and importance of body image disturbance in eating disorders are well established. 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. Brasil Faculdade de Psicologia. Universidade de São Paulo. Inc. Objective This study explores the presence of obsessive-compulsive and delusional features of the ‘Body Image Disturbance’ in anorexia and bulimia nervosa. Swain. the psychopathological nature of this symptom is not yet defined. Faculdade de Medicina. pp. Variables were analyzed with the Fisher’s Exact Test and Mann-Whitney non-parametric test (U). 27-39 © 2006 Nova Science Publishers. Hospital das Clínicas.

A.K. bulimic episodes are mostly originated in the dissatisfaction with the body and in the attempts to reduce body weight. 1995). (DSM-IV) (APA. Despite the fact that the features of obsessiveness in eating disorders have been studied (Pigott et al.. 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’. 1994) as one of the diagnostic criteria for these pathologies. 1991.D. despite the evident cachexia. which they consider as protuberant. Review of the Literature Meyer and Weinroth (1957) noted that patients with anorexia nervosa are excessively concerned with their shape. these episodes would apparently represent the opposite of the excessive eating restriction and fasting seen in anorexia nervosa. D. 1994). Dissatisfaction with body weight and shape seems to motivate several of the behaviors found on subjects with these pathologies. M. or denial of the seriousness of the current low body weight’ (APA. whose diagnostic criterion according to the DSM-IV requires a ‘disturbance in the way in which one’s body weight or shape is experienced. Although the presence and importance of body image disturbance in eating disorders are well established. Krahn. For example. 1994). The essential feature of bulimia nervosa are the recurrent episodes of lack of control over eating. ... especially with their abdominal features. The severest abnormalities occur in anorexia nervosa. what means an attempt to correct a perceived defect in the physical appearance (APA. Discussion The analysis of the psychopathological differences of ‘Body Image Disturbance’ in anorexia and bulimia nervosa has diagnostic implications. However. Zubieta. the psychopathological nature of this symptom is not yet defined. Fenick. Next. 1994). At first. Demitrack. A. J. fourth Edition.. Introduction Body image disturbance is an important clinical feature on eating disorders and was characterized by the Diagnostic and Statistical Manual of Mental Disorders. the research on delusional features or the interface between obsessions/delusions in eating pathologies has to be better explored.28 Simone Mancini Castilho 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.. For the diagnosis of bulimia nervosa the DSM-IV requires that “self-evaluation is unduly influenced by body shape and weight’ (APA. undue influence of body weight or shape on self-evaluation. Bruch (1962) stated that ‘a disturbance in body image of delusional proportions’ would be the central aspect of anorexia nervosa.

we noted that systematized studies assessing the degrees or rates of psychotic symptomatology in patients with eating disorders are scarce. 1997..E. 1995... D. The inverse relationship. In a retrospective study. Weltzin. A. G. On the other hand.. A. Russel. They were selected according to DSM-IV criteria (APA. All anorexic and 3 bulimic patients were hospitalized at the time of the interview. 2. M. G..J.. R.. whereas in one of them they seemed to represent a factitious psychosis.. an increased frequency of eating disorders or symptoms in patients with OCD has been also documented (Thornton. Objectives This study aimed at: 1..H. 1992. according to the DSM-III criteria (APA. Beis. C. that is. Grounds (1982) showed that 5% of patients with anorexia nervosa had brief psychotic episodes. J..E. Among 16 patients these symptoms seemed attributable to an affective or schizoaffective disorder. C. E...M. Solyom.C.C. F. Damluji. 1988.Psychopathological Aspects of Body Image Disturbance on Anorexia … 29 Controlled studies identify high rates of obsessiveness among patients with anorexia and bulimia nervosa.M. 1985). 1992). in these studies structured diagnostic instruments were not used. Lyketsos.. L..S.. Hudson et al. 1994). 1991.... L’heureux. Broocks. C. Pigott. Of note. G.. Miles. C. 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. Paterakis. Cases of schizophrenia or organic psychosis were not identified. Bulik. Kaye et al. P.L. Duchmann... Freeman. and there are studies showing increased diagnostic proportions of obsessivecompulsive disorder (OCD) in eating disorders (Pigott et al. Beidel.. Rubenstein. 1991.. Assessing obsessive.G.A. Pigott et al.F. Murphy. and 16 met criteria for the diagnosis of anorexia nervosa and 11 for bulimia nervosa. Hill.. . N. 1980). Thiel. Ohlmeier. in 17 (13%) out of 130 patients with lifetime diagnosis of anorexia nervosa and/or bulimia nervosa. Jacoby. Lyketsos. J. Comparing both diagnostic groups regarding the mentioned psychopathological features. A. compulsive or delusional features of body image disturbance in patients with anorexia and bulimia nervosa. Method Twenty-seven female patients were interviewed. Schussler. T. (1981) described the clinical features of six patients with anorexia nervosa who had developed associated schizophrenia or schizophreniform disorder. D. J. W... 1982. J.E. (1984) detected psychotic symptoms. We also found studies in the literature which comment on the clinical features present in eating disorders and comorbid psychotic conditions (Ferguson. 1992).L. Kaye. T.... Hsu et al.

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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

Psychopathological Aspects of Body Image Disturbance on Anorexia …

31

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

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

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

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

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

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Simone Mancini Castilho

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

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

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

Psychopathological Aspects of Body Image Disturbance on Anorexia … Compulsive Features According to the Y-BOCS

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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*).

0174* .27% * 9. H.72% 27.1492 .0002* 0.A.0551* 25% 18. Conditions that increase the probability of going on a diet or fasting.75% * 75% * 25% 81..54% 27.18% .0130* Discussion A complex interaction of physiological and psychological factors.L.25% 75% 81.9594 . weight and eating seem to be important risk factors for these pathologies (Fairburn.27% 45. P < .0032* .27% * 0. Doll.75% * 18.0075* . . Compulsive and Delusional Features in the diagnostic groups Anorexia nervosa N = 16 Bulimia nervosa N = 11 54. Welch. 75% 56.45% .7741 .E. O'connor. C.27% * 36. cultural pressures and family demands is involved in the appearance of anorexia nervosa and bulimia nervosa.34 Simone Mancini Castilho Table 1 Obsessive.18% * P 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.25% 45.. such as the concern regarding body shape. 1997).8520 81.A.0081* .25% * 50% * ..25% 50% 56. S.25% * 43..54% 54.18% * 27.G.05.. M.45% 72. Davies.9394 . B.25% * 68.2747 .36% * 18.3048 56.09% * 27.2240 .36% 36.

the phenomenon could be considered an overvalued idea or a delusion if the lack of resistance not be only occasional. non-intrusive idea. however. For example. (1969) described the obsession as a ‘mental event with a subjective feeling of compulsion overcoming an internal resistance’ . In this context... Akiskal. The symptom ‘body image disturbance’ may have some features that deviate from the obsessive concern and bring it closer to overvalued ideas. 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. that is. making physical exercises.S. intellectually and emotionally identify themselves with it. Mullen (1979) also noted that the resistance to an obsession could fluctuate and suggested that. in patients with chronic OCD (Insel. The lack of resistance offered against thoughts and behaviors and the non-intrusive way of experiencing them. If we transport this concept to the . as it stimulates the performing of a diet. at the same time. B.J. weighing oneself or provoking vomits. then this idea could be deemed overvalued or delusional. Not all obsessive or compulsive features are always found in one idea or behavior.T.Psychopathological Aspects of Body Image Disturbance on Anorexia … 35 Once started. behaviors related to weight loss (e. Sometimes. Therefore. that is. differing from the obsessive concern for being a natural. if patients cease to recognize their idea as irrational or egodystonic.g. for instance. fasting. These concerns or images are frequent or almost constant and cause remarkable anxiety in the patients.. patients do not show resistance or insight regarding these thoughts or images.. Mayer-Gross et al. as can be observed. 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. the ‘body image disturbance’ becomes a risk and maintenance factor for the disease.. but a constant feature of the experience. we could be facing a different notion of a typical obsession (Insel.T. M. who try but are not always able to resist to their occurrence. Devlin. whereas. H. Akiskal. it is considered as justified and a normal expression of its nature. the lack of insight or resistance may make a belief or a behavior different from classical obsessions or compulsions. some of which are probable maintainers of the disease (Walsh. Such behaviors are clearly excessive and interfere with the socio-occupational performance of the patients. 1986).R. aiming at relieving the discomfort caused by the idea of being fat. 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. 1998). the emotional syntony or egosyntony with which patients experience it are some of these features. 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. accepted without resistance and which is not seen as senseless by the patient. but added that if the personality as a whole identifies itself with the idea. purging behaviors) cause physiological alterations. in such cases. Similarly to the compulsions there are repeatedly performed voluntary behaviors such as fasting. 1986). experiencing them as natural and reasonable.

Braff. (c) beliefs are idiosyncratic to the patients’ cultural context and (d) they are kept despite evidence or experiences in the opposite sense. without a consensus regarding its nature. Jaspers (1963) provides a formal distinction between prevalent ideas and delusions. 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. 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. 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. Its quality is. He argued that delusions would be better conceived as extreme points along certain dimensions of beliefs. Other remarkable aspect is the bizarreness of the belief or its lack of compatibility with reality. entirely distinct from normal beliefs. 1987). previous history of obesity or the presence of obese family members. in our study. Of note. its quality is similar to strong political. were assessed according to the following dimensions: concern with the belief. is erroneously considered as true. and delusional features of the body image disturbance symptom. and patients with a prevalent idea inevitably act on it. high degree of conviction and irreducibility of the belief shown by some patients. Although both groups had high values in the questions which investigated how obsessive their concerns related to body image were. he says. in fact. due to this strong affective load. such as the degree of conviction. patients might not consider their behaviors dedicated to weight loss excessive. and that. 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. an isolated idea. anorexic patients had higher scores in the questions that assessed compulsive features (6 to 10 in the . 1992). Anorexic and bulimic patients presented high scores in the assessment of obsessive. compulsive.R. The symptom ‘body image disturbance’ has delusional features which. religious or ethical convictions. and it could appear in the mind for understandable reasons. 1991. In that case. such as the fear of gaining weight among subjects with professional requirements of weight control.36 Simone Mancini Castilho symptom ‘body image disturbance’ we may perceive that the resistance of patients to the idea of being fat might not be present in all cases. On the other hand. understandable by the personality and life of the subject. as the personality is identified with the idea. irreducibility. D. origin and taxonomy (Butler. Therefore. Since the hey-day of phenomenology at the end of the 19th and the beginning of the 20th centuries. therefore. delusions having determined features: (a) its content is deemed false or fantastic. differing from them only in degree. regarding the high degree of current malnutrition and weight loss. the idea of being fat or having a big belly would be accepted and defended by patients. By contrast. Roberts. the great concern. resistance and insight. (b) the degree of conviction is firm and absolute. conviction. in a determined and repeated way. delusion has been defined in several ways. loaded and accentuated by a very strong affective state.. there was no difference between the groups in the total scores of these questions (1 to 5 in the Y-BOCS). In this case. The latter. Hemsley.A. insight and bizarreness. 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. P. an overvalued idea is. The study of Jaspers (1963) was incorporated in the current definitions. However..

D. V. Kaye.E. DC: The Association. T.. the difference between them remained. Beck. Comprehensive Psychiatry. W. G. Delusions: a review and integration.T. p.M. 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. 4th. the groups were compared again after the exclusion of this component of the scale.24. Erbaugh.C.. However. Weltzin. revised. such as having a lower correspondence with reality. E.. Diagnostic and statistical manual of mental disorders. Diagnostic and statistical manual of mental disorders. M. R.17. Summing up. Mendelson.. (1961) An inventory for measuring depression. etc. v. Perceptual and conceptual disturbance in anorexia nervosa. Therefore... J. being more vigorously defended by patients and being more concerning for them. v. Ward. bizarreness and concern) than bulimic patients. Washington. behavioral aspects of body image disturbance (weighing oneself. 3rd. Washington... Schizophrenia Bulletin. it is interesting that if we take away the practice of fasting from the list of target symptoms of body image disturbance. but. p. Bulik. p. American Psychiatry Association (1994).187-94. there is no difference between the groups regarding the quality of compulsions.4. Mock. to the severity of the clinical picture of anorexic patients in this study. bizarreness and concern were those responsible for such difference. H. As the assessment of the bizarreness of the belief was performed only by the interviewer.L. Beidel. what could be a source of bias.. 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. Comparative psychopathology of women with bulimia nervosa and obsessive-compulsive disorder. Bruch.Psychopathological Aspects of Body Image Disturbance on Anorexia … 37 Y-BOCS) and delusive characteristics (conviction. looking at the mirror. DC: The Association.262-8.53-63. compared to bulimic patients .ed. Diagnostic and statistical manual of mental disorders. fasting or doing physical exercises to lose weight. v. (1992). Washington.) seem to have a greater compulsive quality (questions 6 to 10 in the Y-BOCS) in patients with anorexia nervosa. Butler. Prospective studies with greater samples and are needed to prove this. Archives of General Psychiatry. 3rd. Psychosomatic Medicine. C. in part. A more careful analysis demonstrated that the components conviction (question 1).W. Braff. (1962).H. (1991).33. References American Psychiatry Association (1980).H.ed. Duchmann.. DC: The Association.ed. . These findings can be related. D.633-47. v. p. American Psychiatry Association (1987). A. nevertheless. This analysis seems relevant to us as fasting would be more similar to an avoidant behavior than to a compulsive behavior proper.

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but is rarely invoked. or translate medical expertise into medical authority. The regime of governmentality within the clinic is shaped by practices which operationalise ‘duty of care’. is ‘the law’. The ‘fiction’ of acting ‘responsibly’.In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. ‘carers’ and patients are mediated through conventions and rules. interactions with staff. ‘control’ (or management) is exercised diffusely. employed so . in a sense. behavioural ‘contracts’. Inc. to make the ‘correct’ choices. to accept the ‘empowerment’ regime that is made even more convincing by the threat of legal intervention. pp. and attitudes to the body) and what Goffman called the ‘moral career’ of the patient (eg learning to play the ‘patient role’. University of Sydney NSW 2006 Australia Abstract Anorexia nervosa is often chronic. Swain. through disciplinary practices embedded in everyday clinic life. such as daily routines of eating and washing. visits and activities. The patient learns to provide consent ‘freely’. at least formally (though the strategic possibilities of orders confers internal authority within the clinical setting). to ‘be’ an ‘anorexic’). we conclude that the regulatory regime that shapes treatment of anorexia nervosa. Instead. The regulatory regime not only touches on such ‘practices’ but also targets ‘identities’ (including self-image. with one of the highest death rates for psychological conditions. Law can compel treatment. 41-61 © 2006 Nova Science Publishers. or which conscript ‘empowerment’ as control. Chapter III Experiences of ‘Control’ in Anorexia Nervosa Treatment: Delayed Coercion. Rather. We argue that it is not the clumsiness of the law. Shadow of Law. that of the ‘recovering’ patient. or show how interactions between ‘experts’. Mim Ingvarson and David Tait Sydney Law School. or Disseminated Power and Control? Terry Carney. regular surveillance and measuring. In time the constraints learned in this way become part of the new role. or the success of less restrictive options which explains why law is so infrequently engaged. based on an interpretation of Foucault.

1996. peaking at about 0. A more neutral term. it is identified by ‘clusters of symptoms and behaviours considered clinically meaningful in terms of course. 2003). Feminists point to socio-political dimensions of anorexia (patriarchy. The patient has become an active participant in the governance of self. but it has strong pejorative overtones. 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. 1999: 37. either in shaping the form in which body image conditions express themselves in different countries (Abusah.5% (or 1% in some US studies) of women aged 15-19 age band (Griffiths.1 Whatever its true ‘character’. intense fasting. becomes part of the new identity. 3 ‘Control’ is an apt term from the sociological perspective. specifically menstruation (Tomkiewicz. 1993). but masks the exercise of legal and social power which brings about that result. like ‘management’ highlights the positive contribution to therapeutic outcomes. or its social and familial origins. Griffiths. means that aggregate mortality figuresof perhaps 1 death annually per million women aged 15-65 (Draper. 1999). its escalation into severe anorexia nervosa is usually accompanied by physiological changes that then limit the person’s awareness of the risks they face. 1996). 2001). Some writers highlight long historical traditions of ascetism. 2000)pales against the equivalent statistic of 61 female suicides per million Australian women (ABS Year Book 1997). like self-flagellation. 2000). The literature is divided about whether anorexia is mainly a pathological condition. may connote a display of devotion and sacrifice (Tait. or pre-disposing some young people to greater risk of anorexia. 2003). Feeney and Clarke. Along with many psychiatric conditions. leading the authors to suggest that. rather than by objective anatomical features (Bruce. And even if some fasting originates in a rational decision. embarking on crusades and other forms of extreme self-discipline. severe anorexia nervosa is experienced by half to 1 percent of women over their lifecourse (Steiger and Séguin. Kohn. Further: Beumont and Carney.42 Terry Carney. Introduction Anorexia nervosa joins other ‘syndromes’ listed in psychiatric manuals like the DSMlV(R) or the ICD 10. where fasting is associated with religious merit and definition of the ‘self’. 1984: 302-308). . seeing eating disorders as one of a series of responses to familial traumas. disempowerment) to explain the reported loss of self esteem and ‘powerlessness’ (Gilmore.2 complicated by treatment resistance and low rates of success (Ben-Tovim. Bray. with one of the highest death and morbidity rates among cognate conditions. 1998). 1993). Anorexia nervosa is life-threatening. 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. Draper. those young people from cultures where the condition is rare may experience a heightened risk of the condition (Alexander. 1996). Mim Ingvarson and David Tait hesitantly at first. outcome and response to treatment’. On this view. However its low prevalence. 2000: 120). or may in some contexts be understood as a ‘rational’ form of behaviour (For a review: Dresser. Others focus on the family and relational context in which the anorexic ‘identity’ is constructed (Young. And resistance to assuming an adult female identity may be reflected in attempts to delay the onset of puberty. Culture too may play a part. while it is a myth to believe that some cultures immunise against the condition. 1984: 297. 1994.

Tait. Under guardianship laws the substitute decision-maker can be any person from a statutory guardian to a member of the person’s family.. Saunders. Tait. less restrictive. 2003).. Saunders. We argue that control is mainly extra-legal (a product of family and clinical rather than legal transactions). 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. andmost cruciallyoften involves transformation of the identity of the patient within the particular social environment in which control finds expression. When mental health law is used. Touyz. 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. 1999). Previous work (Carney. This Chapter reports our data about the way ‘control’ is conceptualised and experienced during the lifecourse of anorexia. and the trajectories and transitions associated with it (See: George. Tait. Noordsy and Clark. Touyz and Ingvarson.Experiences of ‘Control’ in Anorexia Nervosa Treatment 43 Clinicians sometimes turn to law for assistance in compelling hospitalisation of people with treatment resistant or life-threatening severe anorexia nervosa. 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. legislatively 4 Our focus is on sociological insights revealed by taking a lifecourse perspective on the life domains of anorexia. Different laws may be invoked at different times during episodes of hospitalisation or increased management over the course of their treatment (Carney and Saunders. Moreover in the case of anorexia. Some patients are scheduled/committed under mental health laws while others are covered by adult guardianship legislation (Carney. Wakefield et al. 2002) or ‘close management’ (Drake. Saunders. Mercer and Drake. 2003.3 both in formal (legal orders) and ‘informal’ settings where it is synonymous with clinical management regimes like ‘assertive treatment’ (Davis. coupled with insights derived from the work of Erving Goffman and Michael Foucault. Given the legislative and clinical preference for voluntary treatment. . Touyz. Noordsy. Teague. Law is invoked only when other. 1999). Bartels. Carney. those legally sanctioned interventions account for comparatively small proportions (or ‘slices’) of the lifecourse4 of the condition (Carney and Saunders. or to require involuntary nasogastric feeding. 2002). 2003). measures prove inadequate. Wakefield et al. 2004). 2002). including notions of illness as ‘career’ (Aneshensel. 1993. 2003) analysed the experience of anorexia patients. is very diverse in its deployment (ranging from suasion to coercion). the head psychiatrist of the service where a person is receiving treatment makes the decisions about treatment.

Touyz and Carney. 1998: 51). Boyer and Lubell. through threats of negative consequences such as involuntary hospitalisation or being put out of the house. persuasion. since responsibility for assisting with the management of adverse effects of severe anorexia primarily lies with the medical profession. Borum and Wagner. Swartz. 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. 1999: 450). and coercion may be ‘experienced’ in community as well as in hospital settings. Even ‘informal persuasion’ takes many forms in the case of anorexia management. barter. Swartz. 2002: 122). This is unsurprising. blackmail. … (Rathner. A Gradient of Forms of Suasion/coercion. not the legal system. 2002). 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. relatives and co-workers’ (Pescosolido. 2003). relatives. Wakefield. ‘does not tell the whole story of coercion’ in mental health (Hiday.44 Terry Carney. [T]here are various social pressures that family. 1998: 185-86). Legal coercion. schools and (mental) health care personnel use in an attempt to get the sufferer to accept the idea of seeking help: request.5 tends to be a measure of ‘last resort’. . gentle prodding. As discussed further below. ranging from ‘mere invitations’ to ‘verbal brow-beating’ or moral blackmail. as Hiday et al observed. Individuals are ‘”pushed” into care by friends. Swanson. Borum and Wagner. reasoning. through inducements with offers of desired objects or services …. Swanson. enticement. with its notion of ‘mutual obligations’ of clinician/patient (Dresser. 1984: 323). 2002: 124). informal ‘suasion’ is both much more common and more nuanced in its impact on the young woman (Tait. manipulation. bargaining. 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. stronger again in its impact on the person with anorexia are cases of ‘strategic’ use of law. friends. Among clinicians. 1999: 449). Boyer and Lubell. as Rathner observed. a frequent next step up the compliance ladder is to encourage compliance by employing a legal concept like a ‘contract’ (Harlow. depending among other things on the perceived ‘fairness’ of the process (Hiday. Ingvarson. running from: [M]ild persuasive attempts and pleas. just as in mental health generally. Swanson. to strong application of physical force (Hiday. Mim Ingvarson and David Tait sanctioned coercion. 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. deceiving. selective information. Borum and Wagner. Swartz.

with committal retained as the last port of call. Tait. a major public teaching hospital in Sydney. Carney. Twenty five cases with another eating disorder or co-morbid diagnosis were discarded. 2001. Approximately 40% of admissions were for less than three weeks. while for a quarter of the sample there were 4 or more admissions in the period. Almost two thirds of admissions (63 of 96) took place without any indication of clinical consideration of a possible need for coercion. 2004). Of these. Ward. Saunders. 2000). Legally-backed coercion is the exception As more fully reported elsewhere (Carney. Tait and Touyz. Saunders.6 The facility utilised a ‘progressive’ regime that minimised the level of coercion (Carney. . and reportedly used mainly to ‘initiate’ rather than coerce treatment (Newman. 2002). the study found low rates of resort to formal (legally mandated) coercion. 2003).7 within a state jurisdiction where adult guardianship options were available. mapping various factors such as case flows. Treasure and Russell. Tait.Experiences of ‘Control’ in Anorexia Nervosa Treatment 45 treatment (such as adult guardianship). Tait. even though 15 of these cases (28% of the sub-sample). Saunders. and what form of order to seek (Saunders. Bowers and Andersen. deciding if legal coercion was needed. guardianship tends to be favoured over mental health. Touyz and Ingvarson. a. with a mean stay of 49 days (and a maximum of 344 days). or foreshadowed strategically (Carney. Russell and Beumont. On entry to the program clinicians implicitly assessed the required patient ‘status’. Use of Formal ‘Control’ in a Typical Specialist Anorexia Unit. Touyz and Ingvarson. 2003. Formal coercion might have been mentioned by treating doctors. leaving 96 admissions relating to 75 individuals. if both adult guardianship and mental health laws are available. while 19% were people over the age of 30. only to be later followed by its subsequent withdrawal once this ‘leverage’ has achieved the desired goal of ‘voluntary’ acceptance of treatment. duration of treatment stays and use of legally mandated coercion. 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’). 2004).8 6 7 8 Data was extracted for all 119 admissions to the specialist anorexia program of the Royal Prince Alfred hospital (RPA. 1995). Watson. over a period of four and a half years. Slightly over a third (36%) were under the age of 20. Carney. This provided a particularly useful case study of how power is exercised within a relatively low-coercion environment. characteristics of patients. Wakefield. and in another three cases (5%) it was their third admission. One third of the admissions were isolated events within the sample frame. the least popular choice among anorexia clinicians is to obtain a formal legal order to compel treatment (Carney and Saunders. 1999. As revealed in the next section. Touyz and Beumont. 2004). Even lower proportions of coercion (approximately 16% of the samples) were found in the Iowa (US) and Maudsley (UK) studies (Ramsay. and whether to go ahead with obtaining legal backing. were second admissions. in the state of New South Wales).

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. Mental health committal is also commonly used in conjunction with/after guardianship. Forty two percent of legally coerced admissions were of this character.5 yrs) and the non-coerced group (24. Guardianship is seldom used on its own. but mental health committal is popular. The study data revealed that mental health committal is also quite commonly used in conjunction with guardianship. it usually led to an application for an order. By contrast. Mental health committal orders were much more popular with clinicians as a ‘standalone’ order. or subsequent to an earlier order for adult guardianship.5% of 26 admissions backed by a legal order) solely involved adult guardianship.6 yrs). or to make decisions about proposed behavioural therapies (two thirds of such cases in the study). accounting for 44% of all such admissions. 40 cases (62%) were patients on their first or second admission. Coercion is most likely to be considered for chronic cases Formal coercion is understandably considered in more chronic.46 Terry Carney. was the exception: only 3 admissions (11. Mim Ingvarson and David Tait b. 16 of the formally coerced cases involved patients on their 3rd or subsequent admission (72% of this subsample). Number and coercion status of admissions. Guardianship allows appointment of a third party to provide consent to medical treatment (one third of the ‘mixed’ order cases). 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). But adult guardianship. As revealed in the table below. d. 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. Of those where formal coercion was not considered or used. .2 yrs). The mean age at admission was almost identical for the coerced (24. those for whom coercion was considered but not invoked were older (average age 29. while the others were grounded in supervening factors such as depression. on its own. When formal coercion was canvassed by clinicians. Slightly more than half of these were based on the medical complications of anorexia itself (6 of 11 cases). delusional behaviour or threats to the health and safety of the person. as it was in 27 percent of cases.

2002). This phenomenon was detected in anorexia cases by members of the adult guardianship tribunal in the state of New South Wales. and even law/power influencing World Trade Organisation bargaining (Steinberg. . 2002). the management of alleged promiscuous sexual ‘delinquency’ of young women (Ajzenstadt and Steinberg. Indeed. Seven (27%) of the applications over the decade involved more than one application. with only an average of one application a year. Guardianship is lightly used Data for the ten year period 1994-2003. 11 12 13 Personal communication with NSW Guardianship Board members. Australia (‘NSW’). apart from a peak of seven applications in 2000. 1995). As shown in the next table.12 It was further refined by a more detailed review. Statistics supplied by the NSW Guardianship Tribunal. a. and were then allowed to lapse once cooperation was forthcoming. De-identified data extracted by Esther Cho of the Guardianship Tribunal on 8 August 2003. STATUS OF APPLICATIONS ‘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 Year ‘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 Total Withdrawn Adjourned Dismissed GrantedGO 26 6 1 1 18 It can be seen that guardianship was rarely used in the first half of the decade. applications are patchy at best. only three or four applications were made each year in the latter part of the decade. Members observed that guardianship applications were being lodged strategically to persuade patients reluctant to consent to proposed treatment regimes. 2000. or procedural rules impacting on pre-trial civil settlements (Main and Park. Guardianship (GO) Applications 1994-2003. 1992).13 indicated that the tribunal has been lightly used for anorexia cases over much of its history. with recent examples including the strategic influence of law on negotiation of child custody disputes (Jacob. Thurday 11 October 2001. 1979 on divorce bargaining). tracking the history of guardianship applications in respect of anorexia nervosa patients.Experiences of ‘Control’ in Anorexia Nervosa Treatment Tracing ‘Strategic’ (or Shadow of Law) Uses of Formal Coercion 47 The normative character of transactions taking place in the ‘shadow’ of the law has long intrigued researchers (Eg Mnookin and Kornhauser.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. however.

Mim Ingvarson and David Tait b. revealed that several withdrawn cases reappeared in later years. you know. very few applications appear to have been lodged by 14 15 As indicated previously. the sole case in 1995. where such forms of ‘intensive supervision [are] at times provided with the client’s consent and at other times is provided involuntarily’ (Noordsy. 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…. Mercer and Drake. Yeah. before finally being placed on an order in 2003. 2002).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. had her application withdrawn in that year. while family members were the nominal or actual applicants in 8 cases (in 4 withdrawn matters the applicant was ‘to be advised’. Likewise ‘Eve’. Thus the sole case from 1994 (‘Abigail’.15 Unlike most other types of adult guardianship application. ‘Hanna’ saw two applications withdrawn in 1999 and 2001. implying that clinicians had a hand in initiating the matter): data referred to at n 15 above. . 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. And I thought oh great. Fieldwork reports by ‘Fiona’ (not her real name) of another otherwise unrecorded episode suggests that this may understate such cases. Indeed such regimes may occupy the hinterland between community treatment orders and more ‘voluntary’ programs (Davis. We just think you should go to the hospital’. Strategic withdrawals are not always the end of the story Fewer applications were withdrawn than was expected: just six of 26 applications (or 23%). And they said ‘you’ll have to go to the tribunal’ and yeah … What we term the ‘strategic context’. an alternative explanation can be made in terms of regimes such as clinical regimes such as ‘close monitoring’ or ‘assertive treatment’. how can I appeal this or whatever’. And in 1997 another guardianship order was sought (but denied by the Tribunal). I said say ‘I’m not going to. not her real name) appeared on three occasions in all. then. really my head wasn’t there and I really wasn’t there. She reappeared in 1996 when a financial management order was granted (and guardianship adjourned). including whether to rely on the ‘shadow of law’. is pertinent to choice of pathway. withdrawal in 2001) round out these cases of an apparently ‘strategic’ resort to the Tribunal. granted 2000) and ‘Rebecca’ (granted 2000. She had a guardianship application lodged and withdrawn in 1994. 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. But she was placed on guardianship when she reappeared six years later in 2001. For her part.48 Terry Carney. however. well it’s funny ‘cos it said on the envelope it had been delivered by the bailiff and it was in my mail box. as in the case of lodging proceedings which are later withdrawn. Closer study. Clinicians were named as applicants in 14 cases. ‘Martha’ (withdrawn 1999. often adopted with ‘dual disorder’ patients.. 2002). however. 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.

without regard to the wider context and web of relationships within which a patient operatesis likely to be unduly simplistic. His focus is on the ‘techniques’ for the exercise of power. Institutions not commonly thought of as part of the law. churches and jails (Pescosolido. Boyer and Lubell. As Foucault demonstrated. So they said. This suggests that the applications were seen as something that would enable treatment rather than as a challenge to medical authority (also: Newman. Disseminated Power and Control: Towards self-management/control? As we have already seen. Felicity is driven by her violent dislike of a particular clinician at an alternative facility. There are several factors in play here. She decided to ‘comply with what they wanted’. are key players too.Experiences of ‘Control’ in Anorexia Nervosa Treatment 49 friends or family members on their own volition. So an analysis from the standpoint of managers and regulators alone. This combination of disciplinary influencesthe interplay between dislike of a particular clinician. 1999: 455). threats to switch service settings. power is dynamic rather than static. (Emphasis added). and shaped by its point in history. her ‘hatred’ of that other clinician was apparently the more powerful force motivating her (reluctant) compliance. including self-help groups. First. Second. ‘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 …. such as the home or the hospital. 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. and is often highly disseminated rather than always channelled through particular structures. As one commentator observed. 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. 1995: 58). We’re going to tube feed you’. C. Despite being tube fed. and the services with which they are associated. and the . and despite being coerced into acceptance of this course by a legal order (adult guardianship). at least ‘for the time being’. and social service agencies. the treatment system. Russell and Beumont. and of the prospect of the stigma of transfer to a ‘psychiatric’ unit. [d]ealing with any health problem is a social process that is managed through contacts or social networks that individuals have in the community. as foreshadowed by her treatment team. clinicians. may become sites for expression of such poweroften linked in with complex social networks. and the foreshadowing of psychiatric committalwas sufficient to win her grudging compliance. she was fearful of the loss of control of being placed in a locked ward and then physically ‘restrained’. 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. ‘Right.

or as the ‘sovereignty’ of power (Rabinow. It is a truism that law is power. Shearing and Stenning show how Disney World is constructed to ensure that consumers are complicit in their own security (347). and freely chosen (Shearing and Stenning. 1984). power was not so well captured by such metaphors of ‘command and control’. groups. 2000). 2003). 1997).50 Terry Carney. but that its power is mediated in many ways. (Holmes and Gastaldo. 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. For Foucault. communities. conduct or affect people as well as to construct. as in the carer relationship in nursing: Nurses … are in direct contact with individuals. through their interventions. 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. In this view. These ‘subjectivities’ (sometimes called ‘bio-power’) principally include the ‘self’ or ‘identity’ of the patient. a regulatory regime may be experienced as beneficent. 2002). 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. people's subjectivities. The treatment of anorexia nervosa is harder to deliver without coercion than a plunge down Splash Mountain. and such acculturation may facilitate social functioning or the capacity to manage chronic . This is because clinicians may subtly ‘privilege’ the preferred option supposedly ‘chosen’ by the patient (Powers. 2002). While therapeutic interventions lend themselves to analysis from this perspective. Power is shifting and unstable. Working at the junction of the individual and collective body within power relations that promote and recuperate life. this does not displace the legitimate role played by the psychodynamics of some conditions (Glass. even as superficially attractive a goal as pursuit of ‘empowerment’ in therapy can constitute a technique for the exercise of power. So self-images are shaped by these exchanges. 2002). nurses are able. Nursing too involves deploying techniques ranging from ‘disciplining’ to ‘promoting discourses that construct desirable subjectivities’ (Holmes and Gastaldo. and populations [constituting] a powerful group of experts …. or imposition of nasogastric feeding (Carney. Of course care must be taken not to oversimplify the application of this analysis (Cheek and Porter. indeed sometimes even pleasurable. 1997: xvii). to mold. that selfregulation (assisted when necessary by staff dressed up as Mickey Mouse or other characters from the Walt Disney imaginary) combines freedom and security. A space lying between mere gameplaying contestation and the ‘state of domination’ constituted by its expression in legal coercion. Mim Ingvarson and David Tait dialectic of the dialogue of application and resistance to that power. Exchanges which are never neutral but which may be advantageous or ‘controlling’ in character. with the help of other health care professionals. Instead it was located in the ‘governmentality’ space. As Powers has recently argued.

tends to find its expression in the fluidity of the ‘negotiations’ about the relationships forged both in this societal space. That role has been undermined both by the problematic status of ‘disease’ within psychiatry (Dawson. frequently harks back to. who have had an eating disorder. 2002: 123). 1997: 4041). 2003). I’m terrified of ever going there again. however. I think a lot of people do it. the ‘community/family’ space is now much more central. life in the other sphere. Borum and Wagner. 2004). we suggest. or anticipates. 2000). Hospitals (and medicine) no longer serve as the primary agents for ‘clarifying and purifying’ the disease entity. Pearson. of diagnosis. You can kind of keep yourself . One of our qualitative interviews illustrates this interpenetration of the two ‘worlds’. Beumont and Carney. when she said: I know where this is going to end up. It shows that sometimes the legacy of past experience. Swartz. Power as Experienced by Anorexia Patients Consequently. she brought out the sense of being caught in a kind of systemic ‘limbo-land’ or twilight zone in terms of her weight. can leave a more positive legacy of ‘control’ for the future. in hospital again. This is the new site where power and control is experienced by sufferers of conditions like anorexia (Hiday. or anorexia and have been under weight. In-patient care for psychiatric conditions has altered quite dramatically over the last several decades. 1996. the role of access to ‘normalising’ social interactions and supports may be central to its satisfactory management (White. that once was the case when the ‘infection’ model of health was dominant (Foucault. Power in the case of anorexia management. (Emphasis added).. That terror of having control taken off me. as I wouldn’t want to ever go there again. Tait. Johnson and Ellis. Wakefield et al. Bebbington. 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. Saunders. The hospital setting is no longer the primary ‘place of observation. It’s almost like um. That’s the only good thing about the hospital experience.Experiences of ‘Control’ in Anorexia Nervosa Treatment 51 conditions like anorexia (Aneshensel. of clinical and experimental identification [and] immediate intervention’. the prospect of a return to hospital also shapes the lives of those currently living in the community. but also brings out the multiple levels of that relationship. 1999: 597). Moreover the currency used in negotiations within the setting (hospital or community) where the person with anorexia is currently residing. and those within the hospital setting. Swanson. So conditions of life in the community loom large in the life of hospitalised patients. And in similar vein. Turning to her ongoing issues with her weight management. Touyz. Indeed. however unpleasant. and by the relegation of hospitals to brief interludes in the management of conditions like anorexia (Carney. given that lack of ‘insight’ (denial) is a central ingredient of anorexia.

and she thought Kate was doing something to her and directly punishing her for something. which exacerbated the problem. It‘s a pretty miserable way to live. 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. um way too terrified to [end up in] hospital again. she projected her ‘hostility’. I get stuck in this: ‘I’m not totally over it or totally well’. it was ‘the little bitch is only doing it for attention’. And Kate used to dread her visits. who described the onset of her issues with food in the following way: . That sort of thing. So you know. in the sense of maintaining its thrall over her life and her management of the condition. she recalls how her mother presented herself as the ‘victim’ of Kate’s vindictive or ‘attention seeking’ behaviour: But Mum was also. As elaborated by Tess when she was asked how she herself came to understand that her sister was suffering from anorexia.52 Terry Carney. because of the way you’re treated in hospital you kind of afterwards get stuck. it’s hard because I think the system makes it almost like. So power and control can be very subtle and highly nuanced. 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. Kate ‘dreaded’ visits. Um. Kate’s mother. (Emphasis added). and just saw it as. the sister of ‘Kate’ (the patient). 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. but paradoxically ‘controlling’ as well. Blaming herself for ‘failing’ her daughter. I guess there are times where I feel like that. Look. And she couldn’t even come to the hospital. As can be seen from this passage. The interview with ‘Tess’. Mum didn’t know how to deal with it. she found it a great ordeal to visit her in hospital. Likewise in the case of ‘Kelly’. then was a powerful part of this woman’s ‘social context’. where she is describing their mother visiting Kate in the hospital. And when she did she was hostile. 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. 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. Not going to. 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. 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. So in Kate’s case. (Emphasis added). She didn’t have the emotional ability or any type of insight to deal with it. my mother has always been a victim. you know. When she did so. Which is another kick in the guts. As a result.

that of compulsive eating (O'Brien and Bankston. 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. such as the ‘image of self and felt identity’. or the relationship to the ‘significant society’ or institutional complex. just as has proved to be the case with another eating disorder. 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. I’ve tried to talk to my mum. 1999: 53). the associated lifestyle. and a lessening of the web of ‘control’. But for Goffman it was the personal interior which was significant. fluctuating pattern. 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. its legal authority. expression. time to recovery and so forth (Bruce. like. taking into account the longer term context. . The concept of career traditionally focuses on the external attributes of the professional ‘position’ a person holds. 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. when you got home from school or like you weren’t – she was just really really controlling. anorexia is one where the ‘stage’ of the condition is significant. there is a tendency to see this as ‘progress’. the incorporation of which enables a richer understanding to be gained of: [H]ow social factors interact with the risk.Experiences of ‘Control’ in Anorexia Nervosa Treatment Mum’s very controlling about food with all of me and my sisters. 1999). 1961: 119). You weren’t allowed to eat at. 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. Given its often chronic. 53 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. I’ve tried to work it out with her why it was such a big issue for her. She had her own problems. 1984). It was like a little game with my family so I guess we’d all sort of had… Food was just a big issue. at least in terms of age of onset. 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. Again the ‘family food discipline’ is continuing to operate as a form of control into the present day. duration of the episode. course. history of past episodes. and outcomes of mental illness.

or even conspiracy. starting with perceptions of undifferentiated ‘symptoms’ (such as lack of good health). as those who were believed to be supporters become revealed to be allies of psychiatrists (1961. ii) family insulation from outside perspectives serving to delay appreciation of societal attitudes. and iv) those socialised in the ‘alien’ community and who make the transition to values shared by the community at large (id. involving reconstruction of past identities. 1991). 1993). by appointing a person. once this reaction is internalised. 1999: 596). or retrospectively. can displace a person’s previous identity and see that identity reconceived (and processed) according to the expectations and requirements of more powerful players. and who cannot. Our data does not directly capture the early stages of the management of the pre-patient phase. Families were torn between their desire to ‘support’ the family member or to ally themselves with the doctors. such as clinicians and other networks (Aneshensel. The ‘pre-patient’ and the ‘patient’ phases of identity. 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. including the constraints of the role and expectations about how to act as a group of fellow sufferers. iii) late-in-lifecourse discovery of a devalued identity (either prospectively. A trajectory culminatingat its most optimisticin ‘recovery’ following . For instance a former mental patient residing in supported boarding accommodation may develop ‘classifications’ of those who can. Part of that process for a person with anorexia entails convergence towards a new image of the ‘self’. and in relationships to staff (whose transition from general to say psychiatric nursing may exemplify a 'moral career': Caygill. 1961. Goffman shows that the reaction of others to a person’s condition. In his book on Stigma. Boyer and Lubell. the other the subjective experience of the person with the condition (Goffman. 129). 45-49). Goffman wrote of the duality of self-images which emerge. Mim Ingvarson and David Tait b. who can participate in treatment and lifestyle decisions. and development of (medical practitioner-validated’) ‘patient’ roles. leaving the past intact. One aspect of the pre-patient stage that Goffman identifies is the formation of an alliance. independent of both family and treatment team.54 Terry Carney. leading on into possible adoption of a social condition or ‘sick role’. 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. Guardianship can offer one way of addressing this dilemma. 1999: 458). Likewise Talcott Parsons’ work on the ‘illness career’. readily take the next step back into fully independent living (Shaw. 1968: 45). 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. between the medical staff and the family. one representing the viewpoint and values of so-called ‘normal’ society. and the four common ‘patterns’ of response to that dissonance: i) dual acquisition of both perspectives. 1968).

1991). I was putting all my effort into trying to be such a good patient. she kept certain things to herself. I didn’t want to be in there. Not only did she want to be good at ‘anorexia’ she also wanted to be good at being treated for ‘anorexia’. when discussing her relationship with her previous therapist. Fieldwork illustrations of compromised identity. um. perhaps also a more ‘therapeutic’ relationship as well.Experiences of ‘Control’ in Anorexia Nervosa Treatment 55 treatment (Pescosolido. she was concerned to preserve her ‘reputation’. that my reputation somehow had to be salvaged. It was just that if they didn’t accept me then they would transfer me to Royal Melbourne [Hospital]. . 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. These frameworks provide a useful lens for understanding the way some anorexia patients ‘mould’ their behaviour to accommodate preservation of relationships with significant others. set me back in my own way. on my way to recovery really. 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’. as a result of this internalisation of more negative thoughts. and then that whole admission was one I think I mentioned where I was constantly. identification of cause and application of curative treatment’. Her identification with herself as a patient reflects an important transition: no longer a person in denial of being ‘ill’. c. (Emphasis added). So. went against me further down the track big time in myself. and I remember trying to leave once. I had to make sure that um. but I knew I couldn’t leave. First. in that there was more chance for mutual respect to build? Sometimes there is an intersection with the ‘suasive/coercive’ narrative as well however. But one where the network of family. 1999: 443). It is clear that Kate managed the way she presented her ‘public’ self in order not to unduly offend her therapist. There are at least two forces at work in Kate’s mind here. so that in the end I just had to tell her what she wanted to hear to keep her happy. Boyer and Lubell. she has been socialised into acceptance of the ‘sick role’. you know. partners or therapists. I felt desperate. such as family. But it also entailed a moulding of her relationship with the therapist. Rather than fully express her feelings and thoughts. her reputation as a ‘good patient’. of having to prove. Thus ‘Kate’. Obviously this avoided the tension and trauma of what she described as her more ‘provocative’ behaviour. friends and significant ‘others’ may mediate the choice of pathways taken (or resisted) at any one time (Pescosolido. Thus Kate also talked about conforming to clinicians expectations to avoid transfer into the public system: So I’ll just never forget that. she was Chinese. In my own. Kate is at least prepared to talk the language of illness/recovery. my perception of things. even just a little bit. be the good patient. so thaton a superficial level at leastit was a ‘happier’ interaction. (Emphasis added). and she said she’d make me involuntary. And that. So it was like I have to do this. Consistent with the medical model of diagnosis. And. and they put in a psychiatrist in front of me.

at least formally. it is also explicitly targeted at identities. visits and activities. outside the formal legal system and authority structures usually the focus of attention by lawyers. a credible exemplar of a condition. regular surveillance and measuring. playing on what she knew about that facility as well as on her uncertainty about the ‘unknown’. 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. interactions with staff. This includes daily routines of eating and washing. This includes learning to play the ‘patient role’. informal or written ‘contracts’ and other behavioural measures. Her language here seems little different to that of a person on probation. stigma and social control. and developing compliance strategies becomes a major focus of the intervention. Issues of power and control are therefore major ongoing issues in the treatment of the condition. was a subtle but very effective expression of power which helped control her current compliance with her treatment. but she was fearful of a ‘transfer to Royal Melbourne’. through disciplinary practices embedded in everyday life. whether through compliance with therapies or screening information suitable for the ears of . Control is exercised not through the majesty of a court or tribunal order but through the routine practices of the clinic. This includes self-image. enduring the regulatory regime imposed on them becomes a challenge and can be experienced as harsh and threatening. 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. She may not have enjoyed treatment where she was. Mim Ingvarson and David Tait Yet even this is a qualified acceptance: her identity is partly that of the cooperative patient. and the attitudes to the body. The threat of a transfer. For Kate is articulating a coldly rational analysis of the ‘least worst option’. This role may be learned by observing and modeling oneself on peers. From the perspective of patients. Because these future scenarios were playing on her mind at the time. It also shapes what Goffman refers to as the ‘moral career’ of the patient. The second force at work is even more consistent with an analysis in terms of power. She internalised the disseminated forms of control operating in her clinical environment. the law is rarely invoked. to ‘be’ an ‘anorexic’. in part because of the resistance of patients to therapies intended to cure them. And yet. This may be experienced as ingratitude not just from patients themselves (who may be presumed to ‘lack insight’). and all the other rituals of institutional living. Kate decided to be more cooperative. but by feminist groups raising civil liberties objections. 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).56 Terry Carney. But a moral career may also lead to displaying signs of being on the road to recovery. Conclusion Anorexia nervosa remains one of the difficult and frustrating conditions for medical staff. or by responding to the reactions of others. The regulatory regime does not just touch on practices. Obtaining informed consent is an ongoing concern.

to make the ‘correct’ choices. is that the regulatory regimes that shape the treatment of conditions such as anorexia nervosa. Taking on the role of the patient involves ‘participating in reciprocally sustained fictions’ (1961. 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. The patient learns to provide consent ‘freely’. 1996. But many of them are ‘informal’ in the sense that they operate outside. Winick. 142). 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. In time the constraints learned in this way become part of the new role. Freckelton. If intrusive medical and behavioural intervention to re-shape both practices and identities rarely engages the law.Experiences of ‘Control’ in Anorexia Nervosa Treatment 57 therapists. and in a sense. Such a role for the law could perhaps be seen as ‘professional capture’ by those supposedly regulated by a legal regime. to accept the ‘empowerment’ regime that is made even more convincing by the threat of legal intervention. The fiction employed so hesitantly at first becomes part of the new identity. or codes of ethics grounded in international covenants. it became instead a new source of power for medical therapists. how interactions between ‘experts’. the formal legal system. are ‘the law’. Rather than ‘the law’ being something external that imposed itself upon patients and clinicians. and this fiction can best be sustained when legal coercion is not formally employed. 2000. 2003) is whether this somewhat duplicitious alliance between law and medicine really does promote therapeutic outcomes (Wexler and Winick. based on an interpretation of Foucault. How ‘duty of care’ is operationalised in a hospital environment. ‘carers’ and patients are mediated through conventions and rules. strategic lodging or withdrawal of applications. or ‘in the shadow of’. Some of the ‘rules’ are based in part on legislation. based on Goffman’s understanding of the complicity involved in sustaining a role. However there is another interpretation. 2003). This could include foreshadowing. 2002/3. The language of ‘cure’ and ‘recovery’ providing a framework for an ongoing reshaping of identity. The question posed by the therapeutic jurisprudence literature on the work of tribunals and other institutions (McMahon and Wexler. The patient has become an active participant in the governance of self. or use of guardianship to provide substitute consent rather than the more extensive mental health orders. 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. The ‘fiction’ of acting ‘responsibly’ without coercion is an important part of the therapeutic framework in many contemporary treatments. Wexler. If tribunals and courts . that of the ‘recovering’ patient. Indeed the availability of legal measures may ironically reduce the need for physical constraints. constitute. how medical expertise has been translated into medical authority. or an example of how a system set up to protect patient rights had the unintended consequence of strengthening medical authority. how therapies are developed and tested through a scientific process. 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.

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laviano@uniroma1. chronic renal failure.. ITALY Department of Surgery. Inc. NY. thereby increasing morbidity and mortality. Alessandro Laviano. NPY]. pp. cytokines [e. E-mail: alessandro. 00185 Rome. University La Sapienza.. including sepsis. since it contributes to the development of malnutrition. and impinges on quality of life. anorexia does not represent a primary therapeutic target. viale dell'Università 37. Department of Clinical Medicine. TNF] and neurotransmitters [e.. etc.g. 63-90 © 2006 Nova Science Publishers. In chronic diseases. Syracuse. Michael M.. and suggest that most of the hypothalamic neuronal signalling pathways modulating energy intake are involved. University La Sapienza.g. since effective treatment of the underlying disease rapidly ameliorates food intake. Their modes of action do not appear to be separate and distinct. Antonia Cascino and Filippo Rossi-Fanelli Department of Clinical Medicine. including hormones [e. However. USA Abstract Anorexia and reduced food intake are relevant issues in the management of patients suffering from acute and chronic diseases. In acute diseases.g.it . Rome. Chapter IV Secondary Anorexia: A Neglected Issue in the Optimal Management of Patients Suffering from Acute and Chronic Diseases Alessandro Laviano*. SUNY Upstate Medical University. chronic liver failure. leptin]. IL-6. ITALY. Accumulating evidence indicate that anorexia associated to different diseases is multifactorial in its pathogenesis. A number of factors are considered mediators of anorexia. rather they are closely inter-related.In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Meguid. convincing * Correspondence: dr. anorexia impacts on patients’ prognosis. cancer. Swain. neuropeptides [e. tel: +39-06-49973902. serotonin and dopamine]. University Hospital. Fax: +39-06-4440806.g. IL-1.

Cytokine increased expression during disease inhibits the hypothalamus to appropriately respond to peripheral signals. Michael M. If we consider that secondary anorexia characterizes highly prevalent diseases (cancer. Therefore. the anorexia occurring in patients suffering from acute or chronic diseases. syndromes] per se may not be specific of a single disease. ) while secondary anorexia occurs in specific populations.. believe not only that anorexia and anorexia nervosa are synonymous. 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. either acute or chronic. anorexia is a highly prevalent syndrome which heavily impacts on the prognosis of patients suffering . However. but they can’t because they lost their appetite. the overall magnitude of the clinical issue represented by secondary anorexia becomes self-evident. Antonia Cascino and Filippo Rossi-Fanelli evidence suggest that a hierarchical organization exists in which cytokines play a key role. food intake. although the prevalence of anorexia nervosa is raising among young girls in western countries. but some physicians as well. is associated with the loss of appetite. symptoms or constellations of symptoms [i. the clinical problem of reduced appetite and food intake is much more pervasive than that represented by anorexia nervosa alone.64 Alessandro Laviano.. anorectic cancer patients. but more importantly that there is no clinically relevant syndrome characterized by reduced food intake other than anorexia nervosa. achieved via nutritional counselling. Hypothalamic monoaminergic neurotransmission may significantly contribute to these effects. Therefore. or uremic patients. i. In this light. liver cirrhosis. it is much smaller than the prevalence of secondary anorexia. aimed at interfering with cytokine expression or hypothalamic monoaminergic neurotransmission. by persistently activating anorexigenic systems and/or inhibiting prophagic pathways. brain monoamines. almost every disease. Key Words: anorexia. but they force themselves not to eat. Actually. the anorexia syndrome represents a suitable example. Thus. Also. whose perception has become pathologically deranged. chronic diseases. diagnosis is made based on specific combinations of symptoms and signs. since it characterizes the clinical course of different diseases.e. chronic renal failure. malnutrition. Definition In medicine. Indeed. common people. chronic obstructive pulmonary disease. the optimal therapeutic approach to anorectic patients should be based on both changes in dietary habits. and drug therapy. Meguid. or liver cirrhosis patients really would like to eat. triggering the complex neurochemical cascade which leads to the onset of anorexia.e. hypothalamus Introduction Anorexia is a very well-known word among general audience. In this light. anorexia nervosa thus representing the tip of the iceberg. an important difference between anorexia nervosa and secondary anorexia should not be overlooked: young girls suffering from anorexia nervosa do feel hunger.

can be drawn by a recent survey of the European Society of Medical Oncology [2]. it appears that most oncologists recognize the importance of supportive care for patients with advanced cancer. Yet. 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]. liver cirrhosis. cancer anorexia is highly prevalent and clinically relevant. all these changes are believed to help the host organism to fight back the invasion. The conserved energy is then available for the body’s fight against disease. However. while 42% felt that they were inadequately trained to this task. In chronic clinical states. based on their strict interdependence. anorexia does not represent a therapeutic target. Surprisingly. leading very often to reduced food intake. sepsis or influenza infection]. cancer. Nevertheless. An insight on the reasons for their negative attitude toward anorexia. COPD). Second. and that medical oncologists should be expert in the management of physical and psychological symptoms of advanced cancer. 15% of respondents still believed that palliative care begins when medical oncology ends. very often oncologists do not consider it as a symptom deserving investigation and treatment. the host saves energy by not moving around in search for food. As an example.. As a consequence. many are prepared inadequately for these tasks. 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. prompted in the host by internal/external insults.e. the interest of clinicians toward this syndrome is much less than it should be deserved. Anorexia is defined as the loss of the desire to eat. First. almost all of the responding oncologists agreed that all advanced cancer patients should receive concurrent supportive care. Yet. only a minority of respondents reported to collaborate often with a supportive care specialist.. they are often used as synonymous. Interestingly. and this also reduces heat loss that would otherwise occur from increased convection. reduced calorie intake should not be considered as being part of the clinical definition of anorexia. and therefore on his/her prognosis. As a consequence. including immune system activation and increased energy expenditure. Therefore. the clinical relevance of anorexia varies according to the time course of the underlying diseases. the large majority of them being from Europe and involved with advanced cancer patients. chronic renal failure. sepsis) and chronic diseases (i.e. the beneficial effect is usually supposed to be related to a number of mechanisms. As far as anorexia is concerned. Anorexia is among the physiologic responses. and actual participation levels .e. even if they are receiving antitumour therapy. Approximately 900 oncologists responded to the survey. while an astonishing 30% did not disagree with the statement “palliative care specialists steal patients who would otherwise benefit from medical oncology”. since the quick and effective treatment of the underlying disease is the main goal inevitably leading to amelioration of eating behaviour. Initially. In acute clinical states [i.. long lasting anorexia compromises host defence and ultimately delays recovery. Despite the well-known effects of anorexia on patients’ prognosis. Despite this. rather its consequence.Secondary Anorexia 65 from acute (i. and more broadly toward supportive care. despite being beneficial in the beginning.

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]. Diagnostic Tools It is still difficult to clearly define and diagnose anorexia. the diagnosis of anorexia is based on the presence of reduced energy intake. 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. However. 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]. which closely reflect the attitude of clinicians in investigating specific symptoms. In 300 cancer patients. To reliably assess the presence of anorexia. The use of questionnaires to diagnose anorexia is rapidly increasing. Very often. By using case report forms. 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]. Geels et al. 4]. but their training to recognize and treat anorexia is not sufficient. SYMPTOMS early satiety taste alterations smell alterations meat aversion nausea/vomiting Prevalence As a consequence of the difficulties in clearly defining and diagnosing anorexia. it could be concluded that clinicians may be aware of the clinical impact of anorexia. thus highlighting their feasibility and reliability in different clinical settings. On a broader perspective.66 Alessandro Laviano. Patients reporting at least one of these symptoms are defined as anorectic. Michael M. a visual analogue scale is used. since the reduction of ingested calories might be the consequence of dysphagia or depression rather than the sign of anorexia. it may appear advisable to also quantify the degree of anorexia via the administration to the patient of a visual analogue scale. Antonia Cascino and Filippo Rossi-Fanelli commonly are suboptimal. as previously mentioned. Sometimes. Meguid. A clear example is given by the anorexia of cancer. its prevalence in different clinical conditions is yet to be precisely assessed. considering that questionnaires provide only a qualitative assessment of the presence of anorexia. even if this procedure could be misleading. anorexia .

Marchesini et al. Kalantar-Zadeh et al. Based on these alarming figures and considering that 20% of cancer deaths are due to malnutrition per se [10].e. but it must be reminded that it is generally acknowledged that anorexia and reduced food intake are frequently encountered in cancer patients [7].Secondary Anorexia 67 was detected in approximately 13% of patients. i. anorexia is among the most important causes of malnutrition. 9]. the prevalence of anorexia ranges between 60% and 65% [8. Chronic Renal Failure In this clinical setting. This figure might slightly overestimate the actual prevalence of cancer anorexia. are data showing that despite COPD patients have physical and . Recent data indicate that 67% of chronic lung disease patients experience anorexia during the last year of life. i. 38% of the entire cohort [13]. this figure not being much different from the prevalence of anorexia among lung cancer patients. since most patients suffer from breathlessness which affects food intake. Class B or C). 7]. Chronic Obstructive Pulmonary Disease [COPD] In COPD patients. it is reasonable to conclude that many cancer patients are starving to death. using the guiding symptoms previously mentioned. studied a cohort of 331 maintenance hemodialysis outpatients and demonstrated that diminished appetite was reported by 128 patients. Liver Cirrhosis Similarly to what is observed in the course of neoplastic disease. patients suffering from chronic liver failure frequently experience anorexia. assessed the presence of anorexia in 174 patients with advanced liver cirrhosis (Child-Pugh score ≥7. Indeed. It is pervasive in patients on conservative treatment and very common in patients on hemodialysis [12]. the prevalence of anorexia is particularly high. More striking. anorexia is usually the symptom urging the patients to refer to their physicians. Moreover. however. In a recent paper. Prevalence data are more reliable in terminally ill cancer patients.. while using the quality-of-life questionnaire 55% of patients were diagnosed as anorectic [5].e. and its alleviation is perceived as a sign of benign evolution of the disease. 76% [14]. Data obtained show that more than 50% of patients were anorectic [11]. 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. In this subset of patients.

Consequently. which is now becoming a critical endpoint in the management of patients as well as in designing clinical trials [21]. being as reliable in predicting survival as well-defined prognostic factors. 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. peaking at 90% in the last stages of the disease [15]. This issue has been specifically raised in cancer patients. Severe nausea has been reported affecting approximately 10% of CHF patients [16]. 20]. An interesting and emerging aspect of the clinical impact of anorexia is its influence on patients’ quality of life. receive much less attention from health care professionals [14]. including a 4-fold increase in mortality and a greater hospitalization rates [13]. as recently outlined by Jatoi et al. The clinical relevance of anorexia is underscored by its role as an independent prognostic factor in terminally ill cancer patients. friendship is strengthened by sharing the same food. cancer patients. Similar data have been obtained in chronic renal failure: in maintenance hemodialysis patients. Congestive Heart Failure [CHF] In this clinical setting. Meguid. [23]. their symptoms. anorexia and reduced energy intake impinge on quality of life. cancer anorexia should represent a major therapeutic goal and its alleviation should lead to improved quality of life. since it reduces the oral intake of calories thus further promoting skeletal muscle wasting. food and food intake are much more than calories. including Karnofsky Performance Status and Clinical Prediction of Survival [9. the assessment of the prevalence of anorexia is made difficult by the high proportion of patients suffering from dyspnea. Finally. It is selfevident that in humans. in whom anorexia is pervasive and much effort has been devoted to improve food intake. Michael M. Special events are celebrated with food. it exacerbates the detrimental effects of disease-related alterations of protein metabolism on nutritional status. Unfortunately. including anorexia. It contributes to the development of malnutrition and cachexia. Therefore. and patients suffering from other chronic diseases as well. Also. diminished appetite is associated with poor clinical outcome. nutrients and digestion. Clinical Impact The onset of anorexia significantly impacts on the clinical course of the disease. people often discuss of economic opportunities while eating. almost none of the clinical trials reporting improvements in appetite .68 Alessandro Laviano. On the other hand. Antonia Cascino and Filippo Rossi-Fanelli psychosocial needs at least as severe as lung cancer patients. Since cancer anorexia can be effectively treated or at least its severity dampened [22]. the metabolic dysregulation of cachexia [19] sustains and corroborates the neurochemical alterations responsible of anorexia. it would be expected that the alleviation of anorexia should be associated with significantly improved quality of life. eventually leading to increased morbidity and mortality [18]. but the actual prevalence of anorexia may well be higher [17].

the hormone leptin exerts a strong negative influence on food intake. but the precise neurochemical mechanisms are still matter of debate. insufficient reliability and/or complexity of quality of life assessing tools. including undesirable effects of appetite stimulants. because of the psychological value of appetite rather than for its caloric sequelae. insufficient statistical power of the available data. or improved morbidity and mortality. Intuitively. USA.Secondary Anorexia 69 following drug therapy also reported improved quality of life. the arcuate nucleus of the hypothalamus transduces these inputs into neuronal responses and. The authors mailed all nurses employed by hospice programs in Oregon. anorexia might be secondary to defective signals arising from the periphery. via second order neuronal signalling pathways. Pathogenesis of Anorexia The pathogenesis of anorexia is multifactorial and related to disturbances of the central physiological mechanisms controlling food intake. Among the large series of peripheral signals [Table II]. Ganzini et al. 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. anorexia “is important in its own right—independent of global quality of life. However. i. cancer patients complain of different symptoms and relief of anorexia would simply shift symptomatology [23]. Considering that anorexia alleviation has never been demonstrated to lead to enhanced quality of life. due to an error in the transduction process. Alternatively and provocatively. should we care about anorexia in cancer patients? Certainly yes. it could be questioned whether cancer anorexia and starvation to death represent horrifying symptoms to the surviving relatives rather than to the dying patients. insights might be obtained.e. Many possible explanations have been proposed for this apparent inconsistency. and independent of any other clinical end point” [23]. . 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.. into behavioural responses (Figure 1). On the basis of reports by nurses. and analyzed the results. as assessed by a number of different tools. In particular. Role of Peripheral Signals The hypothesis that peripheral signals are involved in the pathogenesis of anorexia is intriguing. or to a disturbance in the activity of the second order neuronal signalling pathways. by understanding how energy intake is physiologically controlled. 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].. the “soretooth-tight-shoe” phenomenon. independent of survival. As brilliantly pointed out by Jatoi et al. this experience somewhat resembling severe anorexia [24].

70 Alessandro Laviano. Antonia Cascino and Filippo Rossi-Fanelli Hypothalamus NPY/AgRP peripheral signals modulation of food intake POMC/CART arcuate nucleus Figure 1: in the hypothalamus. significantly contributed to the debate by showing in . results from animal and clinical studies are controversial [27-29]. More recently. the arcuate nucleus receives information from the periphery and intergrates these inputs to modulate food intake [NPY: neuropeptide Y. and do not seem to support this hypothesis. recognized anorexigenic factors [26]. particularly because its synthesis and secretion appear to be stimulated by cytokines. CART: cocaine-amphetamine related transcript]. However. Michael M. Thus. It reaches the brain and a raise in its circulating levels results in inhibition of energy intake. Meguid. Bing et al. leptin is an intuitive likely mediator of anorexia. 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. POMC: proopiomelanocortin. AgRP: agouti-related protein.

showed that in anorectic cancer patients. When considered together. including brain insulin. anorexigenic peptides. while no difference exists between cancer patients and healthy individuals in the production of leptin by peripheral blood mononuclear cells [31]. However. Sato et al. but its mechanism of action needs to be further elucidated. 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. However. Then. probably via the neurotransmitter serotonin. and result in reduced eating. individual vagal neurons are able to integrate different kinds of signals relevant to ingestion. b) Insulin Food intake triggers a complex cascade of neurochemical events that signal nutrient and energy availability in the central nervous system. CCK is secreted from duodenal cells in response to nutrients in the lumen. phosphatidylinositol 3-kinase pathway. see ref. these data suggest that peripheral leptin synthesis is preserved during disease.. leptin and melanocortins. are highly interactive with insulin in the central nervous system. the CCK signal enters . showed that in chronic liver disease serum leptin appears a passive marker and not a cause of anorexia [34]. Disrupted brain insulin signalling in obesity and diabetes has been proposed. consisting evidence show that brain insulin interacts with different anorexigenic and orexigenic pathways to modulate their activity and thus food intake [for review. they suggest that leptin in these patients may represent a marker of inflammation [32]. c) Cholecystokinin (CCK) CCK is probably the most extensively studied satiety signal. Consistently with animal data. Some of the secreted CCK enters the blood and stimulates the secretion of appropriate enzymes into the duodenum to facilitate digestion. insulin and leptin share a common signaling pathway involved in food intake. Similarly. an endogenous factor that causes a sensation of fullness and reduces the size of an ongoing meal [for review. Brain insulin has anorexigenic effects. and point to a central dysregulation of the physiological feedback loop. Particularly. Therefore. down regulate stimulators. via other branches emanating from the gastric wall. activate anorexigenic factors. CCK influence food intake and particularly meal size. 33]. via a more complex mechanism. However. see ref. i. but intracerebral insulin synthesis has been also demonstrated. 37].e. circulating leptin levels are lower than those of healthy individuals. but its involvement in secondary anorexia received less attention by reasearchers.Secondary Anorexia 71 an animal model that anorexia develops despite the normal regulation of leptin synthesis [30]. Rather. Supporting a common pathogenic mechanism for the anorexia associated with different diseases. Ben-Ari et al. which is simultaneously sensitive to both CCK and other stimuli such as gastric distension. 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. recently demonstrated a possible role for insulin in cytokine-induced anorexia. 35]. using an experimental model [36]. namely the insulin receptor substrate. In the hypothalamus. Mantovani et al. different factors are able to regulate insulin release directly in the hypothalamus. but intracerebral CCK synthesis has been described. Insulin reaches the brain from the periphery.

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

differentially regulate food intake and energy expenditure by interacting with a GLP-1R-dependent pathway [43]. but it cannot be excluded. in which the biochemical partitioning between fatty acid oxidation and synthesis represents a key signal indicating catabolic or anabolic energy status [44]. but their involvement in the pathogenesis of anorexia has so far received little attention. which are structurally distinct. It is therefore tempting to speculate that energy signals could contribute to anorexia. thus suggesting a direct anorexigenic effect. Both GLP-1 and OXM are thought to exert their effects via the GLP-1 receptor [GLP-1R]. Therefore. Many pathways have been described serving as second order neuronal signalling pathways. ligandspecific activation of a common GLP-1R increases the complexity of gut-brain pathways regulating energy homeostasis. possibly via a deranged "sensing" of the energy metabolism during disease. In a recent study. The involvement of GLP-1 and OXM in secondary anorexia has not been investigated. via inhibition of the synthesis of the prophagic factor neuropeptide Y (NPY)[45]. including orexins A and B. ameliorates anorexia in pathophysiological conditions [48]. A number of studies suggest that a metabolic control of food intake also exists. food intake is accompanied by increased intracellular levels of malonyl coenzyme A (malonyl-CoA)[46]. which is involved in fatty acid oxidation. where peripheral signals mainly converge. The mechanism of action need to be better elucidated. Interestingly. 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]. may impact on the neurochemistry in localized brain areas . more studies are needed to verify the involvement of energy signals in anorexia. since they are generated within the hypothalamic neurons controlling energy intake. and particularly alterations of protein turnover. a prophagic mediator [49]. Role of Second Order Neuronal Signalling The hypothalamic arcuate nucleus. the supplementation of carnitine. thus interacting with a number of neuronal populations [25]. but GLP-1 and OXM interact with a number of pathways to modulate food intake. Under physiological conditions. also changes in energy metabolism influence energy intake in a leptin-independent manner via energy signals. energy signals differ from classic peripheral signals. showed that the loss of renal function in Wistar rats reduces hypothalamic orexin A. which is a potent signal reducing food intake. GLP1 and OXM. Energy Signals Similarly to changes in fat mass. fat metabolism is altered leading to decreased fatty acid oxidation [47] and possibly increased intracellular malonyl-CoA levels. Supporting evidence show that during tumour growth. Li et al. Conceptually.Secondary Anorexia 73 reduce food intake when administered centrally. However. projects to other hypothalamic areas. which in turn may contribute to the development of anorexia. including ghrelin and insulin. Also. nor in experimental or human models. Evidence exist suggesting that disease-associated metabolic changes.

Results from studies investigating the role of the hypothalamic anorexigenic pathway POMC/CART in anorexia appear more convincing. This derangement could be triggered by cytokines. However. and the pro-opiomelanocortin [POMC]/cocaine. inhibiting food intake [for review see ref. and similarly to cancer. In chronic renal failure. food intake is restored in tumour bearing animals. the results obtained in animal models and humans are conflicting [52-55]. Because of the central role of these neuronal pathways. which occur in wild type mice [59] Thus. and tumour growth is not accompanied by the development of anorexia and cachexia. it seems that a dissociation exists between NPY mRNA levels and actual NPY levels. when energy intake needs to be initiated. Michael M.. and the development of cachexia is prevented [59. When energy intake needs to be inhibited. Meguid. Similar results have been obtained in melanocortin 4 receptor (MC4-R) knock-out mice. Antonia Cascino and Filippo Rossi-Fanelli [50].e. stimulating food intake. simultaneously inhibiting the POMC/CART pathway. In these mutants. . it is not clear whether NPY should be considered as a mediator or a marker of anorexia. using either its physiological inhibitor (i. peripheral signals interact with two separate neuronal populations within the arcuate nucleus: the NPY/Agouti-related peptide (AgRP) neurons. However. AgRP) or the synthetic compound SHU9119. primarily due to the hyperactivation of the melanocortin system. As a consequence. animal and human studies consistently show a reduction of NPY [49. Unfortunately this line of investigation has been pursued in cancer anorexia only. they were postulated as putative mediators of anorexia. POMC/CART neurons cannot be completely activated because of the lack of this class of receptors. including α-melanocyte stimulating hormone [α-MSH] and corticotropin releasing hormone (CRH). peripheral signals activate the NPY/AgRP pathway. but it is likely that the pathogenic mechanisms hypothesized for cancer anorexia might well be operating during the clinical course of other diseases. they appear to have a role in sustaining and corroborating anorexia. 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. but it is difficult to assess the extent of the involvement. which appear decreased. 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.74 Alessandro Laviano.and amphetamine-regulated transcript (CART) neurons. However. Indeed. while its onset seems to be secondary to the inability of the hypothalamus to recognize and respond appropriately to consistent peripheral signals [51]. Under normal conditions. 25]. These data suggest that NPY is involved in cancer anorexia. In cancer. it appears that secondary anorexia is related to the inability of the hypothalamus to respond appropriately to consistent peripheral signals. 57]. It has been repeatedly demonstrated that by blocking the hypothalamic melanocortin system. 60]. 58]. A number of studies investigated the role of the prophagic signal NPY in the pathogenesis of anorexia. recent data show a decrease of NPY and NPY-immunoreactive neurons in the hypothalamus of anorectic tumour bearing rats [56.

but compelling evidence are lacking. A simplistic view of energy intake regulation is that ingested nutrients are sensed at different levels of the gastrointestinal tract. . it must be acknowledged that studies also exist. In cancer patients. 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 the complex scenario of mutual interactions existing between different peripheral and central factors. neuromodulatory peptides and transmembrane proteins] interact [25]. hormones. Thus. 65]. In chronic renal failure patients. and is integrated in the hypothalamus. since cytokines biological effects are largely mediated by paracrine and autocrine influences. together with that arising from adipose tissue. including the liver. This could be done by inhibition of the NPY/AgRP orexigenic network. 58. rather they suggest their involvement. since the hypothalamus consists of different areas and nuclei. as well as by persistent stimulation of the POMC/CART anorexigenic pathway. hypothalamic serotonin systems have been implicated in the suppression of feeding [70]. satiation and satiety. In the Fischer rat/MCA sarcoma model. 62]. However. is transmitted to the brain via a series of routes [neuronal input. which failed to demonstrate a direct role of cytokines in experimental models of cancer anorexia. where the appropriate behavioral response is triggered. while suggesting the involvement of the nitric oxide system and systemic or local production of eicosanoids [67. cytokines may play a pivotal role in long-term inhibition of feeding by mimicking the hypothalamic effect of excessive negative feedback signalling [69]. the picture is far more complex. its involvement in this process has been repeatedly confirmed. 68]. Now it is clear that serotonin acts in conjunction with neuropeptides and peripheral hormones to bring about physiological states such as hunger. several groups have found increased levels of cytokines [13. Although the exact role of serotonin in the central regulation of food intake and body weight still awaits further clarification. This information.Secondary Anorexia 75 Role of Cytokines A number of studies indicate that cytokines are involved in anorexia [61. Hypothalamic Neuro-Immune Interactions: The Role of Brain Monoamines The mechanisms by which cytokines negatively influence energy intake are currently under investigation. cytokine circulating levels may not reliably reflect their role in determining specific biological responses [66]. peptides]. For several decades. cytokines and anorexia are intuitively connected. In Lobund-Wistar rats bearing prostate adenocarcinoma tumour cells. early anorexia is associated with an upregulation of brain IL-1β mRNA [54]. brain monoamines and particularly brain serotonin appears to play a pivotal role. As proposed by Inui. Actually. and within each of them a set of effectors [neurotransmitters. Serotonin is a monoamine acting as neurotransmitter and involved in different biological responses.

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

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. In humans. . Therefore. Drug Therapy The optimal therapeutic approach to anorexia should be aimed at counteracting its pathogenic mechanisms. Animal studies support this approach. Progestagens [megestrol acetate and medroxyprogesterone acetate] are the first-line therapy for cancer anorexia [69]. nutritional counselling may significantly improve food intake. it would be advisable to target their synthesis and/or activity to effectively treat anorexia and reduced food intake in cancer patients. It is advisable to avoid high-fat food. They are highly effective in relieving the symptoms of cancer anorexia. MPA] Cannabinoids [dronabinol] Corticosteroids [dexamethasone] Dietary Habits In anorectic patients. cannabinoids [83] and corticosteroids [84]. cytokine therapeutic targeting is achieved via agents interfering with their synthesis and release. considering that cytokines appear to represent the factor initiating the complex cascade of neurochemical events eventually leading to the onset of anorexia. since fat delays gastric emptying and thus it may worsen anorexia symptoms. Since changes in taste/smell may occur in anorectic patients. 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. high-dose progestagens have been shown to improve food intake and to a less extent body weight [85]. extremes in temperature and flavour should be avoided [7]. They include progestagens [82].Secondary Anorexia 77 Therapy The detrimental effects of anorexia on nutritional status and quality of life can be counteracted by a well designed therapeutic strategy which includes both nutritional counselling and pharmacological approach (Table III). 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 a recent systematic review of randomised clinical trials.

Thus. dronabinol at a dose of 2. anorectic cancer patients [92]. the infusion of adenosine 5’-triphosphate [ATP] in cancer patients modestly increased weight. dubbed “cytokine traps” after their ability to block cytokines. they have been used in the treatment of cancer anorexia. while the potential side effects discourage their clinical use. Their effects are similar to those obtained by megestrol acetate. recent data show that suramin inhibits chemotherapy-induced apoptosis [93]. and their use may lead to fluid retention. 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]. Corticosteroids are widely used to dampen immune response and cytokine activity. suramin have been demonstrated to significantly reduce cytokine release. the results obtained appear modest. Data obtained show that megestrol acetate and EPA supplement are equally effective in improving body weight. recently compared the orexigenic effects of megestrol acetate and of a caloric supplement enriched with EPA and DHA in weight losing. Unfortunately. Cannabinoids are derivatives of marijuana and particularly dronabinol has been demonstrated to alter cytokine production by human immune cells [89]. More than 400 patients were studied over a period of approximately 3 months. EPA supplementation may represent an effective therapeutic strategy to ameliorate cancer anorexia [91]. thalidomide. In cancer patients. Appetite is similarly enhanced by the two treatments when it is assessed via North Central Cancer Treatment Group Questionnaire. Combination of both treatments does not increase response rate. but its prophagic effects are less evident than those obtained by megestrol actetate [83]. 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]. but corticosteroids have a higher rate of drug discontinuation because of toxicity and/or patient refusal [84]. Similarly. Michael M. Newly synthesised molecules. Cytokine traps consist of fusions between the constant region of IgG and the extracellular domains of two distinct . Exploiting their immunomodulatory effects. Pentoxifylline. 95]. Meguid. improved strength and slowed the decline in quality of life [94. leading to an increase of NPY hypothalamic levels [87] and a possible inhibition of serotonergic activity [88]. However.5 mg twice a day increases food intake. vaginal spotting and sexual dysfunction. they are contraindicated in hormone-dependent tumours. Anti-Cytokine Agents Other molecules exhibit anti-cytokine activity. Jatoi et al. appear more promising.78 Alessandro Laviano. In particular. but megestrol acetate appears superior when appetite is assessed via 4-week Functional Assessment of Anorexia/Cachexia score. thus prompting their testing as anti-anorexia/cachexia agents [82]. deep venous thrombosis.

These encouraging results must be considered as preliminary. Indeed. Anorexia significantly improved after 3 days of treatment only in cancer patients receiving branched-chain amino acids. isonitrogenous standard diet. 28 patients with low plasma albumin levels [<3. Thus. while simultaneously recording their energy intake [97]. After 6 months of BCAA supplementation. and need to be validated in larger trials. tumor-bearing rats were fed with a BCAA-enriched diet. . The results obtained showed that BCAA-enriched diet delayed the development of anorexia by 2 days when compared to standard diet [unpublished observations]. and their feeding behaviour compared with that of tumor-bearing rats receiving an isocaloric. During chronic renal failure. and represent a substantial advance in creating novel therapeutic candidates for cytokine-driven diseases [96]. studied 44 elderly patients on chronic hemodialysis [12]. Interestingly. leading to a significant improvement of energy intake. double-blind. more fascinating results were later obtained in uremia and in liver cirrhosis. The other 16 patients did not complain of anorexia and were classified as the well-nourished group. In BCAA-treated malnourished patients. the reduction of plasma BCAA is associated with the presence of anorexia [12].5 g/dL] were classified as the malnourished group. Then they performed a 12-month. including the branched-chain amino acids. energy intake and nutritional status can be improved. derangements of plasma amino acid profile occur and a reduction of circulating levels of BCAA is frequently observed. Hypothalamic serotonin synthesis depends on the brain availability of its precursor.Secondary Anorexia 79 cytokine receptor components involved in binding the cytokine. Serotonergic hypothalamic neurotransmission may represent a suitable example. Hiroshige et al. placebo-controlled study on the malnourished group. anorectic cancer patients were orally supplemented with branched-chain amino acids or placebo for 7 days. To test this hypothesis. Traps potently block cytokine in vitro and in vivo. Among them. the amino acid tryptophan [76]. Lower plasma levels of BCAA and lower protein and caloric intakes were found in the malnourished group as compared to the well-nourished group. Anti-Serotonergic Agents Cancer anorexia might be therapeutically approached by interfering with the neurochemical events downstream cytokine activation. they also suffered from anorexia. leading to a reduction of hypothalamic serotonin synthesis and release. by artificially increasing the plasma levels of the competing amino acids. Tryptophan crosses the blood-brain barrier via a specific transport mechanism shared with the other neutral amino acids. To further test the clinical relevance of BCAA. a reduction of tryptophan brain entry could be achieved. since they were obtained in a small population during a short study period. Fourteen patients each received daily oral BCAA supplementation [12 g/day] or a placebo in random order in a cross-over trial for 6 months. which in turn would result in amelioration of cancer anorexia. anorexia and poor oral protein and calorie intakes improved within a month concomitant with the improvement of plasma BCAA levels over the values in well-nourished patients. However. It is therefore tempting to speculate that by supplementing uremic patients with BCAA. they confirm the feasibility of interfering with hypothalamic neurotransmission to influence energy intake.

on average. lean body mass] showed a statistically significant increase and mean plasma albumin concentration increased form 3. Also. no significant changes in nutritional parameters were observed during the first 6 months. but the favourable nutritional status persisted for the next 6 months. Treatment groups did not score differently on SF-36 questionnaire at baseline. In patients who remained in the study. The observed improvement of nutritional status and particularly of lean body mass could be explained at least in part by the excitatory effects of serotonin on hypothalamic melanocortin receptors [73]. the need for hospital admission. These data are particularly important because demonstrate that BCAA supplementation results not only in improved food intake but also in improved nutritional status. A multicenter.8 g/dL. it is conceivable that melanocortin receptors are less activated. anorexia. health-related quality of life. the percentage of patients believing that their health had improved during the preceding 12 months had increased from 29% to 52%. laboratory data and Child-Pugh score. positive results were obtained by BCAA supplementation during the subsequent 6 months. In 14 patients initially treated with placebo. When considered together. In particular. Meguid. and the percentage believing that their health had worsened had decreased from 43% to 18%. nutritional parameters and liver function tests were. Its prevalence decreased with BCAA from 52% to 25% and remained unchanged with lactoalbumin and maltodextrins. treatment with BCAA significantly reduced the combined event rates compared with lactoalbumin. After changing BCAA for a placebo. Secondary outcomes were nutritional parameters. and the duration of hospital stay. By reducing brain serotonergic activity via BCAA. far beyond mere increase of energy intake. Physical functioning and role limitation/emotional also improved. Primary outcomes were the prevention of a combined end point [death and deterioration to exclusion criteria]. anorexia and health-related quality of life [as assessed by the SF-36 questionnaire] improved. and mean plasma albumin concentration increased from 3. Interestingly. after 1 year of continuous treatment with BCAA. randomized study comparing 1-year nutritional supplementation with BCAA against lactoalbumin or maltodextrins was recently performed in 174 patients [11]. Michael M. No significant changes were observed in subjects treated with lactoalbumin or maltodextrins. stable or improved during treatment with BCAA and the Child-Pugh score decreased. However. anorexia was reported in more than 50% of all cases and was not different between groups. and need for therapy. there was a shift toward better scoring of health only in subjects actively treated with BCAA. Such encouraging results were replicated also in cirrhotic patients.80 Alessandro Laviano. Finally. spontaneous oral food intake decreased. The average hospital admission rate was lower in the BCAA arm compared with control treatments. with the percent of patients scoring health as poor decreasing from 19% to 3%. Treatment with BCAA had a significant effect on role limitation/physical.2 g/dL to 3.9 g/dL. these data suggest that the anti-serotonergic approach to the treatment of disease-associated anorexia is effective and results in significant clinical outcomes. leading to reduced peripheral muscle wasting. Considering the role of brain serotonin in the pathogenesis of disease-associated anorexia and cachexia. whose function has been linked to cachexia [98]. and other scales improved significantly when compared with baseline. Antonia Cascino and Filippo Rossi-Fanelli anthropometric indices [body fat percentage. antiserotonergic drugs might be as effective as BCAA in improving food intake .3 g/dL to 3. Similarly.

Using in vivo microdialysis. More data support a role for hypothalamic neurotransmission as an effective therapeutic target in the treatment of cancer anorexia. This may be difficult to achieve. Seven anorectic cancer patients received i.v. The need for selectivity may explain the failure of cyproheptadine in the treatment of anorexia in cancer patients [for review see ref. weight loss continued. showed that intrahypothalamic serotonin concentrations are increased in anorectic tumor bearing rats [75]. Patients were not receiving antineoplastic treatment. In the same study. This evidence may give the neurochemical explanation for the results obtained in anorectic cancer patients. but received oral ondansetron. this approach bears some limitations. Although it remains to be ascertained whether in humans chronically administered ghrelin sustains . antiserotonergic drugs must target the specific serotonin receptor involved in the pathogenesis of anorexia. This hypothesis has been recently tested in an acute study [104]. which appear more involved in mediating nausea and emesis rather than in controlling energy balance [70]. Blaha et al. Acute ghrelin infusion resulted in increased energy intake (approximately +30% vs saline infusion) and meal appreciation in all patients studied. ghrelin and their subsequent food intake and meal appreciation recorded. these data are very intriguing and further support the “monoaminergic” approach to the treatment of anorexia. the use of ghrelin in cancer patients must be cautiously considered because of the stimulatory effects of this hormone on GH production. Also. since dopamine levels were also found depressed [75]. the best candidate to this role being the 5-HT(2C) receptor. Secondly. thus prompting more interest on this class of drugs. Firstly. Although not obtained in prospective randomized clinical trials. 99]. suggesting that they were enjoying food more.Secondary Anorexia 81 and nutritional status. then it must reach the hypothalamus in adequate concentrations to block the receptors. it is tempting to speculate that its administration to anorectic cancer patients may enhance their appetite and improve energy intake. provided that the given antiserotonergic drug selectively targets 5-HT(2C) receptors. 102]. Edelman et al. they also showed a more complex derangement of hypothalamic monoaminergic neurotransmission. Unfortunately. Considering the few patients enrolled. large and placebo controlled trials are needed to establish whether these positive results reflected a true orexigenic effect attributable exclusively to ondansetron. Ondansetron is a type 3 serotonergic receptor antagonist widely used in cancer patients in the prevention and treatment of chemotherapy-induced nausea and vomiting. [100] studied 27 patients with advanced cancer and weight loss. which are mediated by the same receptor stimulating appetite [105]. which may lead to the development of side-effects. Promising and in early clinical trials is blockade of type 3 serotonergic receptors. these intriguing data should be considered as preliminary and need confirmation by larger trials. whose food intake has been restored and quality of life improved by the administration of dopamine (L-DOPA) at a dosage ranging from 375 mg/d to 750 mg/d [101. However. but after 1 month of treatment patients scored better on an hedonic scale. However. Ghrelin Considering the orexigenic effects of ghrelin [103]. particularly if adequate brain concentrations are reached only when using suprapharmacologic peripheral doses.

and the prostaglandin E2 receptor EP3 has been identified on serotonergic neuronal cell bodies in the raphe nucleus [114]. nitric oxide and eicosanoid pathways could not be completely alien from the cytokine-monoamine system. Also. the nitric oxide system and the production of eicosanoids might be of importance for the pathogenesis of anorexia. Murray AB. 98: 2502-10 [3] Stubbs RJ. References [1] Murray MJ. Anti-Inflammatory Agents As previously mentioned. The pathogenesis is multifactorial. Also. Conclusion Anorexia is a syndrome which is pervasive among patients suffering from acute and chronic diseases. including indomethacin. 32: 593-6 [2] Cherny NI. Attitudes of medical oncologists toward palliative care for patients with advanced and incurable cancer. Supporting this view. Rowley E. nitric oxide and eicosanoid influences on appetite appear related to serotonin metabolism [112. Thus. et al. which in turn seems to be triggered by cytokine-driven stimulation of hypothalamic serotonergic system. Michael M. but it appears to be related to the hyperactivation of hypothalamic inhibitory pathways. ghrelin infusion increases plasma glucose and decreases plasma insulin [107]. However. Delargy H. Finally. Johnstone AM. Am J Clin Nutr 1979. Catane R. Anorexia of infection as a mechanism of host defense. Meguid. animal and clinical studies show that nitric oxide synthase and cyclooxigenase inhibitors. and particularly cancer anorexia.82 Alessandro Laviano. it must be reminded that acromegalic patients with chronically elevated GH have a small increase in absolute risk of bowel cancer [106]. Elia M. The use of visual analogue scales to assess motivation to eat in human . Stratton R. leading to reduced morbidity and mortality. Antonia Cascino and Filippo Rossi-Fanelli increased GH production. 111]. nitric oxide mechanism may involve tumour growth and thereby secondarily influence appetite. Cancer 2003. decrease tumour growth and improve anorexia [110. Anorexia can be effectively treated. evidence that nitric oxide and eicosanoids act directly on cells in the central nervous system is lacking. However. Finally. it should be always remembered that improving anorexia and energy intake has a positive impact on quality of life. although it is not known whether amelioration of anorexia results in a long-term benefit for patients. However. animal studies seem to anticipate that chronic treatment with this hormone will have little effect on appetite [105]. 113]. glucose is the preferred substrate for cancer cells [108] and sustained hyperglycemia as in diabetic patients has been shown to represent a risk factor for cancer development and mortality [109]. Reid C. Hughes DA.

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This situation is exacerbated by the fact that bulimia is perceived by the public as a disease that only affects girls. Herberhold Klinik fur Kinder und Jugendmedizin der Medizinischen Universitat zu Lubeck. Bräutigam and M. demanding requirements or expectations in the areas of competitive sports. Three Case Reports B. pp. the different therapeutic approaches. muscle building. 91-104 © 2006 Nova Science Publishers. We focus on the patients’ personal histories and the psychological conditions in the parents. 23538 Lubeck. There are triggers for the disorders among boys that are different from those that have been identified among girls. and ideals of physical perfection. Ratzeburger Allee 160.5% among men. 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. one that is more focused on masculine muscular form. Chapter V “I Couldn’t Find the Food I Liked” Anorexia in Boys. We report on three clinical cases that illustrate some of the differences between male and female anorexia and other aspects like the wide range of psychological and physical symptoms. For example. with the result that affected boys often have to struggle with emotions of shame and denial. and kinds of treatment. Discussion of the results encompasses psychodynamic and systemic issues. Inc.9% among women and 6. nearly every tenth person suffering from an eating disorder is male. The lifetime prevalence of any eating disorder has been reported as 17. These include excessive physical activity. . Arbeitsgruppe fur Psychosomatik und Psychotherapie. Abstract The number of boys affected by eating disorders is increasing.In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. a fragile sexual identity. Although adolescent girls are still the group primarily affected by eating disorders. The fact that the numbers for eating disorders among boys are so low is probably due in part to underdiagnosis. boys often exhibit a different form of body image distortion. There are also differences in the pathologies. They also show less shame concerning binge eating. Swain.

Henninger and Lamprecht 2002). So. I should have made no fuss and stuffed myself like you or anyone else.” said the hunger artist. Overall.5. Under the DSM IV criteria. while another describes the pre-pubertal form of male anorexia as the more frequent and the more difficult to treat form of the disease (see Olivry and Corcos 1999). in advance stages. right into the overseer’s ear. which are reflected in various studies. a body image distortion. “We do admire it. Some recent studies have placed the ratio as high as 1:5 (see Woodside 2004).” said the overseer affably. Herberhold “I always wanted you to admire my fasting. The data for pre-pubertal anorexia are particularly inconsistent. lifting his head and speaking.” said the hunger artist. “and why can’t you help it?” “Because. hypothermia. 1987). heart rhythm disorders. and. (2000) distinguish between physical and psychological changes. “but why shouldn’t we admire it?” “Because I have to fast. Toifl et al. 2003). trans. “What a fellow you are. Jacoby et al. with his lips pursed. in girls there is primary amenorrhea. “Well then we don’t admire it. The numbers given for anorexia range from a rate of 19:1 (Jacobs and Isaacs 1987) to 35:13 (Fosson et al. as if for a kiss. (1988) found a hypothalamic pituitary dysfunction and delayed onset of pubertal development.” “If I had found it.” said the hunger artist. bradycardia (unusually slow pulse). manifest in women as amenorrhea and in men as loss of sexual interest and potency. The first group includes circulatory regulatory disorders. the ICD-10 does specify gender-specific disorder symptoms.92 B. Ohzeki et al. and 5) in the case of pre-pubertal onset of the disorder the sequence of pubertal events is delayed – in boys the genitals remain juvenile. the number of young men suffering from a disorder involving binge eating is about four times that of those with anorexia.” said the hunger artist. Bräutigam and M. the prevalence rates given for the disorders vary from study to study. One current study estimates the risk for a girl to be affected by an eating disorder during her adolescence at 17. 4) an endocrine disorder in the hypothalamic-pituitary-gonadal axis. especially for adolescents. In a study of six male youths with anorexia. hypotonia. One paper describes it as rare among boys (Muise et al. and lanugo. The second . The ICD-10 lists 5 major criteria: 1) a BMI (Body Mass Index kg/m2) under 17. purging.” said the overseer.” said the overseer. (1993) investigated changes in eating behavior in boys and girls between the ages of 6-18 and discovered that eating-related problems among boys have a tendency to decrease with age while they increase in girls as they get older. disorders of the circulatory regulatory system. amenorrhea. or appetite suppressants. W and E Muir) Introduction The number of boys and men suffering from eating disorders is potentially on the rise. “because I couldn’t find the food I liked. so that no syllable might be lost. 2) self-induced weight loss brought about through the avoidance of high-calorie foods and/or though selfinduced vomiting.5%. and amenorrhea. anorexia is present when the subject’s body weight is maintained at less than 85% of expected weight and when the subject has a intense fear of gaining weight. despite being underweight. currently approximately every tenth person with an eating disorder is male. 3) a body-image distortion (see Sack. In general. excessive exercise.” (Kafka 1924. I can’t help it.9% and that for boys at 6. electrolyte disorders. believe me. “But you shouldn’t admire it.

The primary age group for the disorder in children and adolescents is that of 11-18 year-olds. in part because in boys and men there is no distinct phenomenon corresponding to amenorrhea. family conflict situations and overly close bonds.e. They also point out that a wide and distinct spectrum of subclinical eating disorders does exist. Resch (1999) gives the following risk factors: high pressure to perform.g. affect men with anorexia to a similar extent that they do women. The DSM-IV distinguishes between restricting-type anorexia and the binge-eating type. such as the inability to stomach certain foods. the body image distortion. Patients with eating disorders report several non-specific food-related symptoms in childhood years. Muise et al. osteoporosis. very early onset of puberty. limited food selection.. Typical psychological and psycho-social characteristics of female anorexia patients are an above-average I. i.. feeling of worthlessness). an inadequate ability to perceive one’s own emotional state. though. in the DSM IV (Schweiger.. As early as kindergarten or primary school years. an altered cognitive perception of the body’s boundaries. Medical complications. the majority of studies agree that the similarities between those symptoms associated with eating disorders in male and female patients outweigh the differences (see Schweiger. The gonadal disorder develops gradually in men and manifests itself in insufficient testosterone secretion and a resulting loss of sexual interest and potency. acute and chronic stress situations (see Garfinkel. and eating behavior in boys identified a strong denial of the presence of excess weight and described the pursuit of the perfect figure as far .“I Couldn’t Find the Food I Liked” Anorexia in Boys.e. with binging and induced vomiting. the adoption of diagnostic criteria less strict than those laid out. as well as heightened separation anxieties and contact disorders in school (see Walitza et al.. Overall. and a high performance orientation.Q. eating disorders can begin even in pre-pubertal children. The latter differs from bulimia in that the diagnosis of bulimia does not apply to cases where patients are underweight. There are. weight. In-depth somatic examinations intended to rule out organic diseases are much more likely to be administered when the patients are undernourished boys (Severin. Peters and Sipos 2003). avoidance of intimate sexual contact. In a review article. Garner 1982) or post traumatic stress disorder. or stomach pains after meals. being overly responsive to the needs of others. such as severe depression somatoform autonomic dysfunction (see Rief 1995). Thus in the field of child psychology. Bruch described anorexia in 1978 as a typical disease of the daughters of well-to-do. (Schweiger 2003). and conflict avoidance in family relationships. (2003) state that the diagnosis of an eating disorder under strict ICD-10 and DSM VI criteria raises serious difficulties. frequent nausea. successful families. Peters and Sipos 2003) has been discussed. e. children can feel too fat and begin restricting eating behavior that may result in their being underweight or growth disorders. and being a twin. Contrary to previous belief. A study of body image. a clinically relevant depressive pathology. for example. e. Benden and Menken 1992). The DSM-IV also distinguishes diagnostically among other types of psychogenic appetite loss that can occur when other psychological disorders are present. body image distortion. a few characteristics specific to boys and men.g. The ICD-10 refers to an atypical anorexia nervosa in cases where one of the major symptoms is missing. i. Three Case Reports 93 group includes conspicuous eating behavior. Eating disorders and anorexia in particular were then and still are considered typically female diseases. 2001). extreme self-esteem issues (marked insecurity.

and the tendency to avoid entanglement. Chambry 2002). Bräutigam and M. compulsive disorders and addiction. Regarding the pre-pubertal form of anorexia among boys. 1997). The affected persons develop a heightened sense for the needs of others and often use it with controlling or manipulative intentions. There has been a higher frequency of homosexual orientation reported among men with bulimia nervosa. there is no definitive indication of a link between homosexual orientation and a more frequent incidence of eating disorders (Woodside 2004). ill-defined borders. The issue of sexual orientation. Olivry and Corcos (1999) allude to the comorbidity and to the case history of the psychological disturbance that . Eating disorders are diagnosed less frequently and in general only when a psychiatric comorbidity is present (Severein. Situations of separation or the disruption of attachments are often described as triggers of the disease in both genders. actions are always carried out with wellmeaning intentions for the other person and are not open to criticism). Eating disorders are more likely to affect boys / men who are involved in physical and sporting activities. we must point out that there is no sufficient indication for a specific familial pattern. In generally. In diagnoses of the families of female eating disorder patients. seems to be a frequent point of conflict (Chyambry 2002. There was one very significant gender difference observed in an examination of attacks of hunger cravings: 78% of girls reported feelings of guilt. (Carlat et al. while 82% of boys considered a figure in the normal weight range to be desirable. Characteristics that are often identified among very heterogeneous families with an anorexic family member are the following: a strong norm-referenced and high-performance orientation. Herberhold less prominent. both of him or herself and of others (Schepker 1993). These include depression. They strive less towards an ideal weight than they do to attain an ideal body.94 B. The reason for this may lie in different gender-specific expectations regarding social rolls or it might trace back to different conflicts and conflict-resolution at an internal-psychological level. this can be linked with the myth of misfortune. In this area too though. the crucial evaluation is as to whether the damaging eating behavior has a specific function within the familial system. including a fragile sexual identity. though the family dynamics do play a significant roll in treatment of eating disorders. typically one that is muscular and powerful. in negative terms. the tendency to over-protectiveness and sacrifice (decisions are always made based on the other person’s interests. However. as does a tendency on the part of the patient to be demanding. The ‘law of harmony’ (peace at all costs) and conflict avoidance are of special importance (see Cierpka and Reich 1997). the fear of separation. Homosexual men exhibit more eating disorder psychopathologies and higher depressivity in comparison to heterosexual men (Russel and Keel 2002). Dalem 2000). Sixty-six percent of girls wanted to achieve a figure under normal weight (1015% underweight). A childish super-ego persists. Anorexia among both boys and girls is seen as a way of coping with stress or. “it ought to be done the right way”. while only 24% of boys mentioned them (Hoffmann-Müller and Amstad 1994). A familial constellation described as typical among eating disorder patients is one with an overprotective mother and absent father (Srenivasan 1978. A premorbid obesity frequently occurs among men and male adolescents. Benden and Menken 1992). as a refusal to confront the conflicts typical of the developmental phase currently being undergone. boys / men who suffer from an eating disorder tend to push themselves to the limit physically rather than to fixate mentally on a specific weight.

) was brought in as an emergency patient for in-patient treatment. Case Report 1 Situation at Admission David (10 yr. He had been given an infusion by his personal physician but had consistently refused to take any other liquids. we have sketched out two vignettes of cases that were treated in another clinic and that fall more into the borderline area of classic eating disorders and hence indicate the broad spectrum of sub-clinical eating disorders that often go unnoticed but nonetheless require treatment. In the case of in-patient treatment of adolescents. In this specific form there is a significant presence of depression and auto-aggressive behavior among boys. They said he would frequently check to see that the door was closed. It is thought that the earlier a treatment begins after the onset of the disease. Since parents often experience the separation as a strain. but that he was not at all interested in his actual weight. He had. Systemic short-term therapy. Dalem 2000). it is recommended that attending staff work with the parents to set up precise conditions for discharge.” Since that time he had eaten less and less. washed his hands relatively frequently. they said. They also noticed that David was extremely thrifty and concerned with cleanliness: he was sickened by the idea of showering at the swimming pool. and needed an unusually long time to perform day-to-day tasks such as tying his . 11 mo. 2002). They reported that David was very concerned about gaining weight. and that his need for activity increased dramatically over the same period. The situation had come to a climax in the preceding month. which was the first time he had been separated from his parents. while the incidence of laxative abuse is described as less probable. According to his parents. David’s parents reported that his weight had fallen from 33 to 28 kg over the previous four weeks. David himself said “nothing in this trip had suited him. combined with elements of behavior therapy. because bulimia in general is viewed as an even more typically female disease than anorexia is. he hadn’t eaten for 2 days and hadn’t drunk anything for one day. His parents felt as though they were “hitting a wall” when they admonished him about eating. He was 149 cm tall. is viewed as an especially effective treatment for adolescents (Blank et al. Below we have attempted to comprehensively describe the course of therapy and psychodynamics in a case report of a boy of just under 11 who suffers from the restricting type of anorexia. The authors also describe a high incidence of narcissistic disorders in the primary attachment figures. been teased and bullied on the trip. They said David had felt very isolated on this trip. All of the studies reviewed stem from the same environment and similar treatment methods for both genders. His parents dated the onset of his weight loss back to a trip taken with his soccer club four months previously. the better chances it has of success (Romeo 1994. not because he was less hungry but because he had decided not to. parental agreement and cooperation is of central importance.“I Couldn’t Find the Food I Liked” Anorexia in Boys. felt guilty about food. The shame affect is seen as a particular problem among male adolescents who suffer from bulimia. Following that. Three Case Reports 95 evinced itself earlier both through problems with food and through phobic-compulsive disturbances. wanting instead to shower at home because it was cleaner there.

he had entered secondary school. In the first conversation David himself reported being sadder than usual. He suffered from chronic obstipation for about 3 months when he was 4. At 15. where he had great difficulties integrating in class. she was described as being somewhat inaccessible. David’s aggressive behavior stopped and he adapted very well. Patient History The pregnancy went without complications. swimming. The parents supported the decision to have their son examined due to his poor physical condition and they expressed their agreement with the conditions of the in-patient treatment (participation in family therapy. David’s father was a decorator by profession. she had suffered from anorexia that abated without therapy. He had been an enthusiastic marathon runner. Three months before his admission. The Inpatient Treatment Environment A multi-discipline team works at the station. and psychiatric and psychological psychotherapists. who no longer lived at home. David listed soccer. teachers. The relationship between David and his sister was good. David suffered from a sleep disorder. a therapeutic educational nurse (Heilerziehungspfleger). he suffered from multiple sclerosis and. David’s paternal grandfather committed suicide 22 years earlier. and he exhibited a markedly strong will that. He was breastfed for 10 months and was on the whole a restive and nervous infant. could not be countered in a strict manner. made up of pediatric nurses. There are twelve treatment positions available for children and adolescents aged . The maternal grandparents had died as a result of excessive alcohol consumption: the grandmother when David’s mother was 8 years old. Bräutigam and M. but had had to give this up five years earlier due to multiple pains for which no somatic cause could be found. He was a relatively good student in terms of his performance in school. a student of education science. handicrafts. but after half a year it receded without any special intervention. cycling. skateboarding. where he integrated quickly. His behavior overall was very defiant. Herberhold shoes. according to his parents. an art therapist. in fact. There are also a physiotherapist and a social worker that can be called in. his parents were shocked at how overadapted his behavior seemed. Family History David had a 22 year-old sister. the grandfather one and a half years before David’s treatment began. At 4 1/2 he started kindergarten. When he started school at six. In first or second grade.” His paternal grandmother was still alive and there was loose contact with her. according to David’s father. and painting as his hobbies.96 B. His statomotoric and speech development progressed normally. David was a planned child. etc). His mother was employed half time in a white-collar job. At times. although he often reacted aggressively to other children. “couldn’t deal with that. his parents confirmed this.

and on elements of the integrative child and adolescent psychotherapy as well. so that he could be agile. particularly David’s father. after an observation phase this was treated with Anafranil. but break . and exerted enormous pressure on his parents to take him back home. his fantasies of greatness and high-performance related themes. became evident. the collaboration was extremely fragile. step-by-step plan to nutritional rehabilitation. in art therapy. in all its intensity and despair. as I record later. Work with the parents was initially quite difficult. With strong therapeutic support however. patients are given a behavioral therapyoriented. due to the suicide of his own father. which he attempted to keep minor. His speech was uniform. A further hurdle in the therapeutic treatment arose in dealing with the paradoxical signals the parents sent David.. but he didn’t know why that was the case. David threatened to take his own life if his parents didn’t take him out of in-patient treatment immediately. They constantly sent conflicting messages: obey the rules. The treatment concept is committed to an integrative method approach. also were partly responsible for the patient not sensing powerful emotions like rage or powerlessness. with little modulation in his voice. They also receive two individual therapy hours per week. The first four weeks of his stay were marked by crises. pulled out his tube himself.e. After two weeks of inpatient stay. serious. Both preferred the idea that their son not be forced into anything and anxiously predicted resistance from him: resistance that promptly emerged. The station specializes in treating somatization and eating disorders. and learn yoga. in physical therapy. they also take part in the depth-psychology oriented group therapy. It was very important to him to be thin though. The fear that something would happen to David at home or that he might die collided with the fear inspired by David’s threat to harm himself. and once a week a parent or family therapy session takes place. but with whom he was also in competition. Treatment of eating disorder patients lasts between a minimum six weeks and a maximum six months. especially during the projective test procedures. As a rule. It was extremely difficult for both parents to decide definitely on the in-patient treatment. who spoke of his illness as something alien. were dominant with David. In the psychological diagnostics. On several occasions. Another central theme seemed to be his relationship with his father. and the fear of and defense against it. Course of the Therapy Our first impression of David was of a precocious. Three Case Reports 97 4 to 17. and his facial expression was rigid. an extreme compulsion to wash manifested itself. depth-psychological. and in his whole behavior. the theme of aggression. to improve their body awareness. individually designed. to whom David wanted to be close.“I Couldn’t Find the Food I Liked” Anorexia in Boys. this threw both parents into panic. Understandably. He said he no longer had an appetite and had to count calories. it draws on behavioral therapy. which. i. the situation defused itself and he grew increasingly willing to cooperate. As soon as it became clear to David that this decision was unequivocal. systemic. David often refused to cooperate. In the individual therapy sessions we sensed mental disturbances and blocks in the counter-transference. both decided to leave David in the in-patient treatment program. very stiff boy. In addition.

David’s parents began to join forces with him to break the hospital rules: they smuggled food in. Herberhold them too. etc. which had cut their contact with their son. his response to this suggestion was positive and he acted upon it. There seemed to be almost no partner level that was separate from the children. and the patient decided.which up until this time had ranged from despair. David’s father was advised to seek individual psychotherapeutic support to confront his own fear pathology.98 B. The latter was primarily understood as an expression of an underlying severe depressive episode. Family Dynamics In the course of the family therapy. Once the weight situation had become less dramatic. a change occurred. age-appropriate. There followed an individual therapy session with David. The father talked about the unbelievable amount of calories that. Bräutigam and M. during the treatment of her son. In individual therapy his behavior developed from that of a precocious. playful behavior. At this level too. of the deterioration of his own body – especially before the background of his father’s suicide – was a central theme for him. David had gained 8 kg and the compulsive pathology had abated to such an extent that the medication could be tapered off. The decisive positive shift in the therapeutic treatment occurred on two levels. to auto-aggression. Both parents were very slender to the point of thinness. When confronted with this. it became clear that she had had only very limited experience with care-giving and continually felt herself to be on the verge of being overburdened within her role as a mother and in her duty to care for others emotionally. The fear. to work with the therapist instead of against her. They reported that in the current situation they could neither comfort nor be gentle with one . David’s sister talked about her own anorexic period during a family session. he had been able to consume without gaining fat during his marathon running days. Both spoke of extreme difficulties in supporting each other and keeping each other grounded. he gained weight and the compulsive behavior lessened. He also became better and better at articulating the fact that he had often felt lonely and isolated from other children. on his own initiative. In the same period. in which he actively demanded therapeutic support in the form of positive signals when something had worked successfully. By the end of the 10-week treatment. food established itself as a significant topic and relevant arena for action. David’s mother became even thinner. intellectualizing and problemconscious narrative behavior to a more childlike. to some extent seemingly paranoid. the parents behaved like anxious and rebellious children. The therapeutic relationship then became so stable that it became possible to establish sustainable cooperation with David and to modify the stimuli plans with him. rigid but also life-sustaining mother. Focusing on this conflict made it possible to transform the opposition into cooperation. The relationship of the parents to one another came across as very sibling-like in character. Initially through a conversation with the parents in which they articulated their anger at the clinic. to aggression directed outwards visibly improved. His mood . he said. over-stayed visiting hours. It was only after the conflict with the parents had been resolved that this became possible. while the clinic and the therapist took over the roll of the strict.

because to do so would cause them to feel guilty about feeling good when their son was in the clinic. David confronted the issue of life and death and these existential questions in his father’s place.12). In our view the disease was triggered by the temporary separation from his parents. and by doing so managed to bring his whole family together and cause them to confront such threatening subjects as fear of loss and separation together. David’s father had kept physically fit through marathon running for years but was ultimately forced to give that up. David. who took part in one family session. This is a self-punishing dynamic typical for families with anorexic children.“I Couldn’t Find the Food I Liked” Anorexia in Boys. autonomy was associated with fear and thus this represented a critical transition. p. it fulfils the function of a familial reapprochement. this represented an extremely critical point of in his life. David’s grandfather had committed suicide because he could no longer tolerate the physical deterioration brought on by his multiple sclerosis. a depressive duty-fulfillment without enthusiasm that is driven by guilt” (Schepker 1993. Once a trusting therapeutic relationship had been established. The family sculpture had something about it that struck outside observers as rather oppressive and constricting but which all of the family members perceived as a pleasant density and physical closeness. claiming that he had not earned them. The sister. David’s self image as that of an athletic boy who wins all competitions also collapsed on this soccer trip. On the one level. For David and his whole family. one that had dominated his father and probably his grandfather as well: can I go on living if I don’t have complete control over my body? This is where the trans-generationally-significant theme expressed itself. that is when it became obvious just how critical and existentially threatening all family members perceived the physical separation from the sister to be. He then became preoccupied with the unvoiced question or fear that he might have the same disease his father had had. David’s pathology began with his entry into a developmental phase that implied more autonomy. articulated her feelings of guilt and ambivalence about having moved out. . the themes of separation and the disruption of bonds dominated the family therapy session. one that could be summed up with the motto: “Do everything for the others. refused to accept gifts from his parents. nothing for yourself. Three Case Reports 99 another. When David’s disorder appeared. it presents a classic autonomy-dependency conflict. Psychodynamics David’s illness must be viewed at different levels. Within the family there was a significant amount of fear associated with these themes: separation was viewed as almost equivalent to death and absolute loss. for his part. and on a third. He lost to other boys. Out of this emerged what was for him an existential question. one that his son picked up on and transformed into a crisis of his own. a situation exacerbated by harassment by the other children and in which David was also confronted with a new environment. David processed this defeat and the separation from his parents with a feeling of guilt. According to family lore. his father was at the same age at which his own father had committed suicide. For David’s father. on another it symbolizes a trans-generationally-significant theme for the paternal line.

climaxing in arson and severely destructive behavior during his last in-patient treatment period.100 B. The early patient history shows normal statomotoric and speech development. He was diagnosed under ICD-10 with a social behavior and emotional disorder (F. With respect to the family history. When his father insisted that he eat his entire serving. toilet training was complete at the end of his first year. . we know that Stefan grew up with his parents as an only child. withdrawn from the relationship with their son. although it was obviously dominant. This case illustrates the way that a diagnosed but incompletely treated eating disorder. sometimes with blows and rescinding television privileges. Stefan reacted by vomiting. in different ways. Case Report 2 Over a four-year period. Stefan’s mother took care of her own ailing mother. reacting with vomiting to milk products in particular. His father became unemployed when Stefan was one and developed an alcohol problem. Stefan witnessed acts of domestic violence perpetrated against his mother and there were isolated violent acts directed against Stefan. Stefan’s parents separated when he turned 10. He also ate and drank very little. As an infant and small child. it is apparent that the somatoform dysfunction with vomiting and nausea was not treated directly until around the end of his tenth year.3) and with a somatoform dysfunction with nausea and vomiting. For years. accompanied with nausea and vomiting. contact with his father was sporadic and irregular. After he turned 10. Stefan (13 yr.) received in-patient psychiatric treatment four times under various diagnoses. In the later patient history. but he was also very much afraid outdoing his father in that arena. He had several stays in the pediatric clinic due to undefined stomach pains and refusal to eat. The mother reacted to this at times by accommodating his wishes or by ignoring the behavior. that cropped up again and again. Stefan’s aggressive behavior in school and at home began to increase. can be transformed into a dissocial disorder in male adolescents with multiple manifestations. 3 mo. the separation was not discussed with Stefan. who died when Stefan was 12. with the onset of puberty and his parents’ separation. The only way Stefan could get his parents attention was by refusing to eat and through the stomach aches. 91. The disorder developed from an earlier interaction disorder that went unrecognized and untreated. He was often involved in fistfights and verbally aggressive towards his mother. Stefan suffered from severe sleep disorders: up until his third year he woke up as often as 20 times at night. Bräutigam and M. She herself suffered from a cerebral tumor with facial paralysis. an expression of the hunger for parental attention and security. This earlier disorder manifested itself as a sleep and feeding disorder. From the various courses of treatment. the fact that Stefan initially had many friends and got along fairly well in school seems significant. From the beginning of his eleventh year. Herberhold David’s illness is also an avowal of his loyalty for his father: David identified with his father very much and tried to emulate him in his athletic endeavors. From then on. Stefan’s introverted self-destructive behavior began to decrease and aggression directed outward became more frequent. It is also evident that both parents had.

93 m tall and weighed 54 kg (BMI 14.5) at admission. Michael’s father and his girlfriend. The eating disorder took the form of a daily battle over eating: Michael was said to throw out his food and often vomit after meals. Among men with bulimia. was treated for three and a half months for a psychogenic eating disorder for which no more exact diagnosis was given. When applying the classification system. with an umbilical cord entanglement at birth. He saw his father regularly on weekends. is 1. those . at which point his paternal grandparents took over his care. for a nascent personality development disorder with anxiety/avoidance personality traits. boys. They do not suffer as much from feelings of guilt regarding food binges. and they strive less towards an ideal weight. A few days before his hospitalization. Overall however. due to psychosocial stress factors on the basis of an early childhood emotional deprivation. 10 mo. socially less competent and conflict-avoiding. old Michael. Boys seem to strive for a less underweight ideal figure than that pursued by girls. Three Case Reports 101 Case Report 3 13 yr. instead pursuing an ideal physique. Summary and Discussion The number of boys and men suffering from eating disorders is increasing. With regard to Michael’s medical history: nicotine and alcohol abuse were known to have taken place during the pregnancy.5% risk of acquiring an eating disorder. Two years later. Girls run a 17. The number of boys with a binge eating form of disorder is four times higher than that suffering from anorexia nervosa. Boys tend to fixate less on a specific weight. His statomotoric development and speech development were delayed. Nutritional problems arose very early on. Questions of sexual orientation play a role among boys with eating disorders more often than they do among girls. the criterion of the abnormal gonadal axis (lowered libido. Michael transferred to another residential school shortly before his hospitalization at the clinic. contact with Michael’s mother broke off completely. a higher frequency of homosexual orientation has been reported. Michael. A recommendation was made that Michael be encouraged to take on more independence and responsibility in the area of practical living. The over-protective child-raising style of the grandmother was discussed as a problem and the high degree of responsibility borne by his father was also raised as an issue during the in-patient treatment. juvenile genitals) is more difficult to operationalize than is amenorrhea.“I Couldn’t Find the Food I Liked” Anorexia in Boys. 6. who had a learning disability. Michael started at a residential school for children with disabilities at age 7. separated. and for stereotyped movement disorders in the form of jactation. usually a muscular and powerful one. which went to term. with whom Michael had had a good relationship. Michael was released after a small weight gain and a decrease in the jactation. the fourteen year-old son of his father’s long-term girlfriend sexually abused him. At eleven. potency.5%. The psychogenic eating disorder was considered to be the reaction of a learning-disabled boy who was extremely anxious/unselfconfident. A weight loss of 6 kg and the intensification of a chronic eating disorder triggered his hospitalization. Michael’s parents separated when he was five years old. who comes from a tall family.

Bräutigam and M. Y.. thus making it a family theme more available to examination. It alternates between restrictive control and the support of developing needs for independence. we have attempted to give an example of a seldom described but probably not so very rare kind of case. DB.CA. Am J Psychiatry. The treatment often takes on the form of a battle. In describing the case of 10 year-old David. Eating disorders among boys are characterized by a wide spectrum of forms of manifestation and causal factors and by a high frequency of sub-clinical disorders in particular. I. (2002) The emergence and treatment of anorexia and bulimia nervosa: A comprehensive and practical model. Katz. Zadik. References Blank. In: Int. This is that of a boy who uses his pathology in an attempt to detach himself from a symbiotic relationship with his father and transform a conflict that actually belongs to his father into one of his own. the aspect of asceticism and the strength drawn from it is used as a way of establishing borders between the subject and the parents or important attachment persons. identity building. In this regard. I. (1978) The golden cage. at the cost of enjoyment.. Cambrigde. This must be made very clear to the patient: the idea is to return control over his life and his decisions to him and to humiliate him as little as possible along the way. 1127-1132 . They should also illustrate the initially atypical contexts in which eating disorders can represent an expression of the psychological distress of a male adolescent. I. a mixture of a resource-oriented and a confrontational approach seemed optimal. one that cannot be won by the therapist with out the patient though it can be won by the patient without the therapist. S. J. 257 – 260 Bruch. DJ.. Med. Camargo. MA: Harvard university Press Carlat.. Z. (1997) Eating disorders in males: a report on 135 patients. which included the general terms set by the clinic. Toker. Mahazri. and assertion of independence. In the restricting type of anorexia nervosa. Herberhold symptoms disorders in both genders have in common outweigh the gender-specific differences. On this basis. but without apportioning blame. The sustainable therapeutic alliance with the parents. and intimacy. primarily supporting work could be done with David in individual therapy. By refusing to eat. was of critical importance in putting the treatment on the road to success. a female anorexic patient is often trying to detach herself from a symbiotic relationship with her mother and thereby to demonstrate – in an extreme and often life-threatening way –having cut the apron strings and gained independence. and Barak. The psychotherapeutic treatment of children and adolescents with anorexic pathologies usually involves walking a tightrope between curbing and permitting autonomy. H. Health. 154. thus providing access to opportunities for change. The children and adolescents in question use the refusal to eat as a way to try to deal with the general developmental tasks of gradual separation. This theme had to be brought out into the open in the family therapy. Herzog. The case vignettes of Stefan and Michael should illustrate the way in which unrecognized or insufficiently treated eating disorders can turn into other disorder profiles. Adolesc. 14. one that respected the family as a functional system but nevertheless recognized dysfunctional entanglements as such. sensuality.102 B.. sexuality.

300-3006 Sack. (2000) Kognitive Verhaltenstherapie bei Anorexia nervosa und Bulimia nervosa. Guilbaud. In: Rev. PsychologieVerlagsUnion Rief. and Jeammet.102 Resch. D. F. Frankfurt a.. et al. M. Benden A. (1993) Eating Attitudes in Boys and Girls aged 6-18 years. Franz (1969) Sämtliche Erzählungen. G. In: Schweizerische Rundschau für Medizin. Weinheim: Beltz. 29. 52. Henniger. Motozumi. M. In: J. Othara. and Abress... 8-14 Schweiger. Thiel. Child Psychol. H. A. E. (2002) Veränderungen im Körperbild und Körpererleben bei essgestörten und nichtessgestörten Patienten im Verlauf einer stationären Psychotherapie. 28.. K.. PsychologieVerlagsUnion Jacobs.561 Sreenivasan. 23. In: Journal of Adolescent Health. Corcos. 159 . (1982) Anorexia nervosa: A multidimensional perspective. C. In: Eat. Psychosomatik. G. Three Case Reports 103 Chambry. 117 – 121 Olivry. 62. (1997) Die familientherapeutische Behandlung von Patientinnen mit Eßstörungen.. 33. 5.150) Psychotherapie der Eßstörung. CJ and Keel. D. 114 – 118 Garfinkel. W. P. T. (2002) L' anorexie mentale masculine: réalités et perspctives. New York: Thieme Severien. (1994) Adolescent boys and anorexia nervosa.. Lerminiaux. 643 – 647 Russell. Bryant-Waugh. B. (1986) Pre-pubertal anorexia nervosa: A retrospective controlled study. and Gotestam KG. 64 – 69 Schepker. In: Arch Dis Childhood. and Lask.. Kinderpsychol. (2003) Essstörungen. Interne.. In: Prax. (2004) Prevalence of eating disorders in female and male adolescents. Weinheim: Beltz. Cierpka. 100. 27. B. 127 . J. Med. In: Psychopathology. Stuttgart. In: Adolescence. U. (2002) Homosxuality as a specific risk facktor for eating disorders in men. Knibbs. and Paul T.and Isaacs. In: La Presse Médicale. Stein. S. Psychiatr. (1994) Die Bedeutung der Schulleistungen bei Jugendlichen mit anorektischen Störungen. 110.. Fischer-Verlag Kjelsas. Bjornstrom. Medizinische Psychologie. Stuttgart: Thieme Dalem. and Corcos. P. 427 . J. 26.435 Ohzeki. and Sipos.. C. and Reich. R. Med. C. Göttingen: Huber Romeo... B. Gewicht und Eßverhalten bei Jugendlichen. In: Fortschr. (1995) Multiple somatoforme Symptome und Hypochondrie: empirische Beiträge zur Diagnostik und Behandlung. 42. and Menken. Peters. and Amstad.. H. Bern. O. M. 1S61 – 1S67 Cierpka. G. F. In: Ann.. In: Int. Piccinin. V.250 Kafka. A. A. 83. (2000) L' Anorexie Mentale Du Garcon. P. J. E. D. and Ansseau. B. 55. K. (2003) Eating disorders in Adolescent Boys: A Review of the Adolescent and Young Adult Literature. H. 559 . (1992) Anorexia nervosa bei Knaben – ein Fallbericht.. M. 31. In: Psychotherapie. Assoc.. Psychiatry. M. New York: Brunner / Mazel Hoffmann-Müller.. G. New York. Hanaki. Med.. and Garner.. (1999) Entwicklungspsychopathologie des Kindes – und Jugendalters. 13 – 25 Muise. E. R. A. (1994) Körperbild. U. (1978) Anorexia in boys.162 . 237 . and Lamprecht.“I Couldn’t Find the Food I Liked” Anorexia in Boys. M. In: Reich. In: Can. and Shiraki. (Hrsg. (1987) Early onset anorexia. M. I.. F. 153. 1051-1057 Fosson. Kinderpsychiat.. Behav. 1337 .1343 Jacobi. Main. W. S. J Eat Disord. (1999) L`anorexie mentale prépubertaire. U. Liege. M.

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

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

Chapter VI

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake, Eating Patterns, Eating Attitudes and Body Image of Brazilian Bulimic Patients
Marle dos Santos Alvarenga1, Fernanda Baeza Scagliusi2 and Sonia Tucunduva Philippi3
Eating Disorders Unit of Clinics Hospital, Department of Psychiatry, Institute of Psychiatry, University of São Paulo 2 School of Physical Education and Sport, University of São Paulo and Eating Disorders Unit of Clinics Hospital, Department of Psychiatry, Institute of Psychiatry, University of São Paulo 3 Department of Nutrition, School of Public Health, University of São Paulo
1

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

106 Methods

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

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

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

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

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

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

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

Eiger et al.. which makes them eat a very limited amount of food and avoid those foods considered by them caloric or “fattening” (the named “forbidden foods”). 1986. 1989). Distorted cognitions about nutrition and feelings of repugnance.436 to 8. 1991... Researches describes that a chaotic eating pattern is present in BN. Mitchell and Laine.. 2003. cookies. APA. which should be performed by a multiprofessional staff aiming to end bulimic behaviors and to alter the patient’s relationship towards food and weight (ADA. Some authors argue that the disturbed eating pattern is a general feature of BN and not only a characteristic of their restrictive diets and binge episodes. The studies conducted in laboratories.585 kcal. The artificial settings and the low ecological validity of these studies may have limited their findings. Baeza Scagliusi and S. 1996. 1996). 2001. Kissileff et al. food aversion... 1993. Hetherington et al. In our studies we divided this term in the following components: food intake (foods that are eaten and their energy and nutrient content).. Kissileff et al. The items more consumed in these binge episodes are those most avoided by the patients due to their fear of gaining weight (for example. Halmi. which explain the difficulties faced in order to normalize their intake (Hetherington et al. eating pattern (general characteristics of the intake.108 M. 1995). Hetherington et al. 2001. F. varying from 69 to 10. Sunday and. Besides their unhealthy food consumption.. 1986. 1993. Sunday and. candies. metabolic units or hospitals (with inpatients) observed in the binges episodes an energy intake varying from 1. These episodes usually lasted 59 minutes and they were composed by 59% of carbohydrates. where the energy consumption can be very high (Reiff. Tucunduva Philippi The interest for this area of research came from the observation that the majority of patients who looked for treatment in our unit had BN and this is an eating disorder marked not only by binge eating and compensatory practices. as . 1992). taboos and prejudices regarding food and weight control (Elmore and Castro. 1992). etc) (Alvarenga et al. 1985. fears. its is known that these patients have other disturbed eating behaviors. Walsh et al.620 kcal (Hadigan et al. They constantly start a new diet. 1989. especially if one considers that the term “nutritional aspects” embodies several different variables. Sunday and Halmi. 1996).. 1994).. The “diet – binge – purge” cycle illustrates the eating pattern of bulimic patients. 1994. 1989). 1994. Wallin et al. 1996).. essentially in developed countries (Hadigan et al. which was generally followed by vomits.. Walsh et al. as difficulties regarding food choice. dos Santos Alvarenga. Halmi.. but the ample difference between the minimal and maximal values shows that there is a great variability in food intake data of bulimic patients. abnormal patterns of hungry and satiety. oscillating between severe dietary restraint and episodes in which the energy intake is extremely high (Wallin et al. hate and incompetence in dealing with food are also features of this disease (Sunday et al. Without the binges patients had a wide range of energy consumption. This restraint leads to a binge eating episode. Nutritional rehabilitation has a key and primary role with regards to treatment objectives. 1994. 1985. chocolates. Mitchell and Laine. APA. 1989.. 43% of lipids and 8% of proteins. The first studies regarding nutritional aspects of BN were conducted between 1980 and 1990. 1989).. This scenario shows that it is hard to study nutritional aspects of BN. Walsh et al. but also by an extremely affected eating behavior (ADA.

we are most interest in eating attitudes. which include the definition of a recovery criteria and follow-up methods. Nevertheless. many follow-up studies utilized recovery predictors and indicated that the frequency of bulimic behavior at baseline was not associated to the outcome (Abraham et al. Food Intake … 109 number.. we created a more specific definition of eating attitudes. Nobakht and Dezhkam.. Fernandéz et al. Lee et al. Fairburn et al.. in which Olmested et al. Keel and Mitchell.EAT-26 (Garner et al. 1996.. based on the statements of Garcia (1999) and Johnson (1985): what.. among others. Although there are many studies using screening tests in several populations (Adami et al. To assess the effects of BN treatment. 1999. 1990) whereas others consider it as just those that did not present any episode (Herzog et al. 2001.EDI (Garner et al. In addition to analyzing the frequency of binge eating and purging episodes. Keel et al. 1997. (1994) found a high score in the subscale of bulimia of EAT-26 (Garner and Garfinkel. Studies to measure outcome are hard to be conducted because of methodological difficulties. outcome measurements and follow-up studies are not conducted systematically in Brazil. According to Steinhausen and Seidel (1993). 1986. The results of some of these tests are analyzed in studies on recovery predictors. 2002.. 1986). Among these aspects. aversion... with whom. there are some standardized tests used to screen patients with eating disorders.. 2003. Maddocks et al.. self-applied scales should be used in prognostic studies. 2002. types and schedules of the meals) and eating attitudes (relationship with food. Bulimic Inventory Test Edinburgh BITE (Henderson and Freeman.. 1996). 1983.. such as Eating Attitudes Test . and what are the feelings related to food. 2003.Effects of Multiprofessional Treatment on Clinical Symptoms. The definition of recovery varies in each study: some considered recovery as those patient that presented bulimic episodes and purging episodes once a month (Pyle et al. even to compare results of healthy individuals to those from ED patients (Behar et al. Nakazato et al. Steinhausen and Seidel... why we eat that. 1983). Bhugra et al. weight at the start of the treatment. 1992). and when we eat.. 1987). 1994. Fahy and Russell. not only because of the scarce number of studies concerning it but also because it seems that it is one of the most disturbed characteristics of BN. 1996).. few studies assessed the scores of individuals with ED post-treatment (Brambilla et al. several factors are used as prognostic predictors: age at the beginning of the disorder. lack of control. The uncertainty remains as to whether the scores attained on these tests return to normal patterns after the remission of ED symptoms. 1983) among the recurrence predictors.. It is also important to ask in what are food choices based on. Maddocks and Kaplan. Due to our interest. few studies have assessed the nutritional progress of bulimic patients and no study has evaluated the effect of a multiprofessional intervention with . Keller et al. Beals. 1993. presence of comorbidities.. Hsu and Holder. 1993). 1997. and Eating Disorder Inventory . 1979) and high score in the interpersonal distrust subscale of the Eating Disorder Inventory-EDI (Garner et al. Although follow-up studies of bulimic patients are commonly carried out in developed countries (Collings and King.. where. for example) (Herzog et al. how. what we think and feel towards food. Leung et al. and where there is difficulty. 1991). 1998. eating behavior and methods used to lose weight (Herzog et al. feelings and beliefs related to food). 1982). 2003). most studies compare the frequency of pre and post treatment bulimic behavior (vomiting episodes. 1992. with what. 1995. in which situation we eat. Also. Ghazal et al. 2000). 2000.. psychosocial aspects. Even in developed countries.

The study was approved by the Committee of Ethics of the Clinics Hospital of the College of Medicine of the University of São Paulo. APA. eating behavior and body image in bulimic patients treated at a center considered to be one of reference in Brazil: the ED Unit of Clinics Hospital of the University of São Paulo. Because of that. ADA. 2000. the unit provided 3 more months of care.. Tucunduva Philippi regards to important BN aspects: relationship and behavior towards food. F. 1994). 1993). as far as we are concerned the food intake of bulimic patients was analyzed only in cross-sectional studies. 1988. Methods Thirty-nine female patients with BN treated at the Eating Disorders Unit of the University of São Paulo (in Brazil) were followed-up. according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders . The few studies that have assessed the effect of treatment on eating behavior used tools such as food diaries and standardized tests such as the Eating Disorder Inventory (Garner et al. 1994).DSMIV (APA. and BN was diagnosed by means of a semi-structured clinical interview. one must remember that these instruments do not encompass the wide concept of food behavior and are frequently limited to the analysis of dietary restraint (Herman and Mack.. treatment consisted of 12 weeks of cognitive behavioral therapy (CBT) – with one weekly consultation with the psychiatrist. Also. So we conducted an follow-up study to assess the effect of multiprofessional intervention on bulimic symptoms. eating patterns. researchers with interest in nutritional aspects of BN have to use other instruments able to approach these aspects in a more comprehensive manner. Because of that. so it is not know if the treatment improves the food consumption of these patients. and this data was used to calculate Body Mass Index (BMI – weight in kg/height2 in meters). this issue requires further study (Whisenant and Smith. . All measures were compared between these phases. This idea is supported by Eckstein-Harmon (1993) who attested the importance of the outcome measurements of nutritional education and rehabilitation in eating disordered outpatients and inpatients.. 1986. At the end of treatment. Therefore. 1975).110 M. Leung et al. immediately after treatment (Phase 2) and three months after treatment (Phase 3). Patients had their weights and heights measured. but in an unstructured form. Subjects were evaluated by a psychiatrist. Measurements were performed at baseline (Phase 1). Baeza Scagliusi and S. the psychology and the nutrition education teams. Patients gave informed consent before participation. Cognitive Behavioral Therapy (CBT) is considered the best technique to treat BN (Agras et al. 2000). Although we presented above these tests as interesting measurement tools. They were also informed that the goal of the study was to evaluate the outcome of the treatment. Whisennat and Smith (1995) interviewed dietitians who worked with ED and stressed the importance of more objective evaluations of the nutritional treatment. dos Santos Alvarenga. 1995). The descriptive data of the patients were collected in this interview. food intake. Bulimia nervosa should be treated by a multiprofessional staff working to end bulimic behaviors and to change patients’ relationship towards food and weight (Gannon and Mitchell.

definitions of hunger and satiety. Nutzunger and Zwann (1990) and Vanderlinden et al. Story. food pyramid. The food records were also used to obtain patients’ energy and nutrient intakes. 1996). Latner and Wilson. which contains data regarding nutritional composition and serving sizes consumed in Brazil. The food intake was converted into energy and nutrient intake by means of the software Virtual Nutri (Version 1. c) the personal meaning of BN. Only the days that were completely recorded were analyzed. Johnson et al. The topics addressed during the nutrition education program were: role of nutrients. 1986).0) (Philippi et al. The goals of the nutritional treatment were to: a) decrease the binge and purging episodes. Weekly nutritional treatment consisted of one hour of nutrition education and 30 minutes of individual counseling based on the food record. c) establish a regular meal pattern.. the amount eaten. The dietitians instructed the patients to register all food consumed. ADA. and f) barriers for change. the prior or the next week diary was utilized. (1989). 12 and 24 were analyzed. if the patient did not describe correctly one meal. but its structure and content followed the models proposed by Fairburn (1981). b) education about food and nutrition. guidance for buying food and how to eat at restaurants and social events. vomits and use of laxatives. number and type of meals consumed. e) correct nutritional deficiencies and f) implant a healthy food intake and behavior (ADA. 2001b) and those described above: a) the kinds of hunger (physical. After the 12 weeks. d) increase food variety. and the schedule and duration of their meals in a food diary (ADA. ineffectiveness of dietary restraint and of restrictive diets. 2001). (1986). The approach can be divided in some key points: a) education about the disease and its implications. they had to specify which ones. If the answer was yes. diuretics and diet pills were obtained through this diary. emotional and social). Food Intake … 111 The number of weeks of treatment was defined arbitrary. b) the beliefs involved in the diet-binge-purge cycle. energy and nutrient requirements. the social and emotional meanings of foods and exchange of ideas about methods and tips to handle difficult situations regarding food. If one patient did not fill her record in one of these weeks. We chose to use the diary from the second week as a baseline measurement because the record from the first week was used by the dietitians to check if the patients were registering their intake and bulimic behaviors in a proper manner. according to the models of Villapiano and Goodman (2001a. 1994. the topics discussed were chosen by patients and/or the professional team such as issues from lay magazines about body and nutrition. 1988. c) reduction of weight concerns. They were also asked to mark if they considered the meal a binge eating episode and if any purging method had been used to compensate it. 1986). healthy weight and build. even suggesting some educative materials. b) minimize dietary restraint. To do so. which described cognitivebehavioral techniques and provided guidelines for nutritional counseling. Patients received one hour and half of psychology consultation. For example. e) mechanisms used in order to copy with the emotions. Lacey (1985). When a patient registered that a meal was . this day was excluded from analysis. d) self-monitoring of the food intake by means of a food record and e) implementation of a healthy eating pattern (Story. d) body image dysfunctions. diaries filled at weeks 2.Effects of Multiprofessional Treatment on Clinical Symptoms. Weekly frequencies of binges. in which the following issues were addressed. 2001.

which measures concern over body image. These subjects were derived from our clinical experience (for example. Restraint Scale (Herman and Mack. 2000). normoenergetic 600–1. Baeza Scagliusi and S.EAT-26 (Garner et al. The scale contained 24 questions about feelings and beliefs regarding food. Gendall et al. insofar as the amount effectively absorbed is not known (Alvarenga et al. . the intake of the following minerals and vitamins were analyzed (using only the meals not followed by vomits): sodium. The instrument had been applied in a previous sample of patients in order to verify if it was clear and easily understandable. and others.. This differentiation (meals followed by vomiting or not) was made because it was impossible to take into account the energy of foods eaten in a meal followed by vomiting. and minimum and maximum values.. 2002). 1986). 1975). 1982). Patients filled in a questionnaire about their eating attitudes and relationship with food specially developed for this population. B6. certain types of food consumed and body image.2. 1987). 6.200–2.0. F. translated to Portuguese by Nunes et al.BITE (Henderson and Freeman.. Significance level adopted was p ≤ 0. We calculated the energy and macronutrient intake from the meals not followed by vomits (named VET) and from those meals followed by vomits (named VOM). Data is presented by phase. 1997. 1997. Kaye et al.BSQ (Cooper et al. Tucunduva Philippi followed by vomits. 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. Statistical analysis was performed using the Statistical Package for Social Sciences (SPSS) software for Windows v. Energy consumption ranges for VOM and VET were defined. this meal was separated from the others. 2003. the Bulimic Inventory Test Edinburgh . 1998. 1975) and the Dutch Eating Behavior Questionnaire (van Strien et al.. as percent frequencies or as mean.. dos Santos Alvarenga. normoenergetic 1. 1983). shape and size. potassium.001Kcal VET: hypoenergetic < 1. behavior during meals.112 M. and hyperenergetic > 1. Woell et al.200 Kcal. and hyperenergetic > 2201 Kcal These VET values were defined according to the mean energy recommendation for young women (+/. translated to Portuguese by Cordás and Hochgraf (1993). which measures the symptoms and the severity of BN. 1989). Trumbo et al. Reference values used were: VOM: hypoenergetic < 600Kcal.199 Kcal. 1987). 1991. magnesium. and hyperenergetic.. (1994). The values obtained were compared to the Dietary Reference Intakes – DRI’s (Institute of Medicine. D and E. Also. 1989. median.. which measures concern over diet. 1993) and would require a very complex physiological study. calcium. and the VOM values were based on studies of the energy content of binges (Elmore and Castro. and the Body Shape Questionnaire .. translated to Portuguese by Cordás and Castilho (1994). Three-Factor Eating Questionnaire (Stunkard and Messick.05. B1. standard deviation. normoenergetic. C.200Kcal) (NRC. They also answered the Eating Attitudes Test . such as Eating Disorder Inventory (Garner et al. in which the values for energy were classified as hypoenergetic.000 Kcal.. iron and vitamins A.

Effects of Multiprofessional Treatment on Clinical Symptoms. BMI and EAT. (2000) found that 26% of the patients abandoned the treatment after approximately five weeks. Most patients belonged to the BN bulimic subtype (90%). Findings and Discussion Thirty-nine patients started the study (Phase 1). physical education teacher. BITE and BSQ scores varied according to the energy intake range (for VET and VOM consumption). at the end of 6 months (Phase 3). the responses to the tests. normoenergetic and hyperenergetic). 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). and the n of each parameter varied. and the last three (sometimes. For the questions regarding the relation with food.5% dropout rate during the entire follow-up. and the Mann-Whitney test was used when the independent variable had only two categories. 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 first three options of answers (always. there were only 15 patients – for a 48. but merely to describe the group profile. 3 patients (15%) had a previous history of anorexia nervosa. and . the Bonferroni test was used to assess which phase would differ from the other. For the questions regarding eating attitudes and beliefs. 20 were still undergoing treatment. the length of the disorder varied from 1 to 20 years. A chi-square test compared the ratio of affirmative responses for these questions between the phases. at the end of 3 months (Phase 2). The data for the 19 patients that quit follow-up from Phase 1 to Phase 2 were not used for analysis. nutrition student. but other outcomes studies also found an elevated dropout rate (Bacaltchuk and Hay. Elmore and Castro. Agras et al. dancer. among the phases. The diaries returned at each phase. 1999. BITE and BSQ scores throughout the phases. 65% had at least started college. 1991). often) were grouped as “frequent thought or feeling”. For example. 25% had professions or activities that demanded a lean body (dietitian. This high rate may have limited our results. Food Intake … 113 Friedman´s test was used to compare the frequency of bulimic behaviors. 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. 70% did not have a partner. the frequency of affirmative or negative responses was calculated.7% dropout rate during treatment and 61. the energy and nutrient intakes and the EAT. The Spearman correlation coefficient was used to determine the existence of correlations between these variables: frequencies of vomiting and binges. BITE and BSQ scores. When significant results were found. In order to analyze the evolution of eating behaviors and relationship toward food throughout the phases. Kruskal-Wallis ANOVA was used to determine if the frequency of bulimic behavior and EAT. very often. rarely. the following approach was adopted.

2000.3 ± 4.1 135..3 pounds). in Brazil there are no primary care services preventing and detecting eating disorders. and 70% were taking antidepressants according to psychiatric evaluation. In the other hand. In this study the sample were patients of the Eating Disorder Unit.. 1992. 1989. Kell et . The mean desirable weight was 15. 1989). These findings are corroborated by other studies of bulimic patients..9 pounds lower than the mean current weight.0 ± 14. 1999). this difference between Brazilian results and the literature may be due to our health care system. Hetherington et al.5 ± 6. 1990. University of São Paulo. Baeza Scagliusi and S.7 ± 6.0 33. 1997.. which illustrated the weight cycling derived from the many times the patients tried to loose weight.. dos Santos Alvarenga.9 ± 3. Hetherington et al. The patients presented a profile similar to those described in the literature as characteristic of bulimic patients: young women. 1994). Table 1 shows other descriptive data. Finally.. 1997. usually when the disease is very severe.. with a high level of education and with a greater prevalence of the purging subtype (Dolan et al. 1994. Table 1. Gendall et al.6 18. Wallin et al.. which also found a higher mean age and a long time of disease (Hadigan et al.. which may explain the higher mean age of our sample. Kissileff et al. unmarried.114 M. 1992). following the restraint/binge/purge cycle of BN (Reiff.. 1992). evidencing the persistent desire to loose weight that is characteristic of BN.7 ± 4. Leung et al. the vacancies are not much and the wait-list is long.9 120. Fitcher et al.3 ± 17. which makes our sample very representative of eating disorders cases in Brazil.2 20. F. This may be due to the long time of the disease and also to the long time that the patients took to seek treatment.9 ± 23. 1986. People from all over the country come to be treated in this unit.. The mean weight’s oscillation in the adulthood was also high (33.3 17. 1994). so the diagnosis of the disorders happens too late..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. at Institute and Department of Psychiatry (a public institution). the initial BMI was normal as appointed by other authors (Gendall et al. 1993. Woell et al. Nevertheless. probably because they felt ashamed of their behaviors or because the lack of awareness about the disorder (Becker et al. This was the first center in Brazil to treat eating disorders and it is still the most known and important center. Wallin et al.5 Although the patients were still young (median age was 25 years).7 22. Tucunduva Philippi actress). Regarding the anthropometrical data.. they were slightly older than the bulimic patients from developed countries – whose age varies between 16 and 20 years (Joergensen.

4 0. 1994). Other purging behavior. 0-13) (0. Food Intake … 115 al. in Phase 3.2 pounds in the historic of bulimic patients.5 (1. and 91. dieting. Even though. 0-20) 1.7% had this result in regard to vomiting episodes. was shown in 100% of the responses below the diagnostic criteria. 0-11) (0.5. Lacey (1983) observed that 80% of these patients completely ended their binge eating and vomiting episodes at the end of 10 sessions of CBT. regarding the number of vomiting episodes per week. The frequency of other compensatory methods (fasting.5. and the medians were zero in all phases. 0-28) (0. 0-9) (0. This type of compensatory method was less utilized than vomiting.4 ± 3.9 0.6 0. There was no significant statistical difference between the phases regarding use of laxatives. in this study. The percentages found are somewhat compatible with the data described in literature. However up until Phase 2. 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.9 0 (0.2 ± 4. diuretics. 0-11) 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).Effects of Multiprofessional Treatment on Clinical Symptoms.3 0.65 ± 1.3 0. such as the use of laxatives. found (1999) a mean weight’s oscillation of 35. Regarding percentage of improvement in the bulimic behaviors assessed.2 0 (0.6 1.55 ± 2. Table 2 shows the progress of binge eating and purging behaviors in the 3 different phases. 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. 0-8) 0. There was a significant statistical difference between Phases 1 and 3. 0-6) (0. The major difference . and between 2 and 3. Table 2 . minimal-maximal)) Phases Weekly frequency of binges 9.3 (0.5 ± 8. the mean number of binge eating episodes per week was below the minimum frequency established by the DSM-IV (APA. while Sunday and Halmi (1996) affirmed that the bulimic recruited in their study had been heavier in the past. and appetite moderators. 0-1) (0. 0-29) 4.6 ± 2.Measures of bulimic behaviors along the follow-up (data presented as mean ± standard deviation (median. 0-7) Weekly Weekly use Weekly use Weekly use frequency of laxatives of diuretics of diet pills of vomits 4.6 1 ± 1. actually.08 ± 0. 1994).4 ± 0. it took more than 12 sessions for patients to significantly cease these behavioral patterns.5* (7. diuretics and diet pills. physical activity) could not be estimated and compared to the DSM-IV criteria (APA.4 ± 3.7* (3.2 ± 6. 0-11) 1 – Before treatment 2 – Immediately after treatment 3 – Three months after treatment *: significantly different from results obtained three months after treatment There was no significant statistical difference between the phases.9 ± 2.5. regarding the frequency of binge eating episodes per week.92 ± 3. 0-3) (0.

(1999)." From this point. Tables 4 and 5 show the energy and nutrient consumption along the treatment phases. that a longer period of treatment and follow-up (at least six months) yields better results. Perhaps it would be very difficult to consider them recovered based on the criteria of non-influence of weight and body shape. in the VET intake (meals not followed by vomits) and in the VOM intake (meals followed by vomits). who would require a longer follow-up to verify a six-month abstinence. (1994). based on the definition by Pyle et al. and 20% do not present significant symptom improvement. It can be seen. as stated by Keel et al. Leung et al. and 9% still suffered from this disease after treatment. This finding is very important. duration of intervals and evaluation methods are defined. There were no significant differences regarding the number of the other meals. (1999) is much more severe: "absence of changed behavior for at least six months. According to the criteria adopted by Maddocks and Kaplan (1991) (less than one episode of binge eating or purging in the last 4 weeks). Regarding recovery after six months. Even so. we cannot assess patients from this study. seems to be a poor prognostic indicator and can be considered one of the best parameters for residual symptoms in these patients. dinners and evening snacks were slightly higher than at baseline. diagnostic criteria. Mitchell et al. of maximum of two episodes of binge eating and purging episodes in the last two weeks of treatment. Tucunduva Philippi was that in Lacey’s study patients spent half a day. even if at low levels. and 45% did not meet the diagnostic criteria for BN according to the frequency of binge eating episodes after 12 weeks. being treated. half of the patients attain full recovery. The criterion proposed by Keel et al. Table 3 presents the number of meals consumed in one week among the treatment phases. and the median number of the afternoon snacks. 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. According to Becker et al. the length of follow-up was short and patients may have had relapse episodes after this period of time. dos Santos Alvarenga. (1999). a comparison of results between studies is very difficult because of the variability of how improvement.116 M. (2000) found an over 50% decrease in bulimic symptoms after 12 CBT sessions. about 30% attain partial recovery. whereas they stayed 3 hours per week at our center. (1996). Nevertheless. which means having lunch everyday. (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. in their review. these patients should be considered already under recovery. We observed that after six months the median number of lunches was 7 (significantly different from Phase 1). the frequency of vomiting episodes. Collings and King (1994) found that 52% of patients fully recovered. . respectively. F. After six months. 39% experienced some symptoms. once a week. (1990). As stated by Herzog et al. these patients presented a "moderate" response. 1987). Baeza Scagliusi and S.3% vomited more than twice a week. 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. According to Olmested et al. and the weight and shape cannot influence how the subject felt. 8. at the end of the following the median number of the breakfasts was 7.

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.415 kcal (range: 1. while the macronutrient consumption seems to follow the American diet pattern. 1989.. Hetherington et al. which is surprising considering that these meals were more likely to be binge episodes. 1989). p = 0.436 – 8.200-11. (1994) and Gendall et al.690 kcal. Other studies found a great variability in the energy content of the binges. we found a range of 460-2. 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. 1994. 12% of proteins and 43% of lipids). these extreme fluctuations in energy intake disconcert the appetite regulation and other physiological functions. (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. Wallin et al.. It seems like that the patients usually eat less energy than necessary. Regarding the energy consumed in the meals followed by vomits (VOM intake). Due to that it is recommended to include as one of goals of the treatment the regularization of the eating pattern. Wallin et al. . (1989) found a mean energy intake of 3. (1989) found that one third of the bulimic patients declared as compulsive episodes with less than 500 kcal (Rosen et al. (1981) observed a mean intake of 3.3 ± 4%.2.03). Gendall et al. Wallin et al. 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. Woell et al. including the binges episodes.. Food Intake … 117 The results showed that the mean intake of energy in the meals not followed by vomits (VET intake) was much lower than the energy consumption recommendation to young women (+/. Trumbo et al. which leads to a binge episode in order to compensate this deficit. According to Gendall et al. but only at baseline (VET intake = 32.. According to Gayle (1998). (1995) observed a mean intake of 762 ± 560 kcal/day. Mitchell et al.394 kcal (range: 1.. Sunday and Halmi (1996) observed that bulimic patients ate less energy than anorexic patients in a weight maintenance phase.1 ± 7%. in order to prevent fluctuations of the bulimic behaviors. The studies regarding eating pattern and nutrient intakes of bulimic patients are diverse. 2002). The author affirms that the low energy intake leads to a loss of control. except for the lipid consumption (in percent contribution to total energy intake). in spite of the great amount of energy consumed subsequently. The median macronutrient profile of the VOM intake was similar to those observed by Woell et al. VOM intake = 35. 1986.200 kcal) (NRC.500 kcal). (1997). This data shows that the energy intake of these meals was not so high. which was higher in the VOM intake. 1995.100 kcal per day. Walsh et al.Effects of Multiprofessional Treatment on Clinical Symptoms.. Woell et al.585 kcal).. On the other hand. 1994. Wallin et al. 1997. Gendall et al. 1998. These great variability among studies was expected.800 kcal in the energy intake. empirical studies noticed a variation of 605-4. while Mitchell and Laine (1985) obtained a mean consumption of 4. We also observed that the macronutrient profile of the VOM intake did not differ much from the macronutrient profile of the VET intake. (1989) in binges (42% of carbohydrates. (1997) found similar results and attested that these patients use the binges episodes to regularize their limited intake.

3 ± 2 (7. 44-65) 50.3 ± 2 (5. 460-2.197. 0-7) Lunch 4. 3-8) Morning snack 2. 0-7) 3.5 ± 7 (1.3 ± 2 (3.9 ± 2 (3.274. 18-40) 31 ± 13 (27. 19-43) 32.5 ± 1 (4.. 641-2. 21-69) 60.1 ± 2 (3. 24-40) 31. 6-17) Carbohydrate intake (%) 47.1 ± 7 (32.9 ± 15 (44.1 ± 3 (28. Trumbo et al.2 ± 7 (35. Tucunduva Philippi Table 3 – Weekly number of meals along the follow-up (data presented as mean ± standard deviation (median.7 ± 3 (60. 7-32) 1.337 ± 519 (1.118 M. Table 4 – Energy and macronutrient content (as percentage contribution to total energy intake) of the meals not followed by vomits. the percentage contribution of each macronutrient to the VET intake was similar to those recommended in Reference Dietary Allowances (NRC.277. 11-65) 4.7 ± 3 (5.5 ± 8 (51. 10-33) 10.211 ± 226 (1.440) 17. 927-1. 1-7) 5.8 ± 6 (49.5 ± 2 (7. 0-9) Dinner 4.2 ± 7 (16.1 ± 2 (6. Baeza Scagliusi and S.131) Protein intake (%) 14.664) 1. 40-60) Lipid intake (%) 32.094) 1. 10-21)* 15. Table 5 – Energy and macronutrient content (as percentage contribution to total energy intake) of the meals followed by vomits. 0-6) 4.0 ± 2 (4. 1989.8 ± 3 (15.320. 22-42) *: significantly different from Phase 3. 44-72) 50. 1-6) 4.475 ± 771 (1. 26-41) 34.6 ± 3 (14.8 ± 10 (23. along the follow-up (data presented as mean + standard deviation (median. 3-7)* 6. minimal-maximal)) Phases 1 – Before treatment 2 – Immediately after treatment 3 – Three months after treatment Total meals Breakfast 25. 0-6) *: significantly different from Phase 3.6 ± 5 (32.7 ± 1 (4. 577-3. 0-7) 6.310 ± 686 17. 5-50) 25. 57-65) Lipid intake (%) 35. 0-9) Evening snack 2.0 ± 2 (3.853) 1. 0-7) 2. minimal-maximal)) Phases 1 – Before treatment 2 – Immediately after treatment 3 – Three months after treatment Energy intake (kcal) 1. . dos Santos Alvarenga.238.6 ± 3 (18.689) (14. 1-8) Afternoon snack 3.4 ± 6 (49.4 ± 2 (4.393.402 ± 707 (1. 37-55) 45. 24-31) In every phase. 13-21) Carbohydrate intake (%) 53.7 ± 2 (5.3 ± 4 (36. 2-7) 3.2 ± 1 (6. 584-2.4 ± 7 (23. 0-6) 4. 0-6) 3.3 ± 2 (2. 0-7)* 5. 337. F.4. minimal-maximal)) Phases 1 – Before treatment 2 – Immediately after treatment 3 – Three months after treatment Energy intake (kcal) Protein intake (%) 1.6 ± 6 (31. 21-43) 28.3 ± 2 (2.1 ± 2 (4. 0-6) 2.4 ± 6 (50. along the follow-up (data presented as mean + standard deviation (median. 12-21) 17.529 ± 945 (1.1 ± 5 (9.

6% 17. and meals with over 1.201 kcal.0% 75.8% 47.005.001 Kcal decreased after 12 weeks and fell to zero after six months. 2003).001 kcal. It was concluded that there was a trend of decrease for hyperenergetic meals followed by vomiting throughout the phases.6% 47.Proportion of subjects classified in each category of energy intake.3% and the mean protein intake with 17. In this chapter. In that study.0% 0% 25. the number of patients increased after 12 weeks and after six months. b : Normoenergetic = Intake between 1. Only a non-significant increase in normoenergetic intake.8% 11.4% 70.200 e 2.0% 31.. c : Hyperenergetic = Intake > 2. f : Hyperenergetic = Intake > 1. Table 6 shows the distribution of patients in each energy intake range. Meals not followed by vomits: a : Hypoenergetic = Intake < 1. p < 0. Table 6 . only protein intake significantly changed (the baseline intake was lower than the intake presented at Phase 3). Food Intake … 119 2002).6% 41. 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). within the phases of the follow-up Energy intake Phase 1 – Before treatment Phase 2 – Immediately after treatment Meals not followed by vomits 52. and a non-significant reduction in hypereneregetic intake were observed.0% 0% Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec Hypoenergetic intaked Normoenergetic intakee Hyperenergetic intakef *: χ2 (2) = 21.9%. In relation to the meals followed by vomiting (VOM).200 kcal. Meals followed by vomits: d : Hypoenergetic = Intake < 600 kcal. Regarding meals of 601-1.199 kcal.Effects of Multiprofessional Treatment on Clinical Symptoms.6% Phase 3 – Three months after treatment 50. e : Normoenergetic = Intake between 600 e 1.8% of the total intake.8% Meals followed by vomits* 21.0% 50.000 Kcal. considering the meals not followed by vomits (VET) and the meals followed by vomits (VOM).0% 11.000 kcal.6% 31. . The values were also similar to those obtained in a prior cross-sectional study conducted with Brazilian bulimic patients (Alvarenga et al.2% 15. 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. the mean carbohydrate intake contributed with 50.32. while the mean lipid consumption contributed with 32. we observed that along the phases.

hypo VOM does not mean that the patient ate less energy than he should at that moment. 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. 1998. and “different” foods. the size of these binge eating episodes also increases. therefore. the terms hypo. however these are patients undergoing treatment. intake of micronutrients was below the recommendations of the Dietary Reference Intakes (Institute of Medicine. and eating more energy than one should. and that. while the most inadequate intakes were found to sodium. potassium and iron It is not possible to affirm that this unhealthy intake is characteristic of bulimic patients. This ratifies that diet restraint is a symptom much more common among BN patients and that it is difficult to eliminate (Keller et al. hyper for VET applied. It is necessary to evaluate why this happened and what could be done to improve the micronutrient intake of these patients. 1997. 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.. These categories were based on the energy content of binges. this may cause a hydroeletrolitic disturbance (Greenfeld et al. to eating less energy than one should. meaning meals with a low intake of energy. less than half of the patients changed. 1995. Elmore and Castro (1991) stated that greater binge eating episodes are more likely to be purged.120 M. eating the right amount of energy. 2000). however. behavior also described by Keller et al. This paper shows that throughout the follow-up stage patients decreased the size of their meals followed by vomits. The same terms were used for VOM. The fact that the sodium and potassium intake was so low is very preoccupant because. calcium. The intake of vitamins and minerals along the phases. normo. respectively. as the length of the disorder progresses. even with significant changes. Tucunduva Philippi As for the nomenclature used to describe the energy intake of these patients. The reduction of guilt declarations when patients ate foods whose consumption they restricted demonstrates greater permissiveness towards these foods. Intake of vitamins A and C was closer to the recommendations. fast food. patients without treatment will present binge eating episodes with higher energetic content. as well their adequacies in relation to the recommended intakes. 2001). It is remarkable that. This result suggests that the nutritional treatment was not able to correct this unhealthy eating pattern. Chart 1 shows the results of frequency of affirmative responses for questions about eating behavior and beliefs. Baeza Scagliusi and S. There was a gradual reduction in statements regarding behavior change after eating sweets. most of them were still feeling guilty and having difficulties in eating the foods regarded as “dangerous”. . F. supposing that meals followed by vomiting are more likely to be binge eating episodes.. In a broad manner. (1992). can be seen in Table 7. when combined with compensatory behaviors as vomiting and use of laxatives and diuretics. More than half of the patients were still practicing some kind of restraint on their diet at the end of the following. with an intermediate intake of energy and with high intake of energy. Lasater and Mehler. This inappropriate pattern of intake did not change throughout the phases. Most probably. 1992). dos Santos Alvarenga. magnesium. Even though.

219 – 1.6. 0. when compared to the recommended intake.0) 0.917) 1. 68 – 4. 43 – 356) 132 ± 39 (133. 0.400 67 58 55 1.4 – 15) 7 ± 3 (6.3 – 2.433) 1. along the treatment phases Nutrient Vitamin A (mcg) Phase 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 Amount consumeda 710 ± 377 (680. 0 – 55) 8 ± 20 (0.4 (0. 598 – 4.8. 2 – 15) 6 ± 3 (5.258) 84 ± 44 (85.8. 0 – 95) 10 ± 15 (1. 196 – 4. 508 – 2. 1. d: Phase 1 – before treatment. 2 – 25) 7 + 5 (5.414) 113 ± 54 (119.1 91 81 58 1.125 (1. 3 – 16) 1.612) 1117 ± 460 (990. 0.632) 774 ± 337 (765.7. minimal-maximal).123.7 (0. 211 – 2.7.5 – 1. .390.9 ± 0. 3 – 12) Recommende Adequacyc d intakeb (%) 89 800 97 140 118 75 112 289 95 1.4 – 2.156 (1. 73 – 199) 1.061.604 ± 1.081) 855 ± 960 (569. 99 – 1. 0. 656 – 2. 19 – 241) 132 ± 79 (116. b: Recommended intake to young women.178) 632 ± 288 (578.625) 1. obtained in the meals not followed by vomits. Food Intake … 121 Table 7 – Micronutrient intake and adequacy. 0 – 22) 9 ± 7 (7.150) 6 ± 4 (5.5) 0.406) 1. 0.265 ± 513 (1. 344 – 1. according to the Dietary Reference Intakes (Institute of Medicine.500 36 43 34 18 37 35 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 : mean ± standard deviation (median.2) 1 ± 0. 16 .8 ± 0.4 – 3. 1 .427.1 – 1.652) 552 ± 289 (481. c: Percent adequacy of the mean intake.8.551 ± 1.8.4 (0.050) 88 ± 74 (69. 483 – 2.236.186) 217 ± 259 (124.4) 0.9 ± 0.128.195 ± 539 (1. e: Phase 2 – immediately after treatment. 60 .Effects of Multiprofessional Treatment on Clinical Symptoms.4 (0.397 ± 669 (1. 0. 2000). 1998. 0 – 68) 7 ± 5 (6.000 86 63 37 310 43 42 34 3.6 (0.4 (0.3 68 72 351 5 199 166 49 15 57 49 65 2. f: Phase 3 – three months after treatment.015 – 2. 0. 1997.7.493 ± 382 (1.992) 1 ± 0.7) 18 ± 29 (0. 27 – 1.9 ± 0.5 – 1.7) 0.

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

Chart 1 - Frequency of affirmative answers to the questions regarding eating attitudes and beliefs towards food, between the treatment phases. Questions Phase 1 – Before treatment 94% 70% Phase 2 – Phase 3- Three Immediately months after after treatment treatment 75% 57% 65% 60%

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?

75% 70% 74% 95%

71% 65% 76% 76%

76% 59% 82% 53%

60% 74%

29% 59%

29% 59%

35% 90%

29% 41%

6% 29%

65%

41%

35%

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

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

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

123

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

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

Chart 2 - Frequency of ‘frequent’ or ‘not frequent’ answers to the questions regarding relationship towards food, between the treatment phases Questions Phase 1 – Before treatment Freq. Infreq. 95% 5% 100% 95% 50% 60% 60% 42% 44% 0% 5% 50% 40% 40% 58% 56% Phase 2 – Phase 3 – Immediately Three months after treatment after treatment Freq. Infreq. Freq. Infreq. 71% 29% 44% 56% 94% 82% 59% 41% 53% 35% 35% 6% 18% 42% 59% 47% 65% 65% 56% 56% 38% 38% 36% 31% 19% 44% 44% 63% 63% 63% 69% 81%

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**
*: p ≤ 0.05; ** p ≤ 0.01

63%

37%

53%

47%

25%

75%

65% 89%

35% 11%

47% 59%

53% 41%

46% 40%

56% 60%

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

Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake …

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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

1. and after one year. This result is similar to that found in the Fahy and Russell (1993) follow-up in which the mean initial score was 14. dos Santos Alvarenga. F.126 M.05 Figure 2 – Percent distribution of the affirmative answers to the question “How do you feel when you go to a restaurant. 6. Q uie t* . 100% 90% 80% 70% 60% 50% 40% 30% 20% 10% 0% Si ttin g* St an W din ith g so me bo dy * Re ad ing W atc hin gT W V ith att en tio n Ta lki ng Phase 2 Phase 3 Al on e Phase 1 *: p < 0. The mean score after six months showed a "clinically significant" group. The scores of the BITE-symptom showed just a "sub-clinical" group after six months of follow-up. showing a still "clinically significant" group. coffee shop or a bar?” Irritated Phase 2 Fearful Phase 3 Nervous There was no significant statistical difference between the phases in regard to the BITE severity scale.1. Tucunduva Philippi was expected.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 *: p < 0. showing positive evolution of these patients. Baeza Scagliusi and S.

5 ± 14 (28. 15-53)†* 25. 6-49)* 17. Currently.8 ± 8 (17..Effects of Multiprofessional Treatment on Clinical Symptoms. there are other tests that have been translated.. an analysis of the evolution of classification based on test scores showed good results. 2005-b). Food Intake … 127 Table 8 . (1993).2) was lower than the 156 described by Hetherington et al.6 ± 40 (149. and BSQ were the only tests that had been translated to Portuguese and that were available to assess BN.. nutritional knowledge (Scagliusi et al. these tests do not diagnose ED. Wolff and Clark.8 ± 8 (23. 1-28) BITE severityc 15.Scores obtained in the scales (EAT. in which weight variations and body dissatisfaction remained present even among asymptomatic patients. BSQ showed significant statistical difference between Phases 1 and 3. 1-28) 15. Notwithstanding. 2005-a). Fernandéz et al. EAT.5. perception and satisfaction with body size and shape (Stunkard’s Figure Rating Scale – Scagliusi et al. BITE and BSQ). and that specific intervention is required to this end.. nowadays it is recommend the use of tests more specifics to the body image aspect that is intended to be measured (Thompson. BITE... Hedges et al. Although we found this improvement in body image issues at the end of the follow-up. Therefore.3 ± 5 (14.5.0 ± 11 (16. . but not as good as the findings for binge eating and purging behavior. 2005-c). so the improvement found in the classification regarding concern over body image through BSQ was surprising. No study showed the evolution of BSQ scores throughout follow-up.6 ± 10 (40. Results show that concern over body image takes more than 12 weeks of CBT to present significant changes. 1998. 11-29)†* 19. which measure the chronic practice of restrictive diets (Restraint Scale – Scagliusi et al. 2006). among others. minimal-maximal)) Phases 1 – Before treatment 2 – Immediately after treatment 3 – Three months after treatment EATa 38. 2-23) 7. For this reason. 1995.1 ± 6 (8. 2-42) BITE symptomsb 23. 2-24) BSQd 145. Some authors (Ramirez and Rosen. they just address some issues and suggest a classification. and between 2 and 3. 2001) declare that traditional CBT is not enough to improve body image in EDs. (1987). The BSQ initial mean score (145.. 1993). When this study was carried out. 99-190)* 132. 2001. but the EDI test has not yet been translated to Portuguese. 48-189)* 109. along the follow-up (data presented as mean + standard deviation (median.2 ± 28 (142. 47-189) † significantly different from the scores obtained immediately after treatment *: significantly different from results obtained three months after treatment. thereby indicating a continuous improvement.5. it is not possible to know if whether overestimation of body size or body dissatisfaction or body disparagement decreased. Steinhausen and Seidel. 2004).5. 3-25) 10. body attitudes (Body Attitudes Questionnaire – Scagliusi et al.6 ± 5 (25.2 ± 44 (103. A series of studies used the Eating Disorders Inventory (EDI) to measure outcome (Brambilla et al. 2003. Using this scale. These results are consistent with those found by Swift et al. one might argue that the BSQ along did not provide much information about what changes did occur in relation to body image.6 ± 6 (5.

According to Maddocks and Kaplan (1991) patients who have been heavier in the past had more chances of presenting worse treatment outcome. are related to a poor outcome or a complication of the disease during follow-up (Agras et al. It is known that these two responses. 1985. and also after six months of follow-up. (1985) and by Fahy and Russell (1993). It seemed that. regardless of the timeframe. at that point. among others factors. the more severe the level of BN symptoms. 1994). even after treatment) are highly prone to experiencing recurrence. and body image.128 M. number of vomiting episodes per week and number of binge eating episodes per week.. (1994) who said that vomiting can be used to control weight. This correlation was no longer true in the following phases. Olmested et al. 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. the greater their concern over body image. After 12 weeks of treatment. These correlations were not present at the beginning. that is. but this became true only after 12 weeks of treatment. BMI. It could be thought that the frequency of binge eating and the frequency of vomiting episodes would present a correlation during all phases. and it seemed that. the stronger the concern of the patient over diet. the number of binge eating episodes had decreased. foods eaten. Bite-severity inventory test and EAT presented a positive correlation only during Phase 2. Tucunduva Philippi Table 9 shows the correlations between BITE. Freeman et al. the greater the number of binge eating episodes per week presented by the patient. This shows that to patients not being treated. suggesting that only at this moment did a greater number of binge eating episodes result in more vomiting episodes.. the higher their EAT score. showing that. the more severe the levels of BN symptoms. This result shows that after being treated. In fact. showing that for these bulimic patients. 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. 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. greater dissatisfaction with body image after treatment and higher EAT scores. and the greater the number of binge eating episodes. EAT and BITEsymptom inventory test presented a positive correlation. stress and affection. Baeza Scagliusi and S. after treatment and follow-up. found in each phase. F. the presence of binge eating and vomiting episodes did not present such a correlation at the beginning of treatment and after six months. This data suggests that these patients (more concerned over food and their body. and not only to compensate binge eating. the bulimic symptoms had somehow changed and no longer had any correlation to the frequency of binge eating episodes. BSQ. EAT and BSQ presented a positive correlation in the 3 phases of the program. After treatment. the higher the BMI.. dos Santos Alvarenga. the symptoms originated from the psychopathology of the disorder and not from inadequate body weight. The severity of BN symptoms at the beginning of treatment was considered a predictor of recurrence by Fahy and Russell (1993). the more severe the patient’s symptoms and BN itself. This finding is supported by Olmested et al. 2000. EAT. as described by Freeman et al. The number of binge eating episodes and BITE-symptom presented a positive correlation just at the beginning of the treatment. . despite the bulimic symptoms.

45* 0.62* 0.13 -0.39 0.03 0.73 0.11 0. the higher the BMI.44 0.47 - -0.Effects of Multiprofessional Treatment on Clinical Symptoms. Food Intake … 129 BMI and BSQ presented a positive correlation after 12 weeks of treatment showing that.10 0.05 -0. the greater the concern over body image.63* 0.10 -0.09 0.48 -0. 2006).19 0.04 0.40 - -0.. the more concerned they are (Hill and Williams.18 *: p ≤ 0.59* BITE BITE Frequency severity symptoms of binges Phase 1 – Before treatment 0. This finding supports the fact that individuals with ED are overly concerned about body image regardless of their weight (Dowson and Henderson.21 0.81* 0.22 0.50* 0.13 0. at this phase.36 0. their concern for the body is the same as what is presented by the overall population: the heavier they are.40 0.28 0.15 0.44* Frequency BodyMass of vomits Index -0. showing that the greater the number of symptoms of BN presented at the end of this period.78* - Phase 3 – Three months after treatment -0.75* 0.01 0. 1998.19 0.44 0.Spearman correlation coefficients between scales scores. This result was not observed at the beginning or after 12 weeks.68* 0. bulimic behaviors and body mass index. insofar as it is the pathological condition that causes this concern.30 0.49 0.28 0.80* - Phase 2 – Immediately after treatment 0.28 0. This finding also shows that treatment can minimize weight-related concerns in individuals who are not overweight. BITE-symptom inventory test and BSQ presented positive correlation only after the sixmonth follow-up. Scagliusi et al.06 0. a: bulimic behaviors are expressed as weekly frequencies. When patients are treated. along the follow-up Scales and EAT measures BSQ EAT BITE severity BITE symptoms Frequency of binges BSQ EAT BITE severity BITE symptoms Frequency of binges BSQ EAT BITE severity BITE symptoms Frequency of binges 0. 2001).01 -0.06 -0.38 0.13 -0.05. the greater the concern of the patient over body image.45 0.20 0.02 0.22 0. Table 9 .08 0.40 0.21 0.48* 0.38 0. It seems that BN symptoms are significantly .13 0.61 0.57* 0.36* 0.20 0.

along the follow-up Energy intake in meals BSQ not followed by vomits BITE severity BITE EAT symptoms Weekly frequency of vomits 13.0 14. c : Hyperenergetic = Intake > 2.8 8.0 10.6 5.0 10.199 kcal.3* 3.5 Phase 2 – Immediately after treatment Phase 3 – Three months after treatment 9.8 5. Table 10 – Mean ranks of the scores and bulimic behaviors.2 6.130 M.9 12.0 11. 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.200 e 2.6 11.9 9.4* 4. the more severe the BN. e : missing value (no subject from this category filled this questionnaire).5 9.5 6. Tucunduva Philippi affected by body image only if the patient still remains highly concerned about his image after six months of treatment.7 5. F.2 8. supporting the presence of vomiting and binge episodes as an indicator of poor prognosis (Olmested et al.0 5.2 10.2 5.07 between the energy categories. 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.5 5. severity measurement by BITE scale considers the frequency of binge eating and vomiting episodes. normoenergetic or hyperenergetic intake.0* 5. As shown by Freeman et al.6* 8..200 kcal.0 10.0 5.6 8. 1996). Fahy and Russell (1993) e Agras et al.7 17.5 8.0 6. d : p = 0.8 13.3 6. Herzog et al.6 6.8 *: significantly different from the others energy categories. 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. BSQ.0 6.6d 7.0 8.3 5. within the same phase.6 Phase 1 – Before treatment Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec Hypoenergetic intake Normoenergetic intakeb a 7. such as the use of drugs and the practice of fasting. b : Normoenergetic = Intake between 1.5 e 8. within each interval of energy intake in meals not followed by vomits.6 e 10. EAT scores. dos Santos Alvarenga. 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. (2000).0 Weekly frequency of binges 11. it seems that the severity of bulimia at the beginning of treatment and after 12 weeks was related to other factors of this test. Actually. Baeza Scagliusi and S. a : Hypoenergetic = Intake < 1. patients with more BN symptoms and more concern about their bodies at the end of the treatment present a higher risk of recurrence. Tables 10 and 11 show BITE-symptom and severity.4* 6. within phase 2. The goal was to assess these different response variables between patients that had hypoenergetic. (1985).201 kcal.8 6.7 7. 1994.7 7..

0 6. In regard to the BITE-symptom. the more severe is her disorder.0 5. and according to them.0 7.0 6.0 8.0 8.0 10.7 6. that is. 1992).0d 7.1 9.0 9. that is.2 5.6 4.0 6.8 10. a : Hypoenergetic = Intake < 600 kcal.1 3. once again. Food Intake … 131 Table 11 – Mean ranks of the scores and bulimic behaviors. Findings show that the scores of BITE-severity were significantly higher in patients with hypoenergetic VET in Phase 3.2 6. In regard to the number of binge eating episodes per week.6 15.6 9. the patient that ate less in Phase 3 presented a more severe case of BN.5* 8. Gendall et al.8 9.001 kcal.8 13.4 8.5 6.0 6.000 kcal.07 in Phase 2). this difference was . within phase 2. d : p = 0. Phase 1 results presented a mean rank very similar to the scores for hypo and normoenergetic VET. this shows that vomiting is used for several reasons not related to the purging of excessive food intake (Olmested et al. the result was significantly higher for patients with hypoenergetic VET intake in Phase 3. however.9 9. even without more binge eating episodes. but very different from the hyperenergetic category. As for the number of vomiting episodes per week. Therefore. (1997) found the same result.5 8.7 Phase 2 – Immediately after treatment Phase 3 – Three months after treatment *: significantly different from the others energy categories. In regard to meals followed by vomiting and BITE-symptom.8 6.4 11. c : Hyperenergetic = Intake > 1. the greater the vomiting episodes.4 Phase 1 – Before treatment Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec Hypoenergetic intakea Normoenergetic intakeb Hyperenergetic intakec Hypoenergetic intake Normoenergetic intakeb a 9.8 5. within each interval of energy intake in meals followed by vomits. it was observed that: those with hypoenergetic intake presented a lower score.0 4.7 2. the more restrictive a patient is. Again. 1994).06 between the energy categories. the less a patient eats.4 9.1 8.0 11.3 11. it was significantly higher for those with hypoenergetic VET intake in Phases 1 and 2 (p = 0. This shows that the greater the food restriction. that food restriction leads to binge eating episodes (Reiff.Effects of Multiprofessional Treatment on Clinical Symptoms.7 5. patients with low energy consumption (in the VOM intake) presented less symptoms.0 12. which proves.9 10.. b : Normoenergetic = Intake between 600 and 1.0 6. along the follow-up Energy intake in meals followed by vomits BSQ BITE severity BITE symptoms EAT Weekly Weekly frequency of frequency vomits of binges 11.5 9. within the same phase. showing that patients with hyperenergetic intake presented more symptoms of BN. the more often the purgation occurs.6 7.2 9.0 13.3 6.0 7.

the less the patient ate (apart from binge eating episodes). Other authors used this method to assess food intake of bulimic patients and considered it a valid instrument (Elmore and Castro.. Baeza Scagliusi and S. In the present research. Goris and Westerterp (2000) observed that confronting subjects with implausible results from a prior diary decreases the errors. she would eat less energy during her meals followed by vomiting. However. In Brazil. 1989). it is believed that the number of patients followed up until the end of the process was sufficient. Even so. Scagliusi et al. was a cross-sectional. 1997. Besides that. (1997) also compared energy intake and clinical variables. Few studies tested strategies to improve the self-report of food intake. who was previously trained. and eventually led to missing values. the number of patients was relatively small. the level of energy intake of meals followed by vomiting did not determine BN symptoms. It is important to note that the method of dietary assessment – food record – has limitations and it is subject to bias. Patients were told to register their intakes soon after them and instructed on how to describe the foods consumed and to estimate portion sizes. We are aware that subjects who fill a food record may change their intake. after treatment. Tucunduva Philippi observed only in Phase 1. Every week. especially by means of not changing the intake during the recording period. F. (2003) verified that confronting the subjects and conducting an intensive training on how to record the intake attenuate the error. probing the patients and instructing them one more time when necessary. some procedures were used in order to improve the record. a dietitian reviewed the diaries when the patients returned them. This data was not followed up in this paper. indicating that. and that body dissatisfaction scores were higher among those consuming meals with less energy intake – indicating severe food restriction. Gayle (1998) affirmed that this method is the only one able to assess energy intake and to identify binges in free-living bulimic subjects. As stated by Woell et al. Moreover. for example (Livingstone and Black. the study by Gendall et al. the more often he purged. The instrument used to assess aspects of eating attitudes and relationship with food was developed for this research based on clinical practice. and they also found that. Phase 2 showed that BSQ scores were lower in patients with hypoenergetic VOM. dos Santos Alvarenga. although it remains high. Woell et al. Some considerations should be made about this study: firstly. 2003). 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. particularly follow-up studies of bulimic patients and nutritional issues.. Gendall et al. Gendall et al. They also found that patients that presented more binge eating episodes had a higher energy intake during these episodes. (1989) even with this bias it is possible to analyze food intake by means of a food diary.132 M. considering that there are few studies on ED in Brazil. Many studies confuse the term eating . However. which may have affected the analysis. 1991. and it became smaller because of the high rate of treatment dropout. and not a follow-up study. all the records were coded and analyzed by only one researcher. We believe that these procedures should have decreased the errors associated to dietary assessment. It can be concluded that if the patient worried less about her body. 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. motivated by feelings of guilty and shame.

without specification of what these behaviors would be. a measure of disinhibition. diuretic and appetite moderator drug use. Using just the nutritional intervention. psychiatric and therapeutic follow-ups would be unethical. are not recommended. the pleasure of eating. 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). restraint and subjective assessment of hunger. due to ethical considerations. EAT and BITE-symptom scores showed a non-symptomatic group. so that the questionnaires that claim to measure behavior. without the due clinical. taking into consideration the means and medians of binge eating and vomiting episodes. Food Intake … 133 behavior with food intake.. Conclusion In summary. and the Dutch Eating Behavior Questionnaire (van Strien et al.. In this manner. in fact only assess if some groups of foods are bought and eaten (Kubik et al.. with the data of this study. Moreover. to which only one of the treatment components is provided. After six months follow-up. Some studies focus on behaviors that are important to EDs. in turn. 1985). based on these results an instrument is being adapted and validated. There are some widely used scales in ED research.Effects of Multiprofessional Treatment on Clinical Symptoms. 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. some positive changes were observed after 12 weeks of CBT: a significant change in the EAT and the BITE-symptom scores. In other researches. like for example vomiting frequency (Martín et al. the results of specific nutritional interventions for the treatment of BN could not be separately tested in controlled studies. food choice. which also measures restraint. but also ignores other pieces of information. 1996). 1986). 1999). cause psychological distress and lead to recurrence. some negative feelings . using only these questionnaires supplies a lot of relevant data. difficulty in handling with hunger. social events. These factors are associated to BN. hidden eating. and there was significant difference in the BSQ score. but they do not encompass the wide range of dysfunctional eating attitudes that this disease implies. This may. control groups. 2003). (1988) which showed that bulimics with poorer prognostic had more abnormal eating behaviors. We believe it is relevant to research these aspects. Although these scales are useful and well developed psychometrically. the positive changes found were: the patients did not meet the diagnostic criteria for BN. like the Restraint Scale (Herman and Mack. and feelings towards food. such as beliefs and perceptions about food. In this manner. some misconceptions about food were reverted (as thinking that eating a little more automatically causes weight gain). Townsend et al. which measures chronic dieting or the switch between periods of restraint and lapses. Also. and assess mainly dietary restraint. as for example in the study of Mitchell et al. food behavior is cited but is not defined. that even the patients whose clinical status becomes normal may still have a complicated relationship with eating and their bodies.. they are limited in scope. as we could note. 2002. the Three-Factor Eating Questionnaire (Stunkard and Messick. but their interrogations only cover the classical symptoms of BN. because they are a part of a total treatment program (Rock and Curran-Celentano. and zero median for laxative. 1975). Today.

F. since measuring the treatment outcome just by verifying changes in the frequency of bulimic symptoms cannot cover the complexity of ED. lack of control and nervousness) while the feeling of tranquility has increased. 1993. This result is preoccupant and should be carefully monitored by dietitians while they treat bulimic patients. Therefore. especially those related to feelings. weight and food in addition to other positive psychological changes. Because it is known that BN is a chronic disorder. It is believed that standardized tests are an effective strategy to assess follow-up of bulimic patients. Sunday and Halmi. we did not find changes in food intake. The main objective of the traditional nutritional approach for BN is to establish a normal eating pattern and to cease the purging practices. cognitive techniques and motivational interviewing to improve the treatment of all features of the eating attitudes of these patients. whether followed by vomiting or not. The obsession with food has also decreased. other measures – such as relationship and attitudes towards food – should be investigated and assessed after the intervention. with a high chance of recurrence. Tucunduva Philippi involving food were reduced (as anxiety. reflected by the lack of pleasure with food and the difficulties in dealing with hunger. Furthermore. 2001). As stated by Levine (1994). as shown by the progress of bulimic symptoms.. 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.134 M. based specially on counseling. They are not ‘ics’ – anorexics or bulimics”. “people with eating disorders are people struggling with fantasies. namely that energy restriction is related to higher frequency of binge eating and purging. based on standardized tests. 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. showed positive progress. and to promote improvements in eating attitudes (ADA. aiming to improve the relation towards body. resulting in a smaller interference of food in patients’ life. anxieties. . 1993). composed by frequent meals rich in nutrient-dense foods. such as energy intake in eating episodes. 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. and coping mechanisms that are established and vigorously reinforced by our culture. 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. New techniques and interventions are required to treat and to alter the relation established by the patient towards food. The assessment of these patients. should aim to help the patient to distinguish behavior related to food and weight from feelings and psychological issues. So dietitians that work with ED should strive to better understand these topics and to seek training in counseling. dos Santos Alvarenga. motives. On the other hand. it is relevant to include measurements of nutritional consumption. Baeza Scagliusi and S. 1996). Nevertheless. It was possible to confirm an important fact. it is necessary to think about recovery in a broader manner. Further nutritional treatment. Treatment should encourage a regular meal pattern. it is remarkable that many disturbed attitudes did not change..

G. In Brazil. It is also relevant to attest that in order to prevent eating disorders specific interventions should be provided to a wide range of people. Body image in early-onset obese patients. 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. Rebecca Cohen. D. tools for measuring eating attitudes. we believe that improvement of eating attitudes and relationship towards food is necessary not only for treatment of eating disorders. especially because they afflict mainly young women. already marked by a poor health status. size acceptance and with strategies to improve relationship towards food.Effects of Multiprofessional Treatment on Clinical Symptoms. Also. Mira. our program of nutritional treatment was improved. 2. 175-80. P. Int J Eat Disord. 1983. since there are too few centers that treat these diseases in Brazil. should be developed and validated. We believe that the first treatment goal is to end bulimic behavior and establish a healthier intake. 87-93. with focus in nutrition education. Adami. Perhaps it is even more necessary to discuss prevention of eating disorders. and the individual counseling has been receiving more attention and time. body image improvement. Food Intake … 135 Based on the results presented in this chapter. M. but also for its prevention. Katie Harkins and Amanda Scott for help with data input. Authors= Notes We thank Cynthia York. Bulimia: a study of outcome. whose aim will be the improvement of eating attitudes and relationship with the body and food. As a research group on nutrition and eating disorders. N. 1997. 2. Jo Wood provided statistical consultation. Scopinaro. especially those focused on feelings. Natalie Demidenko. which could be more aggravate with the presence of an eating disorder. Our research group is now working with the instrument tested in this study. SF. Finally. specially young girls and women. This project was supported by the Departments of Psychiatry and Psychology at the Ottawa Hospital. our data showed that eating disorders are also a reason for concern in an undeveloped country as Brazil. Considering the findings of this research. beliefs and attitudes towards food. Llewellyn-Jones. Dr. Its duration was increased to 18 weeks. B. by providing a more comprehensive care we can be sure that we are treating a person and not a disease. Gandolfo. References Abraham. This new program will be provided to patients after completion of the 18-weeks program. this eating attitudes questionnaire is being adapted and will be psychometrically tested. It is also relevant to note that in order to meet this goal. young women live in a difficult scenario. . We are also developing a new treatment program. Bauer. Eat Weight Disord. Deborah Evans. Our health system needs to be more prepared to deal with this problem. Dr.

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In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Swain. Inc. Chapter VII Actual . lower self concept. and ADBD has been implicated in the clinical literature in the etiology of Bulimia Nervosa (BN. 3Carleton University Abstract It was hypothesized that higher levels of actual-desired BMI discrepency (ADBD) would be associated with higher binge eating symptoms. Monique Potvin-Kent2 and Hany Bissada1. 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). 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. Kanchan Kurichh2. ADBD can be easily assessed by clinicians and may be used as an index of body dissatisfaction and overall self concept. and lower self concept for the BN group. pp.2 1 Ottawa Hospital. Louise Balfour1. and higher body dissatisfaction for a clinical sample of women with Bulimia Nervosa (BN) and Binge Eating Disorder (BED). Casper.3. Fifty-one participants diagnosed with BN and 41 with BED drawn from a clinical sample completed questionnaires assessing eating disorder and general psychopathology.Desired BMI Discrepancy.2. Greater ADBD was related to greater body dissatisfaction for the BN and BED groups. 1996). Those with BN had more self-related pathology. Thompson (1996) argued that discrepancies between actual body size and desired body size is an index of body dissatisfaction (Thompson. 2University of Ottawa. 145-158 © 2006 Nova Science Publishers. Within these clinical . ADBD may be a vulnerability factor for developing an eating disorder for women. Body Dissatisfaction and Self Concept in Women with Bulimia Nervosa and Binge Eating Disorder Giorgio A. 1983).2. Similarly. Tasca1.

studied a sample of lesbians with BN. ADBD was seen as important in women with eating disorder symptoms when desired body weight was lower than actual body weight. In general however. conceptualizations of ADBD. and self evaluation (Tiggeman et al. These studies of general population college women were all suggestive of the role of ADBD for a clinical sample of women with eating disorders. They found that greater ADBD. Garner. 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. Winefield. and found a significant correlation between ADBD and body dissatisfaction. was related to low self evaluation and to lower levels of psychological well being. Post and Crowther. . Drive for Thinness and Interoceptive Awareness scales of the Eating Disorders Inventory –2 (EDI-2. McKinley (1998) found that ADBD was related to body esteem and high body shame. then ADBD likely taps into core issues of ideal self image based on personal or cultural standards. ADBD was defined as a different but related construct to body dissatisfaction. Heffernen (1996). A recent study by Doll and Fairburn (1998) found that women with BN had a greater ADBD than normal controls. 1986. 1985). 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. Body dissatisfaction is specifically related to body shape and size but not necessarily to a self discrepancy. and did not conceptualize ADBD within a broaden psychological context in order to increase our understanding of ADBD’s role in eating disorder pathology. well being. 1991). 1994). Similarly. 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. Tasca. Louise Balfour. 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. 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. Some studies have looked at ADBD among an eating disordered population.. In a sample of undergraduate women. Heffernen’s (1996) study looked at ADBD as a variable of secondary interest. Few studies have looked at the relationship between ADBD and severity of eating disorder symptoms and psychological variables. First. 1973). there is little theoretical formulation for why this particular discrepancy may have an impact on psychological functioning. the impact of ADBD on eating disorder symptomatology has received little empirical attention. In this study. Kanchan Kurichh et al. She also reported higher ADBD among women than among men. defined as Aperceived overweight@. To do so Higgins= (1987) self discrepancy theory is used as a framework. Tiggeman. Winefield and Goldney (1994) looked at the relationship between ADBD and psychological well being among young adults. 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. Snyder (1997) found a significant correlation between perceived overweight and the Body Dissatisfaction. and/or eating disorder symptoms.146 Giorgio A.

resulting in further attempts to attain this ideal. ought self). Higgins (1987) proposed similar notions of discrepancy with regard to the self in his self discrepancy theory. ADBD represents a tangible parallel to actual-desired self discrepancies that is particularly salient to women who are vulnerable to eating disorders. low self esteem. 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. and dissatisfaction with their self and body. Ought self refers to aspects or attributes that one believes one should possess. ADBD could represent a core self related construct for those with eating disorders.e. ideal self and ought self. some women may experience a sense of personal failure. For the purposes of this study. problems with self concept. In a study looking at self discrepancy among college women. or may be internally held standards. Body weight and weight related self perceptions are integral parts of the experience of the self for women with eating disorders. the greater the distress and problems.e. Strauman et al. These standards may be those established as important by others. Ideal self and ought self are self guides that are personal standards that people set up. The emphasis and importance placed on actual weight is a pivotal part of the disorder. ideal self). we hypothesized that the discrepancy between actual and desired BMI for women with BN and BED will be related to eating disorder symptoms. Higgins (1987) suggested that there are several domains of self including the actual self. Because of the parallel. and low self concept. the greater the discrepancy. 1996). Strauman. 1997. Although one could argue that body dissatisfaction may imply some discrepancy from an ideal or standard. Body Dissatisfaction and Self Concept … 147 Self Discrepancy Theory There is an increasing consensus in the literature that Western sociocultural values emphasize thinness and appearance for young women (Heffernan. Vookles. ADBD is a more direct measure of such a discrepancy. Berenstein. With repeated failures at reaching this goal. and eating disorder related psychopathology (Snyder. This may be due to the discrepancy between cultural standards of unrealistic thinness that may be internalized.Actual . especially if it has been internalized by women (i. Chaiken. body dissatisfaction. Actual self refers to aspects and attributes of the self that one actually possesses. and Higgins (1991) found that self discrepencies were related to body dissatisfaction and maladaptive eating in female college students. a culturally sanctioned ideal of thinness is seen as a self guide (i.ideal self discrepancies and body dissatisfaction even after actual BMI was controlled. Moretti and Higgins (1990) found that discrepancies between self guides and actual self can lead to emotional distress and potential emotional problems. or both. 1991).Desired BMI Discrepancy. Snyder (1997) found significant correlations between actual . Ideal self refers to aspect or attributes that one would like to possess. 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. Just as the discrepancy between actual self and self guides is related to psychological distress. .

and Balfour. Problems with self esteem and self concept are also shared among these disorders (Striegel-Moore. Wilson. and Brownell. and Spitzer. (1998) found greater body dissatisfaction among binge eaters than controls. et al. 1997). 1998) and in a clinical sample (Tasca. Of the 92. Hypotheses The first hypothesis for this study was that a greater ADBD. Wing. will be associated with greater binge eating symptoms. women with BN will exhibit more eating disorder and self related problems than women with BED on the measures used in this study. Nelson. Tasca. 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. Second. Ewing. where actual body weight is greater than desired body weight. 1998). and greater body dissatisfaction for women in the BN and BED groups. 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. Dubbert. lower self concept and greater body dissatisfaction than women with BED. and to be a homogeneous group on a number of variables. Although Striegel-Moore et al. Antoniou. greater eating pathology (Yanovski. 2002) those with BED had lower levels of psychopathology than those with BN. Bissada. 1993). 1990). Table 1 presents diagnostic and demographic data of these patients. more binge eating symptoms. Wood. Research has indicated that in a community sample (Hay and Fairburn.148 Giorgio A. . 2002). Wilfley. 1994. other studies have not found the same result (de Zwaan et al. Kern. Method Participants A total of 92 women were assessed as part of this study. 51 patients met diagnostic criteria for BN and 41 met diagnostic criteria for BED.. 1994). Louise Balfour. Results of univariate comparisons of these variables will be discussed below. lower self esteem and greater discrepancy between their current and ideal body size (Striegel-Moore. APA. 1998). Body image disturbance and dissatisfaction is a hallmark symptom of BN (Kearney-Cook and StriegelMoore. Demidenko. Gooding and McDermott. obese people who binge eat compared to obese people who do not binge eat show greater psychopathology (Marcus. Other researchers have found those with BED to be distinct from obese controls. Tasca. 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. We predict that those with BN will have greater ADBD. Elder. For example. lower self concept. 1997). Kanchan Kurichh et al. Bissada.

91 1.93 61.001 d . 1991).47 .001 <.41 5. 10% of all initial consultations (N = 210) referred to the Center were randomly selected and re-evaluated by an independent clinician blind to the diagnosis. the Personality Assessment Inventory (PAI.33 58.96 14.21 13.92 9. a desired BMI was calculated.86 45..019 .91 13.98 14.Actual .07 1.75 sd 9.95 1.26 p <.24 .24 11.64 5.28 3.15 16.59 22.69 0. Measures Actual-Desired BMI Discrepancy (ADBD). patients completed a battery of tests including the Eating Disorders Inventory-2 (EDI-2.00 . patients were asked what their desired weight was.90 .45 .34 46.51 73.58 65.81 Age Actual BMI Desired BMI ADBD Binge Episodes in 28 days Binge Days in 28 days Body Dissatisfaction Self Concept Factor High Self Esteem (Man-G) Low Self Efficacy (DEP-C) Identity Instability (BOR-I) sd 8.25 .88 41. BN (n=51) M 30.31 9. k/m2) was calculated from these.50 F 27.85 7.001 <.63 35.76 17.09 .84 31. medium (>. With Univariate Comparisons and Effect Size (d). 1994).001 <.94 9. Identifying information and diagnostic conclusions were removed from the re-evaluated reports.40 1.89 BED (n=41) M 40. 1991).20).07 20.37 12. Just prior to the consultation. and the Diagnostic Survey of Eating Disorders (DSED. To control for the effect of actual body weight. Actual height and body weight were measured at the time of assessment and Body Mass Index (BMI.74 27.48 . adapted from Johnson and Connors. Morey.786 .41 5.68 Note: Effect sizes (d) are small (>.02 2. The .37 22.18 4.02 17. As a validation check on the diagnosis.09 16.714 .80) effects (Cohen. A referral to one of several treatment options offered by the Center or in the community was often suggested.95 21. 1987).81 28.96 12. Based on this and their actual height.02 15.57 3.06 . the difference between actual and desired BMI was divided by actual BMI.79 70.01 12. As part of the DSED. Garner. 1988).997 .50) or large (>.028 .93 11.69 16. and then desired BMI was subtracted from actual BMI. Body Dissatisfaction and Self Concept … 149 Table 1 Demographic and Clinical Data for Women With Bulimia Nervosa (BN) and Binge Eating Disorder (BED).20 33. Agreement between the independent clinician and the original diagnosis was 86% suggesting a high level of agreement. Procedure Patients were assessed by a psychiatrist or a psychologist.001 .Desired BMI Discrepancy.04 ..00 .52 6. They were then given a DSM-IV multiaxial diagnosis by the psychiatrist or psychologist (APA.238 .

The Depression .Identity Problems (BOR-I) scale and represents vulnerability to environmental stressors. Louise Balfour.92 (Garner. Low self concept is suggested by low scores on MAN-G. Results Initial Inspection of the Data There were no univariate or multivariate outliers in the data. 1991) is a 9-item scale that measures dissatisfaction with overall shape and size. 1994). Body Dissatisfaction The Body Dissatisfaction Scale of the EDI-2 (Garner. Self Concept Morey (1996) described self concept to encompass domains of self esteem. Tasca. (2002) report adequate psychometric properties of PAI scales and subscales for eating disordered populations. Stability of identity was measured by the Borderline . et al. frequency of binges were used for the BN group and days binged was used for the BED group. 1993).Cognitive (DEP-C) scale measured personal competence and perceived control. 1991). and is considered a measure of self efficacy (Morey.150 Giorgio A. 1991). The Mania . Binge Eating Symptoms Objective binges were assessed using the criteria outlined in the Eating Disorder Examination (EDE.Grandiosity (MAN-G) scale was used to assess self esteem. and self efficacy. . all variables had acceptable distributions. High self concept is suggested by high scores on MAN-G and low scores on DEP-C and BOR-I. Tasca. Kanchan Kurichh et al. Table 2 shows the zero order Pearson Product Moment correlations among the variables for each diagnostic group. as an evaluative component of self perception. The number of symptoms over the past 28 days were counted using a calendar recall method.desired BMI / actual BMI] x 100). result was multiplied by 100 so that ADBD was expressed as a percent deviation from actual BMI ([actual BMI . Internal consistency was reported at alpha = . stability of identity. Consistent with DSM-IV (APA. 1991). and high scores on DEP-C and BOR-I. Fairburn and Cooper. Morey. Self Concept was measured by using three scales from the Personality Assessment Inventory (PAI. and there was no multicolinearity among dependent variables. Morey (1996) looked at the configuration of scores on these three scales to assess self concept.

ADBD BN (n=51) -. days binged in the past 28 days (for the BED group).05. and the BOR-I scale load positively.309* Binge symptoms for BN are binge episodes in 28 days. DEP-C and BOR-I scales of the PAI (Morey. (. **p<.100 -. the combined variables (binge episodes.15% and 65.465* * -.175 -.60 respectively). There was a strong association between ADBD and the combined dependent variables (02 = .427** -. and the PAI Self Concept Factor for the BN and BED groups separately.093 . Body Dissatisfaction and Self Concept … 151 Table 2 Correlations among variables for women with Bulimia Nervosa (BN) and Binge Eating Disorder (BED) groups.261 . a self concept factor was created by conducting a principal components factor analysis with no rotation of the MAN-G. *p<.94 respectively).298 . Table 2 shows the correlations . Actual-Desired BMI Difference Bulimia Nervosa Group Using the Wilks= criterion.70 and .Desired BMI Discrepancy.263 -. Also as expected.284* Binge Symptoms1 BN BED Body Dissatisfaction BN BED Binge Symptoms1 Body Dissatisfaction Self Concept 1 BED (n=41) . Therefore. 1988).26% of the variance respectively.062 -. the component matrix had the MAN-G load negatively (-.26) (Cohen. Individual Pearson correlations were calculated to assess for the relationship between ADBD and the number of binge episodes in the past 28 days (for the BN group).Actual . the EDI-2 Body Dissatisfaction Scale. 1991) for both the BN group and the BED group. body dissatisfaction and self concept) were significantly related to the parameter ADBD for the BN group.395. approximate F(3. and consistent with Morey=s (1996) conceptualization. Morey (1996) suggested an analysis of the configuration of three PAI scales in order to assess self concept. one factor emerged for the BN and BED groups separately accounting for 59. this approach does not easily lend itself to using self concept as a continuous variable in a data analysis.01The SPSS General Linear Model (GLM) program was used to perform an overall multivariate analysis among ADBD and all the other variables for each diagnotic group. However.003. As expected. These findings are consistent with Morey=s (1996) configural approach but allows for a single score representing self concept for each participant.84 respectively).223 -. Self Concept Factor As stated. p < . Scores on the self concept factor were reversed so that low scores on this factor represents low self concept and high scores represent high self concept.65 and -. 47) = 5. and for BED are binge days in 28 days.93 and . the DEP-C scale load positively (.

and so the percent discrepancy can be accounted for by the initial difference in weight between the two groups. those with BN were significantly younger.018. it was apparent that the BN group had lower self efficacy (DEP-C). those with BN had significantly lower self concept than the BED group. There were no differences between the BN and BED groups on measures of binge episodes or binge days. so it is possible that the higher BMI of those with BED may account for this difference. 1988). p < . In this study. There were no differences in level of self esteem (MAN-G) between the two groups. had a lower actual BMI and lower desired BMI than those with BED. When the individual scales making up that factor were considered (Table 1). Higher ADBD was significantly related to higher scores on the Body Dissatisfaction Scale and lower scores on the Self Concept Factor. any difference in ADBD is likely due to those with BED weighing significantly more than those with BN. p < . There was also no significant difference between the two groups on the Body Dissatisfaction scale. 37) = 3.88) = 55. p > . and self concept) were significantly related to ADBD for the BED group.24) (Cohen. between ADBD and individual variables for the BN group. There was a strong association between ADBD and the combined variables (02 = . Comparing Bulimia Nervosa to Binge Eating Disorder As indicated in Table 1. The correlation approached significance for the relationship between ADBD and the Self Concept Factor. Binge Eating Disorder Group The Wilks= criterion suggested that the combined variables (binge days. ADBD was not significantly associated with days binged for the BED group. Because older patients may weigh more. body dissatisfaction.50. Those with BED had a significantly higher ADBD than those with BN (Table 1). That is.05). . ADBD was not significantly associated with binge episodes for the BN group. approximate F(3. age was covaried when the groups were compared on actual BMI. Table 2 shows the individual bivariate correlations between ADBD and each of the other variables. Higher ADBD was significantly associated with higher scores on the Body Dissatisfaction Scale. The difference in actual BMI remained significant even when age was covaried in an ANCOVA (F(3. an ANCOVA covarying actual BMI was conducted. and greater identity instability (BOR-I). On the overall Self Concept Factor derived from the PAI.083. To test this. Kanchan Kurichh et al.88) = .791. Louise Balfour. ADBD was calculated as the percent discrepancy from actual BMI. When the variance accounted for by actual BMI was covaried. Tasca.152 Giorgio A. there was no significant difference on ADBD between those with BN and those with BED (F(3.001).

2002). Morey. Specifically. ADBD may be viewed as a potential vulnerability factor for women in developing BN and BED. such as borderline personality disorder. greater ADBD was significantly related to body dissatisfaction and low self concept. with women with BN having lower self concept as measured by the PAI (Morey. such as body dissatisfaction and self concept.Actual . Body Dissatisfaction and Self Concept … 153 Discussion This study looked at ADBD among women with BN and BED. and conceptualized the impact of ADBD on eating disordered women within the framework of self discrepancy theory (Higgins. In self discrepancy theory (Higgins. and that there is a high comorbid diagnosis of self related pathology. those with BN had greater identity instability (BOR-I) and lower self efficacy (DEP-C). 1987) greater actual self vs ideal self dicrepancies predict more emotional discomfort and distress (Moretti and Higgins. 1997). 1991. Despite clinical references to the importance of ADBD (Crowther and Sherwood. The hypothesis that ADBD would be related to higher eating disorder symptoms. allowed for differences to emerge among the diagnostic groups by defining self related problems in broader terms that . ADBD was not related to binge eating symptoms for either the BN or BED groups. this is the first known attempt to look directly at the relationship between ADBD and eating disorder related psychopathology in a clinical sample. Tasca. This is consistent with a study finding no differences between eating disorder diagnostic groups on two measures of self esteem (Griffiths.Desired BMI Discrepancy. and so no support was found for this hypothesis. Prospective studies among adolescent girls using ADBD would provide a stronger test of this hypothesis. MAN-G) only. Had this study focused on self esteem (e.g. and there was a trend toward a correlation with low self concept. For the BED group. In light of internalized social ideals of thinness for women with eating disorders (Striegel-Moore. greater ADBD was associated with greater body dissatisfaction. 1991. Rossiter. et al. It is possible that while ADBD is related to self related experiences. 1993). Agras. and given the results of this study. among those with BN (Dennis and Sansone. Telch and Schneider. 1987). This is consistent with reports in the literature indicating that BN is a more severe disorder than BED (Hay and Fairburn.. et al. higher body dissatisfaction and lower self concept in women with BN and BED was partially supported. differences between groups would not have emerged. This suggested greater self related problems and pathology among those with BN as compared to women with BED. This appears to be paralleled in the ADBD of our eating disordered samples. The Self Concept Factor. 1996). 1999).. especially for eating disordered women for whom body weight and shape are so crucial to self evaluation. 1998. It was clear that for the BN group. ADBD likely results in a number of vulnerabilities such as a sense of personal shortcomings and personal dissatisfaction. it may not be directly related to symptoms of binge eating. 1993). Comparing Bulimia Nervosa and Binge Eating Disorder The clearest difference between the two diagnostic groups in this study was on self concept. 1990).

In our sample. Clinicians could easily calculate the percent deviation from actual BMI. in our BN sample. the mean desired BMI was 22.154 Giorgio A. identity stability and self efficacy. 1991). if an individual with BN had a desired BMI that was less than 21% of their actual BMI. et al (1998) who found greater body dissatisfaction among obese binge eaters than controls. Louise Balfour. The disadvantage is that unique information provided by the individual component scales gets diluted within the overall factor score. The results of this study also indicated that body dissatisfaction among these eating disordered samples were related to ADBD and their associated self discrepancies. our results suggested that this broader construct may be more meaningful to the study of an eating disordered population that self esteem alone. the mean actual BMI in our sample of women with BN was 28. and BOR-I) that parallel Morey=s (1996) configural interpretation of those scales. The prinicpal components analysis produced a factor with loadings from the component scales (MAN-G.59 (21% below actual BMI for the BN group) or less would have a 95% probability of having problems with body dissatisfaction and low self concept. . Interestingly. Clinical Implications of ADBD Using 95% confidence intervals. cutoffs for the percent deviation from individuals= actual BMI were calculated. This is consistent with previous research that found no difference in the number of objective binges between BN and BED samples (Hay and Fairburn. Kanchan Kurichh et al. The advantage of using this approach is that it allows for the creation of a single continuous variable measuring self concept that lends itself to multifactorial analysis. DEP-C. which is almost exactly 21% below the mean BMI for the BN group. 1991) with an eating disordered population. As stated. This result is consistent with the work of StriegelMoore. This result does not support the notion that BED is a less severe than BN when it comes to objective binge eating symptoms. Furthermore. 1998). This broader self construct may be more meaningful to the understanding of an eating disordered population than self esteem alone. suggesting severe problems in this area for the majority of women in both groups. then it would be considered clinically significant.59 and a desired BMI of 22. Tasca. In addition.59. Our study did not find differences in body dissatisfaction between those with BED and BN. There were no differences between the BN and BED groups on the number of binge episodes or days binged over the previous 28-day period. Self Concept Factor To our knowledge this is the first report in the literature using self concept as defined by the PAI (Morey. both diagnostic groups had mean Body Dissatisfaction Scale scores above the clinical cutoff for the EDI-2 (Garner. this is the first report to create a self concept factor based on the configural analysis of self concept from the PAI as suggested by Morey (1996). The means for these two groups in this study were almost identical (Table 1). includes self esteem. For example. A clinical cutoff could be established so that a patient with BN who had a BMI of 28.76.

and also for those with BED. Its assessment is relatively straight forward. Body Dissatisfaction and Self Concept … 155 use the clinical cutoffs suggested by our sample. mood. body dissatisfaction. Longitudinal research starting with an adolescent sample and then following that sample could be done to see if ADBD is a risk factor for developing an eating disorder. but a slightly higher correlation within the BED groups for the same variables(r = -. muscle and low body fat percentage) and not body weight per se may be a more important variable predicting self concept and eating disorder related symptoms. For men. The impact of ADBD found in this study continue to lend importance to the . Similar calculations could be made for the BED group for whom a desired BMI of less than 37% of actual BMI would be considered clinically significant. and McKinley (1998) found higher ADBD among women. the relationship between ADBD likely will be more salient within the clinical and subclinical range of that population. and have an index of how problematic body dissatisfaction and self concept are for those with BN. We do not expect ADBD to be as important an issue for men since cultural standards of unrealistic thinness is more likely to occur with women (Striegel-Moore. Conclusion A theory of ADBD as a self discrepancy is presented that may represent a risk factor for eating disorders among women. Given that ADBD was related to eating disorder related variables in these clinical samples. as our theory suggests. Similarly. However.Desired BMI Discrepancy. and the 95% confidence intervals presented here could be used as cutoffs for clinical samples. the results of this study indicated that ADBD is associated with lower self concept and greater body dissatisfaction. 1993). Targeting ADBD in treatment by focusing on its relevance to eating disordered individuals. Limitations and Future Research The small sample size of the BED group may have reduced the power of some of the analyses. its impact on feelings about their body. ADBD could be an issue targeted in the assessment and treatment of women with BN. and its impact on self concept may allow women with eating disorders to begin to moderate the effects of these discrepancies. 1990). issues related to ideal body shape (e. it would be interesting to see if this discrepancy predicted problems with self concept. and other psychological variables in a female sample in the general population. then we would expect ADBD to be a risk factor for developing an eating disorder for young women but not necessarily for men.298) was not statistically significant. ADBD is a core self discrepancy that leads to negative mood and eating disorder symptoms. One would expect a similar pattern of results in a general population as well.Actual . If. This is particularly apparent in Table 2 where correlations between binge symptoms for the BN group is significantly correlated with Self Concept (r = -.g.284). Self discrepancy theory suggests that a greater discrepancy between actual self and ideal self leads to greater distress and emotional problems (Moretti and Higgins.

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That perspective. and overgeneralized life improvement from thinness. The specific form of one’s maladaptive behavior is a function of learned experiences from one’s environment. the general. by describing key heritable causes of BN. The proposed process is empirically supported and consistent with findings from heritability research. heritable risk from high levels of urgency is likely to become expressed as BN when one learns to expect benefits from eating when distressed and extreme benefits from thinness. are more likely to engage in bulimic behaviors.In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. Thus. Gregory T. Inc. 159-184 © 2006 Nova Science Publishers. The authors propose a specific model that integrates identified heritable and environmental risk factors for BN. is very general: there are many ways in which genes and environment might combine in the risk process. Introduction An important recent advance in understanding bulimia nervosa (BN) has been the recognition that both genetic and environmental factors appear to play roles in the emergence of BN. the tendency to act rashly in response to distress. pp. Cyders University of Kentucky Abstract Heritability studies provide a general framework for understanding risk for bulimia nervosa (BN): liability is a function of both genetic and environmental factors. key environmental . Smith and Melissa A. Swain. Trait urgency. Chapter VIII Integrating Personality and Environmental Risk Factors for Bulimia Nervosa Sarah Fischer. maladaptive behavior pattern (such as BN). Our intent in this chapter is to propose a specific theory of this process. Individuals who learn to expect alleviation of negative mood from eating. of course. is a heritable risk factor that increases the likelihood that one will engage in some form of rash.

the co-twin was eight times as likely as a member of the general population to also be diagnosed with BN (Kendler et al.. and Kendler. (1999) differed from the other reports in also finding moderate effects of common environmental influences.. 1999). Thus.83 (Bulik et al. Kendler. 2000). We argue here that urgency reflects an important part of the heritable component of risk. 2002). and findings from the Australian Twin Registry showed moderate heritability for BN (Wade. and review the empirical evidence supporting it. we will briefly review general evidence for the heritability of BN and for environmental causes of BN. 2003). We propose that the heritable trait of urgency. Sullivan. and very few to no shared environmental influences (Bulik. Cyders causes of BN. Recent studies of the heritability of BN seem to converge on the finding that risk for the disorder has large genetic influences. Findings from two other twin registries are consistent with those from the Virginia Twin Registry. Specific evidence to that effect is (a) concordance of diagnosis in monozygotic twins was significantly greater than that in dizygotic twins. which is the tendency to act rashly when distressed.. estimates of genetic effects for the disorder range from . illustrate how it fits within a gene-environment framework. that due to environmental influences shared among study participants. Typical heritability studies compare monozygotic twins reared together to those reared apart. McGue. Behavioral genetic methods allow researchers to partition the population variance on an attribute three ways: that due to genetic influences. Interestingly. and monozygotic twins to dyzygotic twins. We will then describe our specific model. 2000). To make this argument. The combination of trait urgency and certain kinds of psychosocial learning (indexed as expectancies for the consequences of eating and of dieting). Neale.28 to . large non-shared environmental influences. Various other studies using the Virginia Twin Registry have found similar results for partial syndrome BN. is a general risk factor for addictive/risky behaviors. Heritability of BN and Binge Eating The concept of heritability refers to the proportion of population variance on an attribute that overlaps with genetic variance (Keel and Klump. and for binge eating behavior (Bulik. 1991). and Wade. Neale. Bulik et al. and Iacono. Smith and Melissa A. These effects were not explained by shared environmental features or current contact with the co-twin. and (b) if a member of a monozygotic twin pair was diagnosed with BN. Lake. Sullivan. but not environmental events which one shares with one’s siblings. In their study using the Virginia Twin Registry. Gregory T. and Martin. and mechanisms by which they combine. lead to substantially increased risk for BN. 2000). 2000. MacLean. and that psychosocial learning reflects an important part of the impact of environmental risk. (1991) concluded that approximately 50% of the variability in BN diagnosis is due to additive genetic effects. causes of BN appear to include a genetic preparedness along with unique aspects of an individual’s learning history. Wade et al. Work with the Minnesota Twin Registry found that a large portion of variability in BN is heritable (Klump. According to a meta analysis of these findings. 2003. Adoption studies are also employed. . and that due to environmental events unique to individuals.160 Sarah Fischer. for diagnoses of BN that adhere to strict diagnostic criteria. et al.

at least in part.Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 161 In sum. and perhaps none. and the reinforcement of attractiveness. One obvious implication is that environmental factors are also important influences on the liability for BN. even though risk for BN is heritable. 1985). Very little of the disorder’s variance. the thin ideal for women and body dissatisfaction. A comprehensive model of risk for BN must incorporate genetic risk for the disorder. Evidence for the Role of Environment in the Development of BN The causal role of environmental and cultural factors in BN has. 1985). is influenced by shared environmental factors. depending on environmental and cultural factors. This appears to increase women’s body dissatisfaction (Rodin. In fact. To understand why varying rates of BN can exist. and the general disposition can take varying forms. the importance of appearance in the female gender role. to the fact that Western media images of women seem to be getting thinner and thinner. A different possible mechanism is that there is a genetic risk for a more general behavioral disposition. Among the classic indicators of those factors are the ideal female images presented in the media. These factors. Brownell. the heritable risk appears likely to be of this second form. while average individuals in industrialized nations get bigger and bigger (Wadden. It is also true that the rates of BN appear to have risen in Western cultures in recent decades (Keel and Klump. The British Medical Association (BMA) recently released a statement saying that the media play a large role in the development of both anorexia nervosa (AN) and BN (BMA. One mechanism is that there is a genetic/biological cause of some specific behavior or dysfunction. Images of women in the media are much thinner than the average Western woman. the rates of the disorder vary across time and across cultures. and these images are pervasive. Silberstein. In this model. This assumption is due. . several studies conducted using twin samples in the last fifteen years have converging results: a moderate to large portion of the variance in BN is genetically influenced. 1999). Under such a circumstance. it is important to understand that there are different possible mechanisms of genetic risk. and Foster.1994). When the cause is present.. 2002). in fact. In the case of BN. and a moderate to large portion of the variance is influenced by unique or nonshared environmental effects. Stice summarized a theoretical model for cultural effects on risk for BN (Stice. because although there is heritable risk. 2003). He reviews evidence that the shrinking body size of women in the media is correlated with increases in dieting articles in women’s magazines (Stice. pressure from society on women falls into three categories: the thin-ideal body image for women. Anyone with access to a television or magazines in Western society may plausibly assume that we live in a high risk media environment for disordered eating. 2002). the disorder inevitably occurs. and Striegel-Moore. some researchers suggest that dissatisfaction with one’s body is now normative among Western women (Rodin et al. The Western cultural ideal of attractiveness—the thin ideal--is quite different from the physical reality of most adults. there is no reason to expect the rate of the disorder to vary across time and across contexts. been much more widely emphasized in the literature. appear to promote bulimic behaviors (Stice.

1994). 2002). Attractive people are rated as more intelligent.” A recent meta-analysis by Stice (2002) summarizes findings of prospective longitudinal studies and experimental studies of risk factors for BN. Spangler. endorsing traditional female gender roles is associated with endorsement of the thin ideal. in which women look at media images and compare themselves unfavorably to those images. Body dissatisfaction likely results from social comparison. socially skilled. 2003). So. thinness is associated with attractiveness and femininity. The internalization of this pressure has come to be described as thin-ideal internalization (Stice. and thin-ideal internalization to bulimic symptoms can be construed as evidence that environmental factors influence the development of the disorder.. Thin body shapes are rated as more feminine. 1994). 2002) is thought to be primarily transmitted through media influences. dieting. Roehrig. then it seems there is extreme pressure for women to try to be thin in our society (Stice. The basic paradigm is that women are asked to rate their body dissatisfaction and negative affect both before and after viewing images of thin models. Cyders 1994). Additionally. In addition. A subscription to a teen magazine featuring thin models led to increased bulimic symptoms among girls with low social support (Stice. it is hypothesized that the ideal image of women in Western society is very thin. Body dissatisfaction may mediate the influence of thin-ideal internalization on bulimic symptoms (Stice. Smith and Melissa A. 2004). This risk factor for bulimia (Stice.. and bulimic symptoms themselves. body dissatisfaction. . 2004).162 Sarah Fischer. Thompson. Thin-ideal internalization is considered a risk factor for body dissatisfaction. including thin-ideal internalization. and better qualified for jobs than unattractive people (Feingold. Halliwell and Ditmar (2004) expanded on this model by assessing level of internalization of the thin ideal and how this affected body dissatisfaction in the experimental paradigm. and women who eat less food are rated as more feminine (Stice. Gregory T. Polivy and Herman (2002) stated in a recent review that “the influence of sociocultural factors in the context of eating disorders can be summarized succinctly as the idealization of thinness. Therefore. 2001).08 (Stice. bulimic women endorse the thin ideal more than women without bulimia (Thompson et al. women experience an increase in negative affect and body dissatisfaction. 2002). and Agras. Internalization is defined as “the incorporation of specific values to the point that they become guiding principles” (Thompson et al. 2004). Guarda. there is evidence that attractive people are perceived more positively and receive more reinforcement than do unattractive people. This relationship has been confirmed in the laboratory many times. 2002. 1992). van den Berg. 1994). and level of attractiveness has real consequences in social and work settings. The majority of studies find that after viewing thin models. honest. Women with higher internalization reported greater anxiety after viewing thin model slides. with a significant effect size of . He found that thin-ideal internalization led to increases in bulimic symptoms. The evidence for the relationship of dieting. There is also evidence that thin-ideal internalization is present in girls as young as age nine (Sands and Wardle. If being thin is considered attractive for women. This ideal seems to be associated with gender roles for women. and Heinberg. Body dissatisfaction is defined as negative subjective evaluation of physical attributes (Stice and Shaw.

and at least 50% of them are for food (Strasburger. and are thought to lead to increases in symptoms because the attempts make one vulnerable to disinhibited eating. 1998. Experimental studies have shown that children eat more food and choose junk food more often when watching television with food ads than when watching television without food ads (Halford. 2002). This convergence of cultural phenomena . et al. 2002). Cheskin. Wadden. They also advertise their food products. Stice. typically with an emphasis on fun and taste. As a result. Not surprisingly. 2004). the effect of body dissatisfaction on increased eating disorder symptoms was marginally significant and had an effect size of . American children view an average of 40. Pontin. Killen.Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 163 Body dissatisfaction is an important risk factor for BN because it is hypothesized to lead to the disorder in at least two ways. 1992). attempts to diet. Failure to eat in response to physiological need may result in binge eating (Polivy and Herman. and Taylor. Gillespie. 1999. The food portrayed is often easy-access sugared cereals. which could lead to increased binge eating (Stice and Shaw. Robinson. Today. Additionally. 2002). and Pratt. Correlations between these risk factors (the thin ideal. though. 1997. Meta analytic findings were that body dissatisfaction had a marginally significant effect size of . It should be noted. and (2) it leads to increased negative affect. which then leads to increase in eating disorder symptoms. a relatively new phenomenon in which (a) it is possible to binge on food. 2001). Prospective studies show that measures of dietary restraint efforts predict the onset of binge eating (Stice and Agras. in modern Western culture. and Lowe. therefore. 1997. Western people tend to have an abundance of food. Stice. candy. Hayward. the combination of enticing media messages about food and the easy access to large quantities of food in Western society may create an environment that is conducive to binge eating (Battle and Brownell. and dietary restraint) and bulimic symptoms reflect the association of individual differences in risk with individual differences in symptom levels.000 television commercials per year. but not reduced food consumption. In short. perhaps. 1998.26 on dieting. They appear to measure concern with dieting or. there is evidence that attempts to diet or concern with dieting may serve as a risk factor for bulimic symptoms (Fairburn. 2004). There is. and by offering pre-prepared food (fast food).. 1998. 1985). by increasing fat and sugar content. and a marginally significant effect size of . providers of food compete to make their food products more desirable. The theoretical consequences of body dissatisfaction are that (1) it results in increased dieting. body dissatisfaction. 2002). Presnell. Television watching has been shown to be related to overweight and obesity in both descriptive and experimental studies (Anderson.13 (Stice.14 on negative affect (Stice. Thus. Brown. one exerts cognitive control over one’s eating instead of physiological control. junk food. women are simultaneously exposed to encouragement to eat for non-hunger reasons and given ready access to food. Fisher. and exposed to messages emphasizing the importance of thinness. and Dovey. Crespo. and Spangler. It is perhaps important to recognize that. On this point. that commonly used measures of dietary restraint are not associated with unobtrusive measures of actual caloric intake (Stice. 2002). Heatherton and Polivy. and (b) food is advertised providing pleasures beyond hunger reduction. Bartlett. these individual difference factors operate in a context that is new to human history. When attempting to diet. Attempts to diet are thought to result from internalization of the thin ideal and body dissatisfaction. and fast food.

and we know that environmental risk factors increase risk for the disorder. Gregory T.. Smith and Melissa A. which is thought to stem from social comparisons based on the thin ideal. Two conclusions seems relevant from this literature.164 Sarah Fischer. Therefore. Kaye et al. General Integration of Heritability and Environmental Perspectives From the foregoing. Lehoux.5% (APA. .. Wonderlich. 1994. our current society’s emphasis on thinness and the view that slimness is attractive is thought to contribute to risk for BN through four main mechanisms. body dissatisfaction. Second. Thus. food is prepared to entice consumers beyond their hunger. Bulik et al. there may be several genetic and environmental effects that contribute to the expression of the disorder. To summarize. Thus. Bulik et al. but BN appears only in that small percentage of individuals with enough of the factors to cross the critical threshold. Cyders may help explain the rise in BN rates in the West: if all Western women are exposed to this combination of influences. and it also is thought to lead directly to bulimic symptoms. Third.. 2003. Bulik et al. In the case of BN. the effect of the environment on an individual depends on the genotype of that person (Klump. and food is portrayed as having benefits beyond hunger alleviation. we know there is an inherited risk for BN. individuals who are genetically liable for the disorder will be the ones to develop the disorder. the incidence rate of BN is roughly 2. 2004. concern with dieting or attempts to diet. appear to predict the development of disordered eating. these factors operate in a cultural context in which large amounts of food are readily available. more of the highest risk women are likely to develop BN. which follow from thin-ideal internalization and body dissatisfaction. Fourth. Second. 2000). 2000. This internalization leads to both dieting attempts and body dissatisfaction. and Bulik. The notion is that liability for BN reflects the combination of several genetic and environmental effects. This liability has a normal distribution in the population and is only expressed as the disorder if one’s liability is greater than a particular critical threshold. (2000) go on to argue that a genotype by environment interaction is an important mechanism in increasing risk beyond the threshold. there is considerable evidence that environmental factors increase risk for BN. 2002). each of which likely has a small individual effect. is a risk factor for bulimic symptoms.. (2000) provide a general integration of the two types of causes in their liability threshold risk model. the effect sizes of environmental causes are modest. even if it is high-risk for subclinical eating and dieting problems for women in general. Keel and Klump. Western culture is thought to promote internalization of the thin ideal. An interaction of this type would reconcile the perception that the Western environment is high risk with the awareness that only a small percentage of women develop BN: the environment may be high-risk for a BN diagnosis only among women with high liability. suggesting the need to (a) integrate environmental causal models with genetic ones and (b) explore additional environmental factors. First. Several authors note that this genotype by environment interaction may be an important direction of study for risk for BN (Bulik et al. but will do so only in a high risk environment. Klump et al. Lilenfeld. First. 2002).

A lack of persistence is the inability to remain focused on a task. There is growing evidence that these inconsistent findings occur because the broad construct of impulsivity actually includes several more specific constructs. 1999. In addition. such as binge eating and purging. Descriptions of impulsivity in the DSM-IV include acting without thinking. Fischer. 2001). and we summarize empirical evidence for that integration. Sensation seeking is the tendency to seek out novel and thrilling experiences.’s (2000) model describes. to varying degrees. 1994). Since scales included four different constructs. A number of studies have attempted to relate impulsivity to BN and binge eating. First.related constructs (UPPS-R: Whiteside and Lynam. 2003). impulsivity measures tended to include items reflecting some. which themselves are only moderately related to each other and which account for different phenomena (Evendon. the sensation seeking scale was designed without items measuring a lack of planning. the inability to concentrate. 2002). or all. we believe. specific acts. Prior to their work. We make the argument as follows. of the four constructs. For example. there was built-in inconsistency in measurement (Smith. We propose one specific inherited risk factor (trait urgency) and a set of specific psychosocial learning risk factors (measured as expectancies for reinforcement from eating and from dieting) that. we present a theoretical rationale for focusing on learned expectancies to capture individual differences in environmental risk. is through use of the broad construct of impulsivity. 1999.Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 165 This framework of risk is very general. Petry. are described as impulsive (APA. 2001). Next. Whiteside and Lynam (2001) conducted a factor analysis of several different major selfreport measures of impulsivity and found four factors or impulsivity-related constructs. maladaptive action. Urgency is the tendency to act rashly when faced with distress. The measure was designed to assess each trait uncontaminated by items measuring similar constructs. we present a theoretical integration of urgency and learned expectancies (which includes interaction effects). Impulsivity has often. and Fister. and the proportional representation of different constructs varied from scale to scale. been described as acting without thinking. such as binge eating and substance abuse. we believe trait urgency--the tendency to act rashly when distressed—is the construct that best captures the nature of binge eating and . They developed a self-report inventory to assess these four impulsivity. A lack of deliberation is the tendency to act without thinking. They found that the four scales were only modestly intercorrelated. and we review evidence for its role in relation to BN and binge eating. and the tendency to become easily distracted. Among those four impulsivity-like constructs. operate as risk factors in the way that Bulik et al. we present a theoretical rationale for the consideration of urgency as a risk factor. Urgency as a Risk Factor for BN One of the most common ways researchers have tried to explain rash. but not always. Finally. Whiteside and Lynam. but the findings have been inconclusive and the effect sizes small (Stice. We follow that with empirical evidence for eating and dieting expectancy theory. We then demonstrate that urgency is distinct from other impulsivity-related constructs and heritable.

There are several studies documenting the heritability. Jang and . etc. and Johnson. and Crosby. perhaps by facilitating escape from self-awareness (Heatherton and Baumeister. drink. Spillane. Binge eating has been tied to the avoidance of emotions and the use of distraction (Freeman and Gil. integrative personality trait model: the five factor model of personality. then one is at increased risk for binge eating and BN problems. In Costa and McCrae’s (1992) self-report measure of the five factor model. Bonifazi. Gregory T. if fleeting. 1985). 2001).166 Sarah Fischer. Smith. Weiss. and Jimerson. The five factors include neuroticism. 1992). Steinberg. Paunonen and Ashton. the NEO-PI-R. Binge behavior does not reflect lack of persistence. 1992. In a multi-national twin study of the domains and facets of the NEO-PI-R. and Solyom. They have described this facet as a “craving” factor. 2004). Meidinger. 2001. Cyders bulimic behavior. 2000. It therefore seems quite possible that urgency may be the impulsivity-like construct most relevant to binge eating and BN. distress. Mintz. urgency correlated higher among monozygotic twins than among dizygotic twins (Jang et al. we contend that the propensity to act rashly or maladaptively. but see Davis. 1991). Smyth. Cooper. There is considerable evidence that stress. 1989. Miltenberger. Motives for eating include comforting oneself and distracting oneself from negative emotion (Jackson. relief of negative affect (Deaver. indicating a dyscontrolled impulse to eat. Kaye. 2003). 1986. lack of deliberation is a facet of conscientiousness. 2004). and correlates of this facet (Costa and McCrae. Gwirtzman. nor does it primarily reflect pursuit of new and novel sensations.. 1998. Freeman. agreeableness. those women high in urgency are most likely to act rashly to relieve their distress (Fischer. As we have noted elsewhere.. Freeman and Gil. extraversion. best reflects what clinicians mean when they refer to the impulsivity of binge eating and BN clients. 2002). stability. We also favor trait urgency because of its specificity: rather than referring to general impulsive tendencies. 2003. Smith and Melissa A. and lack of persistence is also a facet of conscientiousness). conscientiousness. 1998). Laboratory induced negative affect leads to increases in eating (Stice. Although there may be a lack of planning component to some binge eating. negative affectivity is an obvious precursor to urgency: among those experiencing negative affect. and Cyders. Tobin. urgency is represented as the impulsivity facet of the broader domain of neuroticism. and negative mood often precede binge eating episodes. Sanftner and Crowther. in press). the idea is that if one has a propensity to act rashly when distressed. and Shephard. Sanftner. Experimental studies indicate that binge eating provides immediate. in response to distress (Costa and McCrae. The other impulsivity-related constructs are represented elsewhere among the five factors (sensation seeking is a facet of extraversion. and openness to experience. in response to distress. The Distinctiveness and Heritability of Urgency Urgency is actually represented as distinct from the other three impulsivity-related constructs in the predominant. McCrae et al. Stress is associated with binge eating on the day that the stress occurred (Crowther. This facet of the neuroticism domain of the NEO-PI-R loaded highly onto the urgency factor in Whiteside and Lynam’s (2001) factor analysis of impulsivity measures. George. and Albino.

. such as problem drinking. while the correlations between interview-assessed urgency and the other constructs.49 (Jang et al. We developed a semi-structured interview based on the UPPS-R. They found that.27. For example. 1992) and with rash.. multimethod (MTMM) study of urgency and the other three impulsivity-related constructs. problems with alcohol use. Flory. 2001).01). self-report assessed urgency was positively correlated with a self-report measure of pathological gambling behavior (r = . 2004a). No other self-report assessed impulsivity construct was associated with pathological gambling. including excessive eating and drinking. p <. We have also recently examined Whiteside and Lynam’s (2001) measure of urgency. interview-assessed urgency correlated with self-report urgency at r = . 2004a). A total of 156 undergraduates completed the semi-structured interview of the UPPS-R. p <. In short.29 for lack of deliberation. and . the heritability estimate for the impulsivity/urgency facet in their two samples was . there is consistent evidence that the urgency/impulsivity facet of the NEO-PI-R correlates with negative mood (Costa and McCrae. We also conducted a multitrait.e. and less religiosity (Paunonen and Ashton. Smith.200. also assessed by interview. Miller. Results of that study supported the convergent and discriminant validity of each construct. Castellani and Rugle (1995) found that cocaine and alcohol abusers scored higher on the urgency/impulsivity facet than a control sample. Correlations between the same construct measured in the two different ways were much higher than were correlations of different constructs measured in the same way. more obesity. and lack of perseverance was also present. and . binge eating. Different means of measuring urgency agree. And.21 for lack of persistence.25.. gambling. controlling for error variance. greater alcohol consumption. For example. 2004a).200).. both interview and self-report assessed urgency had similar relationships to criterion variables. and McCarthy.75. The structure replicated successfully in three different undergraduate samples (with sample sizes ranging from 156 to 1. and a composite measure of eating disorders symptoms..39 with lack of planning. maladaptive actions.30 with lack of persistence. We first sought to replicate the four-factor structure for impulsivity-related constructs that has been operationalized in their UPPS-R (Whiteside and Lynam. urgency’s correlations with the other constructs were .. and self-report measures of various criterion variables. lack of planning. including urgency. urgency is .01). No other interview assessed impulsivity-related constructs were associated with pathological gambling (Fischer et al. For example. in the sample of 1. McCrae and Costa (1994) found long-term stability of the facet.11 with sensation seeking (Fischer. 2004a). 2001). the self-report version of the UPPS-R. Cyders. interview assessed urgency was correlated with self-report pathological gambling (r = . for example. were . and school performance (Fischer et al.03 for sensation seeking (Fischer et al. and Leukefeld (2003) found that the urgency/impulsivity facet was positively related to risky sexual behavior. that variance not shared by the other facets of neuroticism).001. . 1998). in order to examine the potential role of method variance in the assessment of urgency and in its relations with other constructs (Campbell and Fiske.Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 167 colleagues examined the heritability of the specific variance unique to urgency (i. Additionally. 1959). greater tobacco consumption. Evidence for the discriminant validity of urgency from sensation seeking. Lynam. p <. Correlates of the urgency/impulsivity facet include.

Fischer. sensation seeking (r = . or a combination of these two traits. and we have compared its role to that of the other impulsivity-like constructs. 2004a. 2004b). that urgency correlates with various measure of negative affectivity and maladaptive behavior. Smith. Fischer. they have not yet been done with the UPPS-R. One limitation of the meta analysis was that many studies did not use measures designed specifically to differentiate among the four constructs. just as it is in Caucasian samples. In each of four samples of college women. In addition. While cross cultural studies have been conducted using the facets of the NEO-PI-R. and vice versa. a meta-analysis of impulsivity-related constructs found the following magnitudes of relation to bulimic symptoms: urgency (r = .168 Sarah Fischer. that urgency can be measured with either self-report or interview methods.34 (p <. beyond that explained by the other constructs. In a recent sample (n =130 women). and Lander. 2004b. Spillane and Smith (2003) conducted a study of individual difference variables that affect Native American drinking on a reservation where high rates of alcohol abuse are observed. for instance. While environmental factors appeared to affect drinking levels to a large extent. urgency/impulsivity as measured by the NEO-PI-R appears to be comparably heritable in different cultures.02). As noted above. 2004). and that urgency appears to operate similarly across cultures. Saucier and Ostendorf. In other words. One possibility is that urgency may be an interaction of neuroticism and lack of planning impulsivity. Smith. and urgency predicts outcome variables consistently. 1999). However. urgency accounted for an additional 6. There is also evidence that both broad personality traits and specific facets such as impulsivity tend to have the same external correlates in different cultures (Church. 2000.18) (Fischer and Smith. regardless of means of measurement.43). This body of evidence is crucial for the claim we make that urgency reflects an important part of the heritable liability for BN. that urgency is not simply the sum or product of neuroticism and lack of planning.5% of the variance in bulimic symptoms. there is evidence that the unique variance associated with urgency is heritable. there was considerable systematic variance in urgency unexplained by those constructs. Cross-cultural evidence also supports the validity of the construct of urgency.05). The beta weight of urgency was . To summarize. the largest beta weight of all predictors in the model. and Anderson. Anderson. we found that although urgency related to the combination of neuroticism and lack of planning. Fischer and Smith. and Smith. the effect size comparisons likely underestimate the true differences in . urgency correlated highly with binge eating behavior (Fischer. Most recently. None of the other four impulsivity-related constructs correlated meaningfully with binge eating. Therefore. they also found that urgency was positively associated with alcohol use and problem drinking. Cyders distinct from other impulsivity-related constructs regardless of method of assessment. lack of perseverance (r = . The trait of urgency does not seem to be reducible to a combination of neuroticism and lack of planning. Smith and Melissa A. and lack of planning (r = . Urgency’s Relation to Binge Eating and BN We have begun to examine urgency’s relation to binge eating and BN. lack of planning measures may have included some urgency content. Gregory T.18). 2003. instead of a personality construct in its own right.

urgency reflects a general tendency to act rashly in response to distress. Contingencies of reinforcement and punishment clearly exert a powerful influence on behavior (Skinner. Response-outcome expectancies are expectancies that a given behavior will result in a given outcome. Some individuals may learn that drinking alleviates distress. and so are the cognitive mechanism by which prior learning leads to subsequent behavior.Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 169 effects. Stimulus-stimulus expectancies are described as expectations that a given circumstance will be followed by some other specific circumstance. 1952. the trait of urgency does not directly produce binge eating behavior and BN. 1972. actually developed cognitive maps of the maze itself. as a result of learning. Rotter. among impulsivity-like constructs. researchers focused on the learning of behavioral contingencies. Watson. . Therefore. We believe that urgency is best considered a general. Tolman (1932) argued that rats form expectancies about the maze. instead of just learning a series of motor behaviors in response to reinforcement. Of course. described two basic kinds of expectancies: Stimulus-stimulus expectancies and response-outcome expectancies. although they clarify the likelihood that urgency is the one impulsivity-like construct relevant to BN. one’s expectancies summarize one’s learning history. For the promise of this perspective to be realized. Expectancy Theory: Psychosocial Learning In the early part of the 20th century. It is important to note that these findings come from cross-sectional research. Tolman. Therefore. Rather. Essentially. In a nutshell. This finding of the cognitive nature of learning helped pave the way for future cognitive and social learning theories. based on their experiences with it. In other words. prospective and experimental designs that clarify urgency’s possible causal role are essential. others may learn that gambling does so. along with many other researchers to follow (Bolles. and so to explain behavior. MacCorquodale and Meehl. Nonetheless. We have adopted expectancy theory for this purpose. Thus. psychology was captivated by the power of learning models in explaining behavior. he found that rats could just as successfully swim or ride a trolley car through the maze. After teaching rats to run mazes. We suggest that the particular form of “acting out” behavior that results from high urgency is a function of psychosocial learning. He concluded that rats. and those expectancies then influence one’s future behavioral choices. Tolman (1932) advanced learning theory by demonstrating that the content of learning may be more cognitive than strictly behavioral in nature. one forms response-outcome and stimulus-stimulus expectancies. During this time. to understand when urgency is likely to lead to bulimic symptoms. it is necessary to consider psychosocial learning. they do not show a prospective or causal relation between the trait and the disorder. in accounting for binge eating behavior. 1954). as a result of one’s learning history. 1953. distal risk factor for a variety of “acting out” behaviors. the mechanism of learning is that. the findings clearly point to the primary importance of urgency. they knew how the maze was laid out so that they could get to the end by any number of motoric acts. and some may learn that bulimic symptoms can play that role. 1930).

1993. result from extreme learning histories. result from extreme expectancies. eating helps relieve the boredom. Cyders Expectancy theory has become an important construct in many areas of psychology. eating can help me take my mind off my problems. To the degree that some women have come to associate eating with powerful reinforcers. and thinness result in individual differences in expectancies for the consequences of those behaviors.” “I would be more attractive if I were thin. then.” I would feel more capable and confident if I were thin. and risk for alcohol abuse (Goldman. there is substantial support for the notion that learned expectancies are one mechanism by which learning shapes subsequent behavior. Extreme eating and dieting behaviors. Alcohol expectancy theory rests on the idea that alcohol expectancies.. as a result. and so pursue food with greater vigor. Examples of such statements are the following: “When I am feeling depressed or upset. 1990. such as those initiated by Tolman. Smith Goldman. 1990). 1998). gambling behavior (Walters and Contri.170 Sarah Fischer. 1986). Expectancy Theory Applied to Eating Disorders. they hold strong expectancies for reinforcement from thinness. and that. Alcohol expectancy theory is one of the most developed expectancy theories and demonstrates applied support for the idea that expectancies are one mechanism by which learning shapes subsequent behavior. researchers have shown that expectancy theory can also be applied usefully to eating disorders. Smith et al. and Atlas (1998) proposed that learned expectancies for reinforcement from eating may be a mechanism by which one’s learning history leads to overeating and binge eating. 1995). and applied clinical studies. . Smith. affect (Carver and Scheier.” I would feel like I could do whatever I wanted to if I were thin” (Hohlstein et al. Likewise. The central idea is that individuals are exposed to different learning experiences concerning eating. 1998). Gregory T. Smith and Goldman. Recently. Christiansen. 1991.” “When I have nothing to do. which. Hohlstein. The identification of specific eating and dieting expectancies grew out of expectancy statements voiced by both clinical and non-clinical women. appear to be formed prior to drinking onset. Smith and Melissa A. Greenbaum. dieting. including the examination of psychopathology (Alloy and Tabachnick. and they operate to shape her subsequent behavioral choices. the individually different learning histories women have regarding eating. which are useful in predicting early onset problem drinking. 1984)..” “Eating seems to decrease my level of anxiety if I am feeling tense or stressed. dieting. Researchers have also shown that reducing alcohol expectancies can lead to reduced drinking in males (Darkes and Goldman. they hold unusually strong expectancies for reinforcement from eating. and thinness. and Smith. presumably by modeling (Miller. and hence pursue thinness more strongly than do others. To the degree that some women have come to associate thinness with powerful and overly general reinforcers. Brown. in turn. they argued that learned expectancies for reinforcement from dieting and thinness may be a mechanism by which one’s learning history leads to an emphasis on thinness. 1998). Eating and dieting expectancy theory holds that a woman’s learned expectations are the cognitive summaries of her learning history. such as those on alcohol. interpersonal processes (Jones. In sum. In both basic science expectancy studies. 1995). and Christiansen. they form different expectancies for the consequences of those behaviors and states.

Examples include Stice’s (2001) “Slender women are more attractive” and the SATAQ Internalization scale’s “Photographs of thin women make me wish that I were thin. Thus. though not comprehensive. or summarize a set of learning experiences. SATAQ Awareness scale items also seem to reflect precursors to expectancy formation.” These items are different from the preceding ones. These expectancies are then likely to influence their behavior. The items measure the individual’s recognition and endorsement of the social learning message. Conclusions . valid predictor of eating disorder symptom endorsement. 2001). and the body dissatisfaction and drive for thinness subscales from the Eating Disorder Inventory-2 (Garner. Thus. but may also or instead reflect a more global expectancy for the benefits of thinness. 1995). Items such as “People think that the thinner you are.” and “Attractiveness is very important if you want to get ahead in our culture.” From a learning theory perspective. not simply exposure to learning situations. Women who endorse these items strongly apparently feel more strongly about the value of thinness.” seems to reflect exposure to social learning about the benefits of thinness and attractiveness. We chose these measures because each has proved a reliable. which then influence subsequent behavior. the PSPS appears to measure precursors to thinness and dieting expectancies. thinness. In a practical way. the better you look. The more women recognize that message. The social pressure awareness subscale of the SATAQ can also be thought of under the expectancy theory rubric. in the sense that they appear to reflect conclusions on the part of the respondent. If one has felt pressure to lose weight. We offer a representative. or to be thin. From an expectancy theory perspective.Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 171 Understanding Current Measures of Sociocultural nfluence from the Standpoint of Expectancy Theory Many existing measures of sociocultural influences on dieting. The SATAQ item’s reference to a wish to be thinner may reflect the same expectancy (thinness is attractive). one has had a learning experience that will contribute to the expectancies one forms about the benefits of dieting and thinness. 1991). many of them in longitudinal designs (Stice. the Sociocultural Attitudes Toward Appearance Questionnaire (SATAQ. In other words. Consider next items reflecting internalization of the thin ideal. and Stormer. and eating can be though of from the perspective of expectancy theory and thus can be incorporated into this theoretical framework. Thompson. in a sense. 2002). these items appear to ask women to record a learning experience. the scale measures individual differences in one of the causes of expectancy formation. the more likely they will form expectancies for reinforcement from thinness. they serve as markers of likely expectancy endorsement. Items from the PSPS include: “I’ve noticed a strong message from my friends to have a thin body” and “I’ve felt pressure from people I’ve dated to lose weight. that is why scores on the PSPS predict subsequent onset of symptomatology: they contribute to the formation of expectancies. Stice. Heinberg. list of models to demonstrate this fact: the Perceived Sociocultural Pressure Scale (PSPS. The Stice item refers to one specific expectancy for thinness: thinness is more attractive.

and Hill. Smith. each proceeding from a slightly different stage in the psychosocial learning process. dieting. To do this. Demos.172 Sarah Fischer. We believe these constructs should be organized from a learning theory perspective. McCarthy. Simmons. 2002. one late adolescent sample: Simmons et al. By organizing them in this way. body dissatisfaction can be understood as a consequence of one’s learning history. they interviewed both clinical and non-clinical women about their expectancies. and they may reflect the influence of dieting/thinness expectancies. one would likewise be more inclined to value a thinner body. The Body Dissatisfaction subscale of the EDI-2. as crystallized in one’s expectancies for dieting and thinness. (1998) developed measures of expectancies for reinforcement from eating and from dieting/thinness within the framework of the expectancy theory. rather than as individual instruments.” are conclusions one might draw. Hohlstein. they can be seen to be parts of a coherent whole. In this sense. the above examples represent different stages in the psychosocial learning process concerning eating. 2001. If one endorses expectancies for reinforcement from dieting and from thinness more strongly than the average woman. Smith and Melissa A. Smith. Thus. and hence be dissatisfied with one’s own body. expectancies for reinforcement from dieting and thinness could lead to this kind of preoccupation with one’s weight. Cyders of this kind are.. Example items include “I am preoccupied with the desire to be thinner. After a series of test development steps. and Kroll. essentially. McCarthy. endorsements of expectancies that should play a role in influencing subsequent behavior. global scale to the 44-item Thinness and Restricting Expectancy Inventory (TREI). In sum. Gregory T. Items on the Drive for Thinness scale of the EDI-2 are indicative of motivations to be thin. and thinness. they identified five scales to the 34-item Eating Expectancy Inventory (EEI) and one. Understanding the place of each of these constructs within expectancy learning theory both clarifies their connections with each other and produces an integrated theory of symptom acquisition that can be readily understood with the same theoretical tools used for many other psychological phenomena.” and “I exaggerate or magnify the importance of my weight. which includes items such as “I think that my thighs are too large” and “I think my hips are too big. 2002. and Simmons. Smith. The five-factor structure of the EEI and the one-factor structure of the TREI have been replicated in nine samples (four early adolescent female samples: MacBrayer. one college female Caucasian sample and one college female African American sample: Atlas. The Direct Measurement of Expectancies for Reinforcement from Eating and from Dieting/Thinness Hohlstein et al. because psychosocial learning has been shown to be a very powerful and important tool in explaining behavior. .” From an expectancy theory standpoint. the Drive for Thinness subscale appears to reflect consequences of expectancy formation and endorsement of these items may serve as markers of one’s expectancies.

Eating and Thinness expectancy profiles discriminated among anorexic patients. and classification accuracy among the three groups of anorexics. 2002. rmsea=.80. Restraint Scale scores. bulimic patients.95. (2001) found cross-sectional evidence consistent with the hypothesis that various expectancy scales mediate the influences of (a) negative maternal modeling regarding eating. although multifactor solutions also fit well.” There is considerable evidence for the validity of these measures of eating and dieting/thinness expectancies.. (2002) found that expectancies accounted for different symptom variance from that explained by EDI-2 personality risk factors (perfectionism. intercorrelations among putative subscales were all greater than .99. psychiatric controls. Anorexic patients held strong expectancies for the benefits of thinness. and college samples (the latter including men. We focused on early adolescence. Caucasians. along with the expectancy that thinness/dieting leads to overgeneralized self-improvement. and. In these analyses. consistently account for substantial variance in Bulimia Test scores. Spillane. 2004). The next step in testing eating and dieting expectancy theory was to conduct a longitudinal study of expectancy and symptom endorsement. and African Americans). bulimics. and normal controls.” The five-factor structure provided the best goodness-of-fit as compared to alternative factor structures (CFI=. Important content domains included in the TREI are reflected in these sample items: “I feel like I could conquer things more easily if I were thin. interpersonal distrust. MacBrayer et al.40 to r = .62 (Atlas et al. on bulimic symptoms. and leads to feeling out of control. The five-factor structure of the EEI is made up of two positive reinforcement scales (“Eating is pleasurable and useful as a reward” and “Eating enhances cognitive competence”). and one scale assessing the expectancy that “Eating leads to feeling out of control.01).S. alleviate boredom. suggesting the merit of describing one. There were no differences between psychiatric and normal controls. 2001. 2002). women. Simmons et al. 2004. in press). one female and one male: Boerner. correlations generally ranged from r = . which is almost identical to a bulimia nervosa symptom). and Three Factor Eating Questionnaire scores. Hohlstein et al. and unusually low expectancies for the benefits of eating. and ineffectiveness). 1998.Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 173 2002.. and controls was 96% (94% if one does not use the expectancy that eating leads to feeling out of control. and Smith. and that thinness leads to overgeneralized self-improvement. two negative reinforcement scales (“Eating helps manage negative affect” and “Eating alleviates boredom”). and two more college samples. Boerner et al. expectancies that eating helps manage negative affect.” “I would feel more capable and confident if I were thin.. by following a sample of U.” “I would cope better with failures at work or school if I were thin. Anderson. Simmons et al. middle school children from grade 7 through grade 9 (Smith et al. overall factor (“Thinness and restricting food intake lead to overgeneralized self-improvement”).. rmsea = .. late adolescent. Bulimic patients simultaneously held expectancies that eating helps alleviate negative affect and boredom. In early adolescent.” and “I would be more attractive if I were thin. We examined three expectancy scales (eating helps manage . MacBrayer et al..04) The TREI’s one factor solution fit the data well (CFI = . and (b) family teasing about weight.

Gregory T. reciprocal influence phenomenon was observed with early adolescent drinking behavior (Smith et al. 1995). the Bulimia Test-Revised (BULIT-R). The uncontrolled. Thus. which ranged from . eating alleviates boredom. global expectancies. 1998). These findings speak to the value of integrating the many measures of sociocultural influence under an expectancy learning theory umbrella. Analogous to that which has been documented in other areas of psychology. and consequences of expectancies all predict the subsequent onset of bulimic symptomatology. we examined the cross-sectional. multiple regression correlations between the three expectancy scales and the BULIT-R scores.50 range. Cyders negative affect. time-lagged analyses indicated that expectancies correlated with subsequent BUILT-R scores in the . in press). the early empirical work testing eating disorder expectancy theory clearly suggests that eating and dieting expectancies operate in accord with basic expectancy learning theory and very similarly to how expectancies operate in other applied areas.. we utilized structural equation modeling to examine a series of models.40 to . Learned expectancies should predict subsequent changes in symptoms. these longitudinal data provide evidence supporting the application of expectancy theory to eating disorder symptomatology. and symptom level at each time influenced expectancy scores at the subsequent time.96). thin-ideal internalization. because these correlations did not control for prior BULIT-R scores.. The mechanism by which this progression operates is not yet known.60 to . More specifically. Taken together. which in turn predicted yet greater expectancies for reinforcement from both eating and dieting/thinness (Smith et al. . Greater endorsement of expectancies for reinforcement from both dieting and thinness predicted greater bulimic behavior. bulimic women appear to simultaneously hold unrealistic expectancies for reinforcement from both eating and from dieting/thinness (Hohlstein et al. specific expectancies. The overall fit of the model was quite good (Comparative Fit Index = . they could be a product of the high cross-sectional relationships and stable variable scores. and so should predict subsequent changes in expectancies. Reciprocal influences between expectancies and symptom level are consistent with expectancy theory. Smith and Melissa A. The model that best fit the data was one that specified reciprocal influences: expectancies at time 1 influenced symptom level at time 2.69 across three years. However. but it is worth noting that the same kind of positive feedback. and so on: Stice. and symptom level itself brings learning experience. unusually strong learned expectations for reinforcement from eating and from dieting/thinness predict bulimic symptom endorsement. predictive role of expectancy-related constructs (perceived sociocultural pressure. First. successful prospective. When one considers the documented. 2002). and thinness/dieting leads to overgeneralized selfimprovement) and one symptom measure. In order to control for prior BULIT-R scores. there currently exists evidence that precursors to expectancy formation..174 Sarah Fischer. It is interesting to note that the nature of the predictions was of the positive feedback loop variety.

trait urgency is a general risk factor. (2004b) showed that urgency correlated with both alcohol use and binge eating. others from gambling. We have also argued that individual differences in environmental risk can be captured using the expectancy construct. and that eating expectancies correlated with binge eating but not with drinking. Examples of rash action patterns one might develop include binge eating. Which of those action patterns a highly urgent person engages in is a function of the person’s learning history. some individuals form expectancies for distress relief from drinking. resulting in different characteristic forms of rash action (there are. This notion of a general. and gambling behavior. BN. other forms of rash action beyond those listed. it provides substance to the general argument that genetic and environmental factors are both involved. Expectancies for reinforcement from eating and from dieting/thinness are thought to summarize one’s relevant learning history. Fischer et al. heritable liability that can be instantiated in various ways is consistent with what we know about risk for BN. binge eating. perhaps including risky sex or dyscontrolled shopping). cross-sectional studies. and others from binge eating. We emphasize two key dimensions to the urgency-expectancy integration. First. We have demonstrated this process in two recent. First. we attempt to integrate these two risk factors. and for gambling) were behavior-specific. heritable liability of trait urgency. that alcohol expectancies correlated with drinking levels but not with binge eating. Through modeling and experience. too. Second. but problem gamblers had strong . They share the general.Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 175 A Heritable Trait Combines with Psychosocial Learning: Integration of Urgency and Expectancy Risk Models As we noted at the beginning of the chapter. by identifying one specific heritable risk factor and one specific set of environmental risk factors. Since BN rates vary across time and culture. one should be able to show that urgency correlates with each of those action patterns. one general advance in understanding risk for BN is the recognition that both heritable and environmental factors contribute to liability. Our aim is to make this general advance more specific. and that what distinguishes among people with the different action patterns is their different expectancies. In this section. problem gamblers shared trait urgency with binge eaters. For instance. the heritable risk for BN cannot be specific to BN symptomatology: it must involve more general dispositions that can lead to BN under the right environmental circumstances. alcohol use. and problem gambling. Here. no doubt. and so reflect a wide range of learned inputs into one’s eating and dieting predilections. Fischer and Smith (2004a) extended the earlier findings by including gambling behavior. urgency correlated with problem drinking. it suggests a more general integration of dispositional and learning risk factors that may have value beyond the eating disorder field. but their different learning histories cause them to form different expectancies. but the three types of expectancies (for alcohol. We have argued that urgency (the tendency to act rashly or maladaptively when distressed) is one important heritable trait that increases liability for BN. If this model is accurate. for eating. in the sense that it increases one’s likelihood of developing some form of rash/maladaptive action in response to one’s distress. Doing so has two advantages.

their potential implications are clear. 2004b. and it is. is . and we have demonstrated that expectancies differentiate BN patients from others and that expectancies predict the onset of BN symptomatology prospectively among adolescents. shapes the direction and nature of one’s “acting out. A second dimension to the urgency-expectancy integration is that. there must be negative affect (Fischer et al. Evidence is consistent with the possibility that trait urgency is an important part of the heritable liability for BN. Gregory T. there is virtually no relation between the eating expectancy and binge eating. those who expect eating to alleviate negative affect are much more likely to binge eat than are others (Fischer. in press). We have offered a specific theory of the integration of genetic and learned risk. because it likely influences many more syndromes than does urgency.. Individuals experiencing negative affect. in press). and Flory. Fischer et al. Krueger. Other individuals experiencing negative affect tend toward externalizing disorders or rash. important advances in risk for BN are being made. maladaptive actions (Krueger et al. McGue. Cyders gambling expectancies and weak eating expectancies. Evidence from heritability studies indicating the presence of both genetic and environmental risk factors dovetails nicely with empirical demonstrations of the roles of heritable urgency and learned expectancies.” Moreover. 2002. Among individuals low in trait urgency.. we have shown that among individuals high in trait urgency. Of course. In sum. Several avenues of investigation may build on this knowledge. In a series of studies. whereas binge eaters had strong eating expectancies and weak gambling expectancies. but it is one integrated component of such a model. but who are not urgent. negative affectivity may be one part of the risk process. other aspects to the heritable risk for BN. What we are describing is not a comprehensive model of risk for BN. Smith. It seems possible that high levels of trait urgency place one at risk for some form of “acting out” behavior.176 Sarah Fischer. in press). but the risk for BN is increased when urgency is present as well. 2001): they are likely the ones high in urgency (Fischer et al. We have shown that urgency is a general risk factor for maladaptive behavior patterns. represented as expectancies. Negative affectivity appears to be a necessary precursor to high levels of urgency.. Although there are limitations to these findings (their cross-sectional nature and the failure to include identified clinical cases). and we have provided empirical support for the theory. such as depression and anxiety. and Iacono. Anderson. likely tend toward internalizing disorders. There are. So. no doubt. One likely possibility is negative affectivity. What is the precise role of negative affectivity in this process? What other risk factors are also relevant? For instance. The presence of this interaction is quite consistent with the nature of each construct: eating to alleviate negative affect should be much more likely among urgent individuals than among others. 2003. and so heritable dispositions toward negative affectivity are another part of the heritable liability for BN. and that learned expectancies influence the particular form of rash action one chooses. Smith and Melissa A. the notion of dispositional tendencies being shaped into specific behavioral predilections as a result of one’s particular learning experience may well have importance beyond the field of eating disorders. For urgency (rash action in response to subjective distress) to be active. and that one’s learning history.. disposition and learning interact. in the case of binge eating. We have also shown that individual differences in learning can be understood using the expectancy concept. the role of negative affectivity is different.

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Disordered eating and chaotic lifestyle may affect patterns of caries (decay) and gum disease. could theoretically differ to normal flora as a consequence of repeatedly low intra-oral pH secondary to self-induced vomiting (SIV). The mouth is the first part of the digestive system and commonly exhibits signs of disease occurring elsewhere. Parotid salivary gland enlargement and altered salivary composition have been described. Inc. either in dental plaque or saliva. psychiatrists. This chapter reviews the literature and illustrates the clinical problems faced by real cases. dietary and psychiatric/psychological needs of patients. 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. nurses or relatives. be they physicians. 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. pp. 185-204 © 2006 Nova Science Publishers. Nonetheless.In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1 Editor: Pamela I. The presence of gastric acid in the mouth can result in acid erosion. Oral microbial flora. . Chapter IX The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health Alex Milosevic Liverpool University Dental Hospital Liverpool L3 5PS UK Abstract The dental and oral health of individuals with an eating disorder has been largely underinvestigated and ignored as health care professionals focus on the general medical. with disfiguring consequences to the dentition. Prevention will also be discussed. Swain. psychologists.

Glossitis and stomatitis are sometimes early changes in nicotinamide deficiency (pellagra). Blood chemistry revealed a severe anaemia with a Haemoglobin concentration of 7. Saliva Saliva has several important functions in the maintenance of oral health. There are no recorded cases of this in the eating disorders. . The well described swollen bleeding gums present in Vitamin C deficiency or scurvy are a very late stage of the disease and have not been described in the eating disorders. digestive and lubricative actions and. Although the abscess was of dental origin. minor apthous ulceration of the lips and tongue depapillation.5 g/dL) and a decreased total plasma protein concentration of 55 g/L (normal range 62-80g/L) [Keith and Flint. This was associated with angular stomatitis. all the soft tissue membranes such as cheeks and tongue are covered by protective mucous and the teeth themselves are coated by the acquired salivary pellicle. Contrary to an anecdotal report. the potential chronic irritation to the oral mucosa from long term vomiting has not resulted in any reported case of malignant change [Brady. No reports of this in the eating disorders have been made. Furthermore. it was an unusual presentation and the authors believed secondary immuno-deficiency was a predisposing factor. consisting of red. with respect to the mineral content of teeth. 1991]. A tongue abscess was described in a 30-year-old female with anorexia who presented with submandibular tenderness and difficulty swallowing (dysphagia).0g/dL (normal range 11. 1980].186 Alex Milosevic Oro-Dental Effects of the Eating Disorders Soft Tissues Nutritional deficiencies can give rise to a range of health problems but few have specific effects on the oral soft tissues. The salivary functions of lubrication and neutralization of intra-oral acids also termed buffering capacity are probably most important during bouts of self-induced vomiting (SIV). Fewer still are the reports in the literature describing oral lesions related to anorexic or bulimic behaviour. Treatment included an extraction. Angular stomatitis also termed cheilosis. The tongue tip and lateral borders become reddened. 1991]. swollen and occasionally deeply fissured as can the gum margins [Cawson. The inflamed and sore tongue is termed glossitis [Cawson. intravenous antibiotics and a 5-day course of oral penicillin with antifungal cream for the lip commisures [Keith and Flint. The pellicle has a significant role in protecting the tooth from caries and erosion.5-16. Its proteins have protective antibacterial. Cervical lymphadenopathy was not present but proteinuria was. Vitamin B2 (Riboflavin) deficiency is associated with inflammatory and degenerative changes in the mucous membranes of the lips and tongue. saliva can be supersaturated with calcium and phosphate and thus promote remineralisation. 1989]. sore fissures at the angles of the mouth and shiny reddened mucous membranes are characteristic. 1989].

. bulimics and controls were not statistically different.. calcium. 1989]. 1978]. Taylor and Sneddon. 1983]. was not correlated with salivary amylase concentration although significant reductions in amylase levels were found in patients with good treatment outcome but not in those with poor treatment outcome [Kronvall et.at. 1977]. urea nitrogen and albumin were reported to be within normal values although unstimulated salivary values were measured in only one subject [Tylenda et.al. Burke.. Other sialograms performed on a 19-year-old female student [Levin et. Although a very low resting saliva rate was reported. The histological appearance of parotids in malnourished South Africans was of cellular hypertrophy with accumulation of secretory granules.. Although resting salivary flow rates were originally investigated. 1993]. Little is known about the influence of general metabolic disturbance in eating disordered subjects upon salivary function. probably because needle aspiration biopsy and sialography are invasive procedures. Raised salivary amylase in anorexia and bulimia has been reported [Humphries et.al.al. Stimulated and unstimulated salivary concentrations of potassium. Salivary amylase accounts for 55% of the total serum amylase and the rest is of pancreatic origin [Gillard et. 1980]. Stimulated flow rates between anorexics.The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health 187 Initial case reports described salivary parotid gland enlargement in cases of bulimia [Levin et. this was not statistically significant nor would it be clinically significant as stimulated saliva is of greater interest. Hasler. is usually asymptomatic. nuclear displacement and cellular distention [du Plessis. buffering capacity and pH were assessed in both resting and paraffinstimulated saliva in anorexia nervosa [Hellstrom. Any nausea caused by esophageal and stomach distention after a binge eating episode will further stimulate salivation. although some have noted discomfort and can resolve spontaneously and is thus episodic in nature. 1956]. 1980..al.. Flow rate. measured as binge frequency and SIV. Kronval and Theander 1987. 1992]. the 20-year-old female reported by Burke (1986) and on the 26-year-old female reported by Taylor and Sneddon (1987) found no structural abnormality of the gland. 1987]. 1992]. Hempen et al. The mechanism for gland enlargement remains unclear although humoral transmission between the pancreas and parotid was postulated with changes in serum amylase [Kakizaki et. but the mean salivary pH in both eating disorder . stimulated salivary flow is more relevant as salivary flow increases dramatically before vomiting because the medullary centre that controls vomiting is connected to salivary nuclei [Edgar.al.. The severity of abnormal eating behaviours..al.. It seems that parotid gland enlargement is not a consistent feature. Nutritional mumps was used to describe the parotid swelling seen in starvation and malnutrition [Batsakis and McWhirter. 1991]. Chronic malnutrition in Indian children reduced stimulated salivary secretion and buffering capacity and the authors speculated that the low protein diet coupled with low fat favoured reduced salivary buffering capacity [Johansson et. 1986. Most studies have investigated function (see below) rather than structure.al.1987.Others assessed the influence of personality traits on salivary flow but concluded that psychological factors appeared to have no predictive power on salivation despite the evidence to show that depression and anxiety can affect salivation [Millar et. 1982]. The parotid gland sialogram on an 18-year-old female showed a hypertrophic “leafless tree” pattern and the aspiration biopsy demonstrated packed acini with few ducts [Hasler. chloride.al. 1972]. 1982. 1992].

Salivary pH was within the normal range whereas the mean bicarbonate concentration was significantly lower (p<0. A subjective feeling of dry mouth or xerostomia was more frequent among the bulimic group (34%) than controls (10%) despite there being no difference in stimulated flow rates [Rytőmaa et. the gums or gingivae. salivary function is altered in the eating disorders. This is caused by ineffective oral hygiene or plaque control.Touyz et. Bulimics with pathological or unacceptable dental erosion had significantly more viscous saliva compared to bulimics without pathological erosion and the controls see Table 1. The inflammation and subsequent loss of attachment is in response to the microbial flora or dental plaque which may be characterised by specific species or particular virulence factors such that its chronic progressive nature results in tooth loosening and eventual tooth loss. It seems likely that parotid gland hypertrophy is episodic but the clinical picture is very varied with some cases of altered salivary output which is not associated with parotid enlargement. There are. 1991.01) mean stimulated saliva flow rates compared to the control group [Milosevic and Dawson. are collectively termed the periodontium. Bulimics with and without pathological dental erosion had significantly lower (p<0. bleeding gums and called gingivitis. Periodontal Disease The supporting structures of the teeth include the bony socket. 1993]. cP 7. however. Mean whole salivary viscosity measured in Centipoise (cP) according to the presence or absence of pathological erosion Group Bulimics with pathological erosion (N=9) Bulimics without pathological erosion (N=8) Controls (N=10) Salivary viscosity. Overall. Table 1.54) Reduced parotid gland function in bulimia could result in a less watery or serous output and reduced bicarbonate contribution to whole saliva.39 (3. Furthermore. Hence the importance of correct and effective .188 Alex Milosevic groups was significantly lower than the control subjects [Liew et.al.al. Chronic gingivitis can be followed by progress of the inflammatory response to deeper tissues such that bone resorption (loss of attachment) takes place but in certain resistant individuals gingivitis does not lead to periodontitis. few reported cases of significant difficulties associated with this. with the overlying gum.12 (0. Smoking is a co-factor. 1996].46 (0.56) 4. manifest as swollen. a significant reduction in parotid secretion could result in an increased salivary viscosity because of a proportional increase in submandibular and sublingual salivary gland secretion which are more viscous [Milosevic and Dawson.al. 1998]. The first stage of periodontal disease is inflammation of the superficial tissues..43) 4.01) in the two bulimic groups compared to the control group... the cementum layer of the root and the intervening ligament which. 1996].

The initial studies found unremarkable levels of plaque. In 58 subjects with an eating disorder..al. 1991]. fresh fruit juices. Selfinduced vomiting (SIV) is a common purging behaviour in the eating disorders and may produce a similar pattern of erosion as in subjects with GORD or excessive dietary intake of acids. The strength of association between vomiting variables and the outcome of dental erosion has been investigated more recently. The impact of eating disorders upon oral health was initially reported by Hellstrom (1977) and Hurst et al. Carbonated beverages such as cola drinks. It differs to dental caries (decay) in that it does not involve bacterial or plaque acids but does involve dietary or gastric acids having a direct effect upon enamel and dentine. The evidence that periodontitis is worse in the eating disorders is conflicting.al. The presence of plaque and gingivitis was similar in the vomiters and non-vomiters although periodontal bone loss was not assessed [Hellstrom. The increased consumption of these food stuffs increases the risk of erosion although the epidemiological evidence for this is limited. The clinical significance of differences in plaque score and gingivitis around the dental arch is not apparent and probably not important. compared . 1977]. flossing and use of mouth rinses. gingivitis and periodontal disease between eating disordered subjects and controls [Milosevic and Slade. (1977). The approximal plaque index and sulcus bleeding index were significantly higher in the healthy controls compared to the anorexia and bulimia study groups but calibration and the degree of reproducibility of the examiners was not stated although the authors did state that “patients had no loss of attachment” [Philipp et. 1991]. gingivitis and periodontitis. Of the 66 females in study sample.. 1987].. 1977) although no attempt was made to correlate vomiting variables with the outcome of erosion. Inflammation was significantly more common in the non-vomiting group than in the vomiting or regurgitating anorexics [Hurst et. Eroded teeth occurred in a third of cases sampled by Roberts and Li (1987) despite the observation that only 65% of the anorexics vomited compared to all the bulimics. 25 (38%) had significant erosion. In of a sample of 39 anorexics.al. 1990].al. Furthermore. The presence or absence of erosion was related to the duration of vomiting [Simmons et. 1989. buccal erosion due to a high consumption of acid fruits and drinks to relieve thirst was more frequent in vomiting than non-vomiting subjects. 1977. One study found that controls had more surfaces with a plaque score of 0 but the anorexics had significantly more lingual/facial sites with plaque scores of 1 and scores of 2 were similar between the two groups [Liew et. Gastric acid enters the mouth secondary to gastro-oesophageal reflux disease (GORD) or during vomiting. Roberts and Li. More recent results consistently failed to find any difference between plaque. Fresh fruit was eaten in order to induce diarrhoea.al. Altshuler et.The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health 189 oral hygiene procedures which includes tooth brushing ideally with fluoridated toothpaste. 1986]. herbal teas and white wines have been associated with erosion as have fresh fruit and pickled foods.. Dental Erosion Dental erosion is the acid dissolution of tooth substance.. severe lingual-occlusal erosion was reported in 27 subjects (Hellstrom.

Similarly. the frequency of SIV. Table 3. see Table 2 [Milosevic and Slade. 1995]. Relative Risk 3.. p= 0. significant differences were found between the observed frequencies in the absence or presence of pathological tooth wear within the various groups. In the study by Milosevic and Slade.al. 1989].11. Table 2.46. must be involved in determining whether or not erosion occurs.190 Alex Milosevic to 50 age-matched controls. Other factors.at. ns).003.56. [1990]. were not linearly associated (Pearson correlation coefficient) with dental erosion. This result was counter intuitive as it would be expected that more vomiting episodes would lead to increased severity or presence of eroded teeth.3) for the occurrence of dental erosion if subjects have vomited more than 1100 times. Number of cases within groups showing presence or absence of pathological tooth wear Group 1 Bulimics with SIV 14 (42%) 19 (58%) 33 Group 2 Bulimics without SIV 2 (28%) 5 (72%) 7 Group 3 Anorexics 6 (33%) 12 (67%) 18 Group 4 Controls 3 (6%) 47(94%) 50 Row Totals 25 83 108 Pathological erosion/tooth wear present Pathological erosion/tooth wear absent Column Totals It is clear from Table 2 that far more erosion/tooth wear is present in the eating disorder groups compared to the control group. Vomiting duration was only moderately associated with the number of eroded teeth (r=0.01) but the frequency of SIV was not significantly related to dental erosion (r=0. 1991]. From the data in Table 3. the total number of vomiting episodes. Bulimic patients were also found to have more severe erosion compared to anorexics although neither the method used to measure erosion nor the comparison test were stated [Philipp et. p=0.73 Further analysis of the 14 cases in Group 1 found that 11 had 1100 or more vomiting episodes which forms the basis for Table 3. 1989]. its duration and the product of these two variables.73 (95% CI 1. The authors did . Similar results were reported by Altshuler et al. the Relative Risk is 3.. therefore.5. Presence or absence of dental erosion/tooth wear in vomiting bulimics according to total number of vomiting episodes Total number of vomiting episodes <1100 >1100 3 11 14 15 4 19 18 15 33 Pathological tooth wear present Pathological tooth wear absent Column total Chi square = 8. the severity of erosion was no different between those who vomited more frequently compared to those that vomited less frequently [Robb et. The within group proportion with erosion was highest in the vomiting bulimics (group 1) which was also reported in a South African case-control study published in the same year [Jones and Cleaton-Jones. 9.

Dental Caries (Decay) and Its Difference to Dental Erosion Dental decay or caries is caused by the bacterial breakdown of fermentable carbohydrates..al. The commonest surfaces to be severely affected by erosion in subjects with an eating disorder are the palatal (upper inner sites) and occlusal (the biting top surfaces of bicuspids and molars). 1995]. 1993]. Robb et. Dentine sensitivity may be presenting feature. all the teeth are at risk of erosion. acetic and propionic acids. Bacterial plaque acids mainly implicated in the carious process are lactic. over half the bulimics had discovered erosion themselves (12 out of 22) and in a quarter of cases the erosion was diagnosed for the first time by the examiners. Dentine Hypersensitivity Severe enamel erosion may result in exposed dentine. Its management is discussed later. although most workers have assessed its surface or site distribution and compared it to controls groups [Jones and Cleaton-Jones. Mean palatal and labial (front facing sites) exhibited significantly greater erosion in vomiting anorexics and bulimics compared to abstaining anorexics and controls [Robb et..al. 1998]. The authors also reported that abstaining and vomiting anorexics exhibited more lower posterior erosion on buccal (cheek facing surfaces) and occlusal surfaces than controls. This hypothesis has not been proven and others reported that the etiology of the erosion could not be ascertained from its location or distribution [Jarvinen et. This is a different process to acid erosion as the . Both the prevalence and severity of dental erosion were greater in Finnish bulimic subjects compared to controls [Rytőmaa et al.. 1995. Rytőmaa et al.. Milosevic and Slade. Interestingly. The Distribution of Acid Eroded Teeth In any one mouth.. The greater severity of erosion in bulimics compared to anorexics was confirmed in a sample of Australian cases who had six-fold the number of eroded surfaces [Touyz et. 1998]. 1989.al.The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health 191 comment that after six months of SIV most bulimics exhibited one or more eroded tooth surfaces and that after five years all subjects exhibited some erosion. These sites are also eroded in subjects who drink excessive amounts of fruit juice or carbonated beverages and therefore it can be difficult to determine the relative contributions from intrinsic gastric acid and extrinsic dietary acid.. The reason why non-vomiting anorexics had buccal and occlusal erosion is not clear although Scheutzel [1996] believed that extrinsic acids affected the buccal and labial surfaces whereas gastric acid from SIV attacked the palatal and occlusal surfaces. resulting in acidic metabolic by-products which attack a susceptible site on a tooth surface. The most commonly eroded teeth are the upper incisors. 1989. most notably sucrose.al. This can be sensitive to temperature change and normal activities like tooth brushing and drinking become painful. 1992].

1986. This new surface is more readily worn away by tooth grinding habits (bruxism).. Perfectionist tendencies or obsessive-compulsive traits are common in the eating disorders which may manifest as good oral hygiene practices so reducing the risk of caries. (1998) and for DMFT by Touyz et. Bulimic individuals had significantly greater DMF-“value” compared to anorexics and controls. tooth brushing (abrasive processes) and chewing hard foods. Although caries experience was not different in the 27 vomiters compared to the twelve non-vomiters [Hellstrom.192 Alex Milosevic teeth become cavitated and require fillings.al.al. “Clinically detectable” caries occurred in only two cases out of 66 bulimics examined by Simmons et. by contrast. Missing and Filled Teeth) and DMFS (Decayed. The evidence that dental caries is worse in eating disordered individuals than the normal population is slightly conflicting.. The latter authors discussed diet and recognised that the abnormal eating pattern including bouts of high carbohydrate consumption would increase the risk of caries. They thrive under acid conditions and adhere tenaciously to tooth surfaces because not only do they produce acids but very sticky extracellular polysacchharides [Kidd and Joyston-Bechal. No difference in DMFS between eating disorder groups and controls was reported by Milosevic and Slade (1989). Microbiology As discussed in the previous section. Altshuler et.. others reported nonvomiters to have less caries experience [Hurst et al. al. Neither study benefited with a control group and measures for caries and erosion were not validated. dental caries involves microbial plaque acids attacking the tooth surface. Erosion. This is despite the greater theoretical risk associated with haphazard eating habits and increased intake of carbohydrates. is a surface development with loss of the original surface tooth substance and porosity or softening of the remaining surface see Figures 2 and 5. 1991). Streptococcus mutans and Lactobacilli are cariogenic because they are able to produce acid rapidly from fermentable carbohydrates. (1990) and Rytömaa et.al. Missing and Filled Surfaces) were used by Roberts and Li (1987) who concluded that caries experience between anorexics and bulimics was no different and believed neither group were more or less susceptible to dental caries than healthy people. Repeatedly low intra-oral pH from SIV could in theory manifest as an altered oral microbial flora to more aciduric species [Bretz et.al. 1977].al. which was not statistically significant (Jones and Cleaton-Jones. Erosion by contrast occurs when dietary acids “bathe” the whole tooth with resultant thinning of the surface rather than a small area of demineralisation beneath the plaque. The standard measures for decay. Enamel is the initial dental tissue to be involved as it forms the “cap” or covering of the tooth. A further distinguishing feature of dental decay is that enamel caries is a sub-surface phenomenon with the body of the lesion having greater porosity (5-25%) than the surface zone (approximately 1%). 1987]. The mean DMFS scores for a bulimic group and age and sex-matched controls were 27.1 respectively. the literature indicates that dental decay is no worse in eating disordered subjects compared to controls.9 and 19. . 1989). (1993). Overall. 1989]. 1977)]. DMFT (Decayed. although whether the index related to surfaces or teeth is unclear (Philipp et.

The authors demonstrated that Streptococcus sobrinus was capable of producing acid at low pH values.The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health 193 The selective serotonin re-uptake inhibitor. bulimics and controls although the authors failed to state whether they cultured dental plaque or saliva [Touyz et. fluoxetine or Prozac. Salivary bacterial counts of Streptococcus sobrinus were statistically higher in the eating disorder group than in the healthy controls [Bretz et. It is associated with parafunctional tooth clenching and grinding known by dentists as bruxism. The extremely high loads imposed across the teeth and the jaw joint result in tooth wear (attrition) and a clicking joint. Furthermore.al. termed the temporo-mandibular joint (TMJ).. fluoxetine was effective in reducing the frequency of bingeing and purging and salivary levels of Streptococcus sobrinus [Bretz et. 1992]. 1989].al. has been used to reduce binge-eating and vomiting. Bruxism is believed to be a stress relieving mechanism that occurs during sleep in the early hours of the morning.al. Temporo-Mandibular Joint Function and Tooth Grinding (Bruxism) Mouth opening. Perhaps acid erosion of teeth has overshadowed any assessment of dental attrition.. None of these possible reasons have been investigated. If muscle spasm is present. None of the studies on the oral and dental sequelae to the eating disorders have described TMJ dysfunction as a finding despite the hypothetical risk to the joint from frequent wide opening of the mouth during bouts of SIV and stress related bruxism. Lactobacilli and yeast were increased but this was not reflected in greater decay as the DMFS (see above) in the eating disorder group was actually lower than a high risk caries comparison group [Bretz et. These authors offered several explanations for this contradictory result. In a double-blind placebo-controlled trial.. 1993]. pain can also co-exist with limited mouth opening.. 1989]. The TMJ is principally between the articular inferior surface of the squamous temporal bone and the mandibular condyle. .al. 1993]. whereas other streptococci ceased acid production. Neither Streptococcus mutans nor Lactobacillus counts were any different between anorexics. Between the cranially convex glenoid fossa and the condylar head is an intra-articular collagenous fibrous disc of variable thickness that completely divides the jaw joint into upper and lower joint compartments [McKay et. but joint dysfunction is a common and well-recognised problem.al. reduced risk of decay because of the older age of onset of bulimia and a protective effect from greater consumption of dietary fat which protects for decay. It was believed that Streptococcus sobrinus could be a marker of emetic activity and therefore instruct carers on compliance with treatment.. Masseter muscle hypertrophy is a feature of long standing bruxism. including an alteration of microbial virulence secondary to vomiting. salivary levels of Streptococcus mutans. closing and lateral movements are enabled by the jaw joint. Detailed description of the TMJ is beyond the scope of this chapter. which would be difficult to see if erosion was present.

. and related it to the Body Satisfaction Scale and the Eastman Esthetic Index [Milosevic et. 2000.al..al. The influence of poor dental appearance on mental well being has been investigated and the results are contradictory although recent reports concluded that satisfaction with dental appearance was an important factor for psychological health and patients’ expectations of treatment [Albino et.al. In children requesting orthodontic treatment.. 1985]. especially so in dentistry.al. both perceived and desired. Digital depression of the tongue and increased intra-oral pressure to induce vomiting was not therefore the cause of the open bite. 1991].al. Patients with an eating disorder attending dental clinics have a range of problems which may be exacerbated if a dental fixation is present.05). Dental and facial aesthetics were reported to have a very important role in self-esteem and self-image [McLain and Proffit.. Shaw et. 1985].al. not only in adolescence but also into adulthood [Helm et.. 1989. oral and dental problems possibly associated with eating disorders Non-specific Dental caries Gingivitis Chronic Periodontitis Temporo-mandibular joint dysfunction Bruxism Specific Erosion (secondary to SIV) Altered oral microbial flora Altered salivary function including parotid hypertrophy The Inter-Relationship of Psychological Wellbeing and Body Image Distortion with Facial. a recent study measured BID. 1985] whilst body dysmorphic disorder (previously known as dysmorphophobia) has a classic pattern with individuals presenting with a minor or imagined defect and a level of concern that is out of all proporton [Cunningham.al.. yet few studies have assessed the influence of distorted body image on satisfaction with facial and oral features [Cunningham. 2003..52. 1999]. CircumOral and Dental Appearance Facial appearance has universal importance. Whether a general disturbance in body image . Although only a small convenience sample of 15 eating disordered subjects were assessed. The facial. the results indicated that teeth were not associated with body image but the face was associated with an over estimate of body image (rho= +0.al.al. although girls scored significantly lower than boys and the few subjects with prognathic teeth had lower scores than the other malocclusion groups [Klima et. p<0.. 1979]. Certain dental traits in a 15-year follow up study of Danish subjects were found to adversely affect body image and self concept. Birkeland et. 2003]. The presence of an anterior open bite or other dental abnormality was not associated with patient reports of SIV [O’Reilly et. Overall.. In an attempt to understand the influence of facial and dental appearance on body image distortion (BID). It was concluded that dental treatment in anorexia and bulimia may not lead to better perception of body image. 1999]. body image satisfaction did not differ to the control group.194 Alex Milosevic Table 4. Bos et. 2003]. the group over estimated their body image by a mean of 28% and desired to be a mean 25% thinner [Milosevic et.

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health 195 perception and possible dissociation in symptomatology exists such that body image is specific to the body and excludes the teeth and mouth is unclear. 2001]. Referral to another health care professional would be less of a breach of confidentiality as there is an understanding of implied consent for any information disclosed during examination which can be passed on to professional colleagues in order to benefit the patient. Whichever approach is adopted it must be sympathetic and non-judgmental [Kidd and Smith. Finally. patients diagnosed in dental clinics are often younger than those seen in eating disorder clinics and hence have a better prognosis for treatment [Brown and Bonifazi. England. despite the morbidity and mortality associated with the disorder. This was despite 29% having provided dental treatment for a sufferer. Management of the Dental Aspects of Eating Disorders The bulk of the dental literature regarding anorexia and bulimia focuses on issues of management whereas few papers discuss the added difficulty of history taking in these cases.. Another contentious issue for the eating disordered patient is the provision of care in relation to their disorder. is it ethical to refer to a medical practitioner? If the patient is an adolescent is it ethical to inform the child’s parents or guardians that he/she has admitted to an eating disorder? In the latter situation. Treatment is unlikely to succeed in a non-compliant and poorly motivated patient. 1996]. 2001]. Many eating disorder patients are highly secretive or are too embarrassed to admit they have a problem and thus disclosure is not forthcoming [Milosevic. 2003]. 1993]. the general level of knowledge regarding the oral signs of bulimia was very low [Harwood and Newton. History Taking and Ethical Considerations Knowledge of eating disorders by dentists was thought to be important as they may be the first to health care professional to suspect an eating disorder because of the characteristic oral presentation [Burke et. Unfortunately in a survey of 100 dentists working in the county of Kent. taking a relevant medical . Moreover..al.al. However. direct communication with the patient and involvement in all aspects of decision making and treatment planning is very important otherwise feelings of lack of control may become exacerbated [Crossley et. A further and potentially more difficult problem to solve concerns issues of confidentiality and consent [Crossley et. This was an area recommended for further research. 1993]. Some have advocated that treatment is withheld or at least the advanced “comprehensive” procedures are not undertaken until the individual is cured or significant improvement in vomiting behaviour has been achieved [Faine.al. 1999]. 1995]. The ethics of a dentist withholding treatment for a dental problem are uncertain. if the child is deemed competent a breach of confidentiality would be unethical. Should the dentist suspect an eating disorder and question the patient regarding this. The dental management of patients with anorexia and bulimia can be broadly divided into intervention and non-intervention..

but it is unlikely that eating disordered patients would comply with a request percieved to be too intrusive. fructose and maltose have all been associated with dental decay. The Examination Extra-orally. Plaque and gingivitis should be measured with recognised indices and examiners should be calibrated for diagnostic accuracy of scoring criteria. once explanation of the causes of dental erosion are made.. facial muscles and jaw joint function are checked. its progress can be monitored by way of study casts which require an impression. The oral and dental examination should follow a standard protocol for all patients irrespective of the eating disorder. A review one year after initial presentation and comparison with the previously mentioned techniques will help determine if the erosion has progressed. the parotid glands. Such drinking patterns and chaotic eating habits will only serve to increase risk of decay and possibly erosion. patients do not usually complain about them. If erosion is present. the patient needs to be informed about the causes and given appropriate advice as to how to reduce its effects. whereas sucrose. the patient is informed about the oral condition and discussion can ensue as how best to proceed with treatment. Naturally occurring sugars in milk and fruit are virtually non-cariogenic. 1996]. 1994]. Therefore. lest problems with teeth disrupt a thorough examination of all the mouth.196 Alex Milosevic history is mandatory and this may identify other medical conditions unassociated with the eating disorder. The mean intake of diet soda was more than three litres per day in a group of bulimics resident in an inpatient unit [Hetherington et . certainly at the initial presentation. Dental erosion and caries are assessed with the aid of good lighting and dry teeth. glucose. . see Table 5. photographs or a putty index. Both the frequency and quantity of sugar intake should be reduced to lessen the risk of decay [Rugg-Gunn. Diet sheets are helpful in identifying the time and pattern of food consumption. Non-Interventionist Dental Management The dentist can make several recommendations to minimise the effect of dietary acid and vomitus harming the mouth.al. Hygienist phase therapy to professionally remove deposits and instruct on effective plaque control will help lessen the risk of both periodontal health and caries. Radiographs are usually also required. Dental decay can be controlled by correct oral hygiene techniques and dietary advice. Unless the eroded surfaces are visible. Soft tissues and gums (gingivae) should be examined prior to the teeth. Once the dentist has gained all the information.

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health Table 5 Advice to minimise dental problems in eating disorders Raise awareness of the role of plaque and diet in dental caries: • • • 197 The importance of effective plaque control Reduction in frequency of intake of sweet foods.. such as carbonated colas and fresh fruit juice (low calorie drinks are still potentially erosive) Increase consumption of water (carbonated or fizzy water has low erosive potential) Use of a straw will reduce fluid contact with tooth surfaces Monitor intake of fresh fruit and especially acidic fruits such as citrus. Milosevic et.al. Two research groups independently assessed post-vomiting oral hygiene practices with the degree of erosive wear and reported that that the erosion was no worse in the eating disordered subjects who brushed immediately after SIV [Robb et. Interventionist Treatment Application of desensitising pastes on exposed hypersensitive dentine is a short term solution whereas greater durability will be achieved by sealing and impregnating the dentine .al. cider. 1995. chew gum. demineralised dentine is more susceptible to tooth brush abrasion. snacks etc but balance this with any programme to improve weight Maintain close liaison with dietitician/nutritionist Raise awareness of acidic sources in the diet: • • • • • • Reduce intake of acidic drinks. 1997]. mixers (tonic and colas) Vinegar dressing. rinse mouth with water or milk Gentle tooth brushing with a small amount of desensitising or bicarbonate tooth paste after SIV may be safe Check that medication does not provoke dry mouth or nausea For salivary hypofunction/dry mouth • Prescribe neutral artificial saliva or sialogogue pastilles Toothbrushing after vomiting is generally regarded as inadvisable as the softened. pickled foods Post-vomiting methods to increase pH and improve oral milieu: • • After self-induced vomiting (SIV). sour apples Alcohol eg white wine. Eroded palatal sites are probably not easily brushed but buccal sites (facing the cheeks) are more readily abraded..

Furthermore. Also known as dentine bonded crowns. they require minimal preparation of the teeth and are additionally regarded as reversible. The major advantages are its reversibility and ease of use because bonding to the tooth surface precludes the need to cut the tooth. usually with ortho-phosphoric acid. Conventional Ceramo-Metal Crowns These crowns need sufficient tooth structure in order to retain the crown and allow adequate preparation to be made. Given that eroded teeth may have lost significant tooth substance. Dento-Alveolar Compensation A further problem is dento-alveolar compensation secondary to acid erosion. Paradoxically the surface needs to be acid etched. This can only be done in the dental office. Resin Bonded Ceramic Crowns These are an extension of the above method as porcelain or ceramic crowns are attached to eroded teeth using bonding technology. 1996]. comprising quartz filler particles embedded in resin. Despite the teeth getting thinner and shorter. They are indicated where there is greater loss of tooth substance requiring bulk coronal build-up. Thus the cross linkage of resins produces a strong and hard wearing restoration and the resin penetration into dentine and/or enamel gives good to excellent micro-mechanical adhesion. This allows it to be closely matched to patient’s teeth. Composite provides reduction in sensitivity. made in different shades. Placement of Dental Composite Filled Resin One of the most effective methods of replacing worn/eroded surfaces is by way of bonding composite resin. conventional crowns can be difficult. improvement in aesthetics and protection from further erosion. The fitting surface of the crown has to be etched in the laboratory in order for the bonding resin to impregnate the porcelain and thus retain the crown on the tooth [Milosevic and Jones. composite resin is not acid soluble and thus will not dissolve in subjects who continue to engage in SIV. in order to key or roughen the surface so that the bonding resin can penetrate and retain the overlying composite resin which has the same polymeric structure as the bonding resin.198 Alex Milosevic surface with a commercially available un-filled resin. a gap between the upper and lower teeth does not automatically occur as there is a tendency for teeth to re-establish contact and physically erupt to maintain contact with opposing teeth. Dental composite is a tooth coloured filling material. It appears that in some cases the rate of wear .

The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health 199 and eruption are equal. The parotid enlargement is illustrated in figure 1 and the appearance of his teeth is shown in figure 2. . Consequently. During this time the dental erosion progressed. His treatment included an extraction. his oral hygiene was not well maintained and his dietary intake of sugary food continued. He was diagnosed with gingivitis. teeth became carious around the existing restorations resulting in larger restorations and the erosion progressed. caries (decay) and erosion although the latter was attributed to acidic drinks. He attended for review over several years and at one stage presented with bilaterally enlarged parotid salivary glands which was worse on the right. was referred to the dental hospital as he complained of pain and having lost fillings. other teeth became carious and at least one bicuspid became abscessed requiring root canal therapy. This dento-alveolar compensation causes difficulty when patients wish to regain longer teeth as there is no space to do so. the patient stated he had “regurgitated” for the previous six years although he had only received treatment for this for six months. Case 1 This male. although in some individuals it may not occur. By 1996. his medication changed to Fluoxetine. he continued to engage in occasional SIV. Facial view of bilateral enlarged parotid glands in the male described in Case 1. Space can be gained by the interim use of a Dahl appliance or an anterior bite platform. His then medication was Amitryptilline 10mg daily. Unfortunately. It was only after this treatment had been completed that he volunteered he had “psychiatric” problems and had taken an overdose resulting in hospitalisation. Chlorpromazine Hydrochloride and Propranolol with cessation of the Amitryptilline. aged 28 years at initial presentation in 1990. Fig 1. which intrudes the anterior teeth and allows eruption of the posterior teeth. Furthermore. This may take several months and depends on the skeletal and incisal relationships and degree of space needed for build up of the eroded front teeth. both amalgam and tooth coloured restorations as well as hygienist phase therapy and palatal veneers to the upper four incisors.

Fig 3. Note the proud amalgam restoration indicating that tooth substance has dissolved from around the amalgam. was aged 26 years when first seen by the specialist. Intra-oral view of eroded upper teeth in Case 1. On examination. She was not taking any medication although she admitted to SIV over a ten year period. Female aged 26 years. Case 2 This patient. The palate appears to have a hematoma probably caused by the fingers traumatising the soft tissues during bouts of SIV. a female nurse. which is shown in figures 4 and 5. Her main complaint was of the poor dental appearance and inability to incise food because of the significant erosion to the front teeth. She was worried that the teeth would disappear. she had good plaque control and a generally .200 Alex Milosevic Fig 2.

and it can be seen from figure 4 that space is available to lengthen the short upper incisors. This was carried out in stages. showing the pulpal area of the teeth. have proven a valuable method of restoring severely eroded teeth. Indeed. the upper teeth exhibited deeper dentine and the pulps were visible on several teeth. Front view of Case 2 showing the severely eroded front teeth and the inability of the incisors to meet. Sensitivity is likely once most of the dentine has been eroded away. palatal view of the upper teeth. with restoration of the upper six anterior teeth followed by the posterior teeth. coffee. The upper teeth were very eroded whereas the lower teeth less so. . Fig 4. see figure 5. It was decided to restore the upper teeth with resin bonded crowns and use a commercially available kit. Despite the significant erosion. Case 2. red wine etc. dento-alveolar compensation had not occurred. Fig 5. although the margins had stained as the early bonding resin was permeable to food dyes eg tea. The patient was delighted with the result and the crowns. although somewhat experimental at the time of placement. Follow up several years later revealed the crowns had functioned well. Space was not available on three teeth and so these were left untouched.The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health 201 caries free dentition.

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

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

206

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

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

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

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

207

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

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

123. viii. 1. 46. 146. 133. 14. 41. 192. 146. 124. ix. 15. 195 conspiracy. 101. 180. 167. 139 covering. 39. 25. 200 control group. 27. 177. 57. 84. 71. 190 correlation coefficient. 178. 55. 167. 48. 129. 163. 54. 58. 35. 8. 65. 189. 196. 64. 88. 14 control. 109. 152. 110. 133. 16. 24. 80. 120. 115. 192. 34. 191. 180. 106 demographic data. 82 Diagnostic and Statistical Manual of Mental Disorders. 171. 51. 63. 174. 60 confrontation. 134. 128. 9. 185. 9. 93. 125 Denmark. 78 desire. 107. 182. 107. 101 disaster. 46. 34. 12. 5. 8. 172. 176. 9. 193 dietary habits. 187. 76. 49. 153. 37 COPD. 42. 108. 17. 164. 93. 188. 78 corticotropin. 177 diagnostic criteria.208 Index decision making. 195. 43. 18 deprivation. 122. 94. 120. 116. 196. 181 criticism. 33. 54 consumers. 197. 203 dental plaque. 187. 13. 36. 50. 163 conversion. 65. 5. 189. 150. 179 continuity. 196. 35. 27. 192 crisis management. vii. 76. 28. 119 CSF. 150. 93. 115. 102. 41. 77. 193 dentist. ix. 128. 150. 203 dietary fat. 94 cross-sectional study. xi. 142 dental caries. 137. 22. 61. 23 dependent variable. 192. 162. 155. 135. 68. 39 demographic change. 42. 189. 95. 138 consciousness. 19 discipline. 94 conformity. 50 developed countries. 112 digestion. 35. 28. 111. 10. 189. viii. 154 diabetes. 192. 66. 28. 32. 204 differentiation. 54. 76 depression. xi. 102 defense. 151 death. 114. 134. ix. 139 density. 51 cycling. 77. 52. 116. 76. 113. 174. 37. 162. 125. 2. 71 diabetic patients. 106. 65. 12. 96. 134. 175. 196. 46. vii. 19. 136. 41 decay. 170. 148 denial. ix. 82. 20. 28. 73. viii. 79. 157 consensus. 106 context. 94 counseling. 179. 179 correlation. 47. 117 definition. 84 D data analysis. 49. 99. 123. 99 death rate. 112. 96 conflict avoidance. 172 detention. 36 delusions. 6. 91. 190. 120. 60 conviction. 133. 147 disabilities. 2. 123. 114 developed nations. 165. 164. 173. 2. 36. 193. 163. 164. 86. 199 . viii. 6. 128. 197. 31. viii. 94. 18. 113. 13. 134. 15. 117. 114. 38. vii. 66. 4. 185. 93. 141. 177 derivatives. 108. 161. 42. 84. 105. 43. 164. 119. 194. 74 costs. viii. 132. 84. 193. 194 depressive symptoms. 67. 97 deficit. 69. 80. 195 decisions. 10. 160. 87 culture. 149. 171. viii. 163. 16. 117. 81 convergence. 192 controlled trials. 36. 108. 110. 156. 123. 1. 36. 114 cytokines. 163. 12. 56. 53. 2 critical period. 57. 175. 71 direct measure. viii. 184. 163. 192. 112. 4. 53. viii. 111. 185. 41. 147 consent. 173. 54. 2. 22. 113 corticosteroids. 163. 99. 4. 65. 105 deviation. 109. 86 diet. 151 depolarization. ix. 179. 50. 51. 188. 197 consumption patterns. 75. 164 consumption. 94. 3. 19. 64 dietary intake. 78. 116 delusion. 120. 67 coping. 101 disability. 184 currency. 148 dialysis. 117. 196 Department of Health and Human Services. xi. 188. 199 dieting. 106.

6. 153. 26. 95. 109. 27. 88 elderly. 162. 28. 187. 148. 23. 181. 25. 177 endorsements. 159 emotion. 176 dissatisfaction. 153. 161. 164. 100 emotional distress. 78 doctors. 163. 185. 63. 164 dissociation. 20. x. 190. 39. 202 environmental effects. 161. 171. 154. 149. 116. 21. 35. 22. 162. 25. 15. 102. 74. 3. 122. 38. 97. 99 environment. 125. 12. 159. 176. 204 ego. 128. 183. 113. 22. 51. 131. 179. 164. 8. 18. 19. 155. vii. 107. 22. 102. 148. 16 employment. 170. 11. 146. 114. 33. 166. 15. 166 DMF. 192 docosahexaenoic acid. 164 environmental factors. 156. 175. 172 energy consumption. 94. 92. 7. 141. 25. ix. 169. 7. 163 endocrine. 108. 113. 53. 53. 187 disposition. 159. xi. 69. 174. 7. 147. 3. 158. 153. 184. 156. 25. 64. 128. 195 enlargement. 20. 157. 91. 9. 20. 156. 101. 166. 51. 7. 116. 157. 9. 81 down-regulation. 102. 114. 187. 196 displacement. 142. 147. 163. 3. 8. 6 drug therapy. 87 dosage. 193. 92. 153. 37. 34. ix. 133. 153. 172. 178. 28. 45. 180. 180. 181. 99. 111. 165. 157. 103. 116. 120. 187 disorder. 146. 194. 156. 147 emotional state. 163. 131 England. 112. 178 domestic violence. 124 drinking pattern. 140. 130. 168. 160. 107. 140. 11 encouragement. xi. 95. 145. 29. 137. 141. 92. 186. 9. 23. 102 enthusiasm. 155. 163. 25. 140. 45. 93. 189. 109. 189. 192. 137. 60 dizygotic. 135. 128. 166 empathy. 138. 138. 126. 26. 186. 204 diuretic. 119. 29. 131. 39. x. 4. 155. 117. 193. 93 emotions. 66 209 E eating. 1. 199. 115. 195 discomfort. 93. 203. 92. 29. 143. 10. 108. 162. 148. 180. 31. 17. 39. 97. 19. 67. 22. 100. 132. 197 duration. 60. 204 eating disorders. 41. 83 electrolyte. 71 durability. 71. 89. 7. 150. 56. 86. 23. 28. 153. 11. 26. 10. 68. 14. 136. 165. 57. 91. 176. 155. 7. 14. 110. viii. 202. 125. 106. x. 93. 160. 171. 3. 115. 120. ix. 53. 197. 47. 191. 97. 190 dysphagia. 115. 124. 158. 49. 93. 130. 165 duodenum. 134. 156. 135. 148. 203 entanglements. 100. 149. 2. 192. 108. 103. 57. 20. 189. 57. 145. 166. 156. 196 drug abuse. 94. 17. 137. 91. 105. 135. 65. 160. 27. 2. ix. 81. 159. 23. 158. 202. 179 distribution. 194. 164. vii. 29. 174. viii. 167. 44 divorce. 107. 18. 196. 183. 154. 195. 79. 32. 165. 77. 146. 7. 96. 1. 42. 6. 162. 188. 170. 196 drinking patterns. ix. 95. 14. 6. 192. ix. 107. 78. 150. 110. 125. 178. 147. 21. 161. 178. 188. 17. 148. 179. 54 domain. 177. 177. 69 drugs. 21. 29 DSM-IV. 101. 106. 180 DSM-II. 94. x. 27. 195 distress. 133 diversity. 16. 102. viii. 2. 110. 147. 169. 160. 136. 123. 28. x. 134. 169. 133. 140 DSM. 185. 178. x. 23. 30.Index disclosure. 24. 26. 185. 182. 123. 197. 2. 161. 16 . 29. viii. 2. 127. 134. 99. 91. 109. 191. 166 dizygotic twins. 25. 7. 56. 150. 80. 58. 20. 45. 159. 117. 102. 190. 106. 162. 164. 143. 27. 145. 25. 177. 146. 139. 80. 145. 111. 100 dopamine. 141. x. 42. 202. 189. 175. 26. 20. 135. 176. 148. 111. 137. 136. 6. 3. 53. 94 eicosapentaenoic acid. 78 dream. 14. 92 endorphins. 187. 168. 53. 14. 175. 150. 181. 30. 93. 193. 188. 161. 24. 23. x. 92 emergence. 127. 97. 81. 195. xi. 16. 143. 166 emotional disorder. 194. 155. 203. 10. 2. 195. 191. 139. 138. 32. 18. 4. 147. 173. 28. 29 DSM-III. 45. 161. 161. 178. 101. 175 environmental impact. 26. 114. 8. 167. 42. 45.

77. 4. 123. 124. 4. 132. 30. 188. 8 gestures. 102. 76. 63. 100. 48. 200. 63. 49. 75. 33. 34. 80. 6. 97. 35. 74. 189. 178. 99 family therapy. 176 extraction. 200. 166. 165. 74. 72. 68. 80 exercise. 131. 92. ix. 196 fuel. 98. 50. 102. 202 Europe. 13. 191 Euro. 28. 93. 165 food. 99. 113. 83. 50 friends. 164. 189. 55. 192 fibers. 173. 5. 196 . 13. 86. 9. 151. 84. 66. 85 fulfillment. 123 G gambling. 99. 138. 170. 191. 64. 187. 72. 53. 148. 94. 34. 42. 189. 156. 83. 35. 136. 138. 98. 36. 177. 108. 111. 101. 71 epidemic. 52. 101. 17. 71. 142. 68. 134. 123. 76. 164 externalization. 12. 6. 67. 99 environmental influences. 76. 160. 24. 81. 180. 87. 50 exposure. 42. 36. 110. 4. 195 females. 48. 193. 133. 15. 78. 167. 61 gender. 198 Finland. 101. 166 failure. 7 fish. 80. 71 filler particles. 96. 49. 55. 142 fear. 162 fermentable carbohydrates. 16. 81. 36. 173. 54. 123. 92 experimental design. 155. 23. 117. 161. 88 fixation. 93 family environment. 168. 34. 174. 68. 69. 55. 171 expression. 5. 66. 100. 36. 164 Germany. 73. 49. 192. vii. 171 friendship. 77. 1. 139. 197 fluoxetine. 187 fatty acids. 42. xi. 99. 74. 170. 134. 196. 88. 87 exclusion. 198. 163 freedom. 185. 199 extraversion. 147. 124. 197. 122. 71. 106. 169 experts. 192. 173 food products. 77. 72. 134. 65. 202 focusing. 97.210 Index feedback. 163 fasting. 117. 92. 203. 57. 181. 75 feelings. 32. 71. 52. 70. 94. 2. 184 etiology. 102. 141. 84. 74. 136. 185. 125. 175. 106. 204 ethics. 155. 180 externalizing disorders. 56. 163. 49. 63. 72. 73. 83. 87. 180. 199. 179 family conflict. 2. 192 evolution. 183 erosion. 199. 67. 24. 123 fluid. 178. 97. 82. 30. 182. 31. 81. 15. 125. 173. 124. vii epidemiology. 85. 48. 169. 16. 37. 132. 139. viii. 180 enzymes. 122. 75. 179. 30. 165. 160. 24. 102 fast food. 115. 65. 93 excitation. 95. 99. 78. 12. 188. 9. 92. 8 gingivitis. 56 evidence. 159 genotype. 17. 88 fish oil. xi. 122. 36. 5. 100. 111. 179. 135. 196 factor analysis. 193. 110. viii. 112. 81. 186. 186. 117. 162. 50. 32. 108. 98. 15. 68 fructose. 126. 65 everyday life. 92. 163. 44. 194 flora. 179. 76. 123. 181 gender identity. 64. 72. 73. 53. 60. 37. 128. 108. 86. 73. 131. 42. 141. 105. 191. 85. 93. 12 family members. 79. 167. 43. 93. 137. 85. 135. 30. viii. 179. 190. 162. 98. 201 food intake. 51. 94. 189 femininity. 98. 63. 145. 112. 183 gastrointestinal tract. 133. 94. 85. 84. 96. 127 examinations. 162. 75. 20. 98. 74. 67. 136 gene. 132. 142. 65. 109. 176 family. 161. 97 facial muscles. 75 GATT. 133. 2. 188. 35. viii. 196. 64. 164. 71. 87. vii. x. 86. 70. 44. 113. 120. 189. 163. 194 fluctuations. 130 fat. 108. 124. 166 F facial expression. 64. 157. 12. 78. 69. 16. 195 ethnicity. 107. 49. ix. 43. 160 genes.

83. 111 identification. 75. 102. 79. 165. 68. 12. 84 hospitalization. 68. 170. 14. 99. 52. 15 health. 72. 4. 82. 11. 111 guidelines. x. 69. 135. 73. 9. 81. 177. 64. 76. 68. 186 glucose. 56. 101. 85. 56. 107 hip. 32. 34. 176. 42. 79. 167. 63 imagery. 135. 107. 157. 179. 86. x. 188 influence. 185 health problems. 176. 57 grades. 92. 157 impulsive. 113 indication. 165. 106 glossitis. 114. 153. 161 indices. 75. 164 independence. 12. 43. 196 individual differences. 187. 53 immune response. 125 guiding principles. 110 ingestion. 15 granules. 185. 85. 136. 43. 160. 16 homeostasis. 39. 26. 106. 4. 94. 49. 171. 86. 15. 138. 162. 45. 10. 99. 188. 166. 3. 93. 149 hematoma. 71. 189. 85 211 Hong Kong. 13. 95 harm. 139 hopelessness. 89 hypertrophy. 202 inflammation. 183. 174. 191 I iatrogenic. 55. 15. 145. 102 independent variable. 183. 54. 33. xi. 30. 72. 51. 37. 84. 163. 5. 10. 68. 97 hate. 166. 83 hyperglycemia. 78 immune system. 65. 133. 5. 116. 36. viii. 64. 90. 83. 101 host. 51. 68. 59. 50. 107. 162. 65 height. 89. 94. 108. 188 globalization. 2. 46. 50. 132. 6. 94. ix. 120. 202. 181 in vitro. 187. 202 growth. 49. 194 gland. 12. 47. 195. 15. 183 growth hormone. 44. 88. 192. 179 impulsiveness. 186 health psychology. 60. 10. 82 human subjects. ix. 14 health status. 200 hemodialysis. 74. 187 group therapy. 71. 80. 42. 28. 82. xi. 81. 170 identity. 197. 196. 169. 177. 117 governance. 135. 153. 101. 76. 68. 165. 13 infants. 168. 95. 20. 133 gut. 26. 181 impulsivity. 100 idealization. 120. 89 guidance. 45. 35. 78 implementation. 111. 194. 185. xi. 148. 189. 176 induction. 80. 101. 57. xi. 203 heat. 175. 186. 194. 13. 29. 97. 188. 18. 82 goals. 82. 74. 6. 11. 88 incidence. 154. 190. 151. 152.Index girls. 150. 94. 81. 69. 72 H hands. 181. 54. 111. 111. 89 hospice. 36. 75. 86. 7. 187. 56. 179. 171. 70. 124 HE. 71. 8. 11. 6. 26. 14. 70. 72. 173. 28. 65 immunomodulatory. 202 health care professionals. 58. 87 heritability. 172. 91. 204 informed consent. 50. 183. 80. 155. 143 groups. 79. 191. 73. 122. ix. 60 health services. 94 indicators. viii. 153. xi. 88 healing. 146. 173. 36 IL-6. 185. 106. 69. 166. 69. 89. 114. ix. 92. 152. 55. 203 health care. 15 hormone. 87 hypothesis. viii. 2. 72 high school. 10. 91. 16 ICD-. 18. 79. 148. 162 guilt. 181 guilty. 73 . 44. 50. 181 high fat. 95. 153 idiosyncratic. 49. 15. 10. 23. 84. 93. 159. 193 hypothalamus. 69. 195. 67. 50. 3. 162 ideas. 65 heat loss. 59. 31.

viii. 68. 67. 4. 147. 52 life span. 58. 89 integration. 147. 177 intensity. 65. 195 language. 37. 93 insight. 188. 109. 195 interview. 165. 57 lens. 63. 135 insecurity. 90. 36. 17. 13. 153 institutions. 109. 9. 164. 7. 29. 175. 171. 141. 56 laxatives. 87. 29. 22. 4. 186 liability. 165. 88 liver disease. 134. 159. ix. 182 learning process. 102 intravenous antibiotics. 13. 56. 24. 65. 14. 46. 127. 80. viii. 28 internalised. 92. 72. 198 links. 70. 11 input. 4. 43. 181 lifestyle. 154 interval. 160. 169. 164. 185 lifetime. 109. 58 Italy. 161. 159. 101 life course. 1. 71. 30. 146. 186 invading organisms. 57. 6. 120 lead. 202 J Japan. 133. 134. 53. 81. 67 liver function tests. 75. 70. 56. 52. 75 interdependence. 117 jurisdiction. 35. 191 loneliness. 175. 80 location. 12. 176. 85. 54. 169. 110. 84 learning. 95 listening. 133. 71. 10. 85. 179. 163. 15 longitudinal study. viii. 91 ligament. 84. 110. 174. 12. 71. 172 insulation. 136. 120 isolation. 177. 31. 69. 130. 171. viii. 45 justification. 20 iron. 177. 172 legislation. 162. 180 internalizing. 140 laws. 96. 16 interpretation. 169. 56. 182. 23 lipids. 19. 195 L lack of control. 9. 194 lean body mass. 67. 176 interpersonal processes. 94 interaction. 170 interpersonal relations. 79. 176 libido. 168 linkage. 175. 54. 79. 71. 23 jobs. 34. 172. 5. 57. 165. 163. 152. 54. 117 liquids. 55. 108. 170. x. 39. 175 limitation. 182 inhibitor. 76. 160. 164. 15 injury. 190. 97 intent. 51. 112. 110. 131 intervention. 41. 17. 140 Ireland. 14. 56. 80. 55. 55. 156. 75. 88. 174. 100. 159 intentions. 43. 18. 101. 48. 87 liver damage. 2 Israel. 65 interest. 59 leptin. 81. 73. 134. 53. 28. 85. 57. 49. 64. 45 lawyers. 170. 57 instruments. 86 lesions. 80. 110. 93. 168. 168 intimacy. 29. 69. 176. 154. 65 Iran. 173. 175. 41. 82. 164. 187 interface. 65. xi. 188 likelihood. 108. 16 liver. 57. 52. 96 knowledge. 77. 41. 9. 56 internalization. 172. 78. 49. 10. 59 K kindergarten. 76. 43. 63. 165 interaction effects. 64.212 inhibition. 203 interaction effect. 6. 173. x. 41. 193 initiation. viii. 127. ix. 176. 65 instability. 137. 168. 85 liver failure. 11 Index judgment. 162 . 51. 78. 73. 2. 181 Latin America. 167. 165 interactions. 54 insulin. 43. 176. 88 liver cirrhosis. 74. 84. 56. 164.

180 mental health. 199. 65 misconceptions. 167. 98. 103. 163. 161. 91. 171. 123. 123 melts. 116. 118. 148. 132. 186 memory. 203 monozygotic twins. 123. 103. 4. 43. 65. 187 mutual respect. 163. 42 milk. 74. 75 MTMM. 170 malnutrition. 78 monitoring. 101. 183 mood disorder. 111. 67 lying. 168 measures. 52. 41. 182. 69. 68. 140 nausea. 64 loyalty. 163 median. 138 meanings. 42 mental disorder. 170. 187 . 106. 18. 183 models. 120. 118. 41. 133. 18 malaise. 169 moulding. 5 messenger RNA. 59. 101 movement disorders. 50 molecules. 183 men. 48. 83. 3. 47. 23. 168 metabolism. 74. viii. 13. 44. 130. 162. 112. 56. 57. 155. 172. 43. 68. 141. 111. 57. 81. 69. 151. 194 maltose. 78 mass. 68. 68. 111. 166 mood. 195. 134. 196. 165. 139. 102. 179. 15 matrix. 195 mortality rate. 36. 56. 127. 75. 90. 5. 121. 58. 120 major depression. 63. 155. 2. 65 motivation. 43. 75 Middle East. 68. 161 magnesium. 5. 17 morale. 200 melanocyte stimulating hormone. 178. 138. 42. 84. 117. 101 mRNA. 131. 93. 122 membranes. 13. 171. 134. 122. 111. 181 motor behavior. 76. 16. 86 meta analysis. 45 marijuana. 183 media messages. 203 manipulation. 111. 45. 178. 101. 192 meat. 112. 45. 24. 162. 183. 121. 2 males. 116. 187. 174 multiple sclerosis. 82. 77. 44. 173. 100. 100. 183 menstruation. 191. 167 mucosa. 114. 165. 186 mucous membranes. 130. 134 measurement. 1. 63. 36. 73 mass media. 153. 50. 6. 125. 156. 54. 2. 85. 20. 8. 98. 202. 133 medical expertise. 174 moderators. 45. 42. 26. 82. 74 melt. 119. 92. 68. 141. 173. 17. 186 mucous membrane. viii. 53. 197. 150. 73. 186 lymphadenopathy. 93. viii. 44 mapping. 110. 152. 15. 89. 112. 65. viii. 51. 117. 67. 73. viii. 21. 82. 71 lung cancer. 2. 88. 6. 89. 164. 197 minority. 94. 55 movement. 173. 166. 160. 63.Index loss of appetite. 3. ix. 109. 64. 89 methodology. 115 mold. 168. 20. 106. 142. 203 malocclusion. 63. 142. 37. 141. 180. 9. 17. 112. 31. 17. 126. 157 microinjection. 59 mental health professionals. 177. 82. 15. 100 lumen. 129. 19. x. 202. 46. 7. 146. 22 National Research Council. 18. 16 morbidity. 22. 174. 49. 112. 196 management. 110. 186 multidimensional. 169. 133 modeling. 160. 113. 44. 55 N narcissistic personality disorder. vii. 50 lymph. 115. 178 meals. 186 213 M magazines. 138 multiple regression. 175. 56. 96 mumps. 66 media. 195 mortality. 67. 85. 57 medication. 89 lung disease. 180. 85.

184 observations. 142. 177. 182. 74. 168 neurotransmitter. 59. 168. 75 neurotransmitters. 150 output. 71. 151 parental authority. 196. 87 normal distribution. 199. 157. 167. 185. 203 partition. 135. 195 parotid. 69. 84 pancreas. 4. 183. 142. 15. 173. 107. 61 newspapers. 98. 203 parameter. 4. 188 overweight. 72. 188. 1. 71. 72. 183 neurons. 59 nutrients. 83. 54. 18. 35 olanzapine.214 needs. 145. 202 novelty. 71. 157. 178. 166. 63. 56 pellicle. 55. 105. 85 P Pacific. 133. 26. 56 personality. 86. 73. 182 negative consequences. 188. 15. 68. 123. 2. 83. 76. 20 parenting. 71. 147 perfectionism. 186 nicotine. 151 peers. 71. 187 norepinephrine. 71. 166. 99. 179. 82. 111. 75. 63. 71. 36. 54. 58. 11. 87 nurses. 189 periodontitis. 12. 203 personality characteristics. 157 personality factors. 69. 82. 75. xi. 116. vii. 167. 87 neuroticism. 113. 12 parental involvement. 140. 160 passive. 163 oxidation. xi. 101. 114 outliers. 80. 75. 168. 76. 110. 83. 176. 153. 146. 13. 47 New Zealand. 71. 64 . 7. 23. 112. 178. 10. 141. 82. 188. 64 nicotinamide. 18. 164 North America. 82. 155. 96. 100. 24. 166. 74. 69. 196 periodontal disease. 15. 107. 129. 102. 186 peptides. 22. 44 negative mood. 4 nuclei. 75 perceptions. 87 obsessive-compulsive disorder. 87 neuropeptides. 163. 73. 17 openness. 202. 135. 101. 23. 47 nerve. 75. 16. 26. 64. 68. 185 nursing. 87 patient rights. 138. 187. 12. 111 Index orientation. 93. 101. 166. 35. 18. 90 nitric oxide synthase. 25. 16. 42. 189 peripheral blood. 91. 187 nucleus. 11. 13. 168 personal identity. 167. 181. 188. 25. 146. 88 peripheral blood mononuclear cell. 82 pathology. 74. 97. 29 occlusion. 196. 101 nitric oxide. 76. 148. 98. 187 O obesity. 93. 20. 166 organ. 22. 18 parents. 111 nutrition. 65. x. 74. 7. 203 nutritional deficiencies. 187. 134 network. 143. 125. 180. 55. 3. 101 oscillation. 189. 96. 187. 75 New South Wales. 75. ix. 181 personality traits. 108. 10 personality dimensions. 73. 72. 186 penicillin. 50. 36. ix. 199 palliative. 72 nervous system. 140. 69. ix. 25 pain. 4. 57 Pearson correlations. 74. 86. 65 organization. 45. 72. 71. 71. x. 50. 65. 137. 181. 10. 99. 177. 73. 106. 82. ix. 79. 168. 167. 106. x. 4. 25. 71. 93. 194. 198 negative affectivity. 183 pathways. 89 organism. 71 pathogenesis. 70. 76. 21. 203 parotid gland. 18. 95. 173 negotiation. 202 OCD. 159. 29. 88 perseverance. 76. 90 nitrogen. 178. 187. 113. ix. 94. 94. 173 periodontal. 102. 21 personality disorder. 102. ix. 3. 84 nervousness. 73. 179 negative reinforcement. 94. 193.

1. 51. 72 probability. 107. 92 puberty. 139 psychotic symptomatology. vii. 2. 16 psychological phenomena. viii. 7. 59. 97. 97. 49. 93. 58. xi. 139. 186 plasma levels. 197 pharmacological treatment. 4. 37. 15. 115. 21. 82. 134. 198 questioning. 111. 94. 93. 6. 194 psychological pain. 81. 177. 192 porosity. 151 projective test. 68. 149 psychological health. 168. 157. 186 proteinuria. 13 problem drinking. 14. 169. 97. 167. 175. 42. 155. 135. 29 pubertal development. 116. 26. 43. 93. 4. 65. 192 positive correlation. 38 psychosis. 86 pleasure. 193 psychiatric disorders. 4. 50. 44 pH. 172 persuasion. 23. vii. 1. 52. 79. 136. 175. 162. 181 psychoses. 155 psychologist. 7 physical activity. 193 professions. 57. vii. 109. 177 physical education. 97. 37. 168. 3. 50 prediction. 88. 3. 187 power. 192. 110. 88. 76. 23. 139. 165. 108. 85. 80. 14. 103. 173 potassium. 71. 128. 174. 6. 168 preference. 159. 141. 167. 153. 193 planning. 12. 24. 56. 156. 178. 183 primary school. 9. 167. 166. 43. 2. 128. 81. 17. 171. 80. 25. 202 plasma. 169 Q quality of life. 19. 86. 91. 101 psychotherapy. 15. viii. 133. 150 psychopathology. 100. 13. 75. 14. 79. 123. ix. 172 psychological problems. 138 reading. 125 reality. vii. 20 proteins. 17 pharmacotherapy. 16. 170. 129. 135. 177. 2. 20 psychiatric illness. 142 predictors. 113 215 prognosis. 155. 147. 69. 50. 133. 111. 130. 148. 135. 36 photographs. 13 preparation. 187 power relations. 12 placebo. 84 quartz. 15. 161. 134 PM. 79. 77. 185. 117. 2 punishment. 182 pressure. 20. 29 psychosocial stress. 106 phenomenology. 186 protocol. 34. 18. 193. 69 psychological variables. 196 physical abuse. 174. 195 program. 175. 42. 135. 113. 29 psychotic symptoms. 181 predictive validity. 123. 120. 42. 97 prostate. 30. 9. 60. 65. 96. 194. 31. 92. 146. 155. 4. 182 production. 122. 187. 86 protective role. 137. 140. 79. 8 psychiatrist. 43. 161 . 160. 96. 85 pregnancy. 64. 7. 146. viii. 81. 15. 43. 154 problem behavior. 165. 179. 194 rash. 63. 22. 2. 182. 200 population. 196 Prozac. 55. x. 78 poor. 66. 154. 3 psychiatric patients. 17. 136. 22 polyunsaturated fatty acids. 138. 17. 145.Index perspective. 6. 3. 13. 170. 82. 119. 159. 6. 160. 79. 130. 128. 91. 187. 202 psychometric properties. 75. 164. 149 psychology. 80. 45. 157. x. 112. 130 positive feedback. 194 prevention. 117. 106. 174. 188. 129. 93 principle. 110. 156. 174 positive reinforcement. 15. 13. 171. 78. 140. 176 rating scale. 160. 113 physical health. 20. 101 premature death. 11. 81. 179 public health. 89. 195. 56. 47. 36. 146 psychological value. ix. 72. 198 preparedness. 44. 38. 186. 170. 169. 188. x. 69. 133. 78. 5. 11. 112. 128. 71 R range. 169. 45.

80. 160. 112. 147. 24. 53. 169. 108. 165. 81 self. 10. 50. 159. 176. 177. 101. 159. 194 self-monitoring. 18. 186. 153. 191. 56. 175. 86. 5. 42. 125. 177. 54 recovery. 137. 9. 128. 142. 46. 12 repression. 2. 154. 133. 178. 119. 100 selective serotonin reuptake inhibitor. 42. 175. 138. 20. 5. 155. 178. 93. 10. 139. 188 security. 12. 71. 71. 58. 134. 105. 134. 156. 4. 19. 41. 8. 108. 165. 26. 17. 169. 125. 174. 189. 166 self-concept. 130. 194 scurvy. 127. 14. 56 S sacrifice. 12 regulators. 161. 174. 50. 147. 42. 3. 26. 127. 25. 203 self esteem. 150. 16. 107. 28. 3. 41. 142. 21. 178 reinforcers. 38 school. 50. 135. 159. 24. 179. 18. 192. 173. viii. 167. 10. 30. 142. 106 relationship. 154. 10. x. x. 92 right to life. 162. 107. 153. 16. 8. 4. 29. 42. 6. 100 self-discrepancy. 53. 3. 132. 57. 19 self-destructive behavior. 150. 11. 87 recognition. 30. 124. 83 religiosity. 50. 28. 183 satisfaction. 113. 139 reduction. 12 reputation. 3. 194 self-image. 143 self-esteem. 197 salivary glands. 202 schizophrenia. 157. 193. 148. 181. 34. 193. 153. 176. 157. 145. 137. 164. 51. 11. 114. 7. 182 risk-taking. 23. x. 167. 173 school performance. 98. 6. 79. 86. viii. viii. 162. 11. 110. 171. 180. 33. 6. 185. 9. 107. 196 risk factors. xi. 12. 22. 20. 109. 170 relapses. 194 sampling. 38. 203 self-consciousness. 11. 29. 151. 55. 65. 97 resolution. 130. 155. 170. 138. 189. 186 search. 45. 123. 100. 44. 109. 53. 142. 46 saliva. 194. 93. 154. 54. 107. 17. 166. 54. 125. 163. 146. 31 scientific knowledge. 148. 120. 92. 165. 94 resources. 14. 55. 7. 203 reliability. 44. 152. 53. 134. 102. 130. 7. 53. 50 semantics. 66. x. 166. 13. 34. 167 religious beliefs. 44 recall. 101. 35. 5. 6. 39. 65. 183. 147. 101. 198 reflexes. 19 self-regulation. 68. 65 secondary school students. 15 scores. 45. 175. 69 relevance. vii. 153. 49. 9. 20. 13. 132. 8. 2. 93. 173. ix. 100. 5. 162. 168. 6. 50. viii. 167. 66. 192. 112. 133. 141 recurrence. 55. 171. 106. 22. 150 receptors. 55 resins. 123. xi. 163. 54. 187. 111 self-mutilation. 155. 4. 16. 152. 6. 175 reconcile. 93. 109. 157. 93. 13. 54. 12. 174. 154. 19. 146. 182. 109 replacement. 49. 14 routines. 156. 138 secretion. 155. 173. 74. 8. 110 reinforcement. 140. 194. 36. 12. 83 responsibility. 173. 1. 146. 38. 36. viii. 128. 22. 49 rehabilitation. 82. 187. viii. 100. 146. 123. 155. 111. 72 regression. 35. 186. 38 remission. 70. 13. 51. 3. 52. 74. 164. 131. 8. 101 rhythm. 172. 72. 157 self-efficacy. 145. 94 safety. 21 selectivity. 148. 178. 41. 5. 26. 163. 150. 198 resistance. 9. 58 . 2. 103. 2 respiratory. 143. 79. 89. 189. 5. 164 reconstruction. 111. 2. 165. 156 self-awareness. 8 self-destruction. vii. 69. 14.216 Index reasoning. 191. 92. 26. 174. 44. 170. 2. 197. 42. 199 relatives. 12. 188. 173. 181. 96. 96. 151. 161. 199 sample. 9. 185. 109. 162 relationships. 68. 133. 109. 56. 188. 56. 57 risk. 99. 4. 168. 152. 31. 11. 64. 14. 152. 129. 167. 14. 124. 132. 97. 116. x. 56. 167 schooling. 93. 55. 10. 13. 171. 31. 81. 113. 172. 151. 180.

68. 15. 183. 75. 64. 165. 17 summaries. 126. 14. 182 swelling. 52 social control. 57. 174 students. 99. 130. 180 speech. 8 sialogram. 84. 116. 41. 162. 71. 89. 12. 44. 25. 49. 142 strength. 112. 98. 69. 15. 11. 9. 56 survival. 146. 196 suicidal behavior. 165 substance use. 98 significance level. 187 statistics. 167. vii. 166. 90. 13. 70. 26 suicide rate. 63. 16. 12. 163. 100 social class. 7. 150. 172. 49. 97. 71. 8. 150 striae. 187. 71. 69. 6. 7. 15. 6. 69. 164. 84. 95. 112. 112. 8. 57 shares. 170 Sun. 13. 95. 127 standards.Index sensation. x. 14. 167 sexual contact. 2. 187 sibling. 135. 73. 118. 181 shape. 13. 4. 121. 202 signalling. 127. 54 substance abuse. 22. 6. 146. 58. 12 sucrose. 18. 186 strategies. 122 shyness. 2. 15. 37. 165. 187 stomatitis. 154. 88. 4. 181 stages. 12 social behavior. 23 suicidal wishes. 81. 1. 93. 97 sensitivity. 77. 48 suppression. 14 small intestine. 18. 166. 187. 102. 43. 97. 56. 5. 100. 84 surveillance. 12. 178 sensation seeking. 141 solid tumors. 19. 146. vii. ix. 153. 120 software. 111. 147. 92. 112. 69. 140. 90. 128. 166. 191 sexual behavior. 102 shame. 84. 82. 96. 75 signalling pathways. 71. 11. 187. 21. 202. 106. 188. ix. 10. 56. 6. 169. 190. 150. 79. 127. 43. 176 serotonin. 89 supervision. ix. 72. 69. 112. viii. 169. 2. viii. 15. 11. 1. 147 subjective experience. 197 skeletal muscle. 162 217 sodium. 111. 76. 80. 191. 65. 31 sites. 97. 196 sugar. 4. 68. 85. 201 standard deviation. 136. 22. 101 sexuality. 99 suicide attempters. 9. 5. 160 side effects. 58 social environment. 65 series. 17. 2. 96. vii. 169 stomach. ix. 189 streptococci. 67. 69. 167. 15. 2. 17 serum. 203 services. 171 social support. 38. 7. 25. 13 suicide attempts. 93. 5. 170 shaping. 7. 11. 68. 128. 9. 64. 132. 166 spectrum. 168. 54. 101 SPSS. 66. 75. 86. 93 sexual orientation. 87. 93. 193 stressors. 89. 13. 7. 3. 71. 72 smoking. 12. 74. 156. 52 social events. 42. 160 sharing. 68 skills. 155. 178 sensations. 3. 14 suicide. 94. 93. 191. 106 stigma. 75. 114 severity. 68. 10. 95. 56 stimulus. 23 suicidal ideation. 100. ix. 115. 10. 193 stress. 85. 102. 174. 4. 133 social learning. 31. 17. 42. 168. 97 species. 10. 19. 140 social comparison. 157 starvation. 132. 94. 129. 16. 131. x. 183 social context. 100. 35. 11. 11. 192 specificity. 151 stability. 191. 9. 3. 90 somatization. 187 sialography. 24. 189. 28. 26. 137. 78. 18. 20. 204 . 179. 172. 198 separation. 31 structural equation modeling. 91. 23. 19. 3. 63. 132. 107. 98 siblings. 49. 78 sign. 7. 22. 2. 102 sepsis. 166 sensing. 71. 5. 13. 44. 73. 9. 63. 73. 193 sertraline. 166. 73 signals.

164. 67. 99 therapists. 95. 43. 44. 188. 97. 22. 47 transduction. 20. 54. 171. 187 . 174. 64. 106. 72 targets. 60. 86. 100. 65. 69. 133. 27. 56. 72. 24 urea. 87. 193 tricyclic antidepressant. 66. 197 total energy. 153. 116. 139. 36. 80. 31. 1. 89 United States. 145. 88. 10. 74. 131. 116. 180 symptom. 83. 165 threat. 76. 102. 37. 91. 18. 163. 65. viii. 36 teachers. 43. 64. 105. 169. 159. 181 temperature. 127 testosterone. 54. 41. 168. 129. 83 training. 198 teenagers. 161. 201 television. 82 twins. 120. 141. ix. 160 synthesis. 66. 177. 55 terminally ill. 179 television viewing. 16. 181. 33. ix. 83. 196. 192 therapeutic approaches. 95. 137 trend. 98. 67. 11. 16. 70. 50 therapeutic relationship. 16. 77. 75. 82. 199 thinking. 125. 76. 175. 140 uniform. 123. viii. 125. 181 television advertisements. 130. 139. 174. 89. 50. 78 tracking. 186. 35. 125. 97 threats. 91. 191 tension. 182. 140. 90 tumour growth. 55. 189. x. 37. 68. 128. 89. 129. 134. 29. 78. 132. 178 symptoms. 91 therapeutic encounter. 15. 86 tumor growth. 98. 90. 77. 65. 19. 87 T target organs. 54 transactions. 153. 93. 114. 155. 49 threshold. 117. 185. 161. 109. 13. 52. 77. 140 transition to adulthood. 185 umbilical cord. 102. 194 trajectory. 16. 87 tumor. 60. 36. 59. 148. 141 transmission. 135. 192 TNF. 49. 101 UN. 45. 84 test scores. 2. 156. 88. 57 therapy. 97 United Kingdom. 157. 16 therapeutic goal. 99. 151. 71. 183. 56. 16. 196. 47. 19. 2. 8. 30. 16. 139 teaching. 13 tryptophan.218 Index tissue. 48. 169 technology. 12. 154. 29. 86. 11. 123. 119. 155. 177. 168. 92. 55 traumatic experiences. 17. vii. 124. 57. 106. 173. 190. 128. 83. 87. 96. 146. 196. 19. 191. 12 transitions. 4. 41. 64. 73. 112. 25. 200. 147. 97 transformation. 83. 132. 86 tobacco. xi. 65. 69 transference. 22. 167. 8. 149. 94 trust. 117. 56. 136. 98. 173. 41. 13 university students. 73. 35. viii. 109 undernutrition. 134. 24. 33. 32. viii. 30. 174. 58. 171. 75. 136. 115. 199. 181. 191. 198. 130. 68. 8. 96. 12 teeth. 79. 100 tumor cells. 35. 170. 68 therapeutic interventions. 192. 7 treatment methods. 88 TNF-alpha. 146. 18. 192. 110. 83. 71. 163. 42. 162. 172. 16. 79. 142. 67. 183 systems. 55. 86. 193. 180. 179. 45. 133. 137. 11. 63. 141 traits. 106. 153 trial. 47. 133. 118 toxicity. 93 theory. 32. 148. 55. 174. 180. 12. 194. 167 tonic. 46. 87 triggers. 28. ix. 85. 160. 81. 19. 138. 2. 77. 87. 163. 150. 169. 125. 134. 83. 81 taxonomy. 53. 4. 13. 199. 66. 79. 21. 77. 79 trauma. 186. 169. 125. 116. 57. 173. 176. 86 uncertainty. 172. 65. 164 time. 95. 43 transition. 137. 187 transport. 96. 201 U UK. ix. 100. 110. 179 syndrome. ix.

182 values. 55. 133 weight loss. 132. 191. 190 variance.Index 219 V vacancies. 56. 54. 165. 190. 48 women. 131. 154. 36. 135. 166. 112. 181. 51 Western countries. 151. 120 voice. 113. 83. 160 variable. 133. 102. 38. 112. 100. 177. 151. 136. 156. 123. 19. 147. 95. 53. 20. 23. 17. 43. 153. 197 wear. 197. 137. 92. 121. 141. 117. 112. 139. 189. 7 wild type. 163. 22. 8. 167. 203 words. 171 work. 132. 145. 162. 113. 157 weight control. 10. 141. 174 workers. 6. 108. 141. 173. 48. 101. 27. 168. 14. 106. 26. 130. 26. vii. 167. 120. 31. 49. 191 World Health Organization. 153. x. 147. 108. 204 web. 108. 157. 115. 9. 114. 101 weight management. 140. 139. 4. 83. 186. 155. 37. 109. 2. 170. 160. 47. 102 water. 136. 11. 139. 1. 204 vulnerability. 42. 188 W walking. 26 worry. 151. 2. 173. 168. 145. 156. 92 young women. 117 violence. 15. 137. 173 variation. 138. 168. 183 weight gain. 179. 134. 107. 120. vii. 26. 134. 174. 140. 183 validity. 36. 149. 74 withdrawal. 45. 154. 83. 147. 7. 116. 146. 187. 168. 16. 150. 135. 119. 107. 164. 18 viscosity. 21. 193 variability. 71 validation. 178 Y yeast. 155. 117. 203. 24. 57 withdrawals. 154. 119. 7. 146. 173. 178. 53. 179. 161. 169. 152. 112. 85. 162. 190. 116. 172. 114. 193 young men. 150. 136. 171. 108. 31. 114 vagus. 189. 197. 38. 124 WTO. 35. 185. 79. 161. 81. 145. 130. 162. 155. 193 variables. 22. x. 137. 151. xi. 106. 178. 16. 107. 194. 187. 128. 142. 97 voicing. 54. 114. 198. viii. 88. 95. 168. 138. 148. 98. 22. 195. 91. 108. 55 vomiting. 57. 61. 193. 61 X xerostomia. 167. 180. 155 . x. 148. 92. 4. 76. 141. 174. 152. 36. ix. 53. 124. 188 vitamins.