Anorexia Nervosa and Bulimia Nervosa

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, Inc.

New York
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Library of Congress Cataloging-in-Publication Data

Anorexia nervosa and bulimia nervosa : new research / Pamela I. Swain (editor).
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-61668-120-3 (E-Book)
1. Eating disorders. 2. Anorexia nervosa. 3. Bulimia.
[DNLM: 1. Anorexia Nervosa. 2. Bulimia. WM 175 A615 2005] I. Swain, Pamela I.
RC552.E18A55 2005
362.2'5--dc22 2005005548
Published by Nova Science Publishers, Inc. New York

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

Dissatisfaction and Self Concept in Women
with Bulimia Nervosa and Binge Eating Disorder 145
Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh,
Monique Potvin-Kent and Hany Bissada
Chapter VIII Integrating Personality and Environmental
Risk Factors for Bulimia Nervosa 159
Sarah Fischer, Gregory T. Smith and Melissa A. Cyders
Chapter IX The Impact of Anorexia and Bulimia Nervosa
on Oral and Dental Health 185
Alex Milosevic
Index 205
Preface
The abundance of food in the developed countries of the world has seemingly spawned
an epidemic of disorders connected to the food. Extremes such as intensive concern about
one’s body image and total disregard for it have resulted in countries which contain
enormous segments of the population who are either obese and proud of it or bordering on
anorexia nervosa. This new book gathers state-of-the-art research from leading scientists
throughout the world which offers important information on understanding the underlying
causes and discovering the most effective treatments for eating disorders.
Suicide in anorexia nervosa and bulimia nervosa is a major cause of death as reported in
chapter I. Meta-analytic studies have shown that individuals suffering from anorexia nervosa
and bulimia nervosa commit suicide more often than their counterparts in the general
population. The percentage of suicide among patients with eating disorders (not
differentiated) ranges from 1.8% to 7.3%. Risk factors for suicide and attempted suicide
(which in many cases results in successful suicide) in anorexia nervosa and bulimia nervosa
include: purging type, chronic disease, obsessive symptoms, drug abuse, major depression,
lack of impulse control, and low body mass index (BMI) at presentation (for anorexia
nervosa). A few studies have suggested that suicide is the major cause of death among
patients with anorexia nervosa, refuting the assumption that inanition generally threatens the
life of these patients. Data concerning suicide in bulimia nervosa, on the other hand, are still
scarce, as more long-term follow-up studies need to be completed before the risk for bulimia
nervosa may be compared with that for anorexia nervosa. Suicide attempts are easily found
among cohorts of patients with bulimia nervosa, which constitutes a risk factor for completed
suicide. Comorbidity between anorexia nervosa or bulimia nervosa and other psychiatric
disorders is a frequent event, as in the case of affective disorders and personality disorders.
No doubt suicidal behavior is underestimated amongst patients with anorexia nervosa and
bulimia nervosa. Young women are heavily represented among these patients; therefore
suicidal behavior is gender-related. An effort to reconcile with the subject of suicide and a
better evaluation of these patients’ psychopathology should improve suicide prevention
strategies among these individuals. According to World Health Organization estimates,
suicidal behavior and eating disorders are alarming phenomenon among young people.
Preventive strategies of suicide among these patients should include pharmacological
viii Pamela I. Swain
treatments, psychotherapy and school-based interventions involving crisis management, self-

esteem enhancement and the development of coping skills and healthy decision making.
Body image disturbance is an important clinical feature on eating disorders and was
characterized by the Diagnostic and Statistical Manual of Mental Disorders, fourth Edition
(DSM-IV), as one of the diagnostic criteria for these pathologies. Although the presence and
importance of body image disturbance in eating disorders are well established, the
psychopathological nature of this symptom is not yet defined. Chapter II explores the
presence of obsessive-compulsive and delusional features of the ‘Body Image Disturbance’ in
anorexia and bulimia nervosa. Sixteen women with anorexia nervosa and eleven women with
bulimia nervosa were compared regarding their responses to the Yale-Brown Obsessive
Compulsive Scale (Y-BOCS) and to the Delusional Features Assessment Scale. Variables
were analyzed with the Fisher’s Exact Test and Mann-Whitney non-parametric test (U).
Patients with anorexia nervosa had scores significantly higher than bulimic patients in the
Delusional Features Assessment Scale and no differences were found between the groups
regarding obsessive-compulsive features. The analysis of the psychopathological differences
of ‘Body Image Disturbance’ in anorexia and bulimia nervosa has diagnostic implications.
Anorexia nervosa is often chronic, with one of the highest death rates for psychological
conditions. Law can compel treatment, but is rarely invoked, at least formally (though the
strategic possibilities of orders confers internal authority within the clinical setting). Instead,
‘control’ (or management) is exercised diffusely, through disciplinary practices embedded in
everyday clinic life, such as daily routines of eating and washing, behavioural ‘contracts’,
regular surveillance and measuring, interactions with staff, visits and activities. The
regulatory regime not only touches on such ‘practices’ but also targets ‘identities’ (including
self-image, and attitudes to the body) and what Goffman called the ‘moral career’ of the
patient (eg learning to play the ‘patient role’, to ‘be’ an ‘anorexic’). Chapter III argues that it
is not the clumsiness of the law, or the success of less restrictive options which explains why
law is so infrequently engaged. Rather, based on an interpretation of Foucault, the authors
conclude that the regulatory regime that shapes treatment of anorexia nervosa, is ‘the law’, in
a sense. The regime of governmentality within the clinic is shaped by practices which
operationalise ‘duty of care’, or translate medical expertise into medical authority, or show
how interactions between ‘experts’, ‘carers’ and patients are mediated through conventions
and rules, or which conscript ‘empowerment’ as control. The patient learns to provide
consent ‘freely’, to make the ‘correct’ choices, to accept the ‘empowerment’ regime that is
made even more convincing by the threat of legal intervention. In time the constraints learned
in this way become part of the new role, that of the ‘recovering’ patient. The ‘fiction’ of
acting ‘responsibly’, employed so hesitantly at first, becomes part of the new identity. The
patient has become an active participant in the governance of self.
Anorexia and reduced food intake are relevant issues in the management of patients
suffering from acute and chronic diseases, including sepsis, cancer, chronic liver failure,
chronic renal failure, etc. In acute diseases, anorexia does not represent a primary therapeutic
target, since effective treatment of the underlying disease rapidly ameliorates food intake. In
chronic diseases, anorexia impacts on patients’ prognosis, since it contributes to the
development of malnutrition, thereby increasing morbidity and mortality, and impinges on
quality of life. Accumulating evidence indicate that anorexia associated to different diseases
Preface ix
is multifactorial in its pathogenesis, and suggest that most of the hypothalamic neuronal
signalling pathways modulating energy intake are involved. Chapter IV reports a number of
factors are considered mediators of anorexia, including hormones [e.g., leptin], neuropeptides
[e.g., NPY], cytokines [e.g., IL-1, IL-6, TNF] and neurotransmitters [e.g., serotonin and
dopamine]. Their modes of action do not appear to be separate and distinct, rather they are
closely inter-related. However, convincing evidence suggest that a hierarchical organization
exists in which cytokines play a key role, triggering the complex neurochemical cascade
which leads to the onset of anorexia. Cytokine increased expression during disease inhibits
the hypothalamus to appropriately respond to peripheral signals, by persistently activating
anorexigenic systems and/or inhibiting prophagic pathways. Hypothalamic monoaminergic
neurotransmission may significantly contribute to these effects. Thus, the optimal therapeutic
approach to anorectic patients should be based on both changes in dietary habits, achieved
via nutritional counselling, and drug therapy, aimed at interfering with cytokine expression or
hypothalamic monoaminergic neurotransmission.
The number of boys affected by eating disorders is increasing. The fact that the numbers
for eating disorders among boys are so low is probably due in part to underdiagnosis.
Although adolescent girls are still the group primarily affected by eating disorders, nearly
every tenth person suffering from an eating disorder is male. The lifetime prevalence of any
eating disorder has been reported as 17.9% among women and 6.5% among men. There are
triggers for the disorders among boys that are different from those that have been identified
among girls. These include excessive physical activity, a fragile sexual identity, demanding
requirements or expectations in the areas of competitive sports, muscle building, and ideals of
physical perfection. There are also differences in the pathologies. For example, boys often
exhibit a different form of body image distortion, one that is more focused on masculine
muscular form. They also show less shame concerning binge eating. The fact that anorexia
and bulimia are much more difficult to diagnose among boys has led to a situation in which
only the most severe cases are successfully diagnosed. This situation is exacerbated by the
fact that bulimia is perceived by the public as a disease that only affects girls, with the result
that affected boys often have to struggle with emotions of shame and denial. Chapter V
reports on three clinical cases that illustrate some of the differences between male and female
anorexia and other aspects like the wide range of psychological and physical symptoms, the
different therapeutic approaches, and kinds of treatment. The authors focus on the patients’
personal histories and the psychological conditions in the parents. Discussion of the results
encompasses psychodynamic and systemic issues.
Eating disorders (ED) have been treated in Brazil since 1992 with the creation of the ED
Unit of the University of São Paulo, a public service that has treated 1,794 patients, mainly
white, reasonable educated and aged between 21 and 40 years. Food intake and eating
patterns and behaviors are disturbed in bulimia nervosa (BN). Food intake is defined as the
food and nutrients that compose the diet, while eating patterns are the meal frequency,
regularity and schedules, and eating behaviors are the attitudes, beliefs and relationship with
food. In Brazil, the effect of multiprofessional treatment in BN had never been examined.
Even in developed nations, only the frequency of bulimic symptoms has been evaluated. In
chapter VI, the Eating Disorder Inventory, Three-Factor Eating Questionnaire, Dutch Eating
Behavior Questionnaire and Restraint Scale were used to analyze eating behaviors, although
x Pamela I. Swain
these questionnaires focus especially in dietary restraint, leaving the other eating behaviors’
aspects uncovered. Thirty-nine women with BN (according to DSM-IV criteria) were
followed. Treatment was composed by 12 weeks of cognitive-behavior therapy,
pharmacotherapy and nutrition counseling. Measurements were made before and after
treatment, and after three months. Patients recorded their food intake and occurrence of
compulsions and purges in a diary. They fulfilled the EAT, BITE and BSQ, and also an
eating attitudes questionnaire, especially developed for this research. Non-parametric
statistics were used to test for differences among the three moments. The authors observed an
improvement in clinical symptoms; at the end of following 97.5% of the patients did not
fulfill criteria for BN anymore. Scores of EAT, BSQ and BITE-symptoms decreased after
treatment and even more after the later following. Nutrients intake did not alter, even though
energy content of the meals followed by vomit decreased. Number of meals increased and
patients did more meals seated, with company and less anxious. The belief of automatically
gaining weight after a meal, and guilty and worry after eating a “forbidden” food decreased.
Nevertheless, most of them remained hating the hunger sensation, having difficulties with
food choices and not believing that they could have a normal diet and a normal weight. Based
on the questions used to assess eating attitudes, they are now developing an eating attitudes
questionnaire, which will be psychometrically tested. This study supports the idea of the
importance of food issues and behaviors in ED, because even the patients that had a clinical
improvement remained with a complicated relationship with food, which can contribute to
relapses.
As described in chapter VII, it was hypothesized that higher levels of actual-desired BMI
discrepency (ADBD) would be associated with higher binge eating symptoms, lower self
concept, and higher body dissatisfaction for a clinical sample of women with Bulimia
Nervosa (BN) and Binge Eating Disorder (BED). A theoretical frame for ADBD was put
forward based on self discrepancy theory. Also hypothesized was that women with BN would
have greater eating and self related pathology than those with BED. Fifty-one participants
diagnosed with BN and 41 with BED drawn from a clinical sample completed questionnaires
assessing eating disorder and general psychopathology. Greater ADBD was related to greater
body dissatisfaction for the BN and BED groups, and lower self concept for the BN group.
Those with BN had more self-related pathology. ADBD can be easily assessed by clinicians
and may be used as an index of body dissatisfaction and overall self concept. ADBD may be
a vulnerability factor for developing an eating disorder for women.
Heritability studies provide a general framework for understanding risk for bulimia
nervosa (BN): liability is a function of both genetic and environmental factors. Chapter VIII
proposes a specific model that integrates identified heritable and environmental risk factors
for BN. Trait urgency, the tendency to act rashly in response to distress, is a heritable risk
factor that increases the likelihood that one will engage in some form of rash, maladaptive
behavior pattern (such as BN). The specific form of one’s maladaptive behavior is a function
of learned experiences from one’s environment. Individuals who learn to expect alleviation of
negative mood from eating, and overgeneralized life improvement from thinness, are more
likely to engage in bulimic behaviors. Thus, the general, heritable risk from high levels of
urgency is likely to become expressed as BN when one learns to expect benefits from eating
Preface xi
when distressed and extreme benefits from thinness. The proposed process is empirically
supported and consistent with findings from heritability research.
The dental and oral health of individuals with an eating disorder has been largely under-
investigated and ignored as health care professionals focus on the general medical, dietary
and psychiatric/psychological needs of patients. Disordered eating and chaotic lifestyle may
affect patterns of caries (decay) and gum disease. Oral microbial flora, either in dental plaque
or saliva, could theoretically differ to normal flora as a consequence of repeatedly low intra-
oral pH secondary to self-induced vomiting (SIV). Parotid salivary gland enlargement and
altered salivary composition have been described. The presence of gastric acid in the mouth
can result in acid erosion, with disfiguring consequences to the dentition. The impact of
anomalous behaviours such as chaotic eating and self-induced vomiting upon the dental
health of eating disordered subjects may not be apparent to the subjects themselves or their
carers, be they physicians, psychiatrists, psychologists, nurses or relatives. Nonetheless, the
effects upon the teeth can be significant such that it has been postulated that the dentist may
be the first health care professional to suspect an eating disorder in an otherwise healthy
individual. The mouth is the first part of the digestive system and commonly exhibits signs of
disease occurring elsewhere. Chapter IX reviews the literature and illustrates the clinical
problems faced by real cases. Prevention will also be discussed.
In: Anorexia Nervosa and Bulimia Nervosa: New Research ISBN 1-59454-394-1
Editor: Pamela I. Swain, pp. 1-26 © 2006 Nova Science Publishers, Inc.
Chapter I
Suicide in Anorexia Nervosa

and Bulimia Nervosa
Maurizio Pompili1, Paolo Girardi,

Amedeo Ruberto and Roberto Tatarelli
Department of Psychiatry – Sant’Andrea Hospital
University of Rome “La Sapienza” - Italy
Abstract
Suicide in anorexia nervosa and bulimia nervosa is a major cause of death. Meta-analytic
studies have shown that individuals suffering from anorexia nervosa and bulimia nervosa
commit suicide more often than their counterparts in the general population. The
percentage of suicide among patients with eating disorders (not differentiated) ranges
from 1.8% to 7.3%. Risk factors for suicide and attempted suicide (which in many cases
results in successful suicide) in anorexia nervosa and bulimia nervosa include: purging
type, chronic disease, obsessive symptoms, drug abuse, major depression, lack of
impulse control, and low body mass index (BMI) at presentation (for anorexia nervosa).
A few studies have suggested that suicide is the major cause of death among patients
with anorexia nervosa, refuting the assumption that inanition generally threatens the life
of these patients. Data concerning suicide in bulimia nervosa, on the other hand, are still
scarce, as more long-term follow-up studies need to be completed before the risk for
bulimia nervosa may be compared with that for anorexia nervosa. Suicide attempts are
easily found among cohorts of patients with bulimia nervosa, which constitutes a risk
factor for completed suicide. Comorbidity between anorexia nervosa or bulimia nervosa
and other psychiatric disorders is a frequent event, as in the case of affective disorders
and personality disorders. No doubt suicidal behavior is underestimated amongst patients
with anorexia nervosa and bulimia nervosa. Young women are heavily represented
among these patients; therefore suicidal behavior is gender-related. An effort to reconcile
1
Maurizio Pompili, M.D.Sant’Andrea Hospital – Dep. of Psychiatry,University of Rome “La Sapienza”,Via di
Grottarossa, 1035-1039, 00189 Roma – Italy, maurizio.pompili@uniroma1.it
2 Maurizio Pompili, Paolo Girardi, Amedeo Ruberto and Roberto Tatarelli
with the subject of suicide and a better evaluation of these patients’ psychopathology
should improve suicide prevention strategies among these individuals. According to
World Health Organization estimates, suicidal behavior and eating disorders are alarming
phenomenon among young people. Preventive strategies of suicide among these patients
should include pharmacological treatments, psychotherapy and school-based
interventions involving crisis management, self-esteem enhancement and the
development of coping skills and healthy decision making.
Introduction
Suicidal behavior is identified as a major public health problem and a considerable drain
on resources in both primary and secondary health care settings in many countries worldwide.
Suicide is the ninth leading cause of death in the United States for all ages. Among teenagers
and young adults, it is the third most frequent cause of death. Approximately 40,000 to
50,000 Americans die every year by their own hand. According to World Health
Organization estimates, approximately 1 million people died from suicide, and 10 to 20 times
as many attempted suicide worldwide in the year 2000 (WHO, 2000a). This averages out to
one death every 40 seconds and one attempt every three seconds. Youth suicide, the third
leading cause of death among teenagers and young adults, accounts for more deaths in the
United States than natural causes combined for 15 to 24-years-olds, according to the National
Center for Health Statistics (2000). In Europe, according to the WHO Databank, suicidal
behavior among young people has increased over the past thirty years and statistics match
with those of the U.S. Each suicide has a serious impact on at least six other people and the
psychological, social and financial impact of suicide on the family and community is
immeasurable. The World Health Organization (2000b) recognizes suicide as a complex
problem for which there is no single cause, no single reason. It results from a complex
interaction of biological, genetic, psychological, social, cultural and environmental factors.
Shneidman (1985), who is considered the father of suicidology, has proposed the following
definition of suicide: “Currently in the Western world, suicide is a conscious act of self-
induced annihilation, best understood as a multidimensional malaise in a needful individual
who defines an issue for which the suicide is perceived as the best solution”. We shall
continue with another citation by Edwin Shneidman (1993) who suggested “that suicide is
best understood not so much as a movement toward death as it is a movement away from
something and that something is always the same: intolerable emotion, unendurable pain, or
unacceptable anguish. Reduce the level of suffering and the individual will choose to live”.
Profound psychic pain is a major part of the clinical picture, so much so that self-harming
thoughts and behaviors, including self-mutilation, suicidal ideation, gestures and attempts,
may become a way of attempting to cope with this pain and the marked social isolation that
results from eating disorders (Manley and Leichner, 2003). The best way to prevent suicide is
to learn what is causing the distress, the tension and anguish – and the work to treat these
emotions within the suicidal person. Several governments around the world have established
suicide prevention programs. A major reason for this has been the very large increase in
suicide in young people, especially males, seen in many countries. Retrospective studies
indicate that the absolute majority (81-100%) of suicides occurs in subjects with a psychiatric
Suicide in Anorexia Nervosa and Bulimia Nervosa 3
illness, depression being the most common diagnosis (Lonnqvist, 2000). There has been
recent recognition of a very definite increased risk for suicide in girls with eating disorders
(Apter et al., 1995). A few studies suggested that suicide is the major cause of death among
patients with anorexia nervosa (Toltrup et al. 1985; Patton, 1988; Santonastaso, et al. 1991);
refuting the assumption that inanition generally threatens the life of these patients.
The analysis of suicide and attempted suicide in patients suffering from anorexia nervosa
and bulimia nervosa constitutes a focal point for an appropriate comprehension of the
psychopathology of these individuals. People with eating disorders usually evoke the idea of
self-wounding features, aiming at destroying the body slowly rather than through a suicidal
act. This misconception often leads to ignoring the risk of suicide. Few studies, in fact,
analyzed suicidal behavior in-depth among patients with eating disorders, in particular in
patients with anorexia nervosa and bulimia nervosa, and there is no doubt that suicidal
behavior is an underestimated phenomenon.
Great importance can be placed upon the course of the illness and the follow-up period
considered for a correct evaluation of the suicidality among this class of patients (Theander,
1985). According to various authors, suicide occurs not only in the late phases of the illness
but above all in periods of symptomatic remission (Jeammet et al., 1984; Bruch, 1988).
Frequent hospitalizations and, in the case of the anorexic patients, a lower weight at the first
consultation are two predictive factors of suicidal behavior (Morgan and Russell, 1975; Hsu
et al., 1979; Patton, 1988); also, an important risk factor is a later onset of illness (Patton,
1988).
Eating disorders are often comorbid with depression, a feature identifiable in histories of
suicidal individuals (Russell, 1979). Some scholars believe that eating disorders represent a
form of affective disorder (Cantwell et al., 1977; Winokur et al., 1980; Hudson et al., 1983)
and antidepressant medications have been employed. Viesselman and Roig (1985) suggested
that response to an antidepressant does not necessarily mean that the disorder being treated is
depression; patients with eating disorders may be responding to the anti-panic nature of the
drugs rather than to their antidepressant characteristics. Most authors believe that suicidal
behavior among patients with eating disorders is independent of the existence of mood
disorders and stress the existence of suicidal behavior among patients with eating disorders. It
has been suggested that depressive disorders in anorexia nervosa are, in general, secondary to
eating disorders (Ivarsson et al., 2000). It has been stressed that another cause of depression
secondary to anorexia nervosa is reactive distress related to disturbed eating behavior,
concerns about body-image, poor self-esteem, shame and guilt (Halmi et al., 1991; Cooper,
1995). Depression disorders in patients with anorexia nervosa may be related to personality
disorders, which have been shown to have high prevalence in anorexia nervosa patients
(Gartner et al., 1989; Kennedy et al., 1990; Wonderlich et al., 1990; Herzog et al., 1992;
Skodol et al., 1993; Braun et al., 1994; Halmi, 1995), in particular, avoidant, borderline and
obsessive compulsive personality disorders (Piran et al., 1985; Braun et al., 1994; Gillberg et
al., 1995; Halmi et al., 1999). Milos et al. (2004a) investigated comorbidity of psychiatric
disorders with eating disorders. They found that the most common Axis I disorders were
affective, anxiety and substance-related disorders; for Axis II, most common were personality
disorders of cluster C; only subscale B of the Eating Disorder Inventory was associated with
the presence of cluster B disorders. According to these authors the symptomatology of cluster
B patients often impairs patients’ ability to perceive and recognize their own emotional states
and processes, which may in turn decrease the probability that they will endorse items
describing psychopathology. This assumption may explain why these patients are not
represented in studies employing questionnaires, requiring concentration, reading items
carefully, and deciding the most appropriate answer. Spindler and Milos (2004) found that
among bulimic subjects, axes II comorbidity, especially cluster B disorders and to a lesser
degree depressive/negative personality disorders, was associated with a history of inpatient
treatment. History of suicide attempts was also linked to inpatient experience, but not to a
history of underweight. Van Hanswijck de Jonge et al. (2003) reported results of an
investigation among patients with eating disorders. They found that there was a continuum of
severity in borderline personality disorder pathology between the groups of patients with
bulimia nervosa, binge eating and obesity. They observed that personality disorder
difficulties are particularly represented in patients who binge eat. Karwautz et al. (2003)
investigated personality disorders and personality dimensions in anorexia nervosa and found
that cluster analysis based on their Temperament and Character Inventory (TCI) identified a
subgroup of patients characterized by low levels of novelty seeking, self-directedness, and
cooperativeness and high levels of harm avoidance. Bruce et al. (2004) found that women
with bulimia nervosa and comorbid avoidant personality disorder may be characterized by
interpersonal submissiveness and avoidance, affective instability, self-harm and behavioral
inhibition in response to threat. A history of suicide attempts is frequent in women with
diagnosis of anorexia nervosa or bulimia nervosa and major depression. Bulik et al. (1999)
found that in the bulimia nervosa group of their sample, suicide attempts were significantly
more common in subjects with a lifetime diagnosis of major depression; women with
anorexia nervosa, on the other hand, were equally likely to attempt suicide, regardless of the
presence of lifetime major depression. The authors concluded that depression may be a
contributing factor to suicide attempts in bulimia, but previous suicide attempts in the sample
of women with anorexia nervosa presented in the study appear independent of affective
disorders. Women suffering from bulimia nervosa also showed a statistical trend to report a
less severe intention to die. Russell (1979) reported that 87% of patients with eating disorders
also had depressive symptoms and 37% of them had attempted suicide; 45% of these attempts
were serious suicidal gestures. Similar percentages have been reported by Vasselman and
Roig (1985). A higher frequency of death wishes and suicidal feelings in the bulimarexic
group may be due to their feeling more out of control because of the vomiting behavior and
its attendant fear of discovery, shame, secret, or disgust; or it may be a clinical consequence
of the possible increase of bipolar and secondary depression in this group. Also, among
patients of this sample, there was a higher frequency of conduct, antisocial, and hysterical
diagnosis. Patients had planned and carefully thought out their suicide attempts and they told
no one of their plans.
Both anorexia nervosa and bulimia nervosa share the disturbance in the way in which
one’s body or shape is experienced. The body is experienced with intense fear because it may
gain weight or become fat or, as in the case of bulimia nervosa, self-evaluation is unduly
influenced by body shape and weight. Orbach et al. (2001) pointed out that the body is a
source of satisfaction and pleasure that enhances the tendency for life preservation and
attraction to life and serves as a shield against self-destruction, while bodily dissatisfaction
may increase suffering and intensify self-destructive attitudes. Extreme negative life events,
such as physical and mental traumas, can result in great alteration in perception, attitudes,
feelings, and experiences of the body in the form of body rejection, body hate, bodily
detachment, insensivity and indifference to sensation, sense of lack of control, and loss of
bodily boundaries. Such changes may facilitate self-destructive behavior when under stress.
Orbach et al. (2001) investigated a sample of adolescents to examine the relationship between
cognitive and affective attitudes toward the body, body experiences and suicide. They found
that attitudes and feelings toward the body, protection of the body, and body aberration were
the three factors that differentiated the suicidal group and the two nonsuicidal groups. Also,
the sense of lack of control over the body also distinguished the suicidal group from the
normal group. Among this sample, an interrelationship between attraction to death, lack of
body protection, and body aberration emerged. The authors interpreted this result, indicating
that inability or unwillingness to protect the body and dissociative bodily tendencies (body
aberration) are strongly associated with suicidal tendencies. They proposed that enjoyment in
life is strongly linked to good feelings about the body and vice versa. Lack of enjoyment in
life and death wishes are strongly associated with a hateful relationship and lack of comfort
with the body. Suicidal tendencies and body image and experience have been investigated in
a sample of patients with anorexia nervosa and compared to suicidal female adolescent
inpatients (Stein et al., 2003). The authors found that female anorexia inpatients with no
evidence of overt suicidal behavior demonstrated elevated suicidal tendencies that are similar
to those of suicidal psychiatric inpatients. These self-destructive tendencies are highly
associated with a pervasive sense of disturbance of body image and experience. Many
patients with borderline personality disorder suffer from a sense of body alienation that
results from the domination of their body representation by hostile introjects (Maltsberger,
1986). Individuals with anorexia nervosa and bulimia nervosa show a very peculiar attitude
toward their bodies. In one way, they believe that their body is the most precious and
important thing that surrounds them, in another, they fear their body and struggle with it as an
ominous enemy that has to be killed, which deserves a suicidal gesture. Mazza and Reynolds
(2001) investigated self-reported psychopathology in a school-based sample of 456 suicidal
and non-suicidal adolescents. They found that females who engaged in suicidal behavior
reported experiencing significant levels of symptomatology associated with anorexia nervosa;
this led the authors to suggest that body-and self-image may be important factors for
clinicians and mental health professionals to examine when working with suicidal female
adolescents.
Suicide and Attempted Suicide

in Anorexia Nervosa
According to Patton (1988) suicide is the main cause of death among individuals with
anorexia nervosa, typically performed with drug overdose and alcohol. Norring and Sohlberg
(1993) have pointed out that death in anorexia is very often caused by a self-inflicted act
rather than inanition typically performed with drug overdose and alcohol. Sullivan (1995)
derived a crude rate of mortality due to all causes of death of 5.9 % for individuals with
anorexia nervosa. This author analyzed 42 studies (178 deaths in 3066 individuals). In the 38
studies in which the cause of death was specified (N=164), 89 (54%) of the deaths could be
attributed to the complications of an eating disorder, 44 (27%) to suicide, and 31 (19%) to
unknown or other causes. Herzog et al. (2000) found that anorexia nervosa carries a
substantial risk of premature death, and suicide in their sample was significantly higher than
expected. Harris and Barraclough (1997) selected thirteen studies which described cohorts of
anorexic and bulimic patients and performed a meta-analysis. They found that the suicide risk
was 23 times that expected for the combined group, ranging between zero and 100 times. The
suicide risk for anorexia nervosa increased 23 times. Pompili et al. (2004a) also performed a
meta-analytic investigation of cohorts of patients with anorexia nervosa. These authors
selected 10 studies (see table I) and identified suicides which occurred in the follow-up
period of each cohort. They calculated expected suicides in a year in 100,000 individuals if
they all suffered from anorexia nervosa. The authors searched the World Health Statistics
Annual published by the World Health Organization and identified expected suicides in a
year in a population of 100,000 individuals. For each study selected the authors identified
suicide statistics for a specific year and country and used only data applicable to females in
the 14-25 age group. A comparative analysis was performed to ascertain whether suicide
among subjects with anorexia nervosa may be considered a more frequent phenomenon in
comparison to suicide among the general population. The meta-analysis showed that suicide
in anorexia nervosa was, except in one study (Crisp et al., 1992 – St. George’s cohort), a
more frequent phenomenon than their counterparts in the general population. Apter et al.
(1995) found that 10% of their adolescent inpatients met the diagnostic criteria for anorexia
nervosa and that suicidal behavior scores were significantly higher in those with anorexia
nervosa (and conduct disorder) compared to those with anxiety disorders and schizophrenia.
Great differences exist among sub-groups of anorexics. The overall risk of suicide range
from 1.8% (Patton, 1988) to 7.3% (Ratnasuriya et al., 1991).
Patients with binge eating and purgative behavior usually have a weak control over
impulsivity associated with the eating disorder. Among these individuals alcohol and drug
abuse is also widespread. Also, mood disorders seem to affect those who manifest such
behavior more than they do restrictive anorexics (Vandereychen and Pierloot, 1983). In
literature, anorexics with purging behavior are described as those more vulnerable to
affective disorders and poor outcome compared with individuals without purging behavior
(Vandereychen and Pierloot, 1983; Garner et al., 1993).
Suicide attempts are also a prerogative of patients with anorexia nervosa. The
WHO/EURO (Platt et al., 1992) multicenter study defines suicide attempts as “an act with
non fatal outcome, in which the individual deliberately initiates a non-habitual behavior that,
without intervention from others, will cause self-harm, or deliberately ingests a substance in
excess of the prescribed or generally recognized therapeutic dosage, and which is aimed at
realizing changes which the subject derived via actual or expressed physical consequences”.
According to Shneidman (1985) the term attempted suicide should be used only for those
events in which there has been a failure of a conscious effort to end the life. All others – self-
mutilations, excessive dosage of drugs, and other events of this ilk – are, properly speaking,
“quasi-suicidal attempts” or probably, more accurately, “non-suicidal attempts”. Milos et al.
(2004b) found a lifetime prevalence of suicide attempts of 26%, which is four times higher
than the lifetime prevalence found in the general female population in Western countries (ca.
6%) (Weissman et al., 1999; Choquet, 1994) and is comparable to rates previously reported
for eating disorder samples (Corcos et al., 2002; Bulik et al., 1999; Viesselman and Roig,
1985). These authors found that a history of attempted suicide was significantly more
frequent in participants with a purging type disorder (anorexia nervosa and bulimia nervosa),
which is also consistent with the result of the study by Favaro and Santonastaso (1997). The
same study outlined the fact that anorexia nervosa participants were more likely to engage in
suicidal ideation than bulimia nervosa participants. The authors suggested that in anorexia
nervosa, starvation is a form of chronic self-harming behavior and continuously maintaining
underweight generates considerable distress, which might contribute to higher levels of
suicidal ideation in this group. Self-destructive behavior, suicide attempts included, has often
been associated with traumatic experiences in childhood, such as sexual and physical abuse.
In patients with anorexia nervosa suicide attempts and other self-injuring behavior are more
frequently represented in those patients who present binge eating and purging behavior. In
Favaro and Santonastaso’s study (1997), those patients who had attempted suicide were older
than non-attempters, had a longer duration of illness and a greater number of previous failed
treatments. These patients seemed to have a more serious form of anorexia, with lower body
mass index, higher levels of obsessionality and more frequent drug and/or alcohol abuse than
non-attempters.
The personality of anorexic patients has been described as obsessive-compulsive,
introverted, socially insecure and dependent; moreover it has been reported that patients with
anorexia nervosa have typical personality clusters. In a study performed in Japan, Matsunaga
et al. (1998) found that if anorexia nervosa alone was taken into account, DSM-III-R cluster
C was more prevalent; if, instead, anorexia nervosa and bulimia nervosa were considered
together in patients who had both, cluster B and cluster C were both represented; this points
to the role of bulimia nervosa in the identification of individuals belonging to cluster B.
Comorbidity between personality disorders and eating disorders is frequent and it is a major
issue, since the two conditions seem to increase the risk of suicide dramatically. In fact, at
least one-third (31-62%) of people who have committed suicide (Henriksson et al., 1993;
Brent et al., 1994; Lesage et al., 1994; Cheng et, 1997; Foster et al., 1997; Foster et al., 1999)
and up to 77% of suicide attempters (Suominen et al., 1996; Engström et al., 1997; Nimeus et
al., 1997; Ferreira de Castro et al., 1998) have suffered from personality disorders. Suicide
attempters with personality disorders have the highest level of repetition. Comorbidity of
personality disorder with other psychiatric disorders contributes to suicidality, and may
markedly elevate suicide risk (Suominen et al. 2000). Modestin et al. (1997) reported that in
their sample of patients with personality disorders, sexual abuse, physical abuse and the
witnessing of violence were found to be associated with self-destructive and suicidal
behavior of different kinds, including suicide attempts. Virtually all kinds of childhood
traumatic experiences were found to be associated with a history of suicide attempts, even
though the strongest association was found with sexual abuse. The results of this study
confirm these findings in women; only rarely were such associations found in men. The rates
of personality disorders among adolescents who died by suicide have been studied (Links et
al., 2003). In the comprehensive Psychological Autopsy Study in Finland, Marttunen and
colleagues (1994) estimated that 17% of the adolescents aged 13 to 19 years who died by
suicide met criteria for conduct disorder or antisocial personality disorder. Marttunen et al.
(1994) examined adolescents with nonfatal suicidal behavior, and found that approximately
45% of male adolescents and 33% of female adolescents were characterized by antisocial
behavior. Milos et al. (2004b) in their sample of patients with eating disorders found that
cluster B disorders showed a strong association with a history of suicide attempts.
Wonderlich and Swift (1990) reported an association between borderline personality disorder
(which belongs to cluster B) and suicide gestures in eating disorders.
Youssef et al. (2004) investigated a sample of young women through the MMPI-2 and
observed that some scales were risk indicators for suicide. They found that anorexic patients
with antisocial practices are at serious risk for suicide; more subjects have this trait in the
anorexia nervosa restrictive type with suicide attempts than in the same sub-group of
anorexia without suicide attempts. The same authors reported that in the case of anorexia
nervosa purging type, they found the following traits as risk factors for suicide: “hysteria”,
“psychopathic deviate”, “shyness/self-consciousness”, “antisocial practices”,
“obsessiveness”, and “low self-esteem”. Guillon et al. (2003) investigated self-esteem in a
sample of adolescent psychiatric patients. They pointed out that self-esteem can be defined as
an individual’s opinion of him/or herself, or the degree to which one holds attitudes of
acceptance or rejection of oneself. These authors reported that self-esteem has a different role
among the various types of mental disorders. Psychotic disorders were associated with a
relatively intact self-esteem when they were characterized by positive symptoms, whereas
low self-esteem was associated with depression. In this study adolescents with a history of
suicide attempts showed significantly lower self-esteem. This is consistent with Pinto and
Whisman’s (1996) investigation which reported that adolescents who have attempted suicide
have been found to have significantly lower self-esteem than non-suicidal inpatients. Given
the fact that patients with eating disorders usually present low self-esteem we can
hypothesize that rejection of oneself exposes the individual, especially the young one, to a
greater risk of suicide.
Table I – Suicides among various cohorts of patients

with anorexia nervosa. (Pompili et al., 2003 – modified)
Study Sample Follow-up Suicides

Patton, 1988, (UK) 332 10 6
Eckert et al.,1995, (USA) 76 10 0
Herzog et al., 2000, (USA) 136 11 3
Toltrup et al., 1985, (Denmark) 151 16 6
Deter and Herzog, 1994, (Germany) 84 12 2
Corem and Hewitt, 1998, (USA) 571 5 8
Crisp et al.,1992 (St George's) 105 20 1
Crisp et al.,1992, (Aberdee), (UK) 63 20 4
Emborg, 1997 (Denmark) 47 23 5
Kreipe et al., 1989 (USA) 9 6 1
Table II Attempted suicides (A.S.) among cohorts of patients with anorexia nervosa.
The table shows the number of patients that attempted suicide at least once during the
follow-up period or the number of patients that attempted suicide at least once in their
clinical histories (ascertained by scales or questionnaires). (Pompili et al., 2003 –
modified)
Study Sample Follow-up A.S

Viesselman and Roig,1985 (USA) 13 3
Favaro and Santonastaso, 1997 (Italy) 167 6 15
Favaro and Santonastaso, 1996 (Italy) 164 13
Bulik et al., 1999 (USA) 70 3 19
Wiederman and Pryor, 1996 (USA) 59 6
Kreipe et al., 1989 (USA) 49 6 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, 1997). These patients have an extraordinarily high rate of suicide (Favaro and
Santonastaso, 1999). Several studies have reported a lifetime frequency of suicide attempts in
bulimics between 15% and 40% (Favaro and Santonastaso, 1997; Bulik et al., 1999;
Lewinsohn et al., 2000). In a study which investigated 205 bulimic patients, 25% of those
that attempted suicide also had at least one past suicide attempt (1997), which is a major risk
factor for completed suicide. (Kotila and Lönnqvist, 1987). Corcos et al. (2002) presented a
sample of 295 women with bulimia nervosa (202 with BN purging type, 68 with BN non-
purging type and 25 with anorexia nervosa binge eating purging type). These authors found
that the bulimics who had attempted suicide reported suicidal ideation more often during
adolescence and had made their first attempt at this period. They found that more than two-
thirds had suicidal ideation during adolescence and their age at onset of the first eating
disorder had been, on average, one and a half years younger than for subjects with no history
of suicide attempts. Also, those who had been suicidal had a more frequent incidence of live
events such as separation from their family or separation in their family (parental separation
or divorce). Patients with a history of suicidal attempts used laxatives and diuretics more
frequently, had more lifetime depressive disorders, and more lifetime frequencies of
substance use and disorders of conduct (self-injurious behavior, risk-taking behavior,
stealing, running away, pathological lying, or hetero-aggressive behavior. As stated for
anorexia nervosa, the body of evidence suggests that depressive symptoms reported by
patients with bulimia nervosa are secondary, rather than primary phenomena (Cooper and
Fairburn, 1986). Kent et al. (1997) suggested that low self-esteem, which is a characteristic
feature of bulimia nervosa occurring independently of depression and associated with poor
body image, is the factor associated with increased levels of internally directed irritability. In
bulimic patients with a history of suicide attempts, the onset of psychopathology seemed to
have been particularly precocious.
Data concerning suicide in bulimia nervosa are still scarce, as more long-term follow-up
studies need to be completed before the risk for bulimia nervosa may be compared with that
for anorexia nervosa. Yet in some studies suicide seems to be the main cause of death
(Mitchell et al., 1988; Vandereychen and Pieters, 1992).
Among bulimic patients a number of clinical variables have been linked to a greater risk
of suicide, such as late onset, purging behavior, affective disorders, substance and alcohol
abuse and borderline personality characteristics including impulsiveness. Patients with
purging behavior seem to have more severe suicidality and show a greater number of suicide
attempts and self-injurious acts compared with bulimic patients who do not purge
(Viesselman and Roig, 1985; Mitchell, 1992; Shearer et al., 1988). Viesselman and Roig
(1985) found that 20% of the bulimic patients analyzed who had attempted suicide, also had a
diagnosis of major depressive disorder; 11% of these individuals were drug and alcohol
abusers. Sheares et al. (1988) found that suicide attempts were more serious in those patients
who had a borderline personality disorder comorbid with the eating disorder. As stated above,
comorbidity between personality disorders and eating disorders is frequently found among
cohorts of patients. Borderline personality disorder is no doubt extremely frequent in patients
suffering from bulimia nervosa. The incidence of completed suicide in borderline personality
disorder has been unknown until recently (Paris et al., 1989). In two long term follow-up
studies of borderline patients treated in residential settings, McGlashan (1986) and Stone
(1987) found that 3% and 9%, respectively, of borderline go on to complete suicide. Soloff et
al. (2000) found that patients with borderline personality disorder or comorbid disorders
attempted suicide for the first time earlier in life than the depressed patients; no significant
difference in age at the first suicide attempt was found in patients with borderline personality
disorder and patients with comorbid disorders. The suicide intent of the pooled group of
patients with borderline personality disorder had a greater lifetime level of lethality than
those of the depressed patients. In this study, the patients with borderline personality disorder
differed from the depressed patients in having an earlier onset of suicidal behavior, consistent
with the natural history of the disorder, and a higher lifetime number of attempts.
Comorbidity of personality disorder and major depressive episode was associated with an
increased number of suicide attempts. Also, among patients with borderline personality
disorder, impulsivity, assessed as a diagnostic criterion, is associated with the number of
suicide attempts independent of comorbid depression or substance use disorder.
Some authors call for the recognition of a distinct diagnostic subgroup of bulimia
nervosa, such as “multi-impulsive bulimia” or “multi-impulsive personality disorder” (Lacey,
1993; Fichter et al., 1994). This subgroup is usually defined by the existence of at least three
(Lacey, 1993; Fichter et al., 1994) or at least one (Fahy and Eisler, 1993) of the following
behaviors: alcohol or drug abuse, suicide attempts, repeated self-mutilation, sexual
disinhibition, shoplifting. Nagata et al. (2000) investigated a sample of patients with eating
disorders and found that 18% of the 114 bulimic patients showed multi-impulsivity; 80% of
the patients with this features had a history of suicide attempts or self-mutilation prior to the
onset of bulimia nervosa. The authors questioned the hypothesis that impulsivity in bulimia
nervosa is not necessarily part of a comorbid borderline personality disorder; in fact, in their
sample only 27% of the multi-impulsive bulimics met the borderline personality disorder
criterion.
Youssef et al. (2004) found among women with bulimia nervosa purging type a number
of personality traits associated with suicide risk. They observed through the employment of
the MMPI-2 that in bulimic women with suicidal attempts the following scales were risk
indicators: “psychasthenia”, “anger” and “fear”. Favaro and Santonastaso (1997) underlined
the fact that suicide attempts among bulimic patients did not appear to be linked to the
severity of bulimic symptoms in terms of frequency of binge eating and vomiting, but rather
to the presence of purging behavior. Suicide attempts were associated with more serious
psychiatric symptoms and with higher levels of obsessionality. Patients with purging
behavior have a more serious course of illness, as they more frequently experience depressive
symptoms, weight and shape of body preoccupations and have a history of suicide attempts,
drug and alcohol abuse and self-injurious behavior. (Favaro and Santonastaso, 1997; Da
Costa and Halmi, 1992; Dulit et al., 1994; Viesselman and Roig, 1985; Mitchell, 1992).
Suicidality among these patients seems to be increased by the number of compensatory
behaviors that the patients engage in, in order to reduce weight; the more strategies utilized,
the greater the risk of suicide (Favaro and Santonastaso, 1996). Bulimia nervosa is without
doubt linked to self-injury (Dulit et al., 1994; Favazza et al., 1989; Herpertz, 1995). A typical
symptom of bulimia nervosa is self-injuring and self-mutilation; purgative behavior might be
considered a sort of self-wounding action. Patients, in fact, describe this behavior as an
invincible impulse to self-inflict punishment. Van der Kolk et al. (1991) have considered
eating disorders a form of self-destructive behavior similar to suicide attempts and self-
cutting. Self-mutilation should not be considered a feature of suicide behavior but a way to
reduce tension and induce relief (Root and Fallon, 1991); this behavior has also been linked
to a number of dissociative symptoms (Everill et al., 1995). Nevertheless, patients have the
chance to experience their body and look for a sense of reality and their own identity.
However, impulsivity does predict suicidal behavior (Favaro and Santonastaso, 1998).
Table III Attempted suicides (A.S.) among cohorts of patients with bulimia nervosa. The
table shows the number of patients that attempted suicide at least once during the
follow-up period or the number of patients that attempted suicide at least once in their
clinical histories (ascertained by scales or questionnaires). (Pompili et al., 2003 –
modified)
Study sample follow-up A.S.

Viesselman and Roig 1985 (USA) 36
Garfinkel et al., 1980 (Canada) 155 8 36
Favaro and Santonastaso,1997 (Italy) 210 6 38
Bulik et al., 1999 (USA) 152 3 47
Wiederman and Pryor, 1996 (USA) 58 18
Favaro and antonastaso,1998 (Italy) 125 2 23
Raynes et al., 1983 (USA) 15 6
Risk Taking Behavior as Part of Suicide in

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

attempted suicide is about 4% in a United States population attending a primary care clinic,
and its risk, as assessed through the Adverse Childhood Experiences (ACE) scores, increases
with increasing ACE scores (Dube et al., 2001). These scores also correlate with risk-related
behavior, such as alcohol or illicit drug abuse. Onset of problem behavior is at 12 years, rises
to peak until 15 years, and plateaus thereafter (Reynolds and Rob, 1988). Adolescent suicide
attempters report lower levels of parental interest and involvement and belong to more
disrupted families than their nonsuicidal counterparts (Flouri and Buchanan, 2002). A recent
paper (Borawski et al., 2003) investigated two different parenting practices (parental
monitoring and negotiated unsupervised time) and perceived parental trust in the reporting of
health risk behaviors among adolescents. This study clearly stressed the importance of
parents in induction of health risk behavior. Adolescents’ rating their parents as
“affectionless” on the Parental Bonding Instrument (PBI) doubles their risk for suicidal
ideation and triples it for deliberate self-harm. Taken together, these data point at a healthy,
traditional-style family, as the major determinant of protection from risk-related behavior,
which is linked to suicide attempts.
Coordinated efforts are needed when dealing with children or adolescents with suicidal
ideation. Compliance with prescription, either pharmacological or behavioral, is a major issue
in decreasing suicidal risk and this must be assessed and addressed from the first contact with
the patient (Litt et al., 1983). Various approaches were suggested to treat suicidal children
and adolescents; a holistic family technique focuses on children and their parents and aims at
increasing appropriateness of child-parent communication (Pfeffer, 1982); metatherapy, a
psychotherapy based on the collaboration of the parental couple, is supposed to reduce
perceived stigma in children and adolescents, as well as to increase satisfaction with parental
role in parents (Vaz-Leal, 1989). Furthermore, modifying the youth’s perception of his own
parents may be critical in reducing both suicidal thoughts and deliberate self-harm (Martin
and Waite, 1994). Finally, techniques aiming at correction of pathogenic beliefs may prove
useful for adolescents and adults (Weiss and Sampson, 1986).
Self-destructive and risk-taking behavior, although they cannot be classified as suicide
sensu strictu, from part of a broad suicide continuum that may increase premature death in
individuals conforming to this spectrum. Even minimal manifestations of this continuum,
such as drug or alcohol exposure, unprotected sex, and risky driving, displayed to comply
with peer pressure, should not be disregarded, as they could give rise to successful suicide
attempts or impair the organism’s defenses and render the individual more vulnerable to
various noxae. The role of parents is a critical one in this respect. Hence, in managing youths
exhibiting such behavior, care should be taken to involve and educate parents.
Another open issue is those deaths called subintentioned deaths, which may be
represented in individuals with anorexia nervosa and bulimia nervosa. Shneidman et al.
(1961) suggested that motivation is present in some deaths and a comprehensive taxonomy of
death must include components that reflect the role of the individual in his own death. In
particular, an intentioned death is any death in which the decedent plays a direct, conscious
role in affecting his own demise; an unintentioned death is any death in which the decedent
plays no effective role in effecting his own demise. In this discussion it is paramount to
define a subintentioned death, namely a death in which the decedent plays some partial,
covert, or unconscious role in hastening his own demise. Subintentioned deaths are often
identifiable in individuals who manifest poor judgment, excessive risk-taking, abuse of
alcohol, misuse of drugs, self-destructive style of life, disregard of prescribed lifesaving
medical regimen, unprotected sex, driving after alcohol abuse. One may wonder how to
identify deaths from accidents and from suicide, bearing in mind that individuals who die
after an accident may actually have had a role in the occurrence of that accident, acting more
like a suicidal person than a victim of adverse circumstances. Often risk-taking behavior and
adverse circumstance act synchronically and it is very difficult to ascertain whether a death
was suicide or accident (Pompili et al., 2004b). However, in the case of undetermined death,
a conscious act may be lacking or may not be recognized, especially when the individual is
ambivalent in his decision. This leads to a distinction between suicide and subintentional
deaths even if they share various elements. Shneidman (1991, 1993) hypothesized a spectrum
of intentional deaths in which unequivocal completed suicide is the most extreme form of
self-destructive behavior and self-inflicted death should also be recognized in a wide variety
of behaviors which share a dimension called lethality, defined as the probability of a specific
individual’s killing himself (i.e. bringing about his own death) in the immediate future
(today, tomorrow, the next day, the next month). Given the fact that patients with eating
disorders manifest a number of behaviors that do reflect lethality towards themselves and
high risk behaviors, we should emphasize the need to improve recognition of all
manifestations of the suicide spectrum. People who engage in high risk behaviors may
paradoxically be protected from suicide per se, as if they preferred a slow lethal action rather
than a sudden death (Pompili et al., 2004c). Individuals with eating disorders may in some
cases interchange their suicidal wishes with high risk-behaviors, or their unconscious wish to
be dead may play a role in all those deaths that belong to the subintentional category. Deaths
from suicide are underreported because of the tendency to group them as accidental deaths or
deaths from undetermined causes.
Prediction and Prevention of Suicide Among

Patients with Eating Disorders
Suicide prevention among children and adolescents is a high priority due to the fact that
suicide ranks first or second as a cause of death among both boys and girls in the 15 to 19-
year age group in many countries. Given the fact that in many countries and regions most
people in this age group attend school, this appears to be an excellent place to develop
appropriate prevention action. Eating disorders are becoming more prevalent and observable
across cultures. These difficult-to-treat disorders also demonstrate a continuity between
adolescent onset and adult risk for the presence of an eating disorder (Kotler, 2001). The
promotion of children’s health through school is recognized at the international level as an
important means of influencing health behavior. The World Health Organization (2000a;
2000c) defines a “Health-Promoting School” as a school that is constantly strengthening its
capacity to be a healthy setting for living, learning and working. Specifically, these programs
aim to build healthy public policies, create supportive environment, strengthen community
action, foster the development of personal skills, and reorient health services to embrace
health promotion in addition to clinical and curative services (WHO, 2000). Health-
Promoting Schools also help pupils, parents and community members work together to set
priorities and plan actions. They use information about the determinants of health and
wellbeing, as well as leading causes of death and disease and they foster healthy behavior as
well as those that prevent the initiation of important health risks, such as risk taking behavior
in individuals with eating disorders and suicidality among them.
During adolescence, girls have a much higher prevalence of depression and eating
disorders and engage more in suicidal ideation and suicide attempts than boys. Adolescence
is not an easy time psychologically, and adjustment indicators are important, especially in
suicide prevention. Unfortunately, mass media do not help in either the prevention of suicide
or eating disorders. It is believed that a contributing factor in the rise of eating disorders is the
exposure to Western media and its influence on desirable body characteristics. The power of
mass media has been investigated in connection with suicidal behavior. In fact, numerous
studies have considered the association between media reporting and portrayal of suicide and
actual suicidal behavior and ideation (Pirkis and Blood, 2001a,b). Research finds an increase
in suicide by readers or viewers when 1) the number of stories about individual suicide
increases; 2) a particular death is reported at length or in many stories; 3) the story of an
individual death by suicide is placed on the front page or at the beginning of a broadcast; 4)
the headlines about specific suicide death are dramatic (a recent example: “Boy, 10, kills
himself over poor grades”). The media can play a powerful role in educating the public about
suicide prevention as well as in eduating youth about eating disorders. It might be speculated
that those people who are the most vulnerable to mass media’s presentation of desirable body
characteristics are also the most easily influenced by media portrayals of suicide.
Psychotherapy with Suicidal

Anorexic and Bulimic Patients
Psychotherapy with suicidal patients is a real challenge for any clinician. Psychotherapy
has also been employed in the treatment of anorexia nervosa and bulimia nervosa especially
in conjuction with pharmacotherapy. Nevertheless, international literature does not provide
definitive results on the efficacy of psychotherapy in the treatment of such diseases. There are
relatively few evidence-based findings, particularly for the treatment of anorexia nervosa. In
the few studies that have shown the statistical effectiveness of a certain approach, the rate of
failure to respond is typically high and not readily explained by current scientific knowledge
(Hsu, 2004). Psychotherapy may offer a key opportunity to reduce pain. Shneidman (1993)
described what he called “psychache”, meaning an ache in the psyche and suggested that the
key questions to ask a suicidal person are “Where do you hurt?” and “How may I help you?”.
If the function of suicide is to put a stop to an unbearable flow of painful consciusness, then it
follows that the therapist’s main task is to mollify that pain. Shneidman (1993) also pointed
out that the main sources of psychological pain, such as shame, guilt, rage, loneliness,
hopelessness, and so forth, stem from frustrated or thwarted psychological needs. These
psychological needs include the need for achievement, for affiliation, for autonomy, for
counteraction, for exhibition, for nurturance, for order, for understanding. The healing effects
of careful listening to the patient’s story and the development of empathy, so that the patient
feels truly understood, cannot be over-emphasized in this respect. A sound therapeutic
relationship, or working alliance, will go a long way toward preventing repeated suicidal
behavior as the adolescent experiences the feeling of being heard in an important
interpersonal relationship (Manley and Leichner, 2003). Many authors have written about
psychotherapy for patients with anorexia nervosa. Despite different approaches, they believe
that the therapist should be active and should function in the therapeutic encounter as a
parent, teacher, guide and coach. The personality of the therapist is a major therapeutic
element in the treatment of patients with anorexia nervosa (Hsu, 2004). The main goal of a
psychotherapy with anorexic patients is to help the patient get in touch with inner feelings
and experiences, to identify and verbalize them; also therapy should change dysfunctional
thinking which plays an important role in the psychopathology of this disorder.
Psychotherapy with bulimic patients is also a key element of the therapeutic armamentarium;
various therapeutic approaches have been employed, but cognitive behavioral therapy seems
the most effective strategy for these patients. Treatment is active, problem-oriented, semi-
structured, and concerned more with the patient’s present and future than with the past. Yet,
psychotherapy with suicidal patients must take into serious consideration the need of these
patients to escape from unbearable psychological pain and provide a safe and accepting
environment. Also, countertransference reactions play an important role in the management
of suicidal patients. Due to their ability to cause strong emotional feelings, the suicidal
patienta are particularly prone to provoking countertransference reactions. Suicidal patients
generate more anxiety and more feelings of anger. Doctors usually treat patients who
desperately want to live; suicidal patients, in contrast, undermine the very core of the medical
profession by wishing to be dead and by struggling with the therapist who is trying to prevent
this action. Not evey therapist may be an appropriate therapist for suicidal patients.
Insufficient control over counter-transference problems may increase suicide risk in the
patient and suicide may result from an iatrogenic event (Andriola, 1973). In fact, therapists
that are unable to handle strong feelings provoked by suicidal patients cannot conduct proper
therapeutic work with these patients who do not have the opportunity to externalize thei inner
negative feelings to a strong therapeutic figure. Therapists may fear the death of the patient
but at the same time may enhance the risk of a suicidal death.
Anorexic and bulimic patients may be hospitalized especially in the case of severe
medical complications. Hospitalization may carry an extra risk for suicide and staff should
always keep an open mind throughout the entire stay of the patients. A lesson may be learned
from the studies devoted to suicide among inpatients. Crammer (1974) pointed to the
potentially disruptive effects of transitions – for example, initial acclimation toward life or
plans for discharge or rehabilitation. He also emphasized the environmental impact of staff
variables, such as low morale or the absence of key personnel, as well as the need for
effective communication among relevant staff about patients judged as having an increased
risk of suicide. Adverse circumstances such as single-occupancy rooms or the return to a
family in which the patient’s presence represents a severe emotional or financial strain, most
probably add to the suicide risk for a schizophrenic patient. Poor communications about risk
between medical and nursing staff, change in staff, and ward layout have been suggested as
risk factors. According to Crammer (1974) an anti-suicidal ward is one with calm routine,
carried out daily by staff who are themselves unworried and confident of the immediate
future. Their calm is, so to speak, infectious.
Pharmacotherapy and Suicididality in

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

Instituto de Psiquiatria, Hospital das Clínicas, Faculdade de Medicina, Universidade de
São Paulo, São Paulo, Brasil
Faculdade de Psicologia, Universidade São Judas Tadeu, São Paulo, Brasil
Abstract
characterized by the Diagnostic and Statistical Manual of Mental Disorders, fourth
Edition (DSM-IV), as one of the diagnostic criteria for these pathologies. Although the
presence and importance of body image disturbance in eating disorders are well
established, the psychopathological nature of this symptom is not yet defined.
Objective
This study explores the presence of obsessive-compulsive and delusional features of the
‘Body Image Disturbance’ in anorexia and bulimia nervosa.
Method
Sixteen women with anorexia nervosa and eleven women with bulimia nervosa were
compared regarding their responses to the Yale-Brown Obsessive Compulsive Scale (Y-
BOCS) and to the Delusional Features Assessment Scale. Variables were analyzed with
the Fisher’s Exact Test and Mann-Whitney non-parametric test (U).
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.
Discussion
The analysis of the psychopathological differences of ‘Body Image Disturbance’ in

anorexia and bulimia nervosa has diagnostic implications.
Introduction
characterized by the Diagnostic and Statistical Manual of Mental Disorders, fourth Edition,
(DSM-IV) (APA, 1994) as one of the diagnostic criteria for these pathologies. The severest
abnormalities occur in anorexia nervosa, whose diagnostic criterion according to the DSM-IV
requires a ‘disturbance in the way in which one’s body weight or shape is experienced, undue
influence of body weight or shape on self-evaluation, or denial of the seriousness of the
current low body weight’ (APA, 1994). For the diagnosis of bulimia nervosa the DSM-IV
requires that “self-evaluation is unduly influenced by body shape and weight’ (APA, 1994).
Dissatisfaction with body weight and shape seems to motivate several of the behaviors
found on subjects with these pathologies. For example, the essential feature of anorexia
nervosa according to the DSM-IV is ‘a refusal to maintain body weight at or above a
minimally normal weight for age and height’, what means an attempt to correct a perceived
defect in the physical appearance (APA, 1994). The essential feature of bulimia nervosa are
the recurrent episodes of lack of control over eating. At first, these episodes would apparently
represent the opposite of the excessive eating restriction and fasting seen in anorexia nervosa.
However, bulimic episodes are mostly originated in the dissatisfaction with the body and in
the attempts to reduce body weight.
Although the presence and importance of body image disturbance in eating disorders are
well established, the psychopathological nature of this symptom is not yet defined. Despite
the fact that the features of obsessiveness in eating disorders have been studied (Pigott et al.,
1991; Zubieta, J.K.; Demitrack, M.A.; Fenick, A.; Krahn, D.D., 1995), the research on
delusional features or the interface between obsessions/delusions in eating pathologies has to
be better explored.
Review of the Literature
Meyer and Weinroth (1957) noted that patients with anorexia nervosa are excessively
concerned with their shape, especially with their abdominal features, which they consider as
protuberant, despite the evident cachexia. Next, Bruch (1962) stated that ‘a disturbance in
body image of delusional proportions’ would be the central aspect of anorexia nervosa.
Psychopathological Aspects of Body Image Disturbance on Anorexia … 29
Controlled studies identify high rates of obsessiveness among patients with anorexia and
bulimia nervosa, and there are studies showing increased diagnostic proportions of obsessive-
compulsive disorder (OCD) in eating disorders (Pigott et al., 1991; Kaye et al., 1992;
Solyom, L.; Freeman, R.J.; Miles, J.E., 1982; Bulik, C.M.; Beidel, D.C.; Duchmann, E.;
Weltzin, T.E.; Kaye, W.H., 1992).
The inverse relationship, that is, an increased frequency of eating disorders or symptoms
in patients with OCD has been also documented (Thornton, C.; Russel, J., 1997; Thiel, A.;
Broocks, A.; Ohlmeier, M.; Jacoby, G.E.; Schussler, G., 1995; Pigott et al., 1991;
Rubenstein, C.S.; Pigott, T.A.; L’heureux, F.; Hill, J.L.; Murphy, D.L., 1992).
On the other hand, we noted that systematized studies assessing the degrees or rates of
psychotic symptomatology in patients with eating disorders are scarce. Hsu et al. (1981)
described the clinical features of six patients with anorexia nervosa who had developed
associated schizophrenia or schizophreniform disorder. In a retrospective study, Grounds
(1982) showed that 5% of patients with anorexia nervosa had brief psychotic episodes. Of
note, in these studies structured diagnostic instruments were not used. Hudson et al. (1984)
detected psychotic symptoms, according to the DSM-III criteria (APA, 1980), in 17 (13%)
out of 130 patients with lifetime diagnosis of anorexia nervosa and/or bulimia nervosa.
Among 16 patients these symptoms seemed attributable to an affective or schizoaffective
disorder, whereas in one of them they seemed to represent a factitious psychosis. Cases of
schizophrenia or organic psychosis were not identified.
We also found studies in the literature which comment on the clinical features present in
eating disorders and comorbid psychotic conditions (Ferguson, J.M.; Damluji, N.F., 1988;
Lyketsos, G.C.; Paterakis, P.; Beis, A.; Lyketsos, C.G., 1985).
Objectives
This study aimed at:
1. Assessing obsessive, compulsive or delusional features of body image disturbance in

patients with anorexia and bulimia nervosa.
2. Comparing both diagnostic groups regarding the mentioned psychopathological
features.
Method
Twenty-seven female patients were interviewed, all being followed up in the Ambulatory
of Bulimia and Eating Disorders (AMBULIM) of the Psychiatric Institute of the Medical
School of the University of São Paulo. They were selected according to DSM-IV criteria
(APA, 1994), and 16 met criteria for the diagnosis of anorexia nervosa and 11 for bulimia
nervosa. All anorexic and 3 bulimic patients were hospitalized at the time of the interview.
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
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 non-
parametric 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.
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).
Compulsive Features According to the Y-BOCS
The frequency of patients with anorexia nervosa who spend three hours per day or more
with behaviors related to the physical appearance is significantly higher when compared to
patients with bulimia nervosa (81.2% and 27.2%, respectively; P= .05*). The same thing
occurs with the social or professional interference, which was intense or extreme in 43.7% of
anorexic, compared to 9.0% of bulimic patients (P= .008*), with intense or extreme distress
(75% of anorexic and 27.2% of bulimic patients; P= .01*) and small or null degree of control,
reported by 81.2% of anorexic and 36.3% of bulimic patients (P= .007*). There was no
difference between both groups regarding the resistance to the behaviors, reported as always
present or most of the times, in 25% of anorexic and 36.3% of bulimic patients (P= .14).
The group of anorexic patients showed a significantly higher total score in the sum of
questions 1 to 10 of the Y-BOCS (i.e., in the assessment of the obsessive and compulsive
features of body image disturbance), compared to the group of bulimic patients (P = .0398*).
When groups were compared regarding the total score for the questions 1 to 5 (obsessive
features), there were no differences between them (P = .656). Regarding the total score for
questions 6 to 10 (compulsive features) there was a statistically significant predominance of
compulsive features in the group of anorexic patients (P = .0032*). This difference
disappears when we take away ‘fasting’ from the list of target symptoms from which the Y-
BOCS 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*).
Table 1 Obsessive, Compulsive and Delusional Features in the diagnostic groups
Anorexia Bulimia P
nervosa nervosa
N = 16 N = 11
Obsessive Features
Time spent with obsessions(more than 3 hours per day) 75% 54.54% .2240
(question 1 of Y-BOCS)
Social or professional interference (intense or extreme) 56.25% 54.54% .9594
Associated anxiety (intense or extreme) (question 3 of Y- 50% 27.27% .2747
BOCS)
Resistance to obsessions always or most times (question 4 56.25% 45.45% .9394
of Y-BOCS)
Degree of control (mild or none) question 5 of Y-BOCS 75% 72.72% .7741
Compulsive features
Time spent with compulsions (more than 3 hours per day) 81.25% * 27.27% * .0032*
Social or professional interference (intense or extreme) 43.75% * 9.09% * .0081*
Associated anxiety (intense or extreme) (question 8 of Y- 75% * 27.27% * .0174*
BOCS)
Resistance to obsessions always or most times (question 9 25% 36.36% .1492
of Y-BOCS)
Degree of control (mild or none) question 10 of Y-BOCS 81.25% * 36.36% * .0075*
Delusional features
Conviction (being sure regarding the occurrence of her 50% * 18,18% * .0551*
belief) Question 1 of scale for assessment of delusional
features
Conviction (the ignorance of people does not allow them to 25% 18,18% .3048
share her beliefs) Question 2 of scale for assessment of
delusional features
Conviction (patient remains defending completely their 56.25% 45,45% .8520
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 81.25% * 18,18% * 0,0002*
delusional features)
Extreme concern (Question 5 of scale for assessment of 68.75% * 27,27% * 0,0130*
delusional features)
* Statistically significant difference between groups, P < .05.
Discussion
A complex interaction of physiological and psychological factors, cultural pressures and

family demands is involved in the appearance of anorexia nervosa and bulimia nervosa.
Conditions that increase the probability of going on a diet or fasting, such as the concern
regarding body shape, weight and eating seem to be important risk factors for these
pathologies (Fairburn, C.G.; Welch, S.L.; Doll, H.A.; Davies, B.A.; O'connor, M.E., 1997).
Once started, behaviors related to weight loss (e.g., fasting, purging behaviors) cause
physiological alterations, some of which are probable maintainers of the disease (Walsh,
B.T.; Devlin, M.J., 1998).
In this context, the ‘body image disturbance’ becomes a risk and maintenance factor for
the disease, as it stimulates the performing of a diet.
The symptom ‘body image disturbance’ shares several similarities with obsessions as it
is characterized by the recurrent and persistent idea of being fat or the presence of distorted
images about one’s body. These concerns or images are frequent or almost constant and
cause remarkable anxiety in the patients, who try but are not always able to resist to their
occurrence.
Sometimes, however, patients do not show resistance or insight regarding these thoughts
or images, experiencing them as natural and reasonable.
Similarly to the compulsions there are repeatedly performed voluntary behaviors such as
fasting, making physical exercises, weighing oneself or provoking vomits, aiming at relieving
the discomfort caused by the idea of being fat. Such behaviors are clearly excessive and
interfere with the socio-occupational performance of the patients. Behaviors related to body
weight and image differ from compulsions when patients do not consider them exaggerate
and defend the fact of performing these behaviors instead of feeling compelled to accomplish
them.
Not all obsessive or compulsive features are always found in one idea or behavior. For
example, the lack of insight or resistance may make a belief or a behavior different from
classical obsessions or compulsions, as can be observed, for instance, in patients with chronic
OCD (Insel; Akiskal, 1986).
Mayer-Gross et al. (1969) described the obsession as a ‘mental event with a subjective
feeling of compulsion overcoming an internal resistance’ , but added that if the personality as
a whole identifies itself with the idea, then this idea could be deemed overvalued or
delusional. Therefore, if patients cease to recognize their idea as irrational or egodystonic,
that is, intellectually and emotionally identify themselves with it, we could be facing a
different notion of a typical obsession (Insel,T.R.; Akiskal, H.S., 1986). Mullen (1979) also
noted that the resistance to an obsession could fluctuate and suggested that, in such cases, the
phenomenon could be considered an overvalued idea or a delusion if the lack of resistance
not be only occasional, but a constant feature of the experience.
The symptom ‘body image disturbance’ may have some features that deviate from the
obsessive concern and bring it closer to overvalued ideas. The lack of resistance offered
against thoughts and behaviors and the non-intrusive way of experiencing them, that is, the
emotional syntony or egosyntony with which patients experience it are some of these
features.
The concept of an overvalued idea was established by Wernicke (1900) apud McKenna
(1984) who defined it as a solitary belief that determines the subject’s actions at a morbid
degree, whereas, at the same time, it is considered as justified and a normal expression of its
nature. Wernicke was the first one to distinguish overvalued ideas from obsessions showing
that an overvalued idea may arise form adverse experiences that makes them understandable,
differing from the obsessive concern for being a natural, non-intrusive idea, accepted without
resistance and which is not seen as senseless by the patient. If we transport this concept to the
symptom ‘body image disturbance’ we may perceive that the resistance of patients to the idea
of being fat might not be present in all cases. In this case, the idea of being fat or having a big
belly would be accepted and defended by patients, and it could appear in the mind for
understandable reasons, such as the fear of gaining weight among subjects with professional
requirements of weight control, previous history of obesity or the presence of obese family
members. In that case, patients might not consider their behaviors dedicated to weight loss
excessive, reaching to the point of defending this practice, what attenuates its compulsive
character and make them more similar to the actions stemming from an overvalued idea.
Jaspers (1963) provides a formal distinction between prevalent ideas and delusions. The
latter, he says, are the result of a specific abnormal process whose basis is unknown but that
seems to involve a radical transformation in the way by which meanings are associated to
events. Its quality is, therefore, entirely distinct from normal beliefs. By contrast, an
overvalued idea is, in fact, an isolated idea, loaded and accentuated by a very strong affective
state, understandable by the personality and life of the subject, and that, due to this strong
affective load, is erroneously considered as true, as the personality is identified with the idea.
Therefore, its quality is similar to strong political, religious or ethical convictions, differing
from them only in degree. Hamilton (1974) adds that in delusions there is often a discrepancy
between the degree of conviction and the extension in which the belief guides the action, and
patients with a prevalent idea inevitably act on it, in a determined and repeated way.
Since the hey-day of phenomenology at the end of the 19th and the beginning of the 20th
centuries, delusion has been defined in several ways, without a consensus regarding its
nature, origin and taxonomy (Butler; Braff, 1991; Roberts, 1992). The study of Jaspers
(1963) was incorporated in the current definitions, delusions having determined features: (a)
its content is deemed false or fantastic; (b) the degree of conviction is firm and absolute; (c)
beliefs are idiosyncratic to the patients’ cultural context and (d) they are kept despite
evidence or experiences in the opposite sense. However, some problems to apply these
criteria have arisen and Strauss (1969) suggested that the dichotomic classification of beliefs
in delusive and non-delusive was not adequate. He argued that delusions would be better
conceived as extreme points along certain dimensions of beliefs, such as the degree of
conviction, resistance and insight. Delusions were thus proposed to be studied as a
phenomenon that could vary along several dimensions instead of being considered as an all-
or-nothing phenomenon (Garety, P.A.; Hemsley, D.R., 1987).
The symptom ‘body image disturbance’ has delusional features which, in our study, were
assessed according to the following dimensions: concern with the belief, conviction,
irreducibility, insight and bizarreness. Of note, the great concern, high degree of conviction
and irreducibility of the belief shown by some patients. Other remarkable aspect is the
bizarreness of the belief or its lack of compatibility with reality, regarding the high degree of
current malnutrition and weight loss.
Anorexic and bulimic patients presented high scores in the assessment of obsessive,
compulsive, and delusional features of the body image disturbance symptom.
Although both groups had high values in the questions which investigated how obsessive
their concerns related to body image were, there was no difference between the groups in
the total scores of these questions (1 to 5 in the Y-BOCS). On the other hand, anorexic
patients had higher scores in the questions that assessed compulsive features (6 to 10 in the
Y-BOCS) and delusive characteristics (conviction, bizarreness and concern) than bulimic
patients.
Therefore, behavioral aspects of body image disturbance (weighing oneself, looking at
the mirror, fasting or doing physical exercises to lose weight, etc.) seem to have a greater
compulsive quality (questions 6 to 10 in the Y-BOCS) in patients with anorexia nervosa,
compared to bulimic patients . However, it is interesting that if we take away the practice of
fasting from the list of target symptoms of body image disturbance, there is no difference
between the groups regarding the quality of compulsions. This analysis seems relevant to us
as fasting would be more similar to an avoidant behavior than to a compulsive behavior
proper.
Other difference between the groups was the fact that anorexic patients punctuate higher
in the total of questions which assessed delusional features when compared to bulimic ones.
A more careful analysis demonstrated that the components conviction (question 1),
bizarreness and concern were those responsible for such difference. As the assessment of the
bizarreness of the belief was performed only by the interviewer, what could be a source of
bias, the groups were compared again after the exclusion of this component of the scale, but,
nevertheless, the difference between them remained.
Summing up, body image disturbance in anorexic and bulimic patients has the same
quality in obsessive and compulsive aspects and in anorexia nervosa this symptom shows
also some delusional features in higher degree, such as having a lower correspondence with
reality, being more vigorously defended by patients and being more concerning for them.
These findings can be related, in part, to the severity of the clinical picture of anorexic
patients in this study. Prospective studies with greater samples and are needed to prove this.
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Chapter III
Experiences of ‘Control’ in
Anorexia Nervosa Treatment: Delayed
Coercion, Shadow of Law, or
Disseminated Power and Control?
Terry Carney, Mim Ingvarson and David Tait

Sydney Law School, University of Sydney
NSW 2006 Australia
Abstract
Anorexia nervosa is often chronic, with one of the highest death rates for psychological
conditions. Law can compel treatment, but is rarely invoked, at least formally (though the
strategic possibilities of orders confers internal authority within the clinical setting).
Instead, ‘control’ (or management) is exercised diffusely, through disciplinary practices
embedded in everyday clinic life, such as daily routines of eating and washing,
behavioural ‘contracts’, regular surveillance and measuring, interactions with staff, visits
and activities. The regulatory regime not only touches on such ‘practices’ but also targets
‘identities’ (including self-image, and attitudes to the body) and what Goffman called the
‘moral career’ of the patient (eg learning to play the ‘patient role’, to ‘be’ an ‘anorexic’).
We argue that it is not the clumsiness of the law, or the success of less restrictive options
which explains why law is so infrequently engaged. Rather, based on an interpretation of
Foucault, we conclude that the regulatory regime that shapes treatment of anorexia
nervosa, is ‘the law’, in a sense. The regime of governmentality within the clinic is
shaped by practices which operationalise ‘duty of care’, or translate medical expertise
into medical authority, or show how interactions between ‘experts’, ‘carers’ and patients
are mediated through conventions and rules, or which conscript ‘empowerment’ as
control. The patient learns to provide consent ‘freely’, to make the ‘correct’ choices, to
accept the ‘empowerment’ regime that is made even more convincing by the threat of
legal intervention. In time the constraints learned in this way become part of the new
role, that of the ‘recovering’ patient. The ‘fiction’ of acting ‘responsibly’, employed so
42 Terry Carney, Mim Ingvarson and David Tait
hesitantly at first, becomes part of the new identity. The patient has become an active
participant in the governance of self.
Introduction
Anorexia nervosa joins other ‘syndromes’ listed in psychiatric manuals like the DSM-
lV(R) or the ICD 10. Along with many psychiatric conditions, it is identified by ‘clusters of
symptoms and behaviours considered clinically meaningful in terms of course, outcome and
response to treatment’, rather than by objective anatomical features (Bruce, 1999: 37;
Further: Beumont and Carney, 2003).
The literature is divided about whether anorexia is mainly a pathological condition, or
may in some contexts be understood as a ‘rational’ form of behaviour (For a review: Dresser,
1984: 302-308). Some writers highlight long historical traditions of ascetism, where fasting is
associated with religious merit and definition of the ‘self’. On this view, intense fasting, like
self-flagellation, embarking on crusades and other forms of extreme self-discipline, may
connote a display of devotion and sacrifice (Tait, 1993). Others focus on the family and
relational context in which the anorexic ‘identity’ is constructed (Young, 1998), seeing eating
disorders as one of a series of responses to familial traumas. Feminists point to socio-political
dimensions of anorexia (patriarchy, disempowerment) to explain the reported loss of self
esteem and ‘powerlessness’ (Gilmore, 1994; Bray, 1996). And resistance to assuming an
adult female identity may be reflected in attempts to delay the onset of puberty, specifically
menstruation (Tomkiewicz, 2003). Culture too may play a part, either in shaping the form in
which body image conditions express themselves in different countries (Abusah, 1993), or
pre-disposing some young people to greater risk of anorexia.1
Whatever its true ‘character’, or its social and familial origins, severe anorexia nervosa is
experienced by half to 1 percent of women over their lifecourse (Steiger and Séguin, 1999).
And even if some fasting originates in a rational decision, its escalation into severe anorexia
nervosa is usually accompanied by physiological changes that then limit the person’s
awareness of the risks they face. Anorexia nervosa is life-threatening, with one of the highest
death and morbidity rates among cognate conditions,2 complicated by treatment resistance
and low rates of success (Ben-Tovim, 2001).
1
One Australian study which examined the family backgrounds of people with anorexia found an over-
representation of parents from Asia or Europe, and fewer from the Middle East, leading the authors to suggest
that, while it is a myth to believe that some cultures immunise against the condition, those young people from
cultures where the condition is rare may experience a heightened risk of the condition (Alexander, Kohn,
Feeney and Clarke, 2000).
2
Mortality among people diagnosed with anorexia ranges from a low of 4 percent to a more widely accepted
figure of up to one in five (Dresser, 1984: 297; Griffiths, 1996; Draper, 2000: 120). However its low
prevalence, peaking at about 0.5% (or 1% in some US studies) of women aged 15-19 age band (Griffiths,
1996), means that aggregate mortality figuresof perhaps 1 death annually per million women aged 15-65
(Draper, 2000)pales against the equivalent statistic of 61 female suicides per million Australian women
(ABS Year Book 1997). 3 ‘Control’ is an apt term from the sociological perspective, but it has
strong pejorative overtones. A more neutral term, like ‘management’ highlights the positive contribution to
therapeutic outcomes, but masks the exercise of legal and social power which brings about that result.
Experiences of ‘Control’ in Anorexia Nervosa Treatment 43
Clinicians sometimes turn to law for assistance in compelling hospitalisation of people

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

and Control: Where does Formal Coercion Fit in?
The first main insightthat the instruments of social control are quite diverseis
derived from our data on the pattern of deployment of the formal and ‘informal’ measures of
social control of anorexia nervosa patients (Carney, Saunders, Tait, Touyz and Ingvarson,
2004).
Law is invoked only when other, less restrictive, measures prove inadequate. Moreover
in the case of anorexia, those legally sanctioned interventions account for comparatively
small proportions (or ‘slices’) of the lifecourse4 of the condition (Carney and Saunders,
2003). Given the legislative and clinical preference for voluntary treatment, legislatively
4
Our focus is on sociological insights revealed by taking a lifecourse perspective on the life domains of
anorexia, and the trajectories and transitions associated with it (See: George, 1999), including notions of
illness as ‘career’ (Aneshensel, 1999), coupled with insights derived from the work of Erving Goffman
and Michael Foucault.
sanctioned coercion,5 tends to be a measure of ‘last resort’; informal ‘suasion’ is both much
more common and more nuanced in its impact on the young woman (Tait, Ingvarson,
Wakefield, Touyz and Carney, 2003).
This is unsurprising, since responsibility for assisting with the management of adverse
effects of severe anorexia primarily lies with the medical profession, not the legal system, just
as in mental health generally. Legal coercion, as Hiday et al observed, ‘does not tell the
whole story of coercion’ in mental health (Hiday, Swartz, Swanson, Borum and Wagner,
2002: 122). Individuals are ‘”pushed” into care by friends, relatives and co-workers’
(Pescosolido, Boyer and Lubell, 1999: 449).
A Gradient of Forms of Suasion/coercion.
The diversity in the forms of social control able to be deployed in mental health by
clinicians or the law is illustrated by the range of different expressions it may take, running
from:
[M]ild persuasive attempts and pleas, through inducements with offers of desired objects
or services …. through threats of negative consequences such as involuntary
hospitalisation or being put out of the house, to strong application of physical force
(Hiday, Swartz, Swanson, Borum and Wagner, 2002: 124).
Even ‘informal persuasion’ takes many forms in the case of anorexia management,
ranging from ‘mere invitations’ to ‘verbal brow-beating’ or moral blackmail, as Rathner
observed,
[T]here are various social pressures that family, friends, relatives, schools and (mental)
health care personnel use in an attempt to get the sufferer to accept the idea of seeking
help: request, reasoning, persuasion, barter, bargaining, gentle prodding, enticement,
selective information, manipulation, deceiving, blackmail, … (Rathner, 1998: 185-86).
Among clinicians, a frequent next step up the compliance ladder is to encourage

compliance by employing a legal concept like a ‘contract’ (Harlow, 1998: 51), with its notion
of ‘mutual obligations’ of clinician/patient (Dresser, 1984: 323). This may be followed in
mental health settings by a ‘shadow-land’ where people are encouraged into treatment
through ‘foreshadowing’ (or even ‘threatening’) to invoke formal legal measures. Thus 40
percent of ‘voluntary’ patients studied in the MacArthur Coercion Study in the US believed
that they would have been involuntarily committed had they not signed themselves in
(Pescosolido, Boyer and Lubell, 1999: 450).
As discussed further below, stronger again in its impact on the person with anorexia are
cases of ‘strategic’ use of law. This entails strategic lodgement of legal action to compel
5
Perceptions of legal coercion do not necessarily coincide with the legal status of being a voluntary or
involuntary patient, and coercion may be ‘experienced’ in community as well as in hospital settings,
depending among other things on the perceived ‘fairness’ of the process (Hiday, Swartz, Swanson,
Borum and Wagner, 2002).
treatment (such as adult guardianship), only to be later followed by its subsequent withdrawal
once this ‘leverage’ has achieved the desired goal of ‘voluntary’ acceptance of treatment.
Of these, the least popular choice among anorexia clinicians is to obtain a formal legal
order to compel treatment (Carney and Saunders, 2003; Carney, Tait, Saunders, Touyz and
Beumont, 2003). As revealed in the next section, if both adult guardianship and mental health
laws are available, guardianship tends to be favoured over mental health, with committal
retained as the last port of call.
Use of Formal ‘Control’ in a Typical Specialist Anorexia Unit.
A clearer picture of the relationship between formal and informal measures of clinical
management of anorexia is provided by data collected from a specialist Australian anorexia
in-patient facility in the state of New South Wales (‘NSW’).6 The facility utilised a
‘progressive’ regime that minimised the level of coercion (Carney, Wakefield, Tait and
Touyz, 2004),7 within a state jurisdiction where adult guardianship options were available,
and reportedly used mainly to ‘initiate’ rather than coerce treatment (Newman, Russell and
Beumont, 1995).
On entry to the program clinicians implicitly assessed the required patient ‘status’,
deciding if legal coercion was needed, and whether to go ahead with obtaining legal backing,
and what form of order to seek (Saunders, 2001; Carney, 2002). This provided a particularly
useful case study of how power is exercised within a relatively low-coercion environment.
a. Legally-backed coercion is the exception

As more fully reported elsewhere (Carney, Saunders, Tait, Touyz and Ingvarson, 2004),
the study found low rates of resort to formal (legally mandated) coercion. Almost two thirds
of admissions (63 of 96) took place without any indication of clinical consideration of a
possible need for coercion, even though 15 of these cases (28% of the sub-sample), were
second admissions, and in another three cases (5%) it was their third admission.8
6
Data was extracted for all 119 admissions to the specialist anorexia program of the Royal Prince Alfred
hospital (RPA, a major public teaching hospital in Sydney, in the state of New South Wales), over a
period of four and a half years, mapping various factors such as case flows, characteristics of patients,
duration of treatment stays and use of legally mandated coercion. Twenty five cases with another eating
disorder or co-morbid diagnosis were discarded, leaving 96 admissions relating to 75 individuals.
Slightly over a third (36%) were under the age of 20, while 19% were people over the age of 30.
Approximately 40% of admissions were for less than three weeks, with a mean stay of 49 days (and a
maximum of 344 days). One third of the admissions were isolated events within the sample frame, while
for a quarter of the sample there were 4 or more admissions in the period.
7
Even lower proportions of coercion (approximately 16% of the samples) were found in the Iowa (US)
and Maudsley (UK) studies (Ramsay, Ward, Treasure and Russell, 1999; Watson, Bowers and
Andersen, 2000).
8
Formal coercion might have been mentioned by treating doctors, or foreshadowed strategically (Carney,
Saunders, Tait, Touyz and Ingvarson, 2004).
b. Coercion is most likely to be considered for chronic cases

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

1 2 3 4+ Unknown TOTAL
Not coerced 25 (40) 15 (24) 3 (5) 11 (17) 9 63
Considered 2 (29) 1 (14) 0 (0) 1 (14) 3 7
coercion
Coerced 5 (19) 1 (4) 4 (15) 12 (46) 4 26
Total 32 (33) 17 (18) 7 (7) 24 (25) 16 96
c. Guardianship is seldom used on its own, but mental health committal is

popular.
When formal coercion was canvassed by clinicians, as it was in 27 percent of cases, it
usually led to an application for an order. But adult guardianship, on its own, was the
exception: only 3 admissions (11.5% of 26 admissions backed by a legal order) solely
involved adult guardianship.
Mental health committal orders were much more popular with clinicians as a ‘stand-
alone’ order, accounting for 44% of all such admissions. Slightly more than half of these
were based on the medical complications of anorexia itself (6 of 11 cases), while the others
were grounded in supervening factors such as depression, delusional behaviour or threats to
the health and safety of the person.
d. Mental health committal is also commonly used in conjunction with/after

guardianship.
The study data revealed that mental health committal is also quite commonly used in
conjunction with guardianship, or subsequent to an earlier order for adult guardianship. Forty
two percent of legally coerced admissions were of this character.10
9
If age is a proxy for ‘maturity’ (or insight) it would appear that this is not a factor in deciding to obtain a legal
order. The mean age at admission was almost identical for the coerced (24.5 yrs) and the non-coerced group
(24.2 yrs). By contrast, those for whom coercion was considered but not invoked were older (average age 29.6
yrs).
10
Guardianship allows appointment of a third party to provide consent to medical treatment (one third of the
‘mixed’ order cases), or to make decisions about proposed behavioural therapies (two thirds of such cases in
the study).
Tracing ‘Strategic’ (or Shadow of Law) Uses of Formal Coercion
The normative character of transactions taking place in the ‘shadow’ of the law has long
intrigued researchers (Eg Mnookin and Kornhauser, 1979 on divorce bargaining), with recent
examples including the strategic influence of law on negotiation of child custody disputes
(Jacob, 1992), the management of alleged promiscuous sexual ‘delinquency’ of young
women (Ajzenstadt and Steinberg, 1995), or procedural rules impacting on pre-trial civil
settlements (Main and Park, 2000; 2002), and even law/power influencing World Trade
Organisation bargaining (Steinberg, 2002).
This phenomenon was detected in anorexia cases by members of the adult guardianship
tribunal in the state of New South Wales, Australia (‘NSW’). Members observed that
guardianship applications were being lodged strategically to persuade patients reluctant to
consent to proposed treatment regimes, and were then allowed to lapse once cooperation was
forthcoming.11 This was confirmed by initial data showing that nearly a third (four of 13
people, 2 then to be heard) of applications and reviews dealt with in the 2000-2001 period
were withdrawn prior to hearing.12 It was further refined by a more detailed review, tracking
the history of guardianship applications in respect of anorexia nervosa patients.
a. Guardianship is lightly used

Data for the ten year period 1994-2003,13 indicated that the tribunal has been lightly used
for anorexia cases over much of its history. As shown in the next table, applications are
patchy at best.
Guardianship (GO) Applications 1994-2003.
STATUS OF Year Total

APPLICATIONS
‘94 ‘95 ‘96 ‘97 ‘98 ‘99 ‘00 ‘01 ‘02 ‘03
1 1 1 1 1 4 7 4 3 3 26
Withdrawn 1 1 0 0 0 2 0 2 0 0 6
Adjourned 0 0 1 0 0 0 0 0 0 0 1
Dismissed 0 0 0 1 0 0 0 0 0 0 1
GrantedGO 0 0 0 0 1 2 7 2 3 3 18
It can be seen that guardianship was rarely used in the first half of the decade, with only
an average of one application a year. Indeed, apart from a peak of seven applications in 2000,
only three or four applications were made each year in the latter part of the decade.
Seven (27%) of the applications over the decade involved more than one application,
however.
11
Personal communication with NSW Guardianship Board members, Thurday 11 October 2001.
12
Statistics supplied by the NSW Guardianship Tribunal.
13
De-identified data extracted by Esther Cho of the Guardianship Tribunal on 8 August 2003.
b. Strategic withdrawals are not always the end of the story

Fewer applications were withdrawn than was expected: just six of 26 applications (or
23%). Closer study, however, revealed that several withdrawn cases reappeared in later
years.
Thus the sole case from 1994 (‘Abigail’, not her real name) appeared on three occasions
in all. She had a guardianship application lodged and withdrawn in 1994. She reappeared in
1996 when a financial management order was granted (and guardianship adjourned). And in
1997 another guardianship order was sought (but denied by the Tribunal).
Likewise ‘Eve’, the sole case in 1995, had her application withdrawn in that year. But
she was placed on guardianship when she reappeared six years later in 2001. For her part,
‘Hanna’ saw two applications withdrawn in 1999 and 2001, before finally being placed on an
order in 2003. ‘Martha’ (withdrawn 1999, granted 2000) and ‘Rebecca’ (granted 2000,
withdrawal in 2001) round out these cases of an apparently ‘strategic’ resort to the Tribunal.
The remaining two cases where multiple appearances are recordedRachel (GO orders
in 1998 and 2003) and Leah (orders in 1999 and 2003)were the only ones where all
applications are recorded as having proceeded as lodged. Fieldwork reports by ‘Fiona’ (not
her real name) of another otherwise unrecorded episode suggests that this may understate
such cases, however, with paperwork mobilised to trigger acceptance of admission without
leading to a ‘listing’ of the case for hearing:
There was actually an application for an order to appear before a tribunal and all the rest
of it….. Yeah, well it’s funny ‘cos it said on the envelope it had been delivered by the
bailiff and it was in my mail box. And I thought oh great, and so I thought well I don’t
want to go through all that crap and it was at that time that I didn’t really, you know,
really my head wasn’t there and I really wasn’t there.
The first time I was already in hospital when I got the letter so it was a bit late but this
time I got the letter here and that’s when I got my friends who are lawyers and I was
saying ‘what can I do? What can I do?’ They were saying ‘that we don’t think you
should resist. We just think you should go to the hospital’. I said say ‘I’m not going to;
how can I appeal this or whatever’. And they said ‘you’ll have to go to the tribunal’ and
yeah …
What we term the ‘strategic context’, then, is pertinent to choice of pathway, including
whether to rely on the ‘shadow of law’, as in the case of lodging proceedings which are later
withdrawn.14
Another feature of guardianship applications deserves mention: almost all of these were
lodged by (or more usually) on the instigation of the treatment team.15 Unlike most other
types of adult guardianship application, very few applications appear to have been lodged by
14
As indicated previously, an alternative explanation can be made in terms of regimes such as clinical regimes
such as ‘close monitoring’ or ‘assertive treatment’, often adopted with ‘dual disorder’ patients, where such
forms of ‘intensive supervision [are] at times provided with the client’s consent and at other times is provided
involuntarily’ (Noordsy, Mercer and Drake, 2002). Indeed such regimes may occupy the hinterland between
community treatment orders and more ‘voluntary’ programs (Davis, 2002).
15
Clinicians were named as applicants in 14 cases, while family members were the nominal or actual applicants
in 8 cases (in 4 withdrawn matters the applicant was ‘to be advised’, implying that clinicians had a hand in
initiating the matter): data referred to at n 15 above.
friends or family members on their own volition. This suggests that the applications were
seen as something that would enable treatment rather than as a challenge to medical authority
(also: Newman, Russell and Beumont, 1995: 58).
C. Disseminated Power and Control: Towards self-management/control?

As we have already seen, clinicians, and the services with which they are associated, are
key players too. As one commentator observed,
[d]ealing with any health problem is a social process that is managed through contacts or
social networks that individuals have in the community, the treatment system, and social
service agencies, including self-help groups, churches and jails (Pescosolido, Boyer and
Lubell, 1999: 455).
So an analysis from the standpoint of managers and regulators alone, without regard to
the wider context and web of relationships within which a patient operatesis likely to be
unduly simplistic.
Our second main insightthat power and control is a product of interaction between
patient identity and the broader social environmentis best shown in one of our case studies.
‘Felicity’s’ reaction to one episode is described as follows:
I was being seen as an outpatient at [X hospital] by a doctor that I’d … seen at the
Children’s Hospital … And I hated the doctor there … hated him with a passion …. So
they said, ‘Right. We’re going to tube feed you’. And they got the guardianship order out
against me … Because they knew I’d fight it [being tube fed] and pull it out and do
whatever. They threatened to send me to a locked ward where I would be physically
restrained … They threatened to send me to … to the psychiatric unit [at a nearby
hospital]. And that was enough for me … to comply with what they wanted for the time
being. (Emphasis added).
There are several factors in play here.

First, Felicity is driven by her violent dislike of a particular clinician at an alternative
facility. Despite being tube fed, and despite being coerced into acceptance of this course by a
legal order (adult guardianship), her ‘hatred’ of that other clinician was apparently the more
powerful force motivating her (reluctant) compliance.
Second, she was fearful of the loss of control of being placed in a locked ward and then
physically ‘restrained’, and of the prospect of the stigma of transfer to a ‘psychiatric’ unit, as
foreshadowed by her treatment team. This combination of disciplinary influencesthe
interplay between dislike of a particular clinician, threats to switch service settings, and the
foreshadowing of psychiatric committalwas sufficient to win her grudging compliance. She
decided to ‘comply with what they wanted’; at least ‘for the time being’.
As Foucault demonstrated, power is dynamic rather than static, and is often highly
disseminated rather than always channelled through particular structures. Institutions not
commonly thought of as part of the law, such as the home or the hospital, may become sites
for expression of such poweroften linked in with complex social networks, and shaped by
its point in history. His focus is on the ‘techniques’ for the exercise of power, and the
dialectic of the dialogue of application and resistance to that power. It is a truism that law is
power, but that its power is mediated in many ways.
Power is shifting and unstable, and it takes various forms other than the classical
‘disciplinary’ form so sharply expressed in anorexia management in the form of legally
compelled detention for treatment, or imposition of nasogastric feeding (Carney, 2002). For
Foucault, power was not so well captured by such metaphors of ‘command and control’.
Instead it was located in the ‘governmentality’ space. A space lying between mere game-
playing contestation and the ‘state of domination’ constituted by its expression in legal
coercion, or as the ‘sovereignty’ of power (Rabinow, 1997: xvii). In this view, a regulatory
regime may be experienced as beneficent, indeed sometimes even pleasurable, and freely
chosen (Shearing and Stenning, 1984). Shearing and Stenning show how Disney World is
constructed to ensure that consumers are complicit in their own security (347), that self-
regulation (assisted when necessary by staff dressed up as Mickey Mouse or other characters
from the Walt Disney imaginary) combines freedom and security.
The treatment of anorexia nervosa is harder to deliver without coercion than a plunge
down Splash Mountain, but the question posed is still relevant: how can governance be
exercised in a way that is experienced as freely chosen?
Power in ‘Pastoral’ Settings
Power may also take a ‘pastoral’ form of course, as in the carer relationship in nursing:
Nurses … are in direct contact with individuals, groups, communities, and populations
[constituting] a powerful group of experts …. Working at the junction of the individual
and collective body within power relations that promote and recuperate life, nurses are
able, through their interventions, to mold, conduct or affect people as well as to
construct, with the help of other health care professionals, people's subjectivities.
(Holmes and Gastaldo, 2002).
These ‘subjectivities’ (sometimes called ‘bio-power’) principally include the ‘self’ or

‘identity’ of the patient. So self-images are shaped by these exchanges. Exchanges which are
never neutral but which may be advantageous or ‘controlling’ in character.
As Powers has recently argued, even as superficially attractive a goal as pursuit of
‘empowerment’ in therapy can constitute a technique for the exercise of power. This is
because clinicians may subtly ‘privilege’ the preferred option supposedly ‘chosen’ by the
patient (Powers, 2003). Nursing too involves deploying techniques ranging from
‘disciplining’ to ‘promoting discourses that construct desirable subjectivities’ (Holmes and
Gastaldo, 2002).
Of course care must be taken not to oversimplify the application of this analysis (Cheek
and Porter, 1997). While therapeutic interventions lend themselves to analysis from this
perspective, this does not displace the legitimate role played by the psychodynamics of some
conditions (Glass, 2000). Nor does it mean that power and control are inimical to the interests
of the patient: processes of socialisation and formation of identities are shaped by power, and
such acculturation may facilitate social functioning or the capacity to manage chronic
conditions like anorexia (Aneshensel, 1999: 597). Indeed, given that lack of ‘insight’ (denial)
is a central ingredient of anorexia, the role of access to ‘normalising’ social interactions and
supports may be central to its satisfactory management (White, Bebbington, Pearson, Johnson
and Ellis, 2000).
In-patient care for psychiatric conditions has altered quite dramatically over the last
several decades, however. The hospital setting is no longer the primary ‘place of observation,
of diagnosis, of clinical and experimental identification [and] immediate intervention’, that
once was the case when the ‘infection’ model of health was dominant (Foucault, 1997: 40-
41). Hospitals (and medicine) no longer serve as the primary agents for ‘clarifying and
purifying’ the disease entity. That role has been undermined both by the problematic status of
‘disease’ within psychiatry (Dawson, 1996; Beumont and Carney, 2004), and by the
relegation of hospitals to brief interludes in the management of conditions like anorexia
(Carney, Tait, Saunders, Touyz, Wakefield et al., 2003).
Power as Experienced by Anorexia Patients
Consequently, the ‘community/family’ space is now much more central. This is the new
site where power and control is experienced by sufferers of conditions like anorexia (Hiday,
Swartz, Swanson, Borum and Wagner, 2002: 123). Power in the case of anorexia
management, we suggest, tends to find its expression in the fluidity of the ‘negotiations’
about the relationships forged both in this societal space, and those within the hospital
setting.
Moreover the currency used in negotiations within the setting (hospital or community)
where the person with anorexia is currently residing, frequently harks back to, or anticipates,
life in the other sphere. So conditions of life in the community loom large in the life of
hospitalised patients. And in similar vein, the prospect of a return to hospital also shapes the
lives of those currently living in the community.
One of our qualitative interviews illustrates this interpenetration of the two ‘worlds’, but
also brings out the multiple levels of that relationship. It shows that sometimes the legacy of
past experience, however unpleasant, can leave a more positive legacy of ‘control’ for the
future. Kelly’s opinion of the outcome of a previous period of hospitalisation is a case in
point:
I think hospital was good in a way, as I wouldn’t want to ever go there again. That’s the
only good thing about the hospital experience. I’m terrified of ever going there again.
(Emphasis added).
Turning to her ongoing issues with her weight management, she brought out the sense of
being caught in a kind of systemic ‘limbo-land’ or twilight zone in terms of her weight, when
she said:
I know where this is going to end up, in hospital again. That terror of having control
taken off me. It’s almost like um, I think a lot of people do it, who have had an eating
disorder, or anorexia and have been under weight. You can kind of keep yourself
between these safe weights that aren’t perhaps as healthy as they should be but aren’t
going to get you put in hospital. It‘s a pretty miserable way to live. Look, you know, it’s
hard because I think the system makes it almost like, because of the way you’re treated in
hospital you kind of afterwards get stuck. I guess there are times where I feel like that. I
get stuck in this: ‘I’m not totally over it or totally well’. Not going to, um way too
terrified to [end up in] hospital again. (Emphasis added).
As can be seen from this passage, previous unhappy experiences (in this case of
hospitalisation) maintain an element of on-going control or influence over the life course of
the patient with anorexia on return to community living. Kelly’s experience is that this is both
empowering and controlling: empowering in the sense of reminding her of the unpleasant
consequences of an acute episode, but paradoxically ‘controlling’ as well, in the sense of
maintaining its thrall over her life and her management of the condition.
So power and control can be very subtle and highly nuanced.
The interview with ‘Tess’, the sister of ‘Kate’ (the patient), where she is describing their
mother visiting Kate in the hospital, shows the way other more intimate worlds can inter-
relate with each other –
[E]ven in hindsight again you could probably imagine her sense of failure and
everything. And she couldn’t even come to the hospital. And when she did she was
hostile. And Kate used to dread her visits. (Emphasis added).
Kate’s mother, then was a powerful part of this woman’s ‘social context’. Blaming
herself for ‘failing’ her daughter, she found it a great ordeal to visit her in hospital. When she
did so, she projected her ‘hostility’. As a result, Kate ‘dreaded’ visits. As elaborated by Tess
when she was asked how she herself came to understand that her sister was suffering from
anorexia, she recalls how her mother presented herself as the ‘victim’ of Kate’s vindictive or
‘attention seeking’ behaviour:
But Mum was also, Mum didn’t know how to deal with it. She didn’t have the emotional
ability or any type of insight to deal with it. Um, and just saw it as, my mother has
always been a victim, and she thought Kate was doing something to her and directly
punishing her for something. So you know, it was ‘the little bitch is only doing it for
attention’. That sort of thing, which exacerbated the problem.
Kate bought home a Foundation form saying there’s an information night on anorexia
and Mum said ‘what do I want to learn about that shit for’ and she ripped it up in front of
her. Which is another kick in the guts.
So in Kate’s case, one of the most powerful set of forces operating in her social
environment was the presence of her mother and the negative images and tension stemming
from her lack of insight into her daughter’s condition. This was a major complicating or
compounding influencea control or constraint standing in the way of a more therapeutic
acceptance or resolution of her condition.
Likewise in the case of ‘Kelly’, who described the onset of her issues with food in the
following way:
Mum’s very controlling about food with all of me and my sisters. You weren’t allowed to
eat at, like, when you got home from school or like you weren’t – she was just really
really controlling. So we would all of us sneak food from the kitchen from between when
we got home from school and she got home from work and so we’d all like cut the slice
carefully and take it into our room and hide it in the desk draw and hide it for later. It was
like a little game with my family so I guess we’d all sort of had… Food was just a big
issue. I’ve tried to talk to my mum. I’ve tried to work it out with her why it was such a
big issue for her. She had her own problems.
Here the pattern of family ‘culture’ or rules about access to food within the family is
identified as a contributing factor in the emergence and continuation of Kelly’s anorexia.
Again the ‘family food discipline’ is continuing to operate as a form of control into the
present day.
Moral Career
When a young woman does appear to gain greater insight into the anorexia and become
more accepting of treatment interventions and maintenance of minimum weights, there is a
tendency to see this as ‘progress’, and a lessening of the web of ‘control’.
But is it really that she is ‘getting better’ or is she becoming more ‘managed’ and
accepting the authority of her doctors?
a. The ‘stage’ of the life-course of the illness ‘career’?

‘Time’ is a somewhat neglected variable in the sociology of mental health, the
incorporation of which enables a richer understanding to be gained of:
[H]ow social factors interact with the risk, expression, course, and outcomes of mental
illness, taking into account the longer term context, at least in terms of age of onset,
duration of the episode, history of past episodes, time to recovery and so forth (Bruce,
1999: 53).
Given its often chronic, fluctuating pattern, anorexia is one where the ‘stage’ of the
condition is significant. Goffman's term ‘moral career’ is therefore an apt one to apply in
studying this aspect of the changing experience reported by patients over the course of
treatment (Aneshensel, 1999), just as has proved to be the case with another eating disorder,
that of compulsive eating (O'Brien and Bankston, 1984).
The concept of career traditionally focuses on the external attributes of the professional
‘position’ a person holds, its legal authority, the associated lifestyle, or the relationship to the
‘significant society’ or institutional complex. But for Goffman it was the personal interior
which was significant, such as the ‘image of self and felt identity’. Or as he wrote in the essay
on the ‘moral career of the mental patient’:
[My] main concerns will be with the moral aspects of careerthat is, the regular
sequence of changes that career entails in the person's self and in his framework of
imagery for judging himself and others (Goffman, 1961: 119).
b. The ‘pre-patient’ and the ‘patient’ phases of identity.

Goffman distinguished between the ‘pre-patient’ and the ‘patient’ phases of a
sociological transition which he argues can serve to construct one’s ‘self identity’ (Goffman,
1961; 1968). Our data does not directly capture the early stages of the management of the
pre-patient phase, but the resistance to acceptance of anorexia which characterised the state
of mind of patients admitted to the RPA unit offered rich data on the possible transitions
from pre-patient to patient and ‘managed patient’ phases (Pescosolido, Boyer and Lubell,
1999: 458).
Goffman shows that the reaction of others to a person’s condition, once this reaction is
internalised, can displace a person’s previous identity and see that identity reconceived (and
processed) according to the expectations and requirements of more powerful players, such as
clinicians and other networks (Aneshensel, 1999: 596). For instance a former mental patient
residing in supported boarding accommodation may develop ‘classifications’ of those who
can, and who cannot, readily take the next step back into fully independent living (Shaw,
1991). Part of that process for a person with anorexia entails convergence towards a new
image of the ‘self’, including the constraints of the role and expectations about how to act as
a group of fellow sufferers, and in relationships to staff (whose transition from general to say
psychiatric nursing may exemplify a 'moral career': Caygill, 1993).
One aspect of the pre-patient stage that Goffman identifies is the formation of an
alliance, or even conspiracy, between the medical staff and the family. The latter are
persuaded to take on the view of the person presented to them by medical authorities. This
could lead to the person feeling further isolated and betrayed, as those who were believed to
be supporters become revealed to be allies of psychiatrists (1961, 129). Families were torn
between their desire to ‘support’ the family member or to ally themselves with the doctors.
Guardianship can offer one way of addressing this dilemma, by appointing a person,
independent of both family and treatment team, who can participate in treatment and lifestyle
decisions.
In his book on Stigma, Goffman wrote of the duality of self-images which emerge, one
representing the viewpoint and values of so-called ‘normal’ society, the other the subjective
experience of the person with the condition (Goffman, 1968: 45), and the four common
‘patterns’ of response to that dissonance:
i) dual acquisition of both perspectives;

ii) family insulation from outside perspectives serving to delay appreciation of societal
attitudes;
iii) late-in-lifecourse discovery of a devalued identity (either prospectively, leaving the
past intact; or retrospectively, involving reconstruction of past identities; and
iv) those socialised in the ‘alien’ community and who make the transition to values
shared by the community at large (id, 45-49).
Likewise Talcott Parsons’ work on the ‘illness career’, starting with perceptions of
undifferentiated ‘symptoms’ (such as lack of good health), leading on into possible adoption
of a social condition or ‘sick role’, and development of (medical practitioner-validated’)
‘patient’ roles. A trajectory culminatingat its most optimisticin ‘recovery’ following
treatment (Pescosolido, Boyer and Lubell, 1999: 443). But one where the network of family,
friends and significant ‘others’ may mediate the choice of pathways taken (or resisted) at any
one time (Pescosolido, 1991).
c. Fieldwork illustrations of compromised identity.

These frameworks provide a useful lens for understanding the way some anorexia
patients ‘mould’ their behaviour to accommodate preservation of relationships with
significant others, such as family, partners or therapists.
Thus ‘Kate’, when discussing her relationship with her previous therapist, said:
And so I was always used to keeping things to myself because ‘Mary’ said I was being
provocative by voicing how I was feeling or just voicing how I felt about something, my
perception of things, so that in the end I just had to tell her what she wanted to hear to
keep her happy. (Emphasis added).
It is clear that Kate managed the way she presented her ‘public’ self in order not to
unduly offend her therapist. Rather than fully express her feelings and thoughts, she kept
certain things to herself. Obviously this avoided the tension and trauma of what she described
as her more ‘provocative’ behaviour. But it also entailed a moulding of her relationship with
the therapist, so thaton a superficial level at leastit was a ‘happier’ interaction. And, as a
result of this internalisation of more negative thoughts, perhaps also a more ‘therapeutic’
relationship as well, in that there was more chance for mutual respect to build?
Sometimes there is an intersection with the ‘suasive/coercive’ narrative as well however.
Thus Kate also talked about conforming to clinicians expectations to avoid transfer into the
public system:
So I’ll just never forget that, of having to prove, and then that whole admission was one I
think I mentioned where I was constantly, I was putting all my effort into trying to be
such a good patient. I had to make sure that um, you know, that my reputation somehow
had to be salvaged, even just a little bit. And that, um, went against me further down the
track big time in myself. In my own, on my way to recovery really, set me back in my
own way. It was just that if they didn’t accept me then they would transfer me to Royal
Melbourne [Hospital]. I felt desperate, I didn’t want to be in there, but I knew I couldn’t
leave. So, and I remember trying to leave once, and they put in a psychiatrist in front of
me, she was Chinese, and she said she’d make me involuntary. So it was like I have to do
this, be the good patient. (Emphasis added).
There are at least two forces at work in Kate’s mind here.

First, she was concerned to preserve her ‘reputation’; her reputation as a ‘good patient’.
Her identification with herself as a patient reflects an important transition: no longer a person
in denial of being ‘ill’, she has been socialised into acceptance of the ‘sick role’. Consistent
with the medical model of diagnosis, identification of cause and application of curative
treatment’, Kate is at least prepared to talk the language of illness/recovery. Not only did she
want to be good at ‘anorexia’ she also wanted to be good at being treated for ‘anorexia’.
Good enough at ‘anorexia’ to need intensive inpatient care but good enough to be able to stay
at her preferred inpatient care facility and to be considered a ‘good patient’.
Yet even this is a qualified acceptance: her identity is partly that of the cooperative
patient, but it also has strong connotations of acceptance of her present place and regimen of
treatment as an appropriate management of her ‘slightly deviant’ condition. Her language
here seems little different to that of a person on probation, who has reconciled themselves to
the advantage of being a ‘good’ probationer (just as people who are incarcerated usually
become acculturated to being a ‘model’ prisoner).
The second force at work is even more consistent with an analysis in terms of power,
stigma and social control. For Kate is articulating a coldly rational analysis of the ‘least worst
option’. She may not have enjoyed treatment where she was, but she was fearful of a ‘transfer
to Royal Melbourne’. The threat of a transfer, playing on what she knew about that facility as
well as on her uncertainty about the ‘unknown’, was a subtle but very effective expression of
power which helped control her current compliance with her treatment. Because these future
scenarios were playing on her mind at the time, Kate decided to be more cooperative. She
internalised the disseminated forms of control operating in her clinical environment.
This case is a classic illustration of what we mean when we say that power is a product of
the intersection between personal identity (the ‘good patient’) and the highly disseminated
ways in which power is dispersed in society, outside the formal legal system and authority
structures usually the focus of attention by lawyers.
Conclusion
Anorexia nervosa remains one of the difficult and frustrating conditions for medical staff,
in part because of the resistance of patients to therapies intended to cure them. This may be
experienced as ingratitude not just from patients themselves (who may be presumed to ‘lack
insight’), but by feminist groups raising civil liberties objections. Obtaining informed consent
is an ongoing concern, and developing compliance strategies becomes a major focus of the
intervention. From the perspective of patients, enduring the regulatory regime imposed on
them becomes a challenge and can be experienced as harsh and threatening. Issues of power
and control are therefore major ongoing issues in the treatment of the condition.
And yet, the law is rarely invoked, at least formally. Control is exercised not through the
majesty of a court or tribunal order but through the routine practices of the clinic, through
disciplinary practices embedded in everyday life. This includes daily routines of eating and
washing, informal or written ‘contracts’ and other behavioural measures, regular surveillance
and measuring, interactions with staff, visits and activities, and all the other rituals of
institutional living.
The regulatory regime does not just touch on practices; it is also explicitly targeted at
identities. This includes self-image, and the attitudes to the body. It also shapes what
Goffman refers to as the ‘moral career’ of the patient. This includes learning to play the
‘patient role’, to ‘be’ an ‘anorexic’, a credible exemplar of a condition. This role may be
learned by observing and modeling oneself on peers, or by responding to the reactions of
others. But a moral career may also lead to displaying signs of being on the road to recovery,
whether through compliance with therapies or screening information suitable for the ears of
therapists. The language of ‘cure’ and ‘recovery’ providing a framework for an ongoing re-
shaping of identity.
If intrusive medical and behavioural intervention to re-shape both practices and identities
rarely engages the law, the question must be asked – why not? After all this is precisely the
sort of situation where fundamental principles of right to life and right to control over one’s
body come most acutely into collision. Is the law so clumsy that it fails to provide a
mechanism for handling these issues in a timely and sensitive way? Or is the law being
avoided because less restrictive options work most of the time?
Our answer to these questions, based on an interpretation of Foucault, is that the
regulatory regimes that shape the treatment of conditions such as anorexia nervosa,
constitute, and in a sense, are ‘the law’. How ‘duty of care’ is operationalised in a hospital
environment, how medical expertise has been translated into medical authority, how therapies
are developed and tested through a scientific process, how interactions between ‘experts’,
‘carers’ and patients are mediated through conventions and rules, indeed how ‘empowerment’
is conscripted in the service of control―these practices and many more help to shape the
regimes of governmentality that operate within the setting of the eating disorder clinic or
hospital. Some of the ‘rules’ are based in part on legislation, or codes of ethics grounded in
international covenants. But many of them are ‘informal’ in the sense that they operate
outside, or ‘in the shadow of’, the formal legal system.
What was perhaps most interesting about the use of the law for those included in this
study was the way the possibility of legal orders provided a source of authority within the
clinical setting. This could include foreshadowing, strategic lodging or withdrawal of
applications, or use of guardianship to provide substitute consent rather than the more
extensive mental health orders. Rather than ‘the law’ being something external that imposed
itself upon patients and clinicians, it became instead a new source of power for medical
therapists.
Such a role for the law could perhaps be seen as ‘professional capture’ by those
supposedly regulated by a legal regime, or an example of how a system set up to protect
patient rights had the unintended consequence of strengthening medical authority. However
there is another interpretation, based on Goffman’s understanding of the complicity involved
in sustaining a role. Taking on the role of the patient involves ‘participating in reciprocally
sustained fictions’ (1961, 142). The ‘fiction’ of acting ‘responsibly’ without coercion is an
important part of the therapeutic framework in many contemporary treatments, and this
fiction can best be sustained when legal coercion is not formally employed. Indeed the
availability of legal measures may ironically reduce the need for physical constraints. The
patient learns to provide consent ‘freely’, to make the ‘correct’ choices, to accept the
‘empowerment’ regime that is made even more convincing by the threat of legal intervention.
In time the constraints learned in this way become part of the new role, that of the
‘recovering’ patient. The fiction employed so hesitantly at first becomes part of the new
identity. The patient has become an active participant in the governance of self.
The question posed by the therapeutic jurisprudence literature on the work of tribunals
and other institutions (McMahon and Wexler, 2002/3; Freckelton, 2003) is whether this
somewhat duplicitious alliance between law and medicine really does promote therapeutic
outcomes (Wexler and Winick, 1996; Wexler, 2000; Winick, 2003). If tribunals and courts
have become an adjunct to medical authority rather than an independent check on it, how can
we be sure that this authority is subject to appropriate accountability procedures?
‘Control’ so far as anorexia nervosa patients are concerned, is a highly nuanced, and
quite diffuse and diverse concept. It is neither formal legal control, time-delayed imposition
of coercion, nor social control achieved under the thrall (or in the ‘shadow’) of law. It is at
times all of those things and much more.
However the experiences reviewed here might we think best be captured by the label of
‘disseminated power and control’.
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Chapter IV
Secondary Anorexia: A Neglected

Issue in the Optimal Management of
Patients Suffering from Acute and
Chronic Diseases
Alessandro Laviano*, Michael M. Meguid,

Antonia Cascino and Filippo Rossi-Fanelli
Department of Clinical Medicine,
University La Sapienza, Rome, ITALY
Department of Surgery, University Hospital, SUNY Upstate Medical University,
Syracuse, NY, USA
Abstract
Anorexia and reduced food intake are relevant issues in the management of patients
suffering from acute and chronic diseases, including sepsis, cancer, chronic liver failure,
chronic renal failure, etc. In acute diseases, anorexia does not represent a primary
therapeutic target, since effective treatment of the underlying disease rapidly ameliorates
food intake. In chronic diseases, anorexia impacts on patients’ prognosis, since it
contributes to the development of malnutrition, thereby increasing morbidity and
mortality, and impinges on quality of life. Accumulating evidence indicate that anorexia
associated to different diseases is multifactorial in its pathogenesis, and suggest that most
of the hypothalamic neuronal signalling pathways modulating energy intake are
involved. A number of factors are considered mediators of anorexia, including hormones
[e.g., leptin], neuropeptides [e.g., NPY], cytokines [e.g., IL-1, IL-6, TNF] and
neurotransmitters [e.g., serotonin and dopamine]. Their modes of action do not appear to
be separate and distinct, rather they are closely inter-related. However, convincing
*
Correspondence: dr. Alessandro Laviano, Department of Clinical Medicine, University La Sapienza, viale
dell'Università 37, 00185 Rome, ITALY; tel: +39-06-49973902; Fax: +39-06-4440806; E-mail:
alessandro.laviano@uniroma1.it
64 Alessandro Laviano, Michael M. Meguid, Antonia Cascino and Filippo Rossi-Fanelli
evidence suggest that a hierarchical organization exists in which cytokines play a key
role, triggering the complex neurochemical cascade which leads to the onset of anorexia.
Cytokine increased expression during disease inhibits the hypothalamus to appropriately
respond to peripheral signals, by persistently activating anorexigenic systems and/or
inhibiting prophagic pathways. Hypothalamic monoaminergic neurotransmission may
significantly contribute to these effects. Thus, the optimal therapeutic approach to
anorectic patients should be based on both changes in dietary habits, achieved via
nutritional counselling, and drug therapy, aimed at interfering with cytokine expression
or hypothalamic monoaminergic neurotransmission.
Key Words: anorexia, food intake, malnutrition, chronic diseases, brain monoamines,
hypothalamus
Introduction
Anorexia is a very well-known word among general audience. Very often newspapers
and TV news report dramatic stories about young girls who let themselves starve to death
because they could no longer stand their physical shape, whose perception has become
pathologically deranged. Therefore, common people, but some physicians as well, believe not
only that anorexia and anorexia nervosa are synonymous, but more importantly that there is
no clinically relevant syndrome characterized by reduced food intake other than anorexia
nervosa. Actually, the clinical problem of reduced appetite and food intake is much more
pervasive than that represented by anorexia nervosa alone. Indeed, almost every disease,
either acute or chronic, is associated with the loss of appetite. In this light, although the
prevalence of anorexia nervosa is raising among young girls in western countries, it is much
smaller than the prevalence of secondary anorexia, i.e., the anorexia occurring in patients
suffering from acute or chronic diseases. If we consider that secondary anorexia characterizes
highly prevalent diseases (cancer, liver cirrhosis, chronic renal failure, chronic obstructive
pulmonary disease, ) while secondary anorexia occurs in specific populations, the overall
magnitude of the clinical issue represented by secondary anorexia becomes self-evident,
anorexia nervosa thus representing the tip of the iceberg. Also, an important difference
between anorexia nervosa and secondary anorexia should not be overlooked: young girls
suffering from anorexia nervosa do feel hunger, but they force themselves not to eat;
anorectic cancer patients, or uremic patients, or liver cirrhosis patients really would like to
eat, but they can’t because they lost their appetite.
Definition
In medicine, diagnosis is made based on specific combinations of symptoms and signs.

However, symptoms or constellations of symptoms [i.e., syndromes] per se may not be
specific of a single disease. In this light, the anorexia syndrome represents a suitable
example, since it characterizes the clinical course of different diseases. Therefore, anorexia is
a highly prevalent syndrome which heavily impacts on the prognosis of patients suffering
Secondary Anorexia 65
from acute (i.e., sepsis) and chronic diseases (i.e., cancer, liver cirrhosis, chronic renal failure,
COPD).
Anorexia is defined as the loss of the desire to eat, leading very often to reduced food
intake. As a consequence, reduced calorie intake should not be considered as being part of
the clinical definition of anorexia, rather its consequence. However, based on their strict
interdependence, they are often used as synonymous.
Anorexia is among the physiologic responses, including immune system activation and
increased energy expenditure, prompted in the host by internal/external insults. Initially, all
these changes are believed to help the host organism to fight back the invasion. As far as
anorexia is concerned, the beneficial effect is usually supposed to be related to a number of
mechanisms. First, the host saves energy by not moving around in search for food, and this
also reduces heat loss that would otherwise occur from increased convection. The conserved
energy is then available for the body’s fight against disease. Second, the suppression of food
intake during disease may be important in reducing the availability of nutrients essential for
invading organisms and reducing energy expenditure for digestion. The beneficial effect of
the initial anorexia during disease is supported by a classic study in which force-feeding of
experimentally infected mice increased mortality rate [1]. Nevertheless, despite being
beneficial in the beginning, long lasting anorexia compromises host defence and ultimately
delays recovery.
As a consequence, the clinical relevance of anorexia varies according to the time course
of the underlying diseases. In acute clinical states [i.e., sepsis or influenza infection],
anorexia does not represent a therapeutic target, since the quick and effective treatment of the
underlying disease is the main goal inevitably leading to amelioration of eating behaviour. In
chronic clinical states, anorexia should be considered and treated because its long lasting
effects on food intake and quality of life impact on patient’s nutritional and psychological
status, and therefore on his/her prognosis.
Despite the well-known effects of anorexia on patients’ prognosis, the interest of
clinicians toward this syndrome is much less than it should be deserved. As an example,
cancer anorexia is highly prevalent and clinically relevant. Yet, very often oncologists do not
consider it as a symptom deserving investigation and treatment. An insight on the reasons for
their negative attitude toward anorexia, and more broadly toward supportive care, can be
drawn by a recent survey of the European Society of Medical Oncology [2]. Approximately
900 oncologists responded to the survey, the large majority of them being from Europe and
involved with advanced cancer patients. Interestingly, almost all of the responding
oncologists agreed that all advanced cancer patients should receive concurrent supportive
care, even if they are receiving antitumour therapy, and that medical oncologists should be
expert in the management of physical and psychological symptoms of advanced cancer. Yet,
only a minority of respondents reported to collaborate often with a supportive care specialist,
while 42% felt that they were inadequately trained to this task. Surprisingly, 15% of
respondents still believed that palliative care begins when medical oncology ends, while an
astonishing 30% did not disagree with the statement “palliative care specialists steal patients
who would otherwise benefit from medical oncology”. Therefore, it appears that most
oncologists recognize the importance of supportive care for patients with advanced cancer.
Despite this, many are prepared inadequately for these tasks, and actual participation levels
commonly are suboptimal. On a broader perspective, it could be concluded that clinicians

may be aware of the clinical impact of anorexia, but their training to recognize and treat
anorexia is not sufficient.
Diagnostic Tools
It is still difficult to clearly define and diagnose anorexia. Sometimes, a visual analogue
scale is used, which is a useful tool in epidemiological or prospective studies but may prove
quite unreliable if small changes in appetite need to be detected [3]. Very often, the diagnosis
of anorexia is based on the presence of reduced energy intake, even if this procedure could be
misleading, since the reduction of ingested calories might be the consequence of dysphagia or
depression rather than the sign of anorexia, as previously mentioned. To reliably assess the
presence of anorexia, a number of symptoms interfering with food intake and likely related to
changes in the central nervous system control of energy intake has been identified (Table
I)[4]. Patients reporting at least one of these symptoms are defined as anorectic. The use of
questionnaires to diagnose anorexia is rapidly increasing, thus highlighting their feasibility
and reliability in different clinical settings. However, considering that questionnaires provide
only a qualitative assessment of the presence of anorexia, it may appear advisable to also
quantify the degree of anorexia via the administration to the patient of a visual analogue
scale.
Table I: Symptoms interfering with food intake and related to changes in the central
nervous system regulation of energy intake. Patients reporting at least one of these
symptoms are defined as anorectic [see ref. 4].
SYMPTOMS
early satiety
taste alterations
smell alterations
meat aversion
nausea/vomiting
Prevalence
As a consequence of the difficulties in clearly defining and diagnosing anorexia, its

prevalence in different clinical conditions is yet to be precisely assessed. A clear example is
given by the anorexia of cancer. In 300 cancer patients, Geels et al. identified the nine most
common symptoms using patients’ responses to a quality-of-life questionnaire as well as
using graded toxicity data collected on case report forms [5]. By using case report forms,
which closely reflect the attitude of clinicians in investigating specific symptoms, anorexia
was detected in approximately 13% of patients, while using the quality-of-life questionnaire
55% of patients were diagnosed as anorectic [5].
Cancer
An acceptable estimate of the prevalence of cancer anorexia can be derived from a

number of papers which show that approximately 50% of cancer patients upon diagnosis
report abnormalities of eating behaviour [6, 7]. This figure might slightly overestimate the
actual prevalence of cancer anorexia, but it must be reminded that it is generally
acknowledged that anorexia and reduced food intake are frequently encountered in cancer
patients [7]. Moreover, anorexia is usually the symptom urging the patients to refer to their
physicians, and its alleviation is perceived as a sign of benign evolution of the disease.
Prevalence data are more reliable in terminally ill cancer patients. In this subset of
patients, the prevalence of anorexia ranges between 60% and 65% [8, 9]. Based on these
alarming figures and considering that 20% of cancer deaths are due to malnutrition per se
[10], it is reasonable to conclude that many cancer patients are starving to death.
Liver Cirrhosis
Similarly to what is observed in the course of neoplastic disease, patients suffering from
chronic liver failure frequently experience anorexia. In a recent paper, Marchesini et al.
assessed the presence of anorexia in 174 patients with advanced liver cirrhosis (Child-Pugh
score ≥7; Class B or C), using the guiding symptoms previously mentioned. Data obtained
show that more than 50% of patients were anorectic [11].
Chronic Renal Failure
In this clinical setting, anorexia is among the most important causes of malnutrition. It is
pervasive in patients on conservative treatment and very common in patients on hemodialysis
[12]. Indeed, Kalantar-Zadeh et al. studied a cohort of 331 maintenance hemodialysis
outpatients and demonstrated that diminished appetite was reported by 128 patients, i.e., 38%
of the entire cohort [13].
Chronic Obstructive Pulmonary Disease [COPD]
In COPD patients, the prevalence of anorexia is particularly high, since most patients
suffer from breathlessness which affects food intake. Recent data indicate that 67% of
chronic lung disease patients experience anorexia during the last year of life, this figure not
being much different from the prevalence of anorexia among lung cancer patients, i.e. 76%
[14]. More striking, however, are data showing that despite COPD patients have physical and
psychosocial needs at least as severe as lung cancer patients, their symptoms, including
anorexia, receive much less attention from health care professionals [14].
Congestive Heart Failure [CHF]
In this clinical setting, the assessment of the prevalence of anorexia is made difficult by
the high proportion of patients suffering from dyspnea, peaking at 90% in the last stages of
the disease [15]. Severe nausea has been reported affecting approximately 10% of CHF
patients [16], but the actual prevalence of anorexia may well be higher [17].
Clinical Impact
The onset of anorexia significantly impacts on the clinical course of the disease. It
contributes to the development of malnutrition and cachexia, since it reduces the oral intake
of calories thus further promoting skeletal muscle wasting. Also, it exacerbates the
detrimental effects of disease-related alterations of protein metabolism on nutritional status,
eventually leading to increased morbidity and mortality [18]. On the other hand, the
metabolic dysregulation of cachexia [19] sustains and corroborates the neurochemical
alterations responsible of anorexia. The clinical relevance of anorexia is underscored by its
role as an independent prognostic factor in terminally ill cancer patients, being as reliable in
predicting survival as well-defined prognostic factors, including Karnofsky Performance
Status and Clinical Prediction of Survival [9, 20]. Similar data have been obtained in chronic
renal failure: in maintenance hemodialysis patients, diminished appetite is associated with
poor clinical outcome, including a 4-fold increase in mortality and a greater hospitalization
rates [13]. Finally, anorexia and reduced energy intake impinge on quality of life, which is
now becoming a critical endpoint in the management of patients as well as in designing
clinical trials [21].
An interesting and emerging aspect of the clinical impact of anorexia is its influence on
patients’ quality of life. This issue has been specifically raised in cancer patients, in whom
anorexia is pervasive and much effort has been devoted to improve food intake. It is self-
evident that in humans, food and food intake are much more than calories, nutrients and
digestion. Special events are celebrated with food, people often discuss of economic
opportunities while eating, friendship is strengthened by sharing the same food.
Consequently, cancer patients, and patients suffering from other chronic diseases as well,
point to anorexia as one of the most psychologically disturbing symptoms of cancer and
anorexia is frequently found as a major contributor to reduced quality of life. Therefore,
cancer anorexia should represent a major therapeutic goal and its alleviation should lead to
improved quality of life. Since cancer anorexia can be effectively treated or at least its
severity dampened [22], it would be expected that the alleviation of anorexia should be
associated with significantly improved quality of life. Unfortunately, as recently outlined by
Jatoi et al. [23], almost none of the clinical trials reporting improvements in appetite
following drug therapy also reported improved quality of life, as assessed by a number of
different tools.
Many possible explanations have been proposed for this apparent inconsistency,
including undesirable effects of appetite stimulants, insufficient reliability and/or complexity
of quality of life assessing tools, insufficient statistical power of the available data, the “sore-
tooth-tight-shoe” phenomenon, i.e., cancer patients complain of different symptoms and relief
of anorexia would simply shift symptomatology [23]. Alternatively and provocatively, it
could be questioned whether cancer anorexia and starvation to death represent horrifying
symptoms to the surviving relatives rather than to the dying patients. Ganzini et al. recently
conducted a survey to characterize the experience of dying among terminally-ill patients who
make the choice to stop eating and drinking to hasten death, this experience somewhat
resembling severe anorexia [24]. The authors mailed all nurses employed by hospice
programs in Oregon, USA, and analyzed the results. On the basis of reports by nurses,
patients in hospice care who voluntarily choose to refuse food and fluids usually die a “good”
death within two weeks after stopping food and fluids.
Considering that anorexia alleviation has never been demonstrated to lead to enhanced
quality of life, or improved morbidity and mortality, should we care about anorexia in cancer
patients? Certainly yes, because of the psychological value of appetite rather than for its
caloric sequelae. As brilliantly pointed out by Jatoi et al., anorexia “is important in its own
right—independent of global quality of life, independent of survival, and independent of any
other clinical end point” [23].
Pathogenesis of Anorexia
The pathogenesis of anorexia is multifactorial and related to disturbances of the central

physiological mechanisms controlling food intake, but the precise neurochemical
mechanisms are still matter of debate. However, by understanding how energy intake is
physiologically controlled, insights might be obtained.
Under normal conditions energy intake is controlled within the hypothalamus by specific
neuronal populations which integrate peripheral signals conveying information on energy and
adiposity status [25]. In particular, the arcuate nucleus of the hypothalamus transduces these
inputs into neuronal responses and, via second order neuronal signalling pathways, into
behavioural responses (Figure 1). Intuitively, anorexia might be secondary to defective
signals arising from the periphery, due to an error in the transduction process, or to a
disturbance in the activity of the second order neuronal signalling pathways.
Role of Peripheral Signals
The hypothesis that peripheral signals are involved in the pathogenesis of anorexia is
intriguing. Among the large series of peripheral signals [Table II], the hormone leptin exerts
a strong negative influence on food intake.
Hypothalamus
NPY/AgRP
peripheral modulation of
signals food intake
POMC/CART
arcuate nucleus
Figure 1: in the hypothalamus, the arcuate nucleus receives information from the periphery and intergrates
these inputs to modulate food intake [NPY: neuropeptide Y; AgRP: agouti-related protein; POMC: pro-
opiomelanocortin; CART: cocaine-amphetamine related transcript].
Table II: Signals arising from the periphery and influencing food intake
SIGNALS
Adiposity signals leptin
insulin
Gut-derived signals CCK
ghrelin
PYY
glucagon-like peptide-1
oxyntomodulin
Energy signals intracellular malonyl-CoA
Hormones
a) Leptin
Leptin is produced primarily by adipocytes in proportion to body fat. It reaches the brain
and a raise in its circulating levels results in inhibition of energy intake. Thus, leptin is an
intuitive likely mediator of anorexia, particularly because its synthesis and secretion appear to
be stimulated by cytokines, recognized anorexigenic factors [26]. However, results from
animal and clinical studies are controversial [27-29], and do not seem to support this
hypothesis. More recently, Bing et al. significantly contributed to the debate by showing in
an animal model that anorexia develops despite the normal regulation of leptin synthesis [30].
Consistently with animal data, Mantovani et al. showed that in anorectic cancer patients,
circulating leptin levels are lower than those of healthy individuals, while no difference exists
between cancer patients and healthy individuals in the production of leptin by peripheral
blood mononuclear cells [31]. Similar data questioning the role of circulating leptin in the
pathogenesis of anorexia of chronic renal failure patients undergoing dialysis have been
recently published [32, 33]. Rather, they suggest that leptin in these patients may represent a
marker of inflammation [32]. Supporting a common pathogenic mechanism for the anorexia
associated with different diseases, Ben-Ari et al. showed that in chronic liver disease serum
leptin appears a passive marker and not a cause of anorexia [34]. When considered together,
these data suggest that peripheral leptin synthesis is preserved during disease, and point to a
central dysregulation of the physiological feedback loop.
b) Insulin
Food intake triggers a complex cascade of neurochemical events that signal nutrient and
energy availability in the central nervous system, down regulate stimulators, activate
anorexigenic factors, including brain insulin, and result in reduced eating. Insulin reaches the
brain from the periphery, but intracerebral insulin synthesis has been also demonstrated.
Brain insulin has anorexigenic effects, but its mechanism of action needs to be further
elucidated. However, consisting evidence show that brain insulin interacts with different
anorexigenic and orexigenic pathways to modulate their activity and thus food intake [for
review, see ref. 35]. Similarly, different factors are able to regulate insulin release directly in
the hypothalamus. Particularly, leptin and melanocortins, anorexigenic peptides, are highly
interactive with insulin in the central nervous system, probably via the neurotransmitter
serotonin. In the hypothalamus, insulin and leptin share a common signaling pathway
involved in food intake, namely the insulin receptor substrate, phosphatidylinositol 3-kinase
pathway. Disrupted brain insulin signalling in obesity and diabetes has been proposed, but its
involvement in secondary anorexia received less attention by reasearchers. However, Sato et
al. recently demonstrated a possible role for insulin in cytokine-induced anorexia, using an
experimental model [36].
c) Cholecystokinin (CCK)
CCK is probably the most extensively studied satiety signal, i.e., an endogenous factor
that causes a sensation of fullness and reduces the size of an ongoing meal [for review, see
ref. 37]. CCK is secreted from duodenal cells in response to nutrients in the lumen, but
intracerebral CCK synthesis has been described. Some of the secreted CCK enters the blood
and stimulates the secretion of appropriate enzymes into the duodenum to facilitate digestion.
However, CCK influence food intake and particularly meal size, via a more complex
mechanism. Some of the CCK released after nutrients stimulus into the duodenum acts in a
local paracrine manner to stimulate CCK1 receptors on the sensory fibers of the vagus nerves,
which is simultaneously sensitive to both CCK and other stimuli such as gastric distension,
via other branches emanating from the gastric wall. Therefore, individual vagal neurons are
able to integrate different kinds of signals relevant to ingestion. Then, the CCK signal enters
the hindbrain, where it initiates local reflexes and interacts with central pathways to modulate
food intake.
The involvement of CCK in secondary anorexia is debated: it appears unlikely in cancer
anorexia, while contrasting results have been obtained in the anorexia of aging [38, 39].
d) Ghrelin
More recently, the prophagic hormone ghrelin has received considerable interest as a
putative mediator of cancer anorexia. Ghrelin is produced by gastric cells and under
physiological conditions its circulating levels raise before feeding and stimulate food intake
via intra-hypothalamic effects [40]. Consequently, it is conceivable to hypothesize that
during tumour growth ghrelin circulating levels may drop leading to the onset of anorexia.
Unfortunately, recent data obtained in cancer patients show that plasma ghrelin levels are
higher than in healthy individuals, being even higher in patients with cachexia [41]. These
data suggest that anorectic cancer patients might be resistant to the appetite-stimulating
effects of ghrelin. Also, animal data obtained with ghrelin-deficient mice appear to suggest
that ghrelin is not a critical orexigenic factor and, rather, support the hypothesis that ghrelin’s
principle physiological role may be in the determination of the type of metabolic substrate
(i.e., fat vs. carbohydrate) that is used for maintenance of energy balance, particularly under
conditions of high fat intake [42]. Therefore, the impaired ability of target organs, including
the hypothalamus, to respond to ghrelin, rather than the actual circulating levels of the
hormone, appears to mediate cancer anorexia. However, this suggestion does not imply that
supraphysiologic doses of exogenous ghrelin may not be effective in ameliorating anorexia,
although it is likely that this therapeutic approach may progressively worsen ghrelin
resistance of anorectic patients.
e) PYY
PYY is a peptide secreted from the entire gastrointestinal tract [40]. However, the
number of PYY immunoreactive cells increases in the most distal sections of the
gastrointestinal tract, being at a very high level in the rectum. Food intake, but also CCK,
trigger the release of PYY, whose circulating concentrations peak at 1–2 h post ingestion and
are influenced by both the number of calories and the composition of the food consumed.
PYY is present in two forms, PYY [1–36] and PYY [3–36], the latter being the major
circulating form. PYY [3–36] has been shown in normal-weight human volunteers and in
obese subjects to reduce caloric intake by 30%. Interestingly, the effects of PYY are
orexigenic when administered centrally. Considering its anorexigenic properties, PYY
represents a suitable mediator of anorexia, but its role in secondary anorexia has not been
investigated yet.
f] Glucagon-like peptide-1 (GLP-1) and oxyntomodulin (OXM)

GLP-1 and OXM are proglucagon-derived peptides, i.e., derive from the cleavage of the
preproglucagon gene, which is expressed in the central nervous system, in the small intestine
and in the pancreas. OXM and GLP-1 are satiety signals, and they are rapidly released after
food ingestion at levels in proportion to calorie intake [40]. Their anorexigenic effects are
likely mediated by the vagal nerve, as discussed for CCK. However, both GLP-1 and OXM
reduce food intake when administered centrally, thus suggesting a direct anorexigenic effect.
The mechanism of action need to be better elucidated, but GLP-1 and OXM interact with a
number of pathways to modulate food intake, including ghrelin and insulin. Both GLP-1 and
OXM are thought to exert their effects via the GLP-1 receptor [GLP-1R]. Interestingly, GLP-
1 and OXM, which are structurally distinct, differentially regulate food intake and energy
expenditure by interacting with a GLP-1R-dependent pathway [43]. Therefore, ligand-
specific activation of a common GLP-1R increases the complexity of gut-brain pathways
regulating energy homeostasis.
The involvement of GLP-1 and OXM in secondary anorexia has not been investigated,
nor in experimental or human models.
Energy Signals
Similarly to changes in fat mass, also changes in energy metabolism influence energy
intake in a leptin-independent manner via energy signals. Conceptually, energy signals differ
from classic peripheral signals, since they are generated within the hypothalamic neurons
controlling energy intake. A number of studies suggest that a metabolic control of food intake
also exists, in which the biochemical partitioning between fatty acid oxidation and synthesis
represents a key signal indicating catabolic or anabolic energy status [44]. Energy signals are
independent from leptin pathway and they inform the brain on the metabolic switch occurring
at a subcellular level between fatty acid oxidation and synthesis [45]. Under physiological
conditions, food intake is accompanied by increased intracellular levels of malonyl coenzyme
A (malonyl-CoA)[46], which is a potent signal reducing food intake, via inhibition of the
synthesis of the prophagic factor neuropeptide Y (NPY)[45]. It is therefore tempting to
speculate that energy signals could contribute to anorexia, possibly via a deranged "sensing"
of the energy metabolism during disease. Supporting evidence show that during tumour
growth, fat metabolism is altered leading to decreased fatty acid oxidation [47] and possibly
increased intracellular malonyl-CoA levels. Also, the supplementation of carnitine, which is
involved in fatty acid oxidation, ameliorates anorexia in pathophysiological conditions [48].
However, more studies are needed to verify the involvement of energy signals in anorexia.
Role of Second Order Neuronal Signalling
The hypothalamic arcuate nucleus, where peripheral signals mainly converge, projects to
other hypothalamic areas, thus interacting with a number of neuronal populations [25]. Many
pathways have been described serving as second order neuronal signalling pathways,
including orexins A and B, but their involvement in the pathogenesis of anorexia has so far
received little attention, but it cannot be excluded. In a recent study, Li et al. showed that the
loss of renal function in Wistar rats reduces hypothalamic orexin A, a prophagic mediator
[49], which in turn may contribute to the development of anorexia.
Evidence exist suggesting that disease-associated metabolic changes, and particularly
alterations of protein turnover, may impact on the neurochemistry in localized brain areas
[50]. However, they appear to have a role in sustaining and corroborating anorexia, while its
onset seems to be secondary to the inability of the hypothalamus to recognize and respond
appropriately to consistent peripheral signals [51].
Role of Neuropeptides
Consistent and convincing evidence suggest that disease-associated anorexia is brought

about by the derangement of the hypothalamic system transducing peripheral signals into
neuronal responses. Under normal conditions, peripheral signals interact with two separate
neuronal populations within the arcuate nucleus: the NPY/Agouti-related peptide (AgRP)
neurons, stimulating food intake, and the pro-opiomelanocortin [POMC]/cocaine- and
amphetamine-regulated transcript (CART) neurons, inhibiting food intake [for review see ref.
25]. As a consequence, when energy intake needs to be initiated, peripheral signals activate
the NPY/AgRP pathway, simultaneously inhibiting the POMC/CART pathway. When energy
intake needs to be inhibited, peripheral signals inhibit the NPY/AgRP pathway while
simultaneously activating POMC/CART neurons and thus upregulating the expression of a
number of POMC/CART pathway-related factors, including α-melanocyte stimulating
hormone [α-MSH] and corticotropin releasing hormone (CRH).
Because of the central role of these neuronal pathways, they were postulated as putative
mediators of anorexia. A number of studies investigated the role of the prophagic signal NPY
in the pathogenesis of anorexia. In cancer, the results obtained in animal models and humans
are conflicting [52-55]. However, it seems that a dissociation exists between NPY mRNA
levels and actual NPY levels, which appear decreased. Indeed, recent data show a decrease of
NPY and NPY-immunoreactive neurons in the hypothalamus of anorectic tumour bearing rats
[56, 57]. These data suggest that NPY is involved in cancer anorexia, but it is difficult to
assess the extent of the involvement.
In chronic renal failure, animal and human studies consistently show a reduction of NPY
[49, 58]. However, and similarly to cancer, it is not clear whether NPY should be considered
as a mediator or a marker of anorexia.
Results from studies investigating the role of the hypothalamic anorexigenic pathway
POMC/CART in anorexia appear more convincing. Unfortunately this line of investigation
has been pursued in cancer anorexia only, but it is likely that the pathogenic mechanisms
hypothesized for cancer anorexia might well be operating during the clinical course of other
diseases. It has been repeatedly demonstrated that by blocking the hypothalamic melanocortin
system, using either its physiological inhibitor (i.e., AgRP) or the synthetic compound SHU-
9119, food intake is restored in tumour bearing animals, and the development of cachexia is
prevented [59, 60]. Similar results have been obtained in melanocortin 4 receptor (MC4-R)
knock-out mice. In these mutants, POMC/CART neurons cannot be completely activated
because of the lack of this class of receptors, and tumour growth is not accompanied by the
development of anorexia and cachexia, which occur in wild type mice [59]
Thus, it appears that secondary anorexia is related to the inability of the hypothalamus to
respond appropriately to consistent peripheral signals, primarily due to the hyperactivation of
the melanocortin system. This derangement could be triggered by cytokines.
Role of Cytokines
A number of studies indicate that cytokines are involved in anorexia [61, 62]. In the
Fischer rat/MCA sarcoma model, brain interleukin-1 (IL-1) levels inversely correlate with
food intake [63] while intra-hypothalamic IL-1 receptor antagonist microinjection increases
energy intake [64]. In Lobund-Wistar rats bearing prostate adenocarcinoma tumour cells,
early anorexia is associated with an upregulation of brain IL-1β mRNA [54]. In chronic renal
failure patients, several groups have found increased levels of cytokines [13, 58, 65]. In
cancer patients, cytokines and anorexia are intuitively connected, but compelling evidence
are lacking, since cytokines biological effects are largely mediated by paracrine and autocrine
influences. Thus, cytokine circulating levels may not reliably reflect their role in determining
specific biological responses [66], rather they suggest their involvement. However, it must be
acknowledged that studies also exist, which failed to demonstrate a direct role of cytokines in
experimental models of cancer anorexia, while suggesting the involvement of the nitric oxide
system and systemic or local production of eicosanoids [67, 68].
Hypothalamic Neuro-Immune Interactions:

The Role of Brain Monoamines
The mechanisms by which cytokines negatively influence energy intake are currently
under investigation. As proposed by Inui, cytokines may play a pivotal role in long-term
inhibition of feeding by mimicking the hypothalamic effect of excessive negative feedback
signalling [69]. This could be done by inhibition of the NPY/AgRP orexigenic network, as
well as by persistent stimulation of the POMC/CART anorexigenic pathway. In the complex
scenario of mutual interactions existing between different peripheral and central factors, brain
monoamines and particularly brain serotonin appears to play a pivotal role.
A simplistic view of energy intake regulation is that ingested nutrients are sensed at
different levels of the gastrointestinal tract, including the liver. This information, together
with that arising from adipose tissue, is transmitted to the brain via a series of routes
[neuronal input, hormones, peptides], and is integrated in the hypothalamus, where the
appropriate behavioral response is triggered. Actually, the picture is far more complex, since
the hypothalamus consists of different areas and nuclei, and within each of them a set of
effectors [neurotransmitters, neuromodulatory peptides and transmembrane proteins] interact
[25].
For several decades, hypothalamic serotonin systems have been implicated in the
suppression of feeding [70]. Serotonin is a monoamine acting as neurotransmitter and
involved in different biological responses. Although the exact role of serotonin in the central
regulation of food intake and body weight still awaits further clarification, its involvement in
this process has been repeatedly confirmed. Now it is clear that serotonin acts in conjunction
with neuropeptides and peripheral hormones to bring about physiological states such as
hunger, satiation and satiety.
Beside its role in influencing food intake, hypothalamic serotonin appears to impact also
energy expenditure. In a recent report, Ohliger-Frerking et al. studied dorsal raphe nucleus
serotonergic neurons, projecting to the hypothalamus to influence feeding [71]. They showed
that the neurons from obese Zucker rats exhibit both a larger depolarization and increased
firing rate in response to phenylephrine than did cells from lean rats, thus suggesting that
dorsal raphe nucleus serotonergic neurons of obese rats have an enhanced adrenergic drive.
Furthermore, serotonin reduces food intake and augment sympathetic activity, thus promoting
weight loss [72].
Recent data suggest that during disease, hypothalamic serotonergic neurotransmission
may be critical in linking different central anorexigenic pathways, and particularly cytokines
and the melanocortin system. Fenfluramine is a serotonin agonist once widely prescribed in
the treatment of obesity. It has been recently shown that fenfluramine raises hypothalamic
serotonin levels, which in turn activate POMC/CART neurons in the arcuate nucleus,
therefore inducing anorexia and reduced food intake [73]. On the other hand, it is well
documented that cytokines, and particularly IL-1, stimulate the release of hypothalamic
serotonin [74]. Thus, it could be speculated that during disease, cytokines increase
hypothalamic serotonergic activity, which in turn contributes to persistent activation of
POMC/CART neurons, leading to the onset of anorexia and reduced food intake. Supporting
the role of serotonin in the pathogenesis of anorexia, we demonstrated that in anorectic
tumour-bearing animals hypothalamic serotonin levels are increased when compared with
control rats [75]. After tumour removal, hypothalamic serotonin levels normalize and food
intake improves [75]. In the same experimental model, intrahypothalamic microinjections of
mianserin, a serotonin antagonist, improves food intake [64].
In humans, the demonstration of the involvement of brain serotonin in anorexia is more
difficult since serotonergic activity cannot be easily measured in-vivo. Thus, the activity of
hypothalamic serotonergic system is inferred by cerebro-spinal fluid (CSF) levels of
tryptophan. Tryptophan is the precursor of serotonin, whose synthesis is strictly dependent on
the availability of tryptophan [76]. In anorectic cancer patients, plasma and particularly CSF
concentrations of tryptophan are increased when compared to controls and non anorectic
cancer patients [4, 77]. After tumour removal, plasma typtophan normalizes and food intake
improves [66].
Similar data suggesting increased serotonergic activity in the presence of anorexia have
been obtained in patients suffering from chronic renal failure [12, 50, 62] and liver cirrhosis
[78], thus supporting the view that anorexia associated with different diseases may share a
similar pathogenic mechanisms. It must be acknowIedged that partial brain serotonin
depletion and antagonism did not result in improved food intake of tumour bearing animals
[68, 79]. However, it is not clear whether the failure in influencing food intake in these
models could be secondary to the incomplete brain serotonergic depletion or to the lack of
any involvement of serotonin in cancer anorexia [80]. When considered together, we believe
that these data suggest that brain serotonin could represent is a key factor involved in the
pathogenesis of disease-associated anorexia and thus provide an interesting therapeutic
target.
Therapy
The detrimental effects of anorexia on nutritional status and quality of life can be
counteracted by a well designed therapeutic strategy which includes both nutritional
counselling and pharmacological approach (Table III).
Table III: Therapeutic strategies in cancer anorexia
DIETARY COUNSELLING DRUGS

Small but frequent meals Progestagens [MA, MPA]
Energy-dense food Cannabinoids [dronabinol]
Limit fat intake Corticosteroids [dexamethasone]
Avoid extremes in taste
Avoid extremes in smell Pleasant
environment
Presentation of food
Dietary Habits
In anorectic patients, nutritional counselling may significantly improve food intake. Food
intake can be improved by providing small and frequent meals that are energy-dense and easy
to eat. Patients should eat in pleasant surroundings and attention should be given to the
presentation of food. It is advisable to avoid high-fat food, since fat delays gastric emptying
and thus it may worsen anorexia symptoms. Since changes in taste/smell may occur in
anorectic patients, extremes in temperature and flavour should be avoided [7].
Drug Therapy
The optimal therapeutic approach to anorexia should be aimed at counteracting its

pathogenic mechanisms. Therefore, considering that cytokines appear to represent the factor
initiating the complex cascade of neurochemical events eventually leading to the onset of
anorexia, it would be advisable to target their synthesis and/or activity to effectively treat
anorexia and reduced food intake in cancer patients. Animal studies support this approach, by
showing that intrahypothalamic IL-1 blockade as well as systemic TNF inhibition result in
amelioration of anorexia and improved food intake [64, 81]. In humans, cytokine therapeutic
targeting is achieved via agents interfering with their synthesis and release. They include
progestagens [82], cannabinoids [83] and corticosteroids [84].
Progestagens [megestrol acetate and medroxyprogesterone acetate] are the first-line
therapy for cancer anorexia [69]. They are highly effective in relieving the symptoms of
cancer anorexia. In a recent systematic review of randomised clinical trials, high-dose
progestagens have been shown to improve food intake and to a less extent body weight [85].
Their prophagic effect appears to be mediated by the down-regulation of the synthesis and
release of cytokines [86], leading to an increase of NPY hypothalamic levels [87] and a
possible inhibition of serotonergic activity [88]. However, they are contraindicated in
hormone-dependent tumours, and their use may lead to fluid retention, deep venous
thrombosis, vaginal spotting and sexual dysfunction.
Cannabinoids are derivatives of marijuana and particularly dronabinol has been
demonstrated to alter cytokine production by human immune cells [89]. In cancer patients,
dronabinol at a dose of 2.5 mg twice a day increases food intake, but its prophagic effects are
less evident than those obtained by megestrol actetate [83].
Corticosteroids are widely used to dampen immune response and cytokine activity.
Exploiting their immunomodulatory effects, they have been used in the treatment of cancer
anorexia. Their effects are similar to those obtained by megestrol acetate, but corticosteroids
have a higher rate of drug discontinuation because of toxicity and/or patient refusal [84].
Therapy of Anorexia: What’s Next?
Omega-3 Fatty Acids
The n-3 polyunsaturated fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic
acid [DHA] have been shown to suppress production of proinflammatory cytokines and
arachidonic acid-derived mediators [90]. Thus, EPA supplementation may represent an
effective therapeutic strategy to ameliorate cancer anorexia [91]. Jatoi et al. recently
compared the orexigenic effects of megestrol acetate and of a caloric supplement enriched
with EPA and DHA in weight losing, anorectic cancer patients [92]. More than 400 patients
were studied over a period of approximately 3 months. Data obtained show that megestrol
acetate and EPA supplement are equally effective in improving body weight. Appetite is
similarly enhanced by the two treatments when it is assessed via North Central Cancer
Treatment Group Questionnaire, but megestrol acetate appears superior when appetite is
assessed via 4-week Functional Assessment of Anorexia/Cachexia score. Combination of
both treatments does not increase response rate.
Anti-Cytokine Agents
Other molecules exhibit anti-cytokine activity. Pentoxifylline, thalidomide, suramin have

been demonstrated to significantly reduce cytokine release, thus prompting their testing as
anti-anorexia/cachexia agents [82]. Unfortunately, the results obtained appear modest, while
the potential side effects discourage their clinical use. In particular, recent data show that
suramin inhibits chemotherapy-induced apoptosis [93]. Similarly, the infusion of adenosine
5’-triphosphate [ATP] in cancer patients modestly increased weight, improved strength and
slowed the decline in quality of life [94, 95]. Newly synthesised molecules, dubbed “cytokine
traps” after their ability to block cytokines, appear more promising. Cytokine traps consist of
fusions between the constant region of IgG and the extracellular domains of two distinct
cytokine receptor components involved in binding the cytokine. Traps potently block
cytokine in vitro and in vivo, and represent a substantial advance in creating novel therapeutic
candidates for cytokine-driven diseases [96].
Anti-Serotonergic Agents
Cancer anorexia might be therapeutically approached by interfering with the

neurochemical events downstream cytokine activation. Serotonergic hypothalamic
neurotransmission may represent a suitable example. Hypothalamic serotonin synthesis
depends on the brain availability of its precursor, the amino acid tryptophan [76]. Tryptophan
crosses the blood-brain barrier via a specific transport mechanism shared with the other
neutral amino acids, including the branched-chain amino acids. Thus, by artificially
increasing the plasma levels of the competing amino acids, a reduction of tryptophan brain
entry could be achieved, leading to a reduction of hypothalamic serotonin synthesis and
release, which in turn would result in amelioration of cancer anorexia. To test this hypothesis,
tumor-bearing rats were fed with a BCAA-enriched diet, and their feeding behaviour
compared with that of tumor-bearing rats receiving an isocaloric, isonitrogenous standard
diet. The results obtained showed that BCAA-enriched diet delayed the development of
anorexia by 2 days when compared to standard diet [unpublished observations]. To further
test the clinical relevance of BCAA, anorectic cancer patients were orally supplemented with
branched-chain amino acids or placebo for 7 days, while simultaneously recording their
energy intake [97]. Anorexia significantly improved after 3 days of treatment only in cancer
patients receiving branched-chain amino acids, leading to a significant improvement of
energy intake. These encouraging results must be considered as preliminary, since they were
obtained in a small population during a short study period, and need to be validated in larger
trials. However, they confirm the feasibility of interfering with hypothalamic
neurotransmission to influence energy intake. Indeed, more fascinating results were later
obtained in uremia and in liver cirrhosis.
During chronic renal failure, derangements of plasma amino acid profile occur and a
reduction of circulating levels of BCAA is frequently observed. Interestingly, the reduction
of plasma BCAA is associated with the presence of anorexia [12]. It is therefore tempting to
speculate that by supplementing uremic patients with BCAA, energy intake and nutritional
status can be improved. Hiroshige et al. studied 44 elderly patients on chronic hemodialysis
[12]. Among them, 28 patients with low plasma albumin levels [<3.5 g/dL] were classified as
the malnourished group; they also suffered from anorexia. The other 16 patients did not
complain of anorexia and were classified as the well-nourished group. Then they performed a
12-month, double-blind, placebo-controlled study on the malnourished group. Fourteen
patients each received daily oral BCAA supplementation [12 g/day] or a placebo in random
order in a cross-over trial for 6 months. Lower plasma levels of BCAA and lower protein and
caloric intakes were found in the malnourished group as compared to the well-nourished
group. In BCAA-treated malnourished patients, anorexia and poor oral protein and calorie
intakes improved within a month concomitant with the improvement of plasma BCAA levels
over the values in well-nourished patients. After 6 months of BCAA supplementation,
anthropometric indices [body fat percentage, lean body mass] showed a statistically
significant increase and mean plasma albumin concentration increased form 3.3 g/dL to 3.9
g/dL. After changing BCAA for a placebo, spontaneous oral food intake decreased, but the
favourable nutritional status persisted for the next 6 months. In 14 patients initially treated
with placebo, no significant changes in nutritional parameters were observed during the first
6 months. However, positive results were obtained by BCAA supplementation during the
subsequent 6 months, and mean plasma albumin concentration increased from 3.2 g/dL to 3.8
g/dL. These data are particularly important because demonstrate that BCAA supplementation
results not only in improved food intake but also in improved nutritional status. Such
encouraging results were replicated also in cirrhotic patients.
A multicenter, randomized study comparing 1-year nutritional supplementation with
BCAA against lactoalbumin or maltodextrins was recently performed in 174 patients [11].
Primary outcomes were the prevention of a combined end point [death and deterioration to
exclusion criteria], the need for hospital admission, and the duration of hospital stay.
Secondary outcomes were nutritional parameters, laboratory data and Child-Pugh score,
anorexia, health-related quality of life, and need for therapy. Interestingly, treatment with
BCAA significantly reduced the combined event rates compared with lactoalbumin. The
average hospital admission rate was lower in the BCAA arm compared with control
treatments. In patients who remained in the study, nutritional parameters and liver function
tests were, on average, stable or improved during treatment with BCAA and the Child-Pugh
score decreased. Also, anorexia and health-related quality of life [as assessed by the SF-36
questionnaire] improved. In particular, anorexia was reported in more than 50% of all cases
and was not different between groups. Its prevalence decreased with BCAA from 52% to
25% and remained unchanged with lactoalbumin and maltodextrins. Treatment groups did
not score differently on SF-36 questionnaire at baseline. Treatment with BCAA had a
significant effect on role limitation/physical, and other scales improved significantly when
compared with baseline. Physical functioning and role limitation/emotional also improved.
No significant changes were observed in subjects treated with lactoalbumin or maltodextrins.
Finally, there was a shift toward better scoring of health only in subjects actively treated with
BCAA, with the percent of patients scoring health as poor decreasing from 19% to 3%.
Similarly, after 1 year of continuous treatment with BCAA, the percentage of patients
believing that their health had improved during the preceding 12 months had increased from
29% to 52%, and the percentage believing that their health had worsened had decreased from
43% to 18%.
When considered together, these data suggest that the anti-serotonergic approach to the
treatment of disease-associated anorexia is effective and results in significant clinical
outcomes, far beyond mere increase of energy intake. The observed improvement of
nutritional status and particularly of lean body mass could be explained at least in part by the
excitatory effects of serotonin on hypothalamic melanocortin receptors [73], whose function
has been linked to cachexia [98]. By reducing brain serotonergic activity via BCAA, it is
conceivable that melanocortin receptors are less activated, leading to reduced peripheral
muscle wasting.
Considering the role of brain serotonin in the pathogenesis of disease-associated anorexia
and cachexia, antiserotonergic drugs might be as effective as BCAA in improving food intake
and nutritional status. However, this approach bears some limitations. Firstly,
antiserotonergic drugs must target the specific serotonin receptor involved in the
pathogenesis of anorexia, the best candidate to this role being the 5-HT(2C) receptor. The
need for selectivity may explain the failure of cyproheptadine in the treatment of anorexia in
cancer patients [for review see ref. 99]. Secondly, provided that the given antiserotonergic
drug selectively targets 5-HT(2C) receptors, then it must reach the hypothalamus in adequate
concentrations to block the receptors. This may be difficult to achieve, particularly if
adequate brain concentrations are reached only when using suprapharmacologic peripheral
doses, which may lead to the development of side-effects.
Promising and in early clinical trials is blockade of type 3 serotonergic receptors, which
appear more involved in mediating nausea and emesis rather than in controlling energy
balance [70]. Ondansetron is a type 3 serotonergic receptor antagonist widely used in cancer
patients in the prevention and treatment of chemotherapy-induced nausea and vomiting.
Edelman et al. [100] studied 27 patients with advanced cancer and weight loss. Patients were
not receiving antineoplastic treatment, but received oral ondansetron. Unfortunately, weight
loss continued, but after 1 month of treatment patients scored better on an hedonic scale,
suggesting that they were enjoying food more. However, large and placebo controlled trials
are needed to establish whether these positive results reflected a true orexigenic effect
attributable exclusively to ondansetron, thus prompting more interest on this class of drugs.
More data support a role for hypothalamic neurotransmission as an effective therapeutic
target in the treatment of cancer anorexia. Using in vivo microdialysis, Blaha et al. showed
that intrahypothalamic serotonin concentrations are increased in anorectic tumor bearing rats
[75]. In the same study, they also showed a more complex derangement of hypothalamic
monoaminergic neurotransmission, since dopamine levels were also found depressed [75].
This evidence may give the neurochemical explanation for the results obtained in anorectic
cancer patients, whose food intake has been restored and quality of life improved by the
administration of dopamine (L-DOPA) at a dosage ranging from 375 mg/d to 750 mg/d [101,
102]. Although not obtained in prospective randomized clinical trials, these data are very
intriguing and further support the “monoaminergic” approach to the treatment of anorexia.
Ghrelin
Considering the orexigenic effects of ghrelin [103], it is tempting to speculate that its
administration to anorectic cancer patients may enhance their appetite and improve energy
intake. This hypothesis has been recently tested in an acute study [104]. Seven anorectic
cancer patients received i.v. ghrelin and their subsequent food intake and meal appreciation
recorded. Acute ghrelin infusion resulted in increased energy intake (approximately +30% vs
saline infusion) and meal appreciation in all patients studied.
Considering the few patients enrolled, these intriguing data should be considered as
preliminary and need confirmation by larger trials. Also, the use of ghrelin in cancer patients
must be cautiously considered because of the stimulatory effects of this hormone on GH
production, which are mediated by the same receptor stimulating appetite [105]. Although it
remains to be ascertained whether in humans chronically administered ghrelin sustains
increased GH production, it must be reminded that acromegalic patients with chronically

elevated GH have a small increase in absolute risk of bowel cancer [106]. Also, ghrelin
infusion increases plasma glucose and decreases plasma insulin [107]. However, glucose is
the preferred substrate for cancer cells [108] and sustained hyperglycemia as in diabetic
patients has been shown to represent a risk factor for cancer development and mortality
[109]. Finally, animal studies seem to anticipate that chronic treatment with this hormone will
have little effect on appetite [105].
Anti-Inflammatory Agents
As previously mentioned, the nitric oxide system and the production of eicosanoids
might be of importance for the pathogenesis of anorexia, and particularly cancer anorexia.
Supporting this view, animal and clinical studies show that nitric oxide synthase and
cyclooxigenase inhibitors, including indomethacin, decrease tumour growth and improve
anorexia [110, 111]. However, evidence that nitric oxide and eicosanoids act directly on cells
in the central nervous system is lacking. Also, nitric oxide mechanism may involve tumour
growth and thereby secondarily influence appetite. Finally, nitric oxide and eicosanoid
influences on appetite appear related to serotonin metabolism [112, 113], and the
prostaglandin E2 receptor EP3 has been identified on serotonergic neuronal cell bodies in the
raphe nucleus [114]. Thus, nitric oxide and eicosanoid pathways could not be completely
alien from the cytokine-monoamine system.
Conclusion
Anorexia is a syndrome which is pervasive among patients suffering from acute and
chronic diseases. The pathogenesis is multifactorial, but it appears to be related to the
hyperactivation of hypothalamic inhibitory pathways, which in turn seems to be triggered by
cytokine-driven stimulation of hypothalamic serotonergic system. Anorexia can be
effectively treated, although it is not known whether amelioration of anorexia results in a
long-term benefit for patients, leading to reduced morbidity and mortality. However, it should
be always remembered that improving anorexia and energy intake has a positive impact on
quality of life.
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Chapter V
“I Couldn’t Find the Food I Liked”

Anorexia in Boys. Three Case Reports
B. Bräutigam and M. Herberhold

Klinik fur Kinder und Jugendmedizin der Medizinischen Universitat zu Lubeck,
Arbeitsgruppe fur Psychosomatik und Psychotherapie,
Ratzeburger Allee 160, 23538 Lubeck.
Abstract
The number of boys affected by eating disorders is increasing. The fact that the numbers
for eating disorders among boys are so low is probably due in part to underdiagnosis.
Although adolescent girls are still the group primarily affected by eating disorders, nearly
every tenth person suffering from an eating disorder is male. The lifetime prevalence of
any eating disorder has been reported as 17.9% among women and 6.5% among men.
There are triggers for the disorders among boys that are different from those that have
been identified among girls. These include excessive physical activity, a fragile sexual
identity, demanding requirements or expectations in the areas of competitive sports,
muscle building, and ideals of physical perfection. There are also differences in the
pathologies. For example, boys often exhibit a different form of body image distortion,
one that is more focused on masculine muscular form. They also show less shame
concerning binge eating. The fact that anorexia and bulimia are much more difficult to
diagnose among boys has led to a situation in which only the most severe cases are
successfully diagnosed. This situation is exacerbated by the fact that bulimia is perceived
by the public as a disease that only affects girls, with the result that affected boys often
have to struggle with emotions of shame and denial.
We report on three clinical cases that illustrate some of the differences between male and
female anorexia and other aspects like the wide range of psychological and physical
symptoms, the different therapeutic approaches, and kinds of treatment. We focus on the
patients’ personal histories and the psychological conditions in the parents. Discussion of
the results encompasses psychodynamic and systemic issues.
92 B. Bräutigam and M. Herberhold
“I always wanted you to admire my fasting,” said the hunger artist. “We do admire it,”
said the overseer affably. “But you shouldn’t admire it,” said the hunger artist. “Well
then we don’t admire it,” said the overseer, “but why shouldn’t we admire it?”
“Because I have to fast, I can’t help it,” said the hunger artist. “What a fellow you are,”
said the overseer, “and why can’t you help it?” “Because,” said the hunger artist, lifting
his head and speaking, with his lips pursed, as if for a kiss, right into the overseer’s ear,
so that no syllable might be lost, “because I couldn’t find the food I liked.” “If I had
found it, believe me, I should have made no fuss and stuffed myself like you or anyone
else.”
(Kafka 1924, trans. W and E Muir)
Introduction
The number of boys and men suffering from eating disorders is potentially on the rise;
currently approximately every tenth person with an eating disorder is male. Some recent
studies have placed the ratio as high as 1:5 (see Woodside 2004). In general, the prevalence
rates given for the disorders vary from study to study, especially for adolescents. The
numbers given for anorexia range from a rate of 19:1 (Jacobs and Isaacs 1987) to 35:13
(Fosson et al. 1987). One current study estimates the risk for a girl to be affected by an eating
disorder during her adolescence at 17.9% and that for boys at 6.5%. Overall, the number of
young men suffering from a disorder involving binge eating is about four times that of those
with anorexia. The data for pre-pubertal anorexia are particularly inconsistent. One paper
describes it as rare among boys (Muise et al. 2003); while another describes the pre-pubertal
form of male anorexia as the more frequent and the more difficult to treat form of the disease
(see Olivry and Corcos 1999). Ohzeki et al. (1993) investigated changes in eating behavior in
boys and girls between the ages of 6-18 and discovered that eating-related problems among
boys have a tendency to decrease with age while they increase in girls as they get older.
Under the DSM IV criteria, anorexia is present when the subject’s body weight is
maintained at less than 85% of expected weight and when the subject has a intense fear of
gaining weight, despite being underweight; a body image distortion; and amenorrhea. The
ICD-10 lists 5 major criteria: 1) a BMI (Body Mass Index kg/m2) under 17.5; 2) self-induced
weight loss brought about through the avoidance of high-calorie foods and/or though self-
induced vomiting, purging, excessive exercise, or appetite suppressants; 3) a body-image
distortion (see Sack, Henninger and Lamprecht 2002); 4) an endocrine disorder in the
hypothalamic-pituitary-gonadal axis, manifest in women as amenorrhea and in men as loss of
sexual interest and potency; and 5) in the case of pre-pubertal onset of the disorder the
sequence of pubertal events is delayed – in boys the genitals remain juvenile, in girls there is
primary amenorrhea. So, the ICD-10 does specify gender-specific disorder symptoms, which
are reflected in various studies. In a study of six male youths with anorexia, Toifl et al.
(1988) found a hypothalamic pituitary dysfunction and delayed onset of pubertal
development. Jacoby et al. (2000) distinguish between physical and psychological changes.
The first group includes circulatory regulatory disorders; hypotonia; disorders of the
circulatory regulatory system; bradycardia (unusually slow pulse); hypothermia; amenorrhea;
and, in advance stages, heart rhythm disorders, electrolyte disorders, and lanugo. The second
“I Couldn’t Find the Food I Liked” Anorexia in Boys. Three Case Reports 93
group includes conspicuous eating behavior; body image distortion, i.e., an altered cognitive
perception of the body’s boundaries; extreme self-esteem issues (marked insecurity, feeling
of worthlessness); avoidance of intimate sexual contact; and a high performance orientation.
The gonadal disorder develops gradually in men and manifests itself in insufficient
testosterone secretion and a resulting loss of sexual interest and potency. Medical
complications, e.g., osteoporosis, affect men with anorexia to a similar extent that they do
women. (Schweiger 2003). The primary age group for the disorder in children and
adolescents is that of 11-18 year-olds. Resch (1999) gives the following risk factors: high
pressure to perform, an inadequate ability to perceive one’s own emotional state, family
conflict situations and overly close bonds, very early onset of puberty, and being a twin.
Typical psychological and psycho-social characteristics of female anorexia patients are an
above-average I.Q., a clinically relevant depressive pathology, being overly responsive to the
needs of others, and conflict avoidance in family relationships, as well as heightened
separation anxieties and contact disorders in school (see Walitza et al. 2001).
Contrary to previous belief, eating disorders can begin even in pre-pubertal children. As
early as kindergarten or primary school years, children can feel too fat and begin restricting
eating behavior that may result in their being underweight or growth disorders. Patients with
eating disorders report several non-specific food-related symptoms in childhood years, such
as the inability to stomach certain foods, limited food selection, frequent nausea, or stomach
pains after meals. Thus in the field of child psychology, the adoption of diagnostic criteria
less strict than those laid out, for example, in the DSM IV (Schweiger, Peters and Sipos
2003) has been discussed.
The DSM-IV distinguishes between restricting-type anorexia and the binge-eating type,
i.e., with binging and induced vomiting. The latter differs from bulimia in that the diagnosis
of bulimia does not apply to cases where patients are underweight. The ICD-10 refers to an
atypical anorexia nervosa in cases where one of the major symptoms is missing, e.g. the body
image distortion. The DSM-IV also distinguishes diagnostically among other types of
psychogenic appetite loss that can occur when other psychological disorders are present, such
as severe depression somatoform autonomic dysfunction (see Rief 1995), acute and chronic
stress situations (see Garfinkel, Garner 1982) or post traumatic stress disorder.
Bruch described anorexia in 1978 as a typical disease of the daughters of well-to-do,
successful families. Eating disorders and anorexia in particular were then and still are
considered typically female diseases. In-depth somatic examinations intended to rule out
organic diseases are much more likely to be administered when the patients are under-
nourished boys (Severin, Benden and Menken 1992). In a review article, Muise et al. (2003)
state that the diagnosis of an eating disorder under strict ICD-10 and DSM VI criteria raises
serious difficulties, in part because in boys and men there is no distinct phenomenon
corresponding to amenorrhea. They also point out that a wide and distinct spectrum of sub-
clinical eating disorders does exist.
Overall, the majority of studies agree that the similarities between those symptoms
associated with eating disorders in male and female patients outweigh the differences (see
Schweiger, Peters and Sipos 2003). There are, though, a few characteristics specific to boys
and men. A study of body image, weight, and eating behavior in boys identified a strong
denial of the presence of excess weight and described the pursuit of the perfect figure as far
less prominent. Sixty-six percent of girls wanted to achieve a figure under normal weight (10-
15% underweight), while 82% of boys considered a figure in the normal weight range to be
desirable. There was one very significant gender difference observed in an examination of
attacks of hunger cravings: 78% of girls reported feelings of guilt, while only 24% of boys
mentioned them (Hoffmann-Müller and Amstad 1994). The reason for this may lie in
different gender-specific expectations regarding social rolls or it might trace back to different
conflicts and conflict-resolution at an internal-psychological level.
A premorbid obesity frequently occurs among men and male adolescents. Eating
disorders are diagnosed less frequently and in general only when a psychiatric comorbidity is
present (Severein, Benden and Menken 1992). These include depression, compulsive
disorders and addiction. Eating disorders are more likely to affect boys / men who are
involved in physical and sporting activities. In generally, boys / men who suffer from an
eating disorder tend to push themselves to the limit physically rather than to fixate mentally
on a specific weight. They strive less towards an ideal weight than they do to attain an ideal
body, typically one that is muscular and powerful. The issue of sexual orientation, including a
fragile sexual identity, seems to be a frequent point of conflict (Chyambry 2002, Dalem
2000). However, there is no definitive indication of a link between homosexual orientation
and a more frequent incidence of eating disorders (Woodside 2004). There has been a higher
frequency of homosexual orientation reported among men with bulimia nervosa. (Carlat et al.
1997). Homosexual men exhibit more eating disorder psychopathologies and higher
depressivity in comparison to heterosexual men (Russel and Keel 2002). A familial
constellation described as typical among eating disorder patients is one with an
overprotective mother and absent father (Srenivasan 1978; Chambry 2002). In this area too
though, we must point out that there is no sufficient indication for a specific familial pattern,
though the family dynamics do play a significant roll in treatment of eating disorders. In
diagnoses of the families of female eating disorder patients, the crucial evaluation is as to
whether the damaging eating behavior has a specific function within the familial system.
Characteristics that are often identified among very heterogeneous families with an anorexic
family member are the following: a strong norm-referenced and high-performance
orientation, “it ought to be done the right way”; the fear of separation, this can be linked with
the myth of misfortune; the tendency to over-protectiveness and sacrifice (decisions are
always made based on the other person’s interests, actions are always carried out with well-
meaning intentions for the other person and are not open to criticism); ill-defined borders;
and the tendency to avoid entanglement. The ‘law of harmony’ (peace at all costs) and
conflict avoidance are of special importance (see Cierpka and Reich 1997).
Situations of separation or the disruption of attachments are often described as triggers of
the disease in both genders. Anorexia among both boys and girls is seen as a way of coping
with stress or, in negative terms, as a refusal to confront the conflicts typical of the
developmental phase currently being undergone. The affected persons develop a heightened
sense for the needs of others and often use it with controlling or manipulative intentions. A
childish super-ego persists, as does a tendency on the part of the patient to be demanding,
both of him or herself and of others (Schepker 1993).
Regarding the pre-pubertal form of anorexia among boys, Olivry and Corcos (1999)
allude to the comorbidity and to the case history of the psychological disturbance that
evinced itself earlier both through problems with food and through phobic-compulsive
disturbances. The authors also describe a high incidence of narcissistic disorders in the
primary attachment figures. In this specific form there is a significant presence of depression
and auto-aggressive behavior among boys, while the incidence of laxative abuse is described
as less probable. All of the studies reviewed stem from the same environment and similar
treatment methods for both genders. In the case of in-patient treatment of adolescents,
parental agreement and cooperation is of central importance. Since parents often experience
the separation as a strain, it is recommended that attending staff work with the parents to set
up precise conditions for discharge. Systemic short-term therapy, combined with elements of
behavior therapy, is viewed as an especially effective treatment for adolescents (Blank et al.
2002). It is thought that the earlier a treatment begins after the onset of the disease, the better
chances it has of success (Romeo 1994; Dalem 2000). The shame affect is seen as a particular
problem among male adolescents who suffer from bulimia, because bulimia in general is
viewed as an even more typically female disease than anorexia is.
Below we have attempted to comprehensively describe the course of therapy and
psychodynamics in a case report of a boy of just under 11 who suffers from the restricting
type of anorexia. Following that, we have sketched out two vignettes of cases that were
treated in another clinic and that fall more into the borderline area of classic eating disorders
and hence indicate the broad spectrum of sub-clinical eating disorders that often go unnoticed
but nonetheless require treatment.
Case Report 1
Situation at Admission
David (10 yr. 11 mo.) was brought in as an emergency patient for in-patient treatment.
David’s parents reported that his weight had fallen from 33 to 28 kg over the previous four
weeks. He was 149 cm tall. According to his parents, he hadn’t eaten for 2 days and hadn’t
drunk anything for one day. He had been given an infusion by his personal physician but had
consistently refused to take any other liquids. His parents dated the onset of his weight loss
back to a trip taken with his soccer club four months previously. They said David had felt
very isolated on this trip, which was the first time he had been separated from his parents. He
had, they said, been teased and bullied on the trip. David himself said “nothing in this trip
had suited him.” Since that time he had eaten less and less, not because he was less hungry
but because he had decided not to. The situation had come to a climax in the preceding
month. His parents felt as though they were “hitting a wall” when they admonished him about
eating. They reported that David was very concerned about gaining weight, felt guilty about
food, and that his need for activity increased dramatically over the same period, but that he
was not at all interested in his actual weight. They also noticed that David was extremely
thrifty and concerned with cleanliness: he was sickened by the idea of showering at the
swimming pool, wanting instead to shower at home because it was cleaner there. They said
he would frequently check to see that the door was closed, washed his hands relatively
frequently, and needed an unusually long time to perform day-to-day tasks such as tying his
shoes. In the first conversation David himself reported being sadder than usual; his parents
confirmed this. The parents supported the decision to have their son examined due to his poor
physical condition and they expressed their agreement with the conditions of the in-patient
treatment (participation in family therapy, etc).
Patient History
The pregnancy went without complications. David was a planned child. He was breast-
fed for 10 months and was on the whole a restive and nervous infant. His statomotoric and
speech development progressed normally. He suffered from chronic obstipation for about 3
months when he was 4. At 4 1/2 he started kindergarten, where he integrated quickly,
although he often reacted aggressively to other children. His behavior overall was very
defiant, and he exhibited a markedly strong will that, according to his parents, could not be
countered in a strict manner. When he started school at six, David’s aggressive behavior
stopped and he adapted very well. At times, in fact, his parents were shocked at how over-
adapted his behavior seemed. In first or second grade, David suffered from a sleep disorder,
but after half a year it receded without any special intervention. Three months before his
admission, he had entered secondary school, where he had great difficulties integrating in
class. He was a relatively good student in terms of his performance in school. David listed
soccer, skateboarding, swimming, cycling, handicrafts, and painting as his hobbies.
Family History
David had a 22 year-old sister, a student of education science, who no longer lived at
home. At 15, she had suffered from anorexia that abated without therapy. The relationship
between David and his sister was good. His mother was employed half time in a white-collar
job. The maternal grandparents had died as a result of excessive alcohol consumption: the
grandmother when David’s mother was 8 years old, the grandfather one and a half years
before David’s treatment began. David’s father was a decorator by profession. He had been
an enthusiastic marathon runner, but had had to give this up five years earlier due to multiple
pains for which no somatic cause could be found. David’s paternal grandfather committed
suicide 22 years earlier; he suffered from multiple sclerosis and, according to David’s father,
“couldn’t deal with that.” His paternal grandmother was still alive and there was loose
contact with her; she was described as being somewhat inaccessible.
The Inpatient Treatment Environment
A multi-discipline team works at the station, made up of pediatric nurses, a therapeutic

educational nurse (Heilerziehungspfleger), an art therapist, teachers, and psychiatric and
psychological psychotherapists. There are also a physiotherapist and a social worker that can
be called in. There are twelve treatment positions available for children and adolescents aged
4 to 17. The station specializes in treating somatization and eating disorders. The treatment
concept is committed to an integrative method approach; i.e., it draws on behavioral therapy,
depth-psychological, systemic, and on elements of the integrative child and adolescent
psychotherapy as well. Treatment of eating disorder patients lasts between a minimum six
weeks and a maximum six months. As a rule, patients are given a behavioral therapy-
oriented, individually designed, step-by-step plan to nutritional rehabilitation; they also take
part in the depth-psychology oriented group therapy, in art therapy, in physical therapy, and
learn yoga, to improve their body awareness. They also receive two individual therapy hours
per week, and once a week a parent or family therapy session takes place.
Course of the Therapy
Our first impression of David was of a precocious, serious, and in his whole behavior,
very stiff boy, who spoke of his illness as something alien. He said he no longer had an
appetite and had to count calories, but he didn’t know why that was the case. It was very
important to him to be thin though, so that he could be agile. His speech was uniform, with
little modulation in his voice, and his facial expression was rigid. The first four weeks of his
stay were marked by crises. David often refused to cooperate, pulled out his tube himself, and
exerted enormous pressure on his parents to take him back home. After two weeks of in-
patient stay, an extreme compulsion to wash manifested itself; after an observation phase this
was treated with Anafranil.
In the individual therapy sessions we sensed mental disturbances and blocks in the
counter-transference, which, as I record later, also were partly responsible for the patient not
sensing powerful emotions like rage or powerlessness.
In the psychological diagnostics, especially during the projective test procedures, the
theme of aggression, and the fear of and defense against it, were dominant with David.
Another central theme seemed to be his relationship with his father, to whom David wanted
to be close, but with whom he was also in competition. In addition, his fantasies of greatness
and high-performance related themes, which he attempted to keep minor, became evident.
Work with the parents was initially quite difficult; the collaboration was extremely
fragile. It was extremely difficult for both parents to decide definitely on the in-patient
treatment. Both preferred the idea that their son not be forced into anything and anxiously
predicted resistance from him: resistance that promptly emerged, in all its intensity and
despair. On several occasions, David threatened to take his own life if his parents didn’t take
him out of in-patient treatment immediately. Understandably, this threw both parents into
panic, particularly David’s father, due to the suicide of his own father. The fear that
something would happen to David at home or that he might die collided with the fear inspired
by David’s threat to harm himself. With strong therapeutic support however, both decided to
leave David in the in-patient treatment program. As soon as it became clear to David that this
decision was unequivocal, the situation defused itself and he grew increasingly willing to
cooperate.
A further hurdle in the therapeutic treatment arose in dealing with the paradoxical signals
the parents sent David. They constantly sent conflicting messages: obey the rules, but break
them too. Once the weight situation had become less dramatic, David’s parents began to join
forces with him to break the hospital rules: they smuggled food in, over-stayed visiting hours,
etc. When confronted with this, the parents behaved like anxious and rebellious children,
while the clinic and the therapist took over the roll of the strict, rigid but also life-sustaining
mother.
The decisive positive shift in the therapeutic treatment occurred on two levels. Initially
through a conversation with the parents in which they articulated their anger at the clinic,
which had cut their contact with their son. Focusing on this conflict made it possible to
transform the opposition into cooperation. There followed an individual therapy session with
David, in which he actively demanded therapeutic support in the form of positive signals
when something had worked successfully. At this level too, a change occurred, and the
patient decided, on his own initiative, to work with the therapist instead of against her. It was
only after the conflict with the parents had been resolved that this became possible. The
therapeutic relationship then became so stable that it became possible to establish sustainable
cooperation with David and to modify the stimuli plans with him. His mood - which up until
this time had ranged from despair, to auto-aggression, to aggression directed outwards -
visibly improved; he gained weight and the compulsive behavior lessened. In individual
therapy his behavior developed from that of a precocious, intellectualizing and problem-
conscious narrative behavior to a more childlike, age-appropriate, playful behavior. He also
became better and better at articulating the fact that he had often felt lonely and isolated from
other children.
By the end of the 10-week treatment, David had gained 8 kg and the compulsive
pathology had abated to such an extent that the medication could be tapered off. The latter
was primarily understood as an expression of an underlying severe depressive episode.
David’s father was advised to seek individual psychotherapeutic support to confront his own
fear pathology; his response to this suggestion was positive and he acted upon it.
Family Dynamics
In the course of the family therapy, food established itself as a significant topic and
relevant arena for action. Both parents were very slender to the point of thinness; during the
treatment of her son, David’s mother became even thinner. In the same period, it became
clear that she had had only very limited experience with care-giving and continually felt
herself to be on the verge of being overburdened within her role as a mother and in her duty
to care for others emotionally. The father talked about the unbelievable amount of calories
that, he said, he had been able to consume without gaining fat during his marathon running
days. The fear, to some extent seemingly paranoid, of the deterioration of his own body –
especially before the background of his father’s suicide – was a central theme for him.
David’s sister talked about her own anorexic period during a family session.
The relationship of the parents to one another came across as very sibling-like in
character. There seemed to be almost no partner level that was separate from the children.
Both spoke of extreme difficulties in supporting each other and keeping each other grounded.
They reported that in the current situation they could neither comfort nor be gentle with one
another, because to do so would cause them to feel guilty about feeling good when their son
was in the clinic. David, for his part, refused to accept gifts from his parents, claiming that he
had not earned them. This is a self-punishing dynamic typical for families with anorexic
children, one that could be summed up with the motto: “Do everything for the others, nothing
for yourself, a depressive duty-fulfillment without enthusiasm that is driven by guilt”
(Schepker 1993, p.12).
Once a trusting therapeutic relationship had been established, the themes of separation
and the disruption of bonds dominated the family therapy session. Within the family there
was a significant amount of fear associated with these themes: separation was viewed as
almost equivalent to death and absolute loss. The family sculpture had something about it that
struck outside observers as rather oppressive and constricting but which all of the family
members perceived as a pleasant density and physical closeness. The sister, who took part in
one family session, articulated her feelings of guilt and ambivalence about having moved out;
that is when it became obvious just how critical and existentially threatening all family
members perceived the physical separation from the sister to be.
Psychodynamics
David’s illness must be viewed at different levels. On the one level, it presents a classic
autonomy-dependency conflict; on another it symbolizes a trans-generationally-significant
theme for the paternal line; and on a third, it fulfils the function of a familial reapprochement.
David’s pathology began with his entry into a developmental phase that implied more
autonomy. For David and his whole family, autonomy was associated with fear and thus this
represented a critical transition. In our view the disease was triggered by the temporary
separation from his parents, a situation exacerbated by harassment by the other children and
in which David was also confronted with a new environment. David’s self image as that of an
athletic boy who wins all competitions also collapsed on this soccer trip. He lost to other
boys. David processed this defeat and the separation from his parents with a feeling of guilt.
Out of this emerged what was for him an existential question, one that had dominated his
father and probably his grandfather as well: can I go on living if I don’t have complete
control over my body?
This is where the trans-generationally-significant theme expressed itself. According to
family lore, David’s grandfather had committed suicide because he could no longer tolerate
the physical deterioration brought on by his multiple sclerosis. David’s father had kept
physically fit through marathon running for years but was ultimately forced to give that up.
He then became preoccupied with the unvoiced question or fear that he might have the same
disease his father had had. When David’s disorder appeared, his father was at the same age at
which his own father had committed suicide. For David’s father, this represented an
extremely critical point of in his life, one that his son picked up on and transformed into a
crisis of his own. David confronted the issue of life and death and these existential questions
in his father’s place, and by doing so managed to bring his whole family together and cause
them to confront such threatening subjects as fear of loss and separation together.
David’s illness is also an avowal of his loyalty for his father: David identified with his
father very much and tried to emulate him in his athletic endeavors, but he was also very
much afraid outdoing his father in that arena.
Case Report 2
Over a four-year period, Stefan (13 yr. 3 mo.) received in-patient psychiatric treatment
four times under various diagnoses. He was diagnosed under ICD-10 with a social behavior
and emotional disorder (F. 91.3) and with a somatoform dysfunction with nausea and
vomiting.
The early patient history shows normal statomotoric and speech development; toilet
training was complete at the end of his first year. As an infant and small child, Stefan
suffered from severe sleep disorders: up until his third year he woke up as often as 20 times at
night. He also ate and drank very little, reacting with vomiting to milk products in particular.
When his father insisted that he eat his entire serving, Stefan reacted by vomiting.
In the later patient history, the fact that Stefan initially had many friends and got along
fairly well in school seems significant. He had several stays in the pediatric clinic due to
undefined stomach pains and refusal to eat. From the beginning of his eleventh year, Stefan’s
aggressive behavior in school and at home began to increase. He was often involved in
fistfights and verbally aggressive towards his mother. The mother reacted to this at times by
accommodating his wishes or by ignoring the behavior, sometimes with blows and rescinding
television privileges. With respect to the family history, we know that Stefan grew up with
his parents as an only child. His father became unemployed when Stefan was one and
developed an alcohol problem. Stefan witnessed acts of domestic violence perpetrated against
his mother and there were isolated violent acts directed against Stefan. For years, Stefan’s
mother took care of her own ailing mother, who died when Stefan was 12. She herself
suffered from a cerebral tumor with facial paralysis. Stefan’s parents separated when he
turned 10; the separation was not discussed with Stefan. From then on, contact with his father
was sporadic and irregular.
From the various courses of treatment, it is apparent that the somatoform dysfunction
with vomiting and nausea was not treated directly until around the end of his tenth year,
although it was obviously dominant. The disorder developed from an earlier interaction
disorder that went unrecognized and untreated. This earlier disorder manifested itself as a
sleep and feeding disorder. It is also evident that both parents had, in different ways,
withdrawn from the relationship with their son. The only way Stefan could get his parents
attention was by refusing to eat and through the stomach aches, accompanied with nausea and
vomiting, that cropped up again and again. After he turned 10, with the onset of puberty and
his parents’ separation, Stefan’s introverted self-destructive behavior began to decrease and
aggression directed outward became more frequent, climaxing in arson and severely
destructive behavior during his last in-patient treatment period. This case illustrates the way
that a diagnosed but incompletely treated eating disorder, an expression of the hunger for
parental attention and security, can be transformed into a dissocial disorder in male
adolescents with multiple manifestations.
Case Report 3
13 yr. 10 mo. old Michael, who had a learning disability, was treated for three and a half
months for a psychogenic eating disorder for which no more exact diagnosis was given; for a
nascent personality development disorder with anxiety/avoidance personality traits; and for
stereotyped movement disorders in the form of jactation. Michael, who comes from a tall
family, is 1.93 m tall and weighed 54 kg (BMI 14.5) at admission. A weight loss of 6 kg and
the intensification of a chronic eating disorder triggered his hospitalization. The eating
disorder took the form of a daily battle over eating: Michael was said to throw out his food
and often vomit after meals.
With regard to Michael’s medical history: nicotine and alcohol abuse were known to
have taken place during the pregnancy, which went to term, with an umbilical cord
entanglement at birth. Nutritional problems arose very early on. His statomotoric
development and speech development were delayed. Michael’s parents separated when he
was five years old, at which point his paternal grandparents took over his care. Two years
later, contact with Michael’s mother broke off completely. He saw his father regularly on
weekends. Michael started at a residential school for children with disabilities at age 7. At
eleven, the fourteen year-old son of his father’s long-term girlfriend sexually abused him.
Michael transferred to another residential school shortly before his hospitalization at the
clinic. A few days before his hospitalization, Michael’s father and his girlfriend, with whom
Michael had had a good relationship, separated.
The over-protective child-raising style of the grandmother was discussed as a problem
and the high degree of responsibility borne by his father was also raised as an issue during the
in-patient treatment. A recommendation was made that Michael be encouraged to take on
more independence and responsibility in the area of practical living. Michael was released
after a small weight gain and a decrease in the jactation. The psychogenic eating disorder was
considered to be the reaction of a learning-disabled boy who was extremely
anxious/unselfconfident, socially less competent and conflict-avoiding, due to psychosocial
stress factors on the basis of an early childhood emotional deprivation.
Summary and Discussion
The number of boys and men suffering from eating disorders is increasing. Girls run a
17.5% risk of acquiring an eating disorder; boys, 6.5%. The number of boys with a binge
eating form of disorder is four times higher than that suffering from anorexia nervosa. When
applying the classification system, the criterion of the abnormal gonadal axis (lowered libido,
potency, juvenile genitals) is more difficult to operationalize than is amenorrhea. Boys seem
to strive for a less underweight ideal figure than that pursued by girls. They do not suffer as
much from feelings of guilt regarding food binges. Boys tend to fixate less on a specific
weight, and they strive less towards an ideal weight, instead pursuing an ideal physique,
usually a muscular and powerful one. Questions of sexual orientation play a role among boys
with eating disorders more often than they do among girls. Among men with bulimia, a
higher frequency of homosexual orientation has been reported. Overall however, those
symptoms disorders in both genders have in common outweigh the gender-specific

differences. Eating disorders among boys are characterized by a wide spectrum of forms of
manifestation and causal factors and by a high frequency of sub-clinical disorders in
particular. In the restricting type of anorexia nervosa, the aspect of asceticism and the
strength drawn from it is used as a way of establishing borders between the subject and the
parents or important attachment persons. The children and adolescents in question use the
refusal to eat as a way to try to deal with the general developmental tasks of gradual
separation, identity building, and assertion of independence, at the cost of enjoyment,
sensuality, sexuality, and intimacy. By refusing to eat, a female anorexic patient is often
trying to detach herself from a symbiotic relationship with her mother and thereby to
demonstrate – in an extreme and often life-threatening way –having cut the apron strings and
gained independence. In describing the case of 10 year-old David, we have attempted to give
an example of a seldom described but probably not so very rare kind of case. This is that of a
boy who uses his pathology in an attempt to detach himself from a symbiotic relationship
with his father and transform a conflict that actually belongs to his father into one of his own,
thus making it a family theme more available to examination. The sustainable therapeutic
alliance with the parents, which included the general terms set by the clinic, was of critical
importance in putting the treatment on the road to success. On this basis, primarily supporting
work could be done with David in individual therapy. This theme had to be brought out into
the open in the family therapy, but without apportioning blame. In this regard, a mixture of a
resource-oriented and a confrontational approach seemed optimal, one that respected the
family as a functional system but nevertheless recognized dysfunctional entanglements as
such, thus providing access to opportunities for change. The psychotherapeutic treatment of
children and adolescents with anorexic pathologies usually involves walking a tightrope
between curbing and permitting autonomy. It alternates between restrictive control and the
support of developing needs for independence. The treatment often takes on the form of a
battle, one that cannot be won by the therapist with out the patient though it can be won by
the patient without the therapist. This must be made very clear to the patient: the idea is to
return control over his life and his decisions to him and to humiliate him as little as possible
along the way.
The case vignettes of Stefan and Michael should illustrate the way in which
unrecognized or insufficiently treated eating disorders can turn into other disorder profiles.
They should also illustrate the initially atypical contexts in which eating disorders can
represent an expression of the psychological distress of a male adolescent.
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Chapter VI
Effects of Multiprofessional
Treatment on Clinical Symptoms,
Food Intake, Eating Patterns,
Eating Attitudes and Body
Image of Brazilian Bulimic Patients
Marle dos Santos Alvarenga1, Fernanda Baeza Scagliusi2

and Sonia Tucunduva Philippi3
1
Eating Disorders Unit of Clinics Hospital, Department of Psychiatry, Institute of
Psychiatry, University of São Paulo
2
School of Physical Education and Sport, University of São Paulo and Eating Disorders
Unit of Clinics Hospital, Department of Psychiatry, Institute of Psychiatry, University of
São Paulo
3
Department of Nutrition, School of Public Health, University of São Paulo
Abstract
Eating disorders (ED) have been treated in Brazil since 1992 with the creation of the ED
Unit of the University of São Paulo, a public service that has treated 1,794 patients,
mainly white, reasonable educated and aged between 21 and 40 years.
Food intake and eating patterns and behaviors are disturbed in bulimia nervosa (BN).
Food intake is defined as the food and nutrients that compose the diet, while eating
patterns are the meal frequency, regularity and schedules, and eating behaviors are the
attitudes, beliefs and relationship with food. In Brazil, the effect of multiprofessional
treatment in BN had never been examined. Even in developed nations, only the
frequency of bulimic symptoms has been evaluated. The Eating Disorder Inventory,
Three-Factor Eating Questionnaire, Dutch Eating Behavior Questionnaire and Restraint
Scale were used to analyze eating behaviors, although these questionnaires focus
especially in dietary restraint, leaving the other eating behaviors’ aspects uncovered.
106 M. dos Santos Alvarenga, F. Baeza Scagliusi and S. Tucunduva Philippi
Methods
Thirty-nine women with BN (according to DSM-IV criteria) were followed. Treatment

was composed by 12 weeks of cognitive-behavior therapy, pharmacotherapy and
nutrition counseling. Measurements were made before and after treatment, and after three
months. Patients recorded their food intake and occurrence of compulsions and purges in
a diary. They fulfilled the EAT, BITE and BSQ, and also an eating attitudes
questionnaire, especially developed for this research. Non-parametric statistics were used
to test for differences among the three moments.
Results
We observed an improvement in clinical symptoms; at the end of following 97.5% of the

patients did not fulfill criteria for BN anymore. Scores of EAT, BSQ and BITE-
symptoms decreased after treatment and even more after the later following. Nutrients
intake did not alter, even though energy content of the meals followed by vomit
decreased. Number of meals increased and patients did more meals seated, with company
and less anxious. The belief of automatically gaining weight after a meal, and guilty and
worry after eating a “forbidden” food decreased. Nevertheless, most of them remained
hating the hunger sensation, having difficulties with food choices and not believing that
they could have a normal diet and a normal weight.
Conclusion
Based on the questions used to assess eating attitudes, we are now developing an eating
attitudes questionnaire, which will be psychometrically tested. This study supports the
idea of the importance of food issues and behaviors in ED, because even the patients that
had a clinical improvement remained with a complicated relationship with food, which
can contribute to relapses.
Introduction
Just as in other developing countries, Brazil is undergoing a nutritional transition.

Nutritional transition represents the changes that take place for centuries regarding nutritional
patterns that result from shifts in the structure of the diet followed by the population. These
changes are related to economic, social, and demographic changes, and they result in health
changes as well (Popkin, 1993). These transitions can be seen worldwide, given globalization
of current habits and consumption patterns. However, studies show that the pace of change in
countries undergoing less development has been markedly quicker, with a notable
progression from malnutrition to obesity.
Particularly in Brazil, where great economic and demographic changes took place in the
last decades - from 1960 on (Monteiro et al., 2002; 2004) - we see the presence of
malnutrition along with obesity. In many studies regarding nutritional transition obesity and
other chronic diseases are the main focus, but as appointed by Nasser (1988) and Yager
Effects of Multiprofessional Treatment on Clinical Symptoms, Food Intake … 107
(2000) the increasing prevalence of eating disorders (ED) is also a characteristic feature of
nutrition transition.
There are no specific data regarding prevalence of ED in Brazil. Case reports from
developing countries are rare; thus, it gives the wrong impression that these disorders are rare
in non-developed countries (Negrão and Cordás, 1996). It is estimated that the prevalence of
ED in Brazil is similar to that observed in western countries for young women: 0.5% for
anorexia nervosa; 1.0% for bulimia nervosa, and 2-5% if partial syndromes are considered
(Hay, 2002). Anyhow, it is known that the incidence of ED has been increasing in less
developed countries (Nasser et al., 2001). Vilela et al. (2004) used some screening
questionnaires to evaluate the prevalence of possible eating disorders and inappropriate
eating behaviors in Brazilian children and adolescents aged 7 to 19 years old. According to
the Eating Attitudes Test, 13.3% of the sample had inappropriate eating behaviors. Being
female implied in a greater risk of having inadequate eating behaviors (odds ratio = 1.54;
95% confidence interval = 1.16 – 2.05). According to the Bulimic Inventory Test Edinburgh,
1.1% of the sample had a possible diagnosis of bulimia nervosa. Another Brazilian study
assessed the prevalence of abnormal eating behaviors among 513 young women (aged 12 to
29 years) randomly selected (Nunes et al., 2003). Combining scores obtained in the Eating
Attitudes Test and in the Bulimic Inventory Test Edinburgh, it was observed that 10.9% of
the sample presented abnormal eating behaviors, while 23.8% had unusual eating patterns.
Other striking findings were found by Nappo et al. (2002). Investigating a sample of 2,370
Brazilian subjects about the methods used by them in order to lose weight, the authors
observed that 72.4% of the sample had been submitted to some treatment to lose weight, and
79.2% of these had consumed amphetamine-like anorectic drugs. The most interesting fact
was that among these consumers, 60% had a Body Mass Index below 29.9 kg/m2, which
shows that they did not need these drugs and that probably they were consuming them
motivated by physical appearance aspects. Taken together, this data shows that is necessary
to study, prevent and treat eating disorders in Brazil.
Eating disorders have been treated in Brazil since 1992 with the creation of the ED Unit
of Clinics Hospital of the University of São Paulo, which is a public service (visit
http://www.ambulim.org.br for more information about this service). Together with the unit
of ED in children and adolescents and the binge eating disorder (accompanied by obesity)
unit, these services has treated 1,794 patients, mainly females (88.3%), white, reasonable
educated (36.4% completed junior high or high school and 27% had studied for more than
high school) and aged between 21 and 40 years (58.1%). Nowadays some Brazilian groups
work with ED, offering some public assistance (Fontenelle et al., 2003; Negrão and Cordás,
1996) and doing researches (Borges et al., 2002; Nunes et al, 2003; Vilela et al, 2004). It is
important to remind that there are only ten of these centers in Brazil, which certainly is too
little for such populous country (total population: 182 million people – for more information
visit http://www.ibge.gov.br).
The Brazilian studies that focused in nutritional aspects of ED started to be conducted in
1994 as graduate researches of the dietitians that belonged to the Nutrition in Eating
Disorders Study Group (visit http://www.genta.com.br for more information about this group)
(Alvarenga et al., 2003; Dunker and Philippi, 2003; Scagliusi et al., 2005a). Our current
researches focus mainly in bulimia nervosa (BN).
The interest for this area of research came from the observation that the majority of
patients who looked for treatment in our unit had BN and this is an eating disorder marked
not only by binge eating and compensatory practices, but also by an extremely affected eating
behavior (ADA, 2001; APA, 1994). Distorted cognitions about nutrition and feelings of
repugnance, hate and incompetence in dealing with food are also features of this disease
(Sunday et al., 1992).
Nutritional rehabilitation has a key and primary role with regards to treatment objectives,
which should be performed by a multiprofessional staff aiming to end bulimic behaviors and
to alter the patient’s relationship towards food and weight (ADA, 2001; APA, 1994; Eiger et
al., 1996).
The first studies regarding nutritional aspects of BN were conducted between 1980 and
1990, essentially in developed countries (Hadigan et al., 1989; Kissileff et al., 1986; Mitchell
and Laine, 1985; Walsh et al., 1989). Researches describes that a chaotic eating pattern is
present in BN, oscillating between severe dietary restraint and episodes in which the energy
intake is extremely high (Wallin et al., 1995). The “diet – binge – purge” cycle illustrates the
eating pattern of bulimic patients. They constantly start a new diet, which makes them eat a
very limited amount of food and avoid those foods considered by them caloric or “fattening”
(the named “forbidden foods”). This restraint leads to a binge eating episode, where the
energy consumption can be very high (Reiff, 1992). The items more consumed in these binge
episodes are those most avoided by the patients due to their fear of gaining weight (for
example, cookies, chocolates, candies, etc) (Alvarenga et al., 2003; Wallin et al., 1994;
Walsh et al., 1989).
Some authors argue that the disturbed eating pattern is a general feature of BN and not
only a characteristic of their restrictive diets and binge episodes, which explain the
difficulties faced in order to normalize their intake (Hetherington et al., 1993; Sunday and,
Halmi, 1996). Besides their unhealthy food consumption, its is known that these patients
have other disturbed eating behaviors, as difficulties regarding food choice, abnormal
patterns of hungry and satiety, food aversion, fears, taboos and prejudices regarding food and
weight control (Elmore and Castro, 1991; Hetherington et al., 1993; Sunday and Halmi,
1996).
The studies conducted in laboratories, metabolic units or hospitals (with inpatients)
observed in the binges episodes an energy intake varying from 1,436 to 8,585 kcal, which
was generally followed by vomits. These episodes usually lasted 59 minutes and they were
composed by 59% of carbohydrates, 43% of lipids and 8% of proteins. Without the binges
patients had a wide range of energy consumption, varying from 69 to 10,620 kcal (Hadigan et
al., 1989; Hetherington et al., 1994; Kissileff et al., 1986; Mitchell and Laine, 1985; Sunday
and, Halmi, 1996; Walsh et al., 1989). The artificial settings and the low ecological validity
of these studies may have limited their findings, but the ample difference between the
minimal and maximal values shows that there is a great variability in food intake data of
bulimic patients.
This scenario shows that it is hard to study nutritional aspects of BN, especially if one
considers that the term “nutritional aspects” embodies several different variables. In our
studies we divided this term in the following components: food intake (foods that are eaten
and their energy and nutrient content); eating pattern (general characteristics of the intake, as
number, types and schedules of the meals) and eating attitudes (relationship with food,
feelings and beliefs related to food). Among these aspects, we are most interest in eating
attitudes, not only because of the scarce number of studies concerning it but also because it
seems that it is one of the most disturbed characteristics of BN. Due to our interest, we
created a more specific definition of eating attitudes, based on the statements of Garcia
(1999) and Johnson (1985): what, how, with what, with whom, where, and when we eat, why
we eat that, in which situation we eat, what we think and feel towards food. It is also
important to ask in what are food choices based on, and where there is difficulty, lack of
control, aversion, and what are the feelings related to food.
Although follow-up studies of bulimic patients are commonly carried out in developed
countries (Collings and King, 1994; Fahy and Russell, 1993; Keel et al., 1999; Keel and
Mitchell, 1997; Leung et al., 2000; Maddocks et al., 1992), outcome measurements and
follow-up studies are not conducted systematically in Brazil.
Studies to measure outcome are hard to be conducted because of methodological
difficulties, which include the definition of a recovery criteria and follow-up methods. The
definition of recovery varies in each study: some considered recovery as those patient that
presented bulimic episodes and purging episodes once a month (Pyle et al., 1990) whereas
others consider it as just those that did not present any episode (Herzog et al., 1996; Keller et
al., 1992; Maddocks and Kaplan, 1991).
To assess the effects of BN treatment, most studies compare the frequency of pre and
post treatment bulimic behavior (vomiting episodes, for example) (Herzog et al., 1996). In
addition to analyzing the frequency of binge eating and purging episodes, many follow-up
studies utilized recovery predictors and indicated that the frequency of bulimic behavior at
baseline was not associated to the outcome (Abraham et al., 1983; Fairburn et al., 1986; Hsu
and Holder, 1986). Nevertheless, several factors are used as prognostic predictors: age at the
beginning of the disorder, presence of comorbidities, psychosocial aspects, weight at the start
of the treatment, eating behavior and methods used to lose weight (Herzog et al., 1996).
Also, there are some standardized tests used to screen patients with eating disorders, such
as Eating Attitudes Test - EAT-26 (Garner et al., 1982), Bulimic Inventory Test Edinburgh -
BITE (Henderson and Freeman, 1987), and Eating Disorder Inventory - EDI (Garner et al,
1983), among others. The results of some of these tests are analyzed in studies on recovery
predictors, in which Olmested et al. (1994) found a high score in the subscale of bulimia of
EAT-26 (Garner and Garfinkel, 1979) and high score in the interpersonal distrust subscale of
the Eating Disorder Inventory-EDI (Garner et al., 1983) among the recurrence predictors.
According to Steinhausen and Seidel (1993), self-applied scales should be used in prognostic
studies. Although there are many studies using screening tests in several populations (Adami
et al., 1997; Beals, 2002; Bhugra et al., 2003; Ghazal et al., 2001; Lee et al., 2002; Nobakht
and Dezhkam, 2000), even to compare results of healthy individuals to those from ED
patients (Behar et al., 2003; Nakazato et al., 2003), few studies assessed the scores of
individuals with ED post-treatment (Brambilla et al., 1995; Fernandéz et al., 1998;
Steinhausen and Seidel, 1993). The uncertainty remains as to whether the scores attained on
these tests return to normal patterns after the remission of ED symptoms.
Even in developed countries, few studies have assessed the nutritional progress of
bulimic patients and no study has evaluated the effect of a multiprofessional intervention with
regards to important BN aspects: relationship and behavior towards food. Also, as far as we
are concerned the food intake of bulimic patients was analyzed only in cross-sectional
studies, so it is not know if the treatment improves the food consumption of these patients.
Therefore, this issue requires further study (Whisenant and Smith, 1995).
The few studies that have assessed the effect of treatment on eating behavior used tools
such as food diaries and standardized tests such as the Eating Disorder Inventory (Garner et
al., 1993). Although we presented above these tests as interesting measurement tools, one
must remember that these instruments do not encompass the wide concept of food behavior
and are frequently limited to the analysis of dietary restraint (Herman and Mack, 1975).
Because of that, researchers with interest in nutritional aspects of BN have to use other
instruments able to approach these aspects in a more comprehensive manner.
Whisennat and Smith (1995) interviewed dietitians who worked with ED and stressed the
importance of more objective evaluations of the nutritional treatment. This idea is supported
by Eckstein-Harmon (1993) who attested the importance of the outcome measurements of
nutritional education and rehabilitation in eating disordered outpatients and inpatients.
So we conducted an follow-up study to assess the effect of multiprofessional intervention
on bulimic symptoms, food intake, eating patterns, eating behavior and body image in
bulimic patients treated at a center considered to be one of reference in Brazil: the ED Unit of
Clinics Hospital of the University of São Paulo.
Methods
Thirty-nine female patients with BN treated at the Eating Disorders Unit of the
University of São Paulo (in Brazil) were followed-up. Subjects were evaluated by a
psychiatrist, and BN was diagnosed by means of a semi-structured clinical interview,
according to the criteria of the Diagnostic and Statistical Manual of Mental Disorders - DSM-
IV (APA, 1994). The descriptive data of the patients were collected in this interview. Patients
had their weights and heights measured, and this data was used to calculate Body Mass Index
(BMI – weight in kg/height2 in meters).
Patients gave informed consent before participation. They were also informed that the
goal of the study was to evaluate the outcome of the treatment. The study was approved by
the Committee of Ethics of the Clinics Hospital of the College of Medicine of the University
of São Paulo.
Measurements were performed at baseline (Phase 1), immediately after treatment (Phase
2) and three months after treatment (Phase 3). All measures were compared between these
phases.
Bulimia nervosa should be treated by a multiprofessional staff working to end bulimic
behaviors and to change patients’ relationship towards food and weight (Gannon and
Mitchell, 1986; ADA, 1988; APA, 1994). Cognitive Behavioral Therapy (CBT) is considered
the best technique to treat BN (Agras et al., 2000; Leung et al., 2000). Because of that,
treatment consisted of 12 weeks of cognitive behavioral therapy (CBT) – with one weekly
consultation with the psychiatrist, the psychology and the nutrition education teams. At the
end of treatment, the unit provided 3 more months of care, but in an unstructured form.
The number of weeks of treatment was defined arbitrary, but its structure and content
followed the models proposed by Fairburn (1981), Johnson et al. (1986), Lacey (1985),
Nutzunger and Zwann (1990) and Vanderlinden et al. (1989), which described cognitive-
behavioral techniques and provided guidelines for nutritional counseling, even suggesting
some educative materials.
The goals of the nutritional treatment were to: a) decrease the binge and purging
episodes; b) minimize dietary restraint; c) establish a regular meal pattern; d) increase food
variety; e) correct nutritional deficiencies and f) implant a healthy food intake and behavior
(ADA, 1994; ADA, 2001; Latner and Wilson, 2001). The approach can be divided in some
key points: a) education about the disease and its implications; b) education about food and
nutrition; c) reduction of weight concerns; d) self-monitoring of the food intake by means of
a food record and e) implementation of a healthy eating pattern (Story, 1986).
Weekly nutritional treatment consisted of one hour of nutrition education and 30 minutes
of individual counseling based on the food record. The topics addressed during the nutrition
education program were: role of nutrients; energy and nutrient requirements; food pyramid;
ineffectiveness of dietary restraint and of restrictive diets; definitions of hunger and satiety;
healthy weight and build; guidance for buying food and how to eat at restaurants and social
events. After the 12 weeks, the topics discussed were chosen by patients and/or the
professional team such as issues from lay magazines about body and nutrition, the social and
emotional meanings of foods and exchange of ideas about methods and tips to handle
difficult situations regarding food.
Patients received one hour and half of psychology consultation, in which the following
issues were addressed, according to the models of Villapiano and Goodman (2001a; 2001b)
and those described above: a) the kinds of hunger (physical, emotional and social); b) the
beliefs involved in the diet-binge-purge cycle; c) the personal meaning of BN; d) body image
dysfunctions; e) mechanisms used in order to copy with the emotions; and f) barriers for
change.
The dietitians instructed the patients to register all food consumed, the amount eaten, and
the schedule and duration of their meals in a food diary (ADA, 1988; Story, 1986). They
were also asked to mark if they considered the meal a binge eating episode and if any purging
method had been used to compensate it. If the answer was yes, they had to specify which
ones. Weekly frequencies of binges, vomits and use of laxatives, diuretics and diet pills were
obtained through this diary.
The food records were also used to obtain patients’ energy and nutrient intakes, number
and type of meals consumed. To do so, diaries filled at weeks 2, 12 and 24 were analyzed.
We chose to use the diary from the second week as a baseline measurement because the
record from the first week was used by the dietitians to check if the patients were registering
their intake and bulimic behaviors in a proper manner. If one patient did not fill her record in
one of these weeks, the prior or the next week diary was utilized. Only the days that were
completely recorded were analyzed. For example, if the patient did not describe correctly one
meal, this day was excluded from analysis.
The food intake was converted into energy and nutrient intake by means of the software
Virtual Nutri (Version 1.0) (Philippi et al., 1996), which contains data regarding nutritional
composition and serving sizes consumed in Brazil. When a patient registered that a meal was
followed by vomits, this meal was separated from the others. We calculated the energy and
macronutrient intake from the meals not followed by vomits (named VET) and from those
meals followed by vomits (named VOM). This differentiation (meals followed by vomiting
or not) was made because it was impossible to take into account the energy of foods eaten in
a meal followed by vomiting, insofar as the amount effectively absorbed is not known
(Alvarenga et al., 2003; Gendall et al., 1997; Kaye et al., 1993) and would require a very
complex physiological study. Energy consumption ranges for VOM and VET were defined,
in which the values for energy were classified as hypoenergetic, normoenergetic, and
hyperenergetic.
Reference values used were:
VOM: hypoenergetic < 600Kcal; normoenergetic 600–1,000 Kcal; and hyperenergetic >
1,001Kcal
VET: hypoenergetic < 1,199 Kcal; normoenergetic 1,200–2,200 Kcal; and
hyperenergetic > 2201 Kcal
These VET values were defined according to the mean energy recommendation for
young women (+/- 2,200Kcal) (NRC, 1989; Trumbo et al., 2002); and the VOM values were
based on studies of the energy content of binges (Elmore and Castro, 1991; Woell et al.,
1989).
Also, the intake of the following minerals and vitamins were analyzed (using only the
meals not followed by vomits): sodium, potassium, magnesium, calcium, iron and vitamins
A, B1, B6, C, D and E. The values obtained were compared to the Dietary Reference Intakes
– DRI’s (Institute of Medicine, 1997; 1998; 2000).
Patients filled in a questionnaire about their eating attitudes and relationship with food
specially developed for this population. The scale contained 24 questions about feelings and
beliefs regarding food, behavior during meals, and others. These subjects were derived from
our clinical experience (for example, based on the myths and misconceptions about nutrition
that our patients usually declare) and from other questionnaires that in a certain manner
approach eating behavior and EDs, such as Eating Disorder Inventory (Garner et al., 1983),
Restraint Scale (Herman and Mack, 1975), Three-Factor Eating Questionnaire (Stunkard and
Messick, 1975) and the Dutch Eating Behavior Questionnaire (van Strien et al., 1986). The
instrument had been applied in a previous sample of patients in order to verify if it was clear
and easily understandable.
They also answered the Eating Attitudes Test - EAT-26 (Garner et al., 1982), translated
to Portuguese by Nunes et al. (1994), which measures concern over diet, certain types of food
consumed and body image; the Bulimic Inventory Test Edinburgh - BITE (Henderson and
Freeman, 1987), translated to Portuguese by Cordás and Hochgraf (1993), which measures
the symptoms and the severity of BN; and the Body Shape Questionnaire - BSQ (Cooper et
al., 1987), translated to Portuguese by Cordás and Castilho (1994), which measures concern
over body image, shape and size.
Statistical analysis was performed using the Statistical Package for Social Sciences
(SPSS) software for Windows v. 6.0. Data is presented by phase, as percent frequencies or as
mean, standard deviation, median, and minimum and maximum values. Significance level
adopted was p ≤ 0.05.
Friedman´s test was used to compare the frequency of bulimic behaviors, the energy and
nutrient intakes and the EAT, BITE and BSQ scores throughout the phases. When significant
results were found, the Bonferroni test was used to assess which phase would differ from the
other.
The chi-square test was performed to see if there was any difference between the
proportion of individuals in each classification of VET and VOM energy intakes
(hypoenergetic, normoenergetic and hyperenergetic), among the phases. The Wilcoxon
Matched-Pairs Signed-Ranks test was used to check if the macronutrient profile differed
between meals not followed by vomits (VET intake) and meals followed by vomits (VOM
intake).
In order to analyze the evolution of eating behaviors and relationship toward food
throughout the phases, the following approach was adopted. For the questions regarding
eating attitudes and beliefs, the frequency of affirmative or negative responses was
calculated. A chi-square test compared the ratio of affirmative responses for these questions
between the phases. For the questions regarding the relation with food, the first three options
of answers (always, very often, often) were grouped as “frequent thought or feeling”, and the
last three (sometimes, rarely, and never) as “infrequent thought or feeling”. Chi-square test
was also performed to compare the ratio of frequent and infrequent answers for the questions
of relationship towards food between the phases.
The Spearman correlation coefficient was used to determine the existence of correlations
between these variables: frequencies of vomiting and binges, BMI and EAT, BITE and BSQ
scores. Kruskal-Wallis ANOVA was used to determine if the frequency of bulimic behavior
and EAT, BITE and BSQ scores varied according to the energy intake range (for VET and
VOM consumption), and the Mann-Whitney test was used when the independent variable had
only two categories.
Findings and Discussion
Thirty-nine patients started the study (Phase 1); at the end of 3 months (Phase 2), 20 were
still undergoing treatment; at the end of 6 months (Phase 3), there were only 15 patients – for
a 48.7% dropout rate during treatment and 61.5% dropout rate during the entire follow-up.
This high rate may have limited our results, but other outcomes studies also found an
elevated dropout rate (Bacaltchuk and Hay, 1999; Elmore and Castro, 1991). For example,
Agras et al. (2000) found that 26% of the patients abandoned the treatment after
approximately five weeks.
The diaries returned at each phase, the responses to the tests, and the n of each parameter
varied. The data for the 19 patients that quit follow-up from Phase 1 to Phase 2 were not used
for analysis, but merely to describe the group profile.
Most patients belonged to the BN bulimic subtype (90%); the length of the disorder
varied from 1 to 20 years; 3 patients (15%) had a previous history of anorexia nervosa; 70%
did not have a partner; 65% had at least started college; 25% had professions or activities that
demanded a lean body (dietitian, physical education teacher, nutrition student, dancer, and
actress); and 70% were taking antidepressants according to psychiatric evaluation. Table 1
shows other descriptive data.
The patients presented a profile similar to those described in the literature as
characteristic of bulimic patients: young women, unmarried, with a high level of education
and with a greater prevalence of the purging subtype (Dolan et al., 1990; Fitcher et al., 1992;
Gendall et al., 1997; Hetherington et al., 1994).
Table 1- Patients descriptive data at the beginning of treatment (phase 1)
Characteristics Mean ± Standard Deviation

Age (years) 27.7 ± 6.3
Age when dieting started (years) 17.3 ± 4.6
Age when binges started (years) 18.7 ± 4.2
Age when vomiting started (years) 20.5 ± 6.1
Weight (pounds) 135.9 ± 23.7
Body Mass Index (kg/m2) 22.9 ± 3.9
Desirable weight (pounds) 120.0 ± 14.0
Weight variation throughout adulthood (pounds) 33.3 ± 17.5
Although the patients were still young (median age was 25 years), they were slightly
older than the bulimic patients from developed countries – whose age varies between 16 and
20 years (Joergensen, 1992). This may be due to the long time of the disease and also to the
long time that the patients took to seek treatment, probably because they felt ashamed of their
behaviors or because the lack of awareness about the disorder (Becker et al., 1999). These
findings are corroborated by other studies of bulimic patients, which also found a higher
mean age and a long time of disease (Hadigan et al., 1989; Hetherington et al., 1993;
Kissileff et al., 1986; Leung et al., 2000; Wallin et al., 1994; Woell et al., 1989).
Nevertheless, this difference between Brazilian results and the literature may be due to
our health care system. In this study the sample were patients of the Eating Disorder Unit, at
Institute and Department of Psychiatry (a public institution), University of São Paulo. This
was the first center in Brazil to treat eating disorders and it is still the most known and
important center. People from all over the country come to be treated in this unit, which
makes our sample very representative of eating disorders cases in Brazil. In the other hand,
the vacancies are not much and the wait-list is long, which may explain the higher mean age
of our sample. Finally, in Brazil there are no primary care services preventing and detecting
eating disorders, so the diagnosis of the disorders happens too late, usually when the disease
is very severe.
Regarding the anthropometrical data, the initial BMI was normal as appointed by other
authors (Gendall et al., 1997; Wallin et al., 1994). The mean desirable weight was 15.9
pounds lower than the mean current weight, evidencing the persistent desire to loose weight
that is characteristic of BN. The mean weight’s oscillation in the adulthood was also high
(33.3 pounds), which illustrated the weight cycling derived from the many times the patients
tried to loose weight, following the restraint/binge/purge cycle of BN (Reiff, 1992). Kell et
al. found (1999) a mean weight’s oscillation of 35.2 pounds in the historic of bulimic
patients, while Sunday and Halmi (1996) affirmed that the bulimic recruited in their study
had been heavier in the past.
Table 2 shows the progress of binge eating and purging behaviors in the 3 different
phases. There was a significant statistical difference between Phases 1 and 3, and between 2
and 3, regarding the frequency of binge eating episodes per week. However up until Phase 2,
the mean number of binge eating episodes per week met the DSM-IV criteria for bulimic
frequency (minimum of twice a week for at least three months); in Phase 3, the mean number
of binge eating episodes per week was below the minimum frequency established by the
DSM-IV (APA, 1994).
Table 2 - Measures of bulimic behaviors along the follow-up (data presented as mean ±
standard deviation (median; minimal-maximal))
Phases Weekly Weekly

Weekly use Weekly use Weekly use
frequency frequency
of laxatives of diuretics of diet pills
of binges of vomits
1 – Before treatment 9.5 ± 8.5* 4.2 ± 6.6 1 ± 1.6 1.4 ± 3.6 0.55 ± 2.5
(7; 0-29) (1.5; 0-28) (0; 0-6) (0; 0-13) (0; 0-11)
2 – Immediately after 4.2 ± 4.7* 2.4 ± 3.4 0.9 ± 2.3 0.65 ± 1.9
0
treatment (3.5; 0-20) (0; 0-11) (0; 0-9) (0; 0-8)
3 – Three months 1.6 ± 2.3 0.4 ± 0.9 0.08 ± 0.3 0.92 ± 3.2
0
after treatment (0.5; 0-7) (0; 0-3) (0; 0-1) (0; 0-11)
*: significantly different from results obtained three months after treatment
There was no significant statistical difference between the phases, regarding the number
of vomiting episodes per week. Even though, the median of vomiting episodes was zero in
Phase 2 and at Phase 3 the mean value was below the minimum frequency demanded by
DSM-IV.
There was no significant statistical difference between the phases regarding use of
laxatives, diuretics and diet pills. This type of compensatory method was less utilized than
vomiting, and the medians were zero in all phases.
Regarding percentage of improvement in the bulimic behaviors assessed, there was clear
improvement in the binge eating and purging symptoms at the end of the six-month follow-
up: 75% of the patients had a frequency of binge eating bellow that one that fulfill diagnostic
criteria, and 91.7% had this result in regard to vomiting episodes. Other purging behavior,
such as the use of laxatives, diuretics, and appetite moderators, was shown in 100% of the
responses below the diagnostic criteria. The frequency of other compensatory methods
(fasting, dieting, physical activity) could not be estimated and compared to the DSM-IV
criteria (APA, 1994).
The percentages found are somewhat compatible with the data described in literature.
Lacey (1983) observed that 80% of these patients completely ended their binge eating and
vomiting episodes at the end of 10 sessions of CBT; actually, in this study, it took more than
12 sessions for patients to significantly cease these behavioral patterns. The major difference
was that in Lacey’s study patients spent half a day, once a week, being treated, whereas they
stayed 3 hours per week at our center.
Mitchell et al. (1988) found that 75% of patients had improved their eating behavior
(without defining what kind of changes had taken place) and that 60% did not show bulimic
behavior after treatment. Collings and King (1994) found that 52% of patients fully
recovered, 39% experienced some symptoms, and 9% still suffered from this disease after
treatment. Leung et al. (2000) found an over 50% decrease in bulimic symptoms after 12
CBT sessions. This data can be compared to the findings for this study: 60% did not meet the
diagnostic criteria for BN according to the frequency of vomiting after 12 weeks, and 45%
did not meet the diagnostic criteria for BN according to the frequency of binge eating
episodes after 12 weeks.
After six months, 8.3% vomited more than twice a week. This finding is very important.
According to Olmested et al. (1994), the frequency of vomiting episodes, even if at low
levels, seems to be a poor prognostic indicator and can be considered one of the best
parameters for residual symptoms in these patients.
It can be seen, as stated by Keel et al. (1999), that a longer period of treatment and
follow-up (at least six months) yields better results. Nevertheless, the length of follow-up was
short and patients may have had relapse episodes after this period of time. Regarding
recovery after six months, based on the definition by Pyle et al. (1990), of maximum of two
episodes of binge eating and purging episodes in the last two weeks of treatment, these
patients should be considered already under recovery. According to the criteria adopted by
Maddocks and Kaplan (1991) (less than one episode of binge eating or purging in the last 4
weeks), these patients presented a "moderate" response. One needs to consider that BN is
known for being a disorder with poor prognostics because most patients remain with
symptoms at the end of treatment (Garner, 1987). According to Becker et al. (1999), half of
the patients attain full recovery, about 30% attain partial recovery, and 20% do not present
significant symptom improvement.
The criterion proposed by Keel et al. (1999) is much more severe: "absence of changed
behavior for at least six months, and the weight and shape cannot influence how the subject
felt." From this point, we cannot assess patients from this study, who would require a longer
follow-up to verify a six-month abstinence. Perhaps it would be very difficult to consider
them recovered based on the criteria of non-influence of weight and body shape. As stated by
Herzog et al. (1996), in their review, a comparison of results between studies is very difficult
because of the variability of how improvement, diagnostic criteria, duration of intervals and
evaluation methods are defined.
Table 3 presents the number of meals consumed in one week among the treatment
phases. We observed that after six months the median number of lunches was 7 (significantly
different from Phase 1), which means having lunch everyday. There were no significant
differences regarding the number of the other meals. Even so, at the end of the following the
median number of the breakfasts was 7, and the median number of the afternoon snacks,
dinners and evening snacks were slightly higher than at baseline.
Tables 4 and 5 show the energy and nutrient consumption along the treatment phases, in
the VET intake (meals not followed by vomits) and in the VOM intake (meals followed by
vomits), respectively.
The results showed that the mean intake of energy in the meals not followed by vomits
(VET intake) was much lower than the energy consumption recommendation to young
women (+/- 2,200 kcal) (NRC, 1989; Trumbo et al., 2002). Wallin et al. (1994) and Gendall
et al. (1997) found similar results and attested that these patients use the binges episodes to
regularize their limited intake. It seems like that the patients usually eat less energy than
necessary, which leads to a binge episode in order to compensate this deficit.
The studies regarding eating pattern and nutrient intakes of bulimic patients are diverse.
According to Gendall et al. (1997), empirical studies noticed a variation of 605-4,800 kcal in
the energy intake, while the macronutrient consumption seems to follow the American diet
pattern. Woell et al. (1989) found a mean energy intake of 3,100 kcal per day, including the
binges episodes. On the other hand, Wallin et al. (1995) observed a mean intake of 762 ± 560
kcal/day. Sunday and Halmi (1996) observed that bulimic patients ate less energy than
anorexic patients in a weight maintenance phase.
These great variability among studies was expected, since it is known that bulimic
patients tend to have an atypical and chaotic food intake which varies between the restrictive
and the compensatory phases or between the “regular” meals and the binge episodes (Gayle,
1998; Gendall et al., 1997; Hetherington et al., 1994; Wallin et al., 1994; Wallin et al., 1995;
Walsh et al., 1989). According to Gayle (1998), these extreme fluctuations in energy intake
disconcert the appetite regulation and other physiological functions. The author affirms that
the low energy intake leads to a loss of control, in spite of the great amount of energy
consumed subsequently. Due to that it is recommended to include as one of goals of the
treatment the regularization of the eating pattern, in order to prevent fluctuations of the
bulimic behaviors.
Regarding the energy consumed in the meals followed by vomits (VOM intake), we
found a range of 460-2,690 kcal. This data shows that the energy intake of these meals was
not so high, which is surprising considering that these meals were more likely to be binge
episodes. Woell et al. (1989) found that one third of the bulimic patients declared as
compulsive episodes with less than 500 kcal (Rosen et al., 1986, obtained a very similar
finding) and that this judgment depends not only of the amount of food or energy consumed
but also of the type of food and the psychological state of the patient. Other studies found a
great variability in the energy content of the binges. Mitchell et al. (1981) observed a mean
intake of 3,415 kcal (range: 1,200-11,500 kcal), while Mitchell and Laine (1985) obtained a
mean consumption of 4,394 kcal (range: 1,436 – 8,585 kcal). Elmore and Castro (1991)
affirmed that the greater binges are more likely to be purged and that patients with longer
time of disease had even greater binges. Gendall et al. (1997) declared that the binges that
happen more frequently have greater energy content and also that although compulsive meals
have more energetic value than the non-compulsive ones they do not have different
macronutrient composition.
The median macronutrient profile of the VOM intake was similar to those observed by
Woell et al. (1989) in binges (42% of carbohydrates, 12% of proteins and 43% of lipids). We
also observed that the macronutrient profile of the VOM intake did not differ much from the
macronutrient profile of the VET intake, except for the lipid consumption (in percent
contribution to total energy intake), which was higher in the VOM intake, but only at
baseline (VET intake = 32.1 ± 7%; VOM intake = 35.3 ± 4%, p = 0.03).
Table 3 – Weekly number of meals along the follow-up (data presented as mean ±
Phases Total meals Breakfast Morning Lunch Afternoon Dinner Evening

snack snack snack
1 – Before 25.8 ± 10 4.1 ± 2 2.9 ± 2 4.3 ± 2 3.4 ± 2 4.5 ± 1 2.3 ± 2
treatment (23; 5-50) (4; 0-6) (3; 0-6) (5; 0-7)* (4; 0-6) (4; 2-7) (3; 0-6)
2 – Immediately 25.4 ± 7 4.7 ± 2 2.3 ± 2 5.2 ± 1 4.0 ± 2 3.7 ± 1 3.1 ± 2
after treatment (23; 18-40) (5; 0-7) (2; 0-7) (6; 3-7)* (4; 1-6) (4; 1-7) (3; 0-7)
3 – Three months 31 ± 13 6.3 ± 2 2.3 ± 2 6.5 ± 2 4.7 ± 3 5.1 ± 2 3.0 ± 2
after treatment (27; 11-65) (7; 3-8) (2; 0-7) (7; 1-8) (5; 0-9) (6; 0-9) (3; 0-6)
*: significantly different from Phase 3.
Table 4 – Energy and macronutrient content (as percentage contribution to total energy
intake) of the meals not followed by vomits, along the follow-up (data presented as mean
+ standard deviation (median; minimal-maximal))
Phases Energy intake Protein Carbohydrate Lipid intake

(kcal) intake (%) intake (%) (%)
1 – Before treatment 1,529 ± 945 14.6 ± 3 53.5 ± 8 32.1 ± 7
(1,197; 337- 4,094) (14; 10-21)* (51; 44-72) (32; 19-43)
2 – Immediately after 1,475 ± 771 15.8 ± 3 50.8 ± 6 32.6 ± 5
treatment (1,277; 577-3,853) (15; 12-21) (49; 44-65) (32; 24-40)
3 – Three months after 1,337 ± 519 17.6 ± 3 50.4 ± 6 31.6 ± 6
treatment (1,393; 641-2,131) (18; 13-21) (50; 40-60) (31; 22-42)
*: significantly different from Phase 3.
Table 5 – Energy and macronutrient content (as percentage contribution to total energy
intake) of the meals followed by vomits, along the follow-up (data presented as mean +
Phases Energy intake (kcal) Protein Carbohydrate Lipid intake

intake (%) intake (%) (%)
1 – Before treatment 1,310 ± 686 17.5 ± 7 47.4 ± 6 35.3 ± 4
(1,274; 460-2,689) (14; 7-32) (49; 37-55) (36; 26-41)
2 – Immediately after 1,402 ± 707 17.2 ± 7 45.9 ± 15 34.2 ± 7

treatment (1,320; 584-2,664) (16; 10-33) (44; 21-69) (35; 21-43)
3 – Three months after 1,211 ± 226 10.1 ± 5 60.7 ± 3 28.1 ± 3

treatment (1,238; 927-1,440) (9; 6-17) (60; 57-65) (28; 24-31)
In every phase, the percentage contribution of each macronutrient to the VET intake was
similar to those recommended in Reference Dietary Allowances (NRC, 1989; Trumbo et al.,
2002). The values were also similar to those obtained in a prior cross-sectional study
conducted with Brazilian bulimic patients (Alvarenga et al., 2003). In that study, the mean
carbohydrate intake contributed with 50.8% of the total intake, while the mean lipid
consumption contributed with 32.3% and the mean protein intake with 17.9%. In this chapter,
we observed that along the phases, only protein intake significantly changed (the baseline
intake was lower than the intake presented at Phase 3).
Table 6 shows the distribution of patients in each energy intake range, considering the
meals not followed by vomits (VET) and the meals followed by vomits (VOM).
Table 6 - Proportion of subjects classified in each category of energy intake, within the
phases of the follow-up
Energy intake Phase 1 – Before Phase 2 – Phase 3 – Three

treatment Immediately after months after
treatment treatment
Meals not followed by vomits
Hypoenergetic intakea 52.6% 47.0% 50.0%
Normoenergetic intakeb 31.6% 41.2% 50.0%
Hyperenergetic intakec 15.8% 11.8% 0%
Meals followed by vomits*
Hypoenergetic intaked 21.0% 11.8% 25.0%
Normoenergetic intakee 47.4% 70.6% 75.0%
Hyperenergetic intakef 31.6% 17.6% 0%
*: χ2 (2) = 21.32; p < 0.005.
Meals not followed by vomits:
a
: Hypoenergetic = Intake < 1,199 kcal.
b
: Normoenergetic = Intake between 1,200 e 2,200 kcal.
c
: Hyperenergetic = Intake > 2,201 kcal.
Meals followed by vomits:
d
: Hypoenergetic = Intake < 600 kcal.
e
: Normoenergetic = Intake between 600 e 1,000 kcal.
f
The results indicated that there was no significant change in the number of patients in
each category in regard to energy intake of meals not followed by vomiting (VET). Only a
non-significant increase in normoenergetic intake, and a non-significant reduction in
hypereneregetic intake were observed.
In relation to the meals followed by vomiting (VOM), the number of patients that
presented episodes with an intake less than or equal to 600 Kcal decreased by half after 12
weeks of treatment and then increased after six months. Regarding meals of 601-1,000 Kcal,
the number of patients increased after 12 weeks and after six months, and meals with over
1,001 Kcal decreased after 12 weeks and fell to zero after six months. It was concluded that
there was a trend of decrease for hyperenergetic meals followed by vomiting throughout the
phases.
As for the nomenclature used to describe the energy intake of these patients, the terms
hypo, normo, hyper for VET applied, respectively, to eating less energy than one should,
eating the right amount of energy, and eating more energy than one should. The same terms
were used for VOM, meaning meals with a low intake of energy, with an intermediate intake
of energy and with high intake of energy; therefore, hypo VOM does not mean that the
patient ate less energy than he should at that moment. These categories were based on the
energy content of binges, supposing that meals followed by vomiting are more likely to be
binge eating episodes. Even though, one must also consider that not only binges are followed
by vomiting (since regular meals also can be followed by vomiting) and not all binge
episodes are followed by vomiting.
Elmore and Castro (1991) stated that greater binge eating episodes are more likely to be
purged, and that, as the length of the disorder progresses, the size of these binge eating
episodes also increases. This paper shows that throughout the follow-up stage patients
decreased the size of their meals followed by vomits, however these are patients undergoing
treatment. Most probably, patients without treatment will present binge eating episodes with
higher energetic content.
The intake of vitamins and minerals along the phases, as well their adequacies in relation
to the recommended intakes, can be seen in Table 7.
In a broad manner, intake of micronutrients was below the recommendations of the
Dietary Reference Intakes (Institute of Medicine, 1997; 1998; 2000). Intake of vitamins A
and C was closer to the recommendations, while the most inadequate intakes were found to
sodium, calcium, magnesium, potassium and iron It is not possible to affirm that this
unhealthy intake is characteristic of bulimic patients, because since we did not have a control
group we could not know if the intake of healthy young women is so inadequate as the
patients’ intake. The fact that the sodium and potassium intake was so low is very
preoccupant because, when combined with compensatory behaviors as vomiting and use of
laxatives and diuretics, this may cause a hydroeletrolitic disturbance (Greenfeld et al., 1995;
Lasater and Mehler, 2001).
This inappropriate pattern of intake did not change throughout the phases. This result
suggests that the nutritional treatment was not able to correct this unhealthy eating pattern. It
is necessary to evaluate why this happened and what could be done to improve the
micronutrient intake of these patients.
Chart 1 shows the results of frequency of affirmative responses for questions about
eating behavior and beliefs. The reduction of guilt declarations when patients ate foods
whose consumption they restricted demonstrates greater permissiveness towards these foods.
There was a gradual reduction in statements regarding behavior change after eating sweets,
fast food, and “different” foods; however, less than half of the patients changed. It is
remarkable that, even with significant changes, most of them were still feeling guilty and
having difficulties in eating the foods regarded as “dangerous”, behavior also described by
Keller et al. (1992).
More than half of the patients were still practicing some kind of restraint on their diet at
the end of the following. This ratifies that diet restraint is a symptom much more common
among BN patients and that it is difficult to eliminate (Keller et al., 1992).
Table 7 – Micronutrient intake and adequacy, obtained in the meals not followed by
vomits, along the treatment phases
Recommende Adequacyc
Nutrient Phase Amount consumeda
d intakeb (%)
1d 710 ± 377 (680; 27 – 1,632) 89
Vitamin A (mcg) 2e 774 ± 337 (765; 219 – 1,612) 800 97
3f 1117 ± 460 (990; 656 – 2,050) 140
1d 88 ± 74 (69; 1 - 258) 118
Vitamin C (mg) 2e 84 ± 44 (85; 16 - 186) 75 112
3f 217 ± 259 (124; 60 - 992) 289
1d 1 ± 0.7 (0.7; 0.4 – 3.2) 95
Thiamin (mg) 2e 1 ± 0.6 (0.8; 0.3 – 2.7) 1.1 91
3f 0.9 ± 0.4 (0.7; 0.5 – 1.5) 81
1d 0.8 ± 0.4 (0.7; 0.1 – 1.4) 58
Vitamin B6 (mg) 2e 0.9 ± 0.4 (0.8; 0.4 – 2.0) 1.3 68
3f 0.9 ± 0.4 (0.8; 0.5 – 1.7) 72
1d 18 ± 29 (0.8; 0 – 95) 351
Vitamin D (mcg) 2e 10 ± 15 (1; 0 – 55) 5 199
3f 8 ± 20 (0.6; 0 – 68) 166
1d 7 ± 5 (6; 0 – 22) 49
Vitamin E (mg) 2e 9 ± 7 (7; 2 – 25) 15 57
3f 7 + 5 (5; 3 – 16) 49
1d 1,551 ± 1,156 (1,236; 68 – 4,406) 65
Sodium (mg) 2e 1,604 ± 1,125 (1,123; 598 – 4,917) 2,400 67
3f 1,397 ± 669 (1,427; 483 – 2,652) 58
1d 552 ± 289 (481; 99 – 1,081) 55
Calcium (mg) 2e 855 ± 960 (569; 196 – 4,178) 1,000 86
3f 632 ± 288 (578; 344 – 1,414) 63
1d 113 ± 54 (119; 19 – 241) 37
Magnesium (mg) 2e 132 ± 79 (116; 43 – 356) 310 43
3f 132 ± 39 (133; 73 – 199) 42
1d 1,195 ± 539 (1,128; 211 – 2,433) 34
Potassium (mg) 2e 1,265 ± 513 (1,061; 508 – 2,625) 3,500 36
3f 1,493 ± 382 (1,390; 1,015 – 2,150) 43
1d 6 ± 4 (5; 0.4 – 15) 34
Iron (mg) 2e 7 ± 3 (6; 2 – 15) 18 37
3f 6 ± 3 (5; 3 – 12) 35
a
: mean ± standard deviation (median; minimal-maximal).
b: Recommended intake to young women, according to the Dietary Reference Intakes (Institute of
Medicine, 1997; 1998; 2000).
c: Percent adequacy of the mean intake, when compared to the recommended intake.
d: Phase 1 – before treatment.
e: Phase 2 – immediately after treatment.
f: Phase 3 – three months after treatment.
Chart 1 - Frequency of affirmative answers to the questions regarding eating attitudes

and beliefs towards food, between the treatment phases.
Questions Phase 1 – Phase 2 – Phase 3- Three

Before Immediately months after
treatment after treatment treatment
Do you make any restrictions in your 94% 75% 57%
regular diet?
Do you feel guilty whenever you eat one 70% 65% 60%
of the foods that you try to cut from your
diet?*
Do you feel pleasure when you eat? 75% 71% 76%
Do you like cooking? 70% 65% 59%
Do you usually eat the meals that you 74% 76% 82%
prepare?
When you eat sweets, fast-foods, pizza, 95% 76% 53%
or when you go to aparty, do you eat in a
different manner?**
Does it bother you to eat in the presence 60% 29% 29%
of other people?a
Do you believe that there is a 74% 59% 59%
combination of food that is dangerously
“fattening”?
Do you believe that there is a food or 35% 29% 6%
some thing that “melts” fat? a
Do you believe that overeating in one 90% 41% 29%
meal or in special occasion automatically
makes you put on weight?***
Do you believe that not eating for one 65% 41% 35%
day or eating a liquid diet can make you
lose weight?
*: 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
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 well-
known 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.
Chart 2 - Frequency of ‘frequent’ or ‘not frequent’ answers to the questions regarding

relationship towards food, between the treatment phases
Questions Phase 1 – Phase 2 – Phase 3 –

Before Immediately Three months
treatment after treatment after treatment
Freq. Infreq. Freq. Infreq. Freq. Infreq.
I worry all the time about what I am 95% 5% 71% 29% 44% 56%
going to eat**
I worry all the time with my 100% 0% 94% 6% 56% 44%
weight**
I feel fat despite what I eat** 95% 5% 82% 18% 56% 44%
I hate feeling hungry 50% 50% 59% 42% 38% 63%
It is hard for me to choose what to 60% 40% 41% 59% 38% 63%
eat
I wish I did not have the need to eat 60% 40% 53% 47% 36% 63%
I dream of a pill that would replace 42% 58% 35% 65% 31% 69%
food
I don’t believe I’ll ever be able to 44% 56% 35% 65% 19% 81%
follow a regular
intake and achieve a regular weight
In a situation in which there is much 63% 37% 53% 47% 25% 75%
food, such as
parties and buffets, I get nervous
and/or lose control*
Whenever I have a problem, I look 65% 35% 47% 53% 46% 56%
for food
My eating habits have a great 89% 11% 59% 41% 40% 60%
interference in my life as a whole**
*: p ≤ 0.05; ** p ≤ 0.01
Regarding the question of feeling nervous or loosing control in situations with abundant
food, the most important reduction took place only at the end of the six months, indicating
that longer treatment is needed for patients to gain confidence and ease to eat in any situation.
The analysis of the question about “the way you eat” interfering greatly in their lives as a
whole demonstrated a significant change, although 40% of the patients were still answering
positively after six months, indicating that to a subgroup, BN represented the complex role of
food in human life. There were no significant shifts in the question related to looking for food
whenever they have a problem. This suggests that food still performed many different roles in
the lives of these patients, as an expression of feelings and impulses and “a means of external
adaptation and an attempt at internal control” (Johnson and Maddi, 1988). Thus, faced with
many possibilities, ED patients choose weight control and, therefore food control, as a way of
life. Changing this behavior pattern seems to demand much more than 12 weeks of CBT and
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
was expected. The scores of the BITE-symptom showed just a "sub-clinical" group after six
months of follow-up, showing positive evolution of these patients.
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
ing
ng
V
*
e
g
t*
g*
on
dy
din
tio
gT
uie
lki
ttin
ad
Al
en
bo
an
Ta
Q
hin
Re
Si
att
me
St
atc
ith
so
W
ith
Phase 1 Phase 2 Phase 3

W
*: p < 0.05
Figure 1 – Percent distribution of the affirmative answers to the question “How do you usually eat your
meals?”
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
At ease* Anxious* Irritated Fearful Nervous
Phase 1 Phase 2 Phase 3
*: p < 0.05
Figure 2 – Percent distribution of the affirmative answers to the question “How do you feel when you go to a
restaurant, coffee shop or a bar?”
There was no significant statistical difference between the phases in regard to the BITE
severity scale. The mean score after six months showed a "clinically significant" group. This
result is similar to that found in the Fahy and Russell (1993) follow-up in which the mean
initial score was 14.1, and after one year, 6.1, showing a still "clinically significant" group.
Table 8 - Scores obtained in the scales (EAT, BITE and BSQ), along the follow-up (data
presented as mean + standard deviation (median; minimal-maximal))
Phases EATa BITE BITE severityc BSQd

symptomsb
1 – Before treatment 38.6 ± 10 23.6 ± 5 15.3 ± 5 145.2 ± 28
(40; 15-53)†* (25; 11-29)†* (14; 3-25) (142; 99-190)*
2 – Immediately after 25.5 ± 14 19.8 ± 8 10.1 ± 6 132.6 ± 40
treatment (28; 6-49)* (23; 1-28) (8; 2-23) (149; 48-189)*
3 – Three months after 17.0 ± 11 15.8 ± 8 7.6 ± 6 109.2 ± 44
treatment (16.5; 2-42) (17.5; 1-28) (5.5; 2-24) (103.5; 47-189)
† significantly different from the scores obtained immediately after treatment
*: significantly different from results obtained three months after treatment.
BSQ showed significant statistical difference between Phases 1 and 3, and between 2 and
3, thereby indicating a continuous improvement. The BSQ initial mean score (145.2) was
lower than the 156 described by Hetherington et al. (1993). No study showed the evolution of
BSQ scores throughout follow-up. Results show that concern over body image takes more
than 12 weeks of CBT to present significant changes. These results are consistent with those
found by Swift et al. (1987), in which weight variations and body dissatisfaction remained
present even among asymptomatic patients. Some authors (Ramirez and Rosen, 2001; Wolff
and Clark, 2001) declare that traditional CBT is not enough to improve body image in EDs,
and that specific intervention is required to this end, so the improvement found in the
classification regarding concern over body image through BSQ was surprising. Although we
found this improvement in body image issues at the end of the follow-up, one might argue
that the BSQ along did not provide much information about what changes did occur in
relation to body image. Using this scale, it is not possible to know if whether overestimation
of body size or body dissatisfaction or body disparagement decreased. For this reason,
nowadays it is recommend the use of tests more specifics to the body image aspect that is
intended to be measured (Thompson, 2004).
A series of studies used the Eating Disorders Inventory (EDI) to measure outcome
(Brambilla et al., 1995; Fernandéz et al., 1998; Hedges et al., 2003; Steinhausen and Seidel,
1993), but the EDI test has not yet been translated to Portuguese. When this study was carried
out, BITE, EAT, and BSQ were the only tests that had been translated to Portuguese and that
were available to assess BN. Currently, there are other tests that have been translated, which
measure the chronic practice of restrictive diets (Restraint Scale – Scagliusi et al., 2005-a),
body attitudes (Body Attitudes Questionnaire – Scagliusi et al., 2005-c), perception and
satisfaction with body size and shape (Stunkard’s Figure Rating Scale – Scagliusi et al.,
2006), nutritional knowledge (Scagliusi et al., 2005-b), among others.
Therefore, an analysis of the evolution of classification based on test scores showed good
results, but not as good as the findings for binge eating and purging behavior.
Notwithstanding, these tests do not diagnose ED, they just address some issues and suggest a
classification.
Table 9 shows the correlations between BITE, EAT, BSQ, BMI, number of vomiting
episodes per week and number of binge eating episodes per week, found in each phase. EAT
and BSQ presented a positive correlation in the 3 phases of the program, showing that for
these bulimic patients, the higher their EAT score, the greater their concern over body image,
regardless of the timeframe. It is known that these two responses, greater dissatisfaction with
body image after treatment and higher EAT scores, are related to a poor outcome or a
complication of the disease during follow-up (Agras et al., 2000; Freeman et al., 1985;
Olmested et al., 1994).
The number of binge eating episodes and BITE-symptom presented a positive correlation
just at the beginning of the treatment, showing that, at that point, the more severe the level of
BN symptoms, the greater the number of binge eating episodes per week presented by the
patient. The severity of BN symptoms at the beginning of treatment was considered a
predictor of recurrence by Fahy and Russell (1993). This correlation was no longer true in the
following phases, and it seemed that, after treatment and follow-up, the bulimic symptoms
had somehow changed and no longer had any correlation to the frequency of binge eating
episodes. It seemed that, despite the bulimic symptoms, the number of binge eating episodes
had decreased.
Positive correlations between BMI and BITE-symptom inventory test and between BMI
and number of binge eating episodes per week were found just at the beginning of treatment.
This shows that to patients not being treated, the higher the BMI, the more severe the levels
of BN symptoms, and the greater the number of binge eating episodes. According to
Maddocks and Kaplan (1991) patients who have been heavier in the past had more chances of
presenting worse treatment outcome. After treatment, it was concluded that patients with a
higher BMI no longer presented the more severe levels of BN symptoms nor presented higher
frequency of binge eating episodes, that is, the symptoms originated from the
psychopathology of the disorder and not from inadequate body weight.
After 12 weeks of treatment, and also after six months of follow-up, EAT and BITE-
symptom inventory test presented a positive correlation. Bite-severity inventory test and EAT
presented a positive correlation only during Phase 2. These correlations were not present at
the beginning. This result shows that after being treated, the stronger the concern of the
patient over diet, foods eaten, and body image, the more severe the patient’s symptoms and
BN itself. The study also suggests that the severity of BN was not related to the level of
concern over food and body at the beginning and after 6 months of treatment. This data
suggests that these patients (more concerned over food and their body, even after treatment)
are highly prone to experiencing recurrence, as described by Freeman et al. (1985) and by
Fahy and Russell (1993).
It could be thought that the frequency of binge eating and the frequency of vomiting
episodes would present a correlation during all phases, but this became true only after 12
weeks of treatment, suggesting that only at this moment did a greater number of binge eating
episodes result in more vomiting episodes. In fact, the presence of binge eating and vomiting
episodes did not present such a correlation at the beginning of treatment and after six months.
This finding is supported by Olmested et al. (1994) who said that vomiting can be used to
control weight, stress and affection, among others factors, and not only to compensate binge
eating.
BMI and BSQ presented a positive correlation after 12 weeks of treatment showing that,
at this phase, the higher the BMI, the greater the concern over body image. This finding
supports the fact that individuals with ED are overly concerned about body image regardless
of their weight (Dowson and Henderson, 2001), insofar as it is the pathological condition that
causes this concern. When patients are treated, their concern for the body is the same as what
is presented by the overall population: the heavier they are, the more concerned they are (Hill
and Williams, 1998; Scagliusi et al., 2006). This finding also shows that treatment can
minimize weight-related concerns in individuals who are not overweight.
Table 9 - Spearman correlation coefficients between scales scores, bulimic behaviors

and body mass index, along the follow-up
Scales and EAT BITE BITE Frequency Frequency BodyMass

measures severity symptoms of binges of vomits Index
Phase 1 – Before treatment
BSQ 0.59* 0.28 0.44 0.38 -0.20 0.06
EAT - 0.40 0.06 0.22 0.10 -0.13
BITE severity - - 0.44 0.38 -0.13 0.19
BITE - - - 0.44* -0.11 0.45*
symptoms
Frequency of - - - - 0.20 0.57*
binges
Phase 2 – Immediately after treatment
BSQ 0.80* 0.45 0.48 -0.01 -0.05 0.50*
EAT - 0.63* 0.75* 0.13 -0.19 0.36*
BITE severity - - 0.61 0.22 0.21 0.02
BITE - - - 0.40 0.36 0.39
symptoms
Frequency of - - - - 0.48* 0.09
binges
Phase 3 – Three months after treatment
BSQ 0.78* -0.04 0.73 0.15 -0.08 0.10
EAT - 0.21 0.81* 0.30 0.03 0.01
BITE severity - - 0.28 0.62* 0.68* -0.40
BITE - - - 0.47 0.28 0.13
symptoms
Frequency of - - - - 0.49 -0.18
binges
*: p ≤ 0.05; a: bulimic behaviors are expressed as weekly frequencies.
BITE-symptom inventory test and BSQ presented positive correlation only after the six-
month follow-up, showing that the greater the number of symptoms of BN presented at the
end of this period, the greater the concern of the patient over body image. This result was not
observed at the beginning or after 12 weeks. It seems that BN symptoms are significantly
affected by body image only if the patient still remains highly concerned about his image
after six months of treatment. As shown by Freeman et al. (1985), Fahy and Russell (1993) e
Agras et al. (2000), patients with more BN symptoms and more concern about their bodies at
the end of the treatment present a higher risk of recurrence.
Only after six months of follow-up was any positive correlation found between BITE-
severity scale and the number of vomiting episodes per week and between this scale and
weekly frequency of binges, showing that the more vomiting and binge episodes after this
length of treatment, the more severe the BN. It can be said that a patient that still presents a
significant number of vomiting and binge episodes after six months of treatment has more
severe and more treatment-resistant bulimia, supporting the presence of vomiting and binge
episodes as an indicator of poor prognosis (Olmested et al., 1994; Herzog et al., 1996).
Actually, severity measurement by BITE scale considers the frequency of binge eating
and vomiting episodes, among others (use of drugs and fasting). Since the number of binge
eating and vomiting episodes presented positive correlation with the BITE-severity score
only after six months, it seems that the severity of bulimia at the beginning of treatment and
after 12 weeks was related to other factors of this test, such as the use of drugs and the
practice of fasting.
Tables 10 and 11 show BITE-symptom and severity, BSQ, EAT scores, and the number
of binge eating and vomiting episodes per week according to the energetic intake ranges for
VOM and VET in each of the 3 phases. The goal was to assess these different response
variables between patients that had hypoenergetic, normoenergetic or hyperenergetic intake.
Table 10 – Mean ranks of the scores and bulimic behaviors, within each interval of
energy intake in meals not followed by vomits, along the follow-up
Energy intake in meals BSQ BITE BITE EAT Weekly Weekly

not followed by vomits severity symptoms frequency of frequency of
vomits binges
Hypoenergetic intakea 7.9 10.0 8.6* 10.8 13.4* 11.2
Normoenergetic intakeb 9.8 10.0 8.7 8.8 6.8 6.0
Hyperenergetic intakec 13.7 10.0 17.3 6.3 5.0 14.0
Hypoenergetic intakea 5.6 6.6 6.5 5.2 11.6d 10.6
Hyperenergetic intakec 12.0 e e
9.0 5.5 11.0
a
Hypoenergetic intake 5.7 9.3* 7.2 6.5 8.0* 8.4*
*: significantly different from the others energy categories, within the same phase.
a
: Hypoenergetic = Intake < 1,199 kcal.
b
: Normoenergetic = Intake between 1,200 e 2,200 kcal.
c
d
: p = 0.07 between the energy categories, within phase 2.
e
: missing value (no subject from this category filled this questionnaire).
Table 11 – Mean ranks of the scores and bulimic behaviors, within each interval of
energy intake in meals followed by vomits, along the follow-up
Energy intake in meals BSQ BITE BITE EAT Weekly Weekly

followed by vomits severity symptoms frequency of frequency
vomits of binges
Hypoenergetic intakea 9.6 9.4 5.5* 11.5 11.0 8.9
Hypoenergetic intakea 2.0d 4.0 3.0 4.5 5.5 10.0
a
Hypoenergetic intake 7.3 8.8 8.0 9.0 6.8 6.7
*: significantly different from the others energy categories, within the same phase.
a
: Hypoenergetic = Intake < 600 kcal.
b
: Normoenergetic = Intake between 600 and 1,000 kcal.
c
d
: p = 0.06 between the energy categories, within phase 2.
Findings show that the scores of BITE-severity were significantly higher in patients with
hypoenergetic VET in Phase 3. Therefore, the patient that ate less in Phase 3 presented a
more severe case of BN; that is, the more restrictive a patient is, the more severe is her
disorder.
In regard to the BITE-symptom, Phase 1 results presented a mean rank very similar to the
scores for hypo and normoenergetic VET, but very different from the hyperenergetic
category, showing that patients with hyperenergetic intake presented more symptoms of BN.
As for the number of vomiting episodes per week, it was significantly higher for those
with hypoenergetic VET intake in Phases 1 and 2 (p = 0.07 in Phase 2). This shows that the
greater the food restriction, the greater the vomiting episodes, even without more binge eating
episodes. Again, this shows that vomiting is used for several reasons not related to the
purging of excessive food intake (Olmested et al., 1994). Gendall et al. (1997) found the
same result, and according to them, the less a patient eats, the more often the purgation
occurs.
In regard to the number of binge eating episodes per week, the result was significantly
higher for patients with hypoenergetic VET intake in Phase 3, which proves, once again, that
food restriction leads to binge eating episodes (Reiff, 1992).
In regard to meals followed by vomiting and BITE-symptom, it was observed that: those
with hypoenergetic intake presented a lower score, that is, patients with low energy
consumption (in the VOM intake) presented less symptoms; however, this difference was
observed only in Phase 1, indicating that, after treatment, the level of energy intake of meals
followed by vomiting did not determine BN symptoms.
Phase 2 showed that BSQ scores were lower in patients with hypoenergetic VOM. It can
be concluded that if the patient worried less about her body, she would eat less energy during
her meals followed by vomiting.
Gendall et al. (1997) also compared energy intake and clinical variables, and they also
found that, the less the patient ate (apart from binge eating episodes), the more often he
purged. They also found that patients that presented more binge eating episodes had a higher
energy intake during these episodes, and that body dissatisfaction scores were higher among
those consuming meals with less energy intake – indicating severe food restriction. This data
was not followed up in this paper. However, the study by Gendall et al. was a cross-sectional,
and not a follow-up study.
Some considerations should be made about this study: firstly, the number of patients was
relatively small, and it became smaller because of the high rate of treatment dropout.
However, it is believed that the number of patients followed up until the end of the process
was sufficient, considering that there are few studies on ED in Brazil, particularly follow-up
studies of bulimic patients and nutritional issues. The number of patients that filled in the
tests and food diaries in Phases 2 and 3 of the follow-up was also low because of dropouts,
and eventually led to missing values, which may have affected the analysis.
It is important to note that the method of dietary assessment – food record – has
limitations and it is subject to bias. Even so, Gayle (1998) affirmed that this method is the
only one able to assess energy intake and to identify binges in free-living bulimic subjects.
We are aware that subjects who fill a food record may change their intake, motivated by
feelings of guilty and shame. Besides that, one still has to consider that the process of coding
the food consumption may have mistakes and that the software used to convert food intake
into nutrient intake may not have values for all foods consumed, for example (Livingstone
and Black, 2003).
Few studies tested strategies to improve the self-report of food intake, especially by
means of not changing the intake during the recording period. Goris and Westerterp (2000)
observed that confronting subjects with implausible results from a prior diary decreases the
errors. In Brazil, Scagliusi et al. (2003) verified that confronting the subjects and conducting
an intensive training on how to record the intake attenuate the error, although it remains high.
In the present research, some procedures were used in order to improve the record.
Patients were told to register their intakes soon after them and instructed on how to describe
the foods consumed and to estimate portion sizes. Every week, a dietitian reviewed the
diaries when the patients returned them, probing the patients and instructing them one more
time when necessary. Moreover, all the records were coded and analyzed by only one
researcher, who was previously trained. We believe that these procedures should have
decreased the errors associated to dietary assessment. As stated by Woell et al. (1989) even
with this bias it is possible to analyze food intake by means of a food diary. Other authors
used this method to assess food intake of bulimic patients and considered it a valid instrument
(Elmore and Castro, 1991; Gendall et al., 1997; Woell et al., 1989).
The instrument used to assess aspects of eating attitudes and relationship with food was
developed for this research based on clinical practice. Many studies confuse the term eating
behavior with food intake, so that the questionnaires that claim to measure behavior, in fact
only assess if some groups of foods are bought and eaten (Kubik et al., 2002; Townsend et
al., 2003). In other researches, food behavior is cited but is not defined, as for example in the
study of Mitchell et al. (1988) which showed that bulimics with poorer prognostic had more
abnormal eating behaviors, without specification of what these behaviors would be. Some
studies focus on behaviors that are important to EDs, but their interrogations only cover the
classical symptoms of BN, like for example vomiting frequency (Martín et al., 1999). There
are some widely used scales in ED research, like the Restraint Scale (Herman and Mack,
1975), which measures chronic dieting or the switch between periods of restraint and lapses,
the Three-Factor Eating Questionnaire (Stunkard and Messick, 1985), a measure of
disinhibition, restraint and subjective assessment of hunger, and the Dutch Eating Behavior
Questionnaire (van Strien et al., 1986), which also measures restraint. Although these scales
are useful and well developed psychometrically, they are limited in scope, and assess mainly
dietary restraint. These factors are associated to BN, but they do not encompass the wide
range of dysfunctional eating attitudes that this disease implies. In this manner, using only
these questionnaires supplies a lot of relevant data, but also ignores other pieces of
information, such as beliefs and perceptions about food, the pleasure of eating, hidden eating,
difficulty in handling with hunger, social events, food choice, and feelings towards food. We
believe it is relevant to research these aspects, as we could note, with the data of this study,
that even the patients whose clinical status becomes normal may still have a complicated
relationship with eating and their bodies. This may, in turn, cause psychological distress and
lead to recurrence. In this manner, the questions utilized in this research served as a starting
point for the development of a specific tool to measure eating attitudes in patients with EDs.
Today, based on these results an instrument is being adapted and validated.
Moreover, the results of specific nutritional interventions for the treatment of BN could
not be separately tested in controlled studies, because they are a part of a total treatment
program (Rock and Curran-Celentano, 1996). Using just the nutritional intervention, without
the due clinical, psychiatric and therapeutic follow-ups would be unethical. Also, due to
ethical considerations, control groups, to which only one of the treatment components is
provided, are not recommended.
Conclusion
In summary, some positive changes were observed after 12 weeks of CBT: a significant
change in the EAT and the BITE-symptom scores, and zero median for laxative, diuretic and
appetite moderator drug use. After six months follow-up, the positive changes found were:
the patients did not meet the diagnostic criteria for BN, taking into consideration the means
and medians of binge eating and vomiting episodes; EAT and BITE-symptom scores showed
a non-symptomatic group; and there was significant difference in the BSQ score.
Regarding eating behaviors and relationship toward foods the following improves were
observed: guilty after eating ‘forbidden foods’ decreased (as well as the behavior while and
after eating these foods improved), some misconceptions about food were reverted (as
thinking that eating a little more automatically causes weight gain), some negative feelings
involving food were reduced (as anxiety, lack of control and nervousness) while the feeling
of tranquility has increased. The obsession with food has also decreased, resulting in a
smaller interference of food in patients’ life. Nevertheless, it is remarkable that many
disturbed attitudes did not change, especially those related to feelings, reflected by the lack of
pleasure with food and the difficulties in dealing with hunger.
On the other hand, we did not find changes in food intake. This result is preoccupant and
should be carefully monitored by dietitians while they treat bulimic patients. Treatment
should encourage a regular meal pattern, composed by frequent meals rich in nutrient-dense
foods.
The assessment of these patients, based on standardized tests, showed positive progress,
as shown by the progress of bulimic symptoms. The use of standardized score tests and data
regarding bulimic behavior and energy intake allowed for a clearer understanding of the
pattern of the disease and its prognosis. It was possible to confirm an important fact, namely
that energy restriction is related to higher frequency of binge eating and purging.
It is believed that standardized tests are an effective strategy to assess follow-up of
bulimic patients, since measuring the treatment outcome just by verifying changes in the
frequency of bulimic symptoms cannot cover the complexity of ED. Furthermore, it is
relevant to include measurements of nutritional consumption, such as energy intake in eating
episodes, whether followed by vomiting or not. Because it is known that BN is a chronic
disorder, with a high chance of recurrence, it is necessary to think about recovery in a broader
manner, aiming to improve the relation towards body, weight and food in addition to other
positive psychological changes.
The main objective of the traditional nutritional approach for BN is to establish a normal
eating pattern and to cease the purging practices. Further nutritional treatment, based
specially on counseling, should aim to help the patient to distinguish behavior related to food
and weight from feelings and psychological issues, and to promote improvements in eating
attitudes (ADA, 2001). New techniques and interventions are required to treat and to alter the
relation established by the patient towards food.
In-depth knowledge about eating attitudes is necessary to design a nutritional
intervention able to improve the quality of the diet of these patients and also to promote
behavioral changes (Hetherington et al., 1993; Sunday and Halmi, 1996). Researchers and
practitioners need to understand and treat all the disordered eating aspects presented by
patients with BN and not only the bulimic episodes that define this syndrome (Hetherington
et al., 1993). Therefore, other measures – such as relationship and attitudes towards food –
should be investigated and assessed after the intervention. We believe that this kind of
comprehensive treatment is necessarily long and can be conducted only if the professionals
involved have a broad understanding of all meanings that food (and also the disease) has. As
stated by Levine (1994), “people with eating disorders are people struggling with fantasies,
motives, anxieties, and coping mechanisms that are established and vigorously reinforced by
our culture. They are not ‘ics’ – anorexics or bulimics”. So dietitians that work with ED
should strive to better understand these topics and to seek training in counseling, cognitive
techniques and motivational interviewing to improve the treatment of all features of the
eating attitudes of these patients.
Based on the results presented in this chapter, our program of nutritional treatment was
improved. Its duration was increased to 18 weeks, and the individual counseling has been
receiving more attention and time. We are also developing a new treatment program, whose
aim will be the improvement of eating attitudes and relationship with the body and food. This
new program will be provided to patients after completion of the 18-weeks program. We
believe that the first treatment goal is to end bulimic behavior and establish a healthier intake,
but if we do not provide a deeper understanding of all food and body issues that the patient
presents it is very likely to have a relapse. Also, by providing a more comprehensive care we
can be sure that we are treating a person and not a disease.
It is also relevant to note that in order to meet this goal, tools for measuring eating
attitudes, especially those focused on feelings, beliefs and attitudes towards food, should be
developed and validated. Our research group is now working with the instrument tested in
this study. Considering the findings of this research, this eating attitudes questionnaire is
being adapted and will be psychometrically tested.
Finally, our data showed that eating disorders are also a reason for concern in an
undeveloped country as Brazil. Our health system needs to be more prepared to deal with this
problem, since there are too few centers that treat these diseases in Brazil. Perhaps it is even
more necessary to discuss prevention of eating disorders, especially because they afflict
mainly young women. In Brazil, young women live in a difficult scenario, already marked by
a poor health status, which could be more aggravate with the presence of an eating disorder.
It is also relevant to attest that in order to prevent eating disorders specific interventions
should be provided to a wide range of people, specially young girls and women, with focus in
nutrition education, body image improvement, size acceptance and with strategies to improve
relationship towards food. As a research group on nutrition and eating disorders, we believe
that improvement of eating attitudes and relationship towards food is necessary not only for
treatment of eating disorders, but also for its prevention.
Authors= Notes
We thank Cynthia York, Dr. Rebecca Cohen, Natalie Demidenko, Deborah Evans, Katie
Harkins and Amanda Scott for help with data input. Dr. Jo Wood provided statistical
consultation. This project was supported by the Departments of Psychiatry and Psychology at
the Ottawa Hospital.
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Chapter VII
Actual - Desired BMI Discrepancy, Body

Dissatisfaction and Self Concept in
Women with Bulimia Nervosa and
Binge Eating Disorder
Giorgio A. Tasca1,2,3, Louise Balfour1,2, Kanchan Kurichh2,

Monique Potvin-Kent2 and Hany Bissada1,2
1
Ottawa Hospital, 2University of Ottawa, 3Carleton University
Abstract
It was hypothesized that higher levels of actual-desired BMI discrepency (ADBD) would
be associated with higher binge eating symptoms, lower self concept, and higher body
dissatisfaction for a clinical sample of women with Bulimia Nervosa (BN) and Binge
Eating Disorder (BED). A theoretical frame for ADBD was put forward based on self
discrepancy theory. Also hypothesized was that women with BN would have greater
eating and self related pathology than those with BED. Fifty-one participants diagnosed
with BN and 41 with BED drawn from a clinical sample completed questionnaires
assessing eating disorder and general psychopathology. Greater ADBD was related to
greater body dissatisfaction for the BN and BED groups, and lower self concept for the
BN group. Those with BN had more self-related pathology. ADBD can be easily
assessed by clinicians and may be used as an index of body dissatisfaction and overall
self concept. ADBD may be a vulnerability factor for developing an eating disorder for
women.
Researchers have identified actual-desired body weight discrepancy (ADBD) among

those with eating disorders as an important variable in the clinical assessment of eating
disorder symptoms (Crowther and Sherwood, 1997), and ADBD has been implicated in the
clinical literature in the etiology of Bulimia Nervosa (BN; Casper, 1983). Similarly,
Thompson (1996) argued that discrepancies between actual body size and desired body size
is an index of body dissatisfaction (Thompson, 1996). Within these clinical
146 Giorgio A. Tasca, Louise Balfour, Kanchan Kurichh et al.
conceptualizations of ADBD, there is little theoretical formulation for why this particular
discrepancy may have an impact on psychological functioning, well being, and/or eating
disorder symptoms. A notable exception is McKinley (1998) who suggested that the negative
impact of ADBD on the body esteem of college women is a result of internalized cultural
standards encouraging negative body experiences. In general however, the impact of ADBD
on eating disorder symptomatology has received little empirical attention.
Tiggeman, Winefield, Winefield and Goldney (1994) looked at the relationship between
ADBD and psychological well being among young adults. They found that greater ADBD,
defined as Aperceived overweight@, was related to low self evaluation and to lower levels of
psychological well being. In a sample of undergraduate women, McKinley (1998) found that
ADBD was related to body esteem and high body shame. She also reported higher ADBD
among women than among men. Snyder (1997) found a significant correlation between
perceived overweight and the Body Dissatisfaction, Drive for Thinness and Interoceptive
Awareness scales of the Eating Disorders Inventory –2 (EDI-2; Garner, 1991). These studies
of general population college women were all suggestive of the role of ADBD for a clinical
sample of women with eating disorders.
Some studies have looked at ADBD among an eating disordered population. A recent
study by Doll and Fairburn (1998) found that women with BN had a greater ADBD than
normal controls. Similarly, studies have found that adolescent girls with BN and severe binge
eating reported greater ADBD than those with mild binge eating and normal controls
(Crowther and Chernyk, 1986; Post and Crowther, 1985). Few studies have looked at the
relationship between ADBD and severity of eating disorder symptoms and psychological
variables. Heffernen (1996), studied a sample of lesbians with BN, and found a significant
correlation between ADBD and body dissatisfaction. Heffernen’s (1996) study looked at
ADBD as a variable of secondary interest, and did not conceptualize ADBD within a broaden
psychological context in order to increase our understanding of ADBD’s role in eating
disorder pathology.
The current study looked at the importance of assessing for ADBD in a clinical context
and developed a conceptual understanding of this variable as a potential risk factor for eating
disorders (Casper, 1973). ADBD was seen as important in women with eating disorder
symptoms when desired body weight was lower than actual body weight. ADBD was defined
as a different but related construct to body dissatisfaction. Body dissatisfaction is specifically
related to body shape and size but not necessarily to a self discrepancy. Because ADBD was
defined in terms of a discrepancy between one=s weight and one=s personal ideal or what is
proscribed as an ideal, then ADBD likely taps into core issues of ideal self image based on
personal or cultural standards, and self evaluation (Tiggeman et al., 1994). In this study,
ADBD’s relationship with eating disorder symptoms and psychological sequelae of eating
disorders in a clinical sample of women diagnosed with BN or with BED was studied. First, a
theoretical formulation of how ADBD may be an important predictor of eating disorder
symptoms and psychological problems in women with BN or BED is proposed. To do so
Higgins= (1987) self discrepancy theory is used as a framework.
Actual - Desired BMI Discrepancy, Body Dissatisfaction and Self Concept … 147
Self Discrepancy Theory
There is an increasing consensus in the literature that Western sociocultural values

emphasize thinness and appearance for young women (Heffernan, 1996). Striegel-Moore
(1993) argued that the internalization of these values as ideals among women constitute a risk
factor for the development of an eating disorder. This may be due to the discrepancy between
cultural standards of unrealistic thinness that may be internalized, and actual BMI and body
shape that generally do not meet these standards. This discrepancy likely leads to a sense of
not living up to a social standard among some women, resulting in further attempts to attain
this ideal. With repeated failures at reaching this goal, some women may experience a sense
of personal failure, low self esteem, and dissatisfaction with their self and body.
Higgins (1987) proposed similar notions of discrepancy with regard to the self in his self
discrepancy theory. Higgins (1987) suggested that there are several domains of self including
the actual self, ideal self and ought self. Actual self refers to aspects and attributes of the self
that one actually possesses. Ideal self refers to aspect or attributes that one would like to
possess. Ought self refers to aspects or attributes that one believes one should possess. Ideal
self and ought self are self guides that are personal standards that people set up. These
standards may be those established as important by others, or may be internally held
standards, or both. For the purposes of this study, a culturally sanctioned ideal of thinness is
seen as a self guide (i.e. ought self), especially if it has been internalized by women (i.e. ideal
self).
Moretti and Higgins (1990) found that discrepancies between self guides and actual self
can lead to emotional distress and potential emotional problems; the greater the discrepancy,
the greater the distress and problems. In a study looking at self discrepancy among college
women, Strauman, Vookles, Berenstein, Chaiken, and Higgins (1991) found that self
discrepencies were related to body dissatisfaction and maladaptive eating in female college
students. Snyder (1997) found significant correlations between actual - ideal self
discrepancies and body dissatisfaction even after actual BMI was controlled.
Body weight and weight related self perceptions are integral parts of the experience of
the self for women with eating disorders. The emphasis and importance placed on actual
weight is a pivotal part of the disorder. Just as the discrepancy between actual self and self
guides is related to psychological distress, problems with self concept, and eating disorder
related psychopathology (Snyder, 1997; Strauman et al, 1991), we hypothesized that the
discrepancy between actual and desired BMI for women with BN and BED will be related to
eating disorder symptoms, body dissatisfaction, and low self concept. ADBD represents a
tangible parallel to actual-desired self discrepancies that is particularly salient to women who
are vulnerable to eating disorders. Because of the parallel, ADBD could represent a core self
related construct for those with eating disorders. Although one could argue that body
dissatisfaction may imply some discrepancy from an ideal or standard, ADBD is a more
direct measure of such a discrepancy.
Bulimia Nervosa and Binge Eating Disorder
BED has recently been included as a diagnosis requiring further research in the
Diagnostic and Statistical Manual for Mental Disorders (DSM-IV; APA, 1994). Research has
indicated that in a community sample (Hay and Fairburn, 1998) and in a clinical sample
(Tasca, Wood, Demidenko, Bissada, 2002) those with BED had lower levels of
psychopathology than those with BN. Other researchers have found those with BED to be
distinct from obese controls, and to be a homogeneous group on a number of variables. For
example, obese people who binge eat compared to obese people who do not binge eat show
greater psychopathology (Marcus, Wing, Ewing, Kern, Gooding and McDermott, 1990),
greater eating pathology (Yanovski, Nelson, Dubbert, and Spitzer, 1993), lower self esteem
and greater discrepancy between their current and ideal body size (Striegel-Moore, Wilson,
Wilfley, Elder, and Brownell, 1998). Although Striegel-Moore et al, (1998) found greater
body dissatisfaction among binge eaters than controls, other studies have not found the same
result (de Zwaan et al, 1994; Antoniou, Tasca, Bissada, and Balfour, 2002). Binge eating is a
symptom held in common between BN and BED and often the criteria for evaluating binge
eating is similar for both disorders (Walsh and Garner, 1997). Problems with self esteem and
self concept are also shared among these disorders (Striegel-Moore, et al., 1998). Body image
disturbance and dissatisfaction is a hallmark symptom of BN (Kearney-Cook and Striegel-
Moore, 1997).
Hypotheses
The first hypothesis for this study was that a greater ADBD, where actual body weight is
greater than desired body weight, will be associated with greater binge eating symptoms,
lower self concept, and greater body dissatisfaction for women in the BN and BED groups.
Second, women with BN will exhibit more eating disorder and self related problems than
women with BED on the measures used in this study. We predict that those with BN will
have greater ADBD, more binge eating symptoms, lower self concept and greater body
dissatisfaction than women with BED.
Method
Participants
A total of 92 women were assessed as part of this study. These were patients referred by
family physicians to a consultation service of a center for the treatment of eating disorders in
a medium sized urban setting. Of the 92, 51 patients met diagnostic criteria for BN and 41
met diagnostic criteria for BED. Table 1 presents diagnostic and demographic data of these
patients. Results of univariate comparisons of these variables will be discussed below.
Table 1 Demographic and Clinical Data for Women With Bulimia Nervosa (BN) and
Binge Eating Disorder (BED), With Univariate Comparisons and Effect Size (d).
BN BED
(n=51) (n=41)
M sd M sd F p d
Age 30.81 8.85 40.88 9.92 27.33 <.001 .95
Actual BMI 28.59 7.28 41.74 9.41 58.84 <.001 1.24
Desired BMI 22.76 3.21 27.20 5.37 31.63 <.001 .91
ADBD 17.69 13.02 33.15 12.07 35.47 <.001 1.04
Binge Episodes in 28 days 16.96 15.94 16.98 20.31 .00 .997 .00
Binge Days in 28 days 14.95 9.52 14.37 9.64 .07 .786 .06
Body Dissatisfaction 21.02 6.90 22.57 5.40 1.41 .238 - .25
Self Concept Factor 2.86 .93 3.34 1.01 5.69 .019 .48
High Self Esteem (Man-G) 45.51 11.02 46.58 12.09 0.18 .714 - .09
Low Self Efficacy (DEP-C) 73.79 17.24 65.93 16.91 4.96 .028 .45
Identity Instability (BOR-I) 70.89 11.75 61.81 13.50 12.26 .001 .68
Note: Effect sizes (d) are small (>.20), medium (>.50) or large (>.80) effects (Cohen, 1988).
Procedure
Patients were assessed by a psychiatrist or a psychologist. Just prior to the consultation,

patients completed a battery of tests including the Eating Disorders Inventory-2 (EDI-2;
Garner, 1991), the Personality Assessment Inventory (PAI; Morey, 1991), and the Diagnostic
Survey of Eating Disorders (DSED; adapted from Johnson and Connors, 1987). They were
then given a DSM-IV multiaxial diagnosis by the psychiatrist or psychologist (APA, 1994).
A referral to one of several treatment options offered by the Center or in the community was
often suggested. As a validation check on the diagnosis, 10% of all initial consultations (N =
210) referred to the Center were randomly selected and re-evaluated by an independent
clinician blind to the diagnosis. Identifying information and diagnostic conclusions were
removed from the re-evaluated reports. Agreement between the independent clinician and the
original diagnosis was 86% suggesting a high level of agreement.
Measures
Actual-Desired BMI Discrepancy (ADBD).
Actual height and body weight were measured at the time of assessment and Body Mass
Index (BMI; k/m2) was calculated from these. As part of the DSED, patients were asked what
their desired weight was. Based on this and their actual height, a desired BMI was calculated,
and then desired BMI was subtracted from actual BMI. To control for the effect of actual
body weight, the difference between actual and desired BMI was divided by actual BMI. The
result was multiplied by 100 so that ADBD was expressed as a percent deviation from actual
BMI ([actual BMI - desired BMI / actual BMI] x 100).
Binge Eating Symptoms
Objective binges were assessed using the criteria outlined in the Eating Disorder
Examination (EDE; Fairburn and Cooper, 1993). Consistent with DSM-IV (APA, 1994),
frequency of binges were used for the BN group and days binged was used for the BED
group. The number of symptoms over the past 28 days were counted using a calendar recall
method.
Body Dissatisfaction
The Body Dissatisfaction Scale of the EDI-2 (Garner, 1991) is a 9-item scale that
measures dissatisfaction with overall shape and size. Internal consistency was reported at
alpha = .92 (Garner, 1991).
Self Concept
Morey (1996) described self concept to encompass domains of self esteem, stability of
identity, and self efficacy. Self Concept was measured by using three scales from the
Personality Assessment Inventory (PAI; Morey, 1991). The Mania - Grandiosity (MAN-G)
scale was used to assess self esteem, as an evaluative component of self perception. The
Depression - Cognitive (DEP-C) scale measured personal competence and perceived control,
and is considered a measure of self efficacy (Morey, 1991). Stability of identity was
measured by the Borderline - Identity Problems (BOR-I) scale and represents vulnerability to
environmental stressors. Morey (1996) looked at the configuration of scores on these three
scales to assess self concept. High self concept is suggested by high scores on MAN-G and
low scores on DEP-C and BOR-I. Low self concept is suggested by low scores on MAN-G,
and high scores on DEP-C and BOR-I. Tasca, et al. (2002) report adequate psychometric
properties of PAI scales and subscales for eating disordered populations.
Results
Initial Inspection of the Data
There were no univariate or multivariate outliers in the data, all variables had acceptable
distributions, and there was no multicolinearity among dependent variables. Table 2 shows
the zero order Pearson Product Moment correlations among the variables for each diagnostic
group.
Table 2 Correlations among variables for women with Bulimia Nervosa (BN) and Binge
Eating Disorder (BED) groups.
ADBD Binge Symptoms1 Body Dissatisfaction

BN BED BN BED BN BED
(n=51) (n=41)
Binge Symptoms1 -.093 .261
Body Dissatisfaction .465* * .427** .175 -.062
Self Concept -.284* -.298 -.100 -.223 -.263 -.309*
1
Binge symptoms for BN are binge episodes in 28 days, and for BED are binge days in 28 days.
*p<.05, **p<.01The SPSS General Linear Model (GLM) program was used to perform an overall
multivariate analysis among ADBD and all the other variables for each diagnotic group. Individual
Pearson correlations were calculated to assess for the relationship between ADBD and the number
of binge episodes in the past 28 days (for the BN group), days binged in the past 28 days (for the
BED group), the EDI-2 Body Dissatisfaction Scale, and the PAI Self Concept Factor for the BN
and BED groups separately.
Self Concept Factor
As stated, Morey (1996) suggested an analysis of the configuration of three PAI scales in
order to assess self concept. However, this approach does not easily lend itself to using self
concept as a continuous variable in a data analysis. Therefore, a self concept factor was
created by conducting a principal components factor analysis with no rotation of the MAN-G,
DEP-C and BOR-I scales of the PAI (Morey, 1991) for both the BN group and the BED
group. As expected, and consistent with Morey=s (1996) conceptualization, one factor
emerged for the BN and BED groups separately accounting for 59.15% and 65.26% of the
variance respectively. Also as expected, the component matrix had the MAN-G load
negatively (-.65 and -.60 respectively), the DEP-C scale load positively (.93 and .94
respectively), and the BOR-I scale load positively, (.70 and .84 respectively). These findings
are consistent with Morey=s (1996) configural approach but allows for a single score
representing self concept for each participant. Scores on the self concept factor were reversed
so that low scores on this factor represents low self concept and high scores represent high
self concept.
Actual-Desired BMI Difference
Bulimia Nervosa Group
Using the Wilks= criterion, the combined variables (binge episodes, body dissatisfaction
and self concept) were significantly related to the parameter ADBD for the BN group,
approximate F(3, 47) = 5.395, p < .003. There was a strong association between ADBD and
the combined dependent variables (02 = .26) (Cohen, 1988). Table 2 shows the correlations
between ADBD and individual variables for the BN group. Higher ADBD was significantly
related to higher scores on the Body Dissatisfaction Scale and lower scores on the Self
Concept Factor. ADBD was not significantly associated with binge episodes for the BN
group.
Binge Eating Disorder Group
The Wilks= criterion suggested that the combined variables (binge days, body
dissatisfaction, and self concept) were significantly related to ADBD for the BED group,
approximate F(3, 37) = 3.791, p < .018. There was a strong association between ADBD and
the combined variables (02 = .24) (Cohen, 1988). Table 2 shows the individual bivariate
correlations between ADBD and each of the other variables. Higher ADBD was significantly
associated with higher scores on the Body Dissatisfaction Scale. The correlation approached
significance for the relationship between ADBD and the Self Concept Factor. ADBD was not
significantly associated with days binged for the BED group.
Comparing Bulimia Nervosa

to Binge Eating Disorder
As indicated in Table 1, those with BN were significantly younger, had a lower actual
BMI and lower desired BMI than those with BED. Because older patients may weigh more,
age was covaried when the groups were compared on actual BMI. The difference in actual
BMI remained significant even when age was covaried in an ANCOVA (F(3,88) = 55.50, p <
.001). Those with BED had a significantly higher ADBD than those with BN (Table 1). In
this study, ADBD was calculated as the percent discrepancy from actual BMI, so it is
possible that the higher BMI of those with BED may account for this difference. To test this,
an ANCOVA covarying actual BMI was conducted. When the variance accounted for by
actual BMI was covaried, there was no significant difference on ADBD between those with
BN and those with BED (F(3,88) = .083, p > .05). That is, any difference in ADBD is likely
due to those with BED weighing significantly more than those with BN, and so the percent
discrepancy can be accounted for by the initial difference in weight between the two groups.
There were no differences between the BN and BED groups on measures of binge episodes
or binge days. There was also no significant difference between the two groups on the Body
Dissatisfaction scale.
On the overall Self Concept Factor derived from the PAI, those with BN had
significantly lower self concept than the BED group. When the individual scales making up
that factor were considered (Table 1), it was apparent that the BN group had lower self
efficacy (DEP-C), and greater identity instability (BOR-I). There were no differences in level
of self esteem (MAN-G) between the two groups.
Discussion
This study looked at ADBD among women with BN and BED, and conceptualized the
impact of ADBD on eating disordered women within the framework of self discrepancy
theory (Higgins, 1987). Despite clinical references to the importance of ADBD (Crowther
and Sherwood, 1997), this is the first known attempt to look directly at the relationship
between ADBD and eating disorder related psychopathology in a clinical sample. The
hypothesis that ADBD would be related to higher eating disorder symptoms, higher body
dissatisfaction and lower self concept in women with BN and BED was partially supported. It
was clear that for the BN group, greater ADBD was significantly related to body
dissatisfaction and low self concept. For the BED group, greater ADBD was associated with
greater body dissatisfaction, and there was a trend toward a correlation with low self concept.
In self discrepancy theory (Higgins, 1987) greater actual self vs ideal self dicrepancies
predict more emotional discomfort and distress (Moretti and Higgins, 1990). This appears to
be paralleled in the ADBD of our eating disordered samples. ADBD likely results in a
number of vulnerabilities such as a sense of personal shortcomings and personal
dissatisfaction, especially for eating disordered women for whom body weight and shape are
so crucial to self evaluation. In light of internalized social ideals of thinness for women with
eating disorders (Striegel-Moore, 1993), and given the results of this study, ADBD may be
viewed as a potential vulnerability factor for women in developing BN and BED. Prospective
studies among adolescent girls using ADBD would provide a stronger test of this hypothesis.
ADBD was not related to binge eating symptoms for either the BN or BED groups, and
so no support was found for this hypothesis. It is possible that while ADBD is related to self
related experiences, such as body dissatisfaction and self concept, it may not be directly
related to symptoms of binge eating.
Comparing Bulimia Nervosa

and Binge Eating Disorder
The clearest difference between the two diagnostic groups in this study was on self
concept, with women with BN having lower self concept as measured by the PAI (Morey,
1991; Morey, 1996). Specifically, those with BN had greater identity instability (BOR-I) and
lower self efficacy (DEP-C). This suggested greater self related problems and pathology
among those with BN as compared to women with BED. This is consistent with reports in the
literature indicating that BN is a more severe disorder than BED (Hay and Fairburn, 1998;
Tasca, et al., 2002), and that there is a high comorbid diagnosis of self related pathology,
such as borderline personality disorder, among those with BN (Dennis and Sansone, 1991;
Rossiter, Agras, Telch and Schneider, 1993). Had this study focused on self esteem (e.g.
MAN-G) only, differences between groups would not have emerged. This is consistent with a
study finding no differences between eating disorder diagnostic groups on two measures of
self esteem (Griffiths, et al., 1999). The Self Concept Factor, allowed for differences to
emerge among the diagnostic groups by defining self related problems in broader terms that
includes self esteem, identity stability and self efficacy. This broader self construct may be
more meaningful to the understanding of an eating disordered population than self esteem
alone.
There were no differences between the BN and BED groups on the number of binge
episodes or days binged over the previous 28-day period. This is consistent with previous
research that found no difference in the number of objective binges between BN and BED
samples (Hay and Fairburn, 1998). The means for these two groups in this study were almost
identical (Table 1). This result does not support the notion that BED is a less severe than BN
when it comes to objective binge eating symptoms.
Our study did not find differences in body dissatisfaction between those with BED and
BN. In addition, both diagnostic groups had mean Body Dissatisfaction Scale scores above
the clinical cutoff for the EDI-2 (Garner, 1991), suggesting severe problems in this area for
the majority of women in both groups. This result is consistent with the work of Striegel-
Moore, et al (1998) who found greater body dissatisfaction among obese binge eaters than
controls. The results of this study also indicated that body dissatisfaction among these eating
disordered samples were related to ADBD and their associated self discrepancies.
Self Concept Factor
To our knowledge this is the first report in the literature using self concept as defined by
the PAI (Morey, 1991) with an eating disordered population. As stated, our results suggested
that this broader construct may be more meaningful to the study of an eating disordered
population that self esteem alone. Furthermore, this is the first report to create a self concept
factor based on the configural analysis of self concept from the PAI as suggested by Morey
(1996). The prinicpal components analysis produced a factor with loadings from the
component scales (MAN-G, DEP-C, and BOR-I) that parallel Morey=s (1996) configural
interpretation of those scales. The advantage of using this approach is that it allows for the
creation of a single continuous variable measuring self concept that lends itself to
multifactorial analysis. The disadvantage is that unique information provided by the
individual component scales gets diluted within the overall factor score.
Clinical Implications of ADBD
Using 95% confidence intervals, cutoffs for the percent deviation from individuals=
actual BMI were calculated. In our sample, if an individual with BN had a desired BMI that
was less than 21% of their actual BMI, then it would be considered clinically significant. For
example, the mean actual BMI in our sample of women with BN was 28.59. A clinical cutoff
could be established so that a patient with BN who had a BMI of 28.59 and a desired BMI of
22.59 (21% below actual BMI for the BN group) or less would have a 95% probability of
having problems with body dissatisfaction and low self concept. Interestingly, in our BN
sample, the mean desired BMI was 22.76, which is almost exactly 21% below the mean BMI
for the BN group. Clinicians could easily calculate the percent deviation from actual BMI,
use the clinical cutoffs suggested by our sample, and have an index of how problematic body
dissatisfaction and self concept are for those with BN. Similar calculations could be made for
the BED group for whom a desired BMI of less than 37% of actual BMI would be considered
clinically significant.
Limitations and Future Research
The small sample size of the BED group may have reduced the power of some of the
analyses. This is particularly apparent in Table 2 where correlations between binge symptoms
for the BN group is significantly correlated with Self Concept (r = -.284), but a slightly
higher correlation within the BED groups for the same variables(r = -.298) was not
statistically significant.
Given that ADBD was related to eating disorder related variables in these clinical
samples, it would be interesting to see if this discrepancy predicted problems with self
concept, body dissatisfaction, mood, and other psychological variables in a female sample in
the general population. One would expect a similar pattern of results in a general population
as well. However, the relationship between ADBD likely will be more salient within the
clinical and subclinical range of that population. Longitudinal research starting with an
adolescent sample and then following that sample could be done to see if ADBD is a risk
factor for developing an eating disorder. We do not expect ADBD to be as important an issue
for men since cultural standards of unrealistic thinness is more likely to occur with women
(Striegel-Moore, 1993), and McKinley (1998) found higher ADBD among women. If, as our
theory suggests, ADBD is a core self discrepancy that leads to negative mood and eating
disorder symptoms, then we would expect ADBD to be a risk factor for developing an eating
disorder for young women but not necessarily for men. For men, issues related to ideal body
shape (e.g. muscle and low body fat percentage) and not body weight per se may be a more
important variable predicting self concept and eating disorder related symptoms.
Conclusion
A theory of ADBD as a self discrepancy is presented that may represent a risk factor for
eating disorders among women. Self discrepancy theory suggests that a greater discrepancy
between actual self and ideal self leads to greater distress and emotional problems (Moretti
and Higgins, 1990). Similarly, the results of this study indicated that ADBD is associated
with lower self concept and greater body dissatisfaction. ADBD could be an issue targeted in
the assessment and treatment of women with BN, and also for those with BED. Its assessment
is relatively straight forward, and the 95% confidence intervals presented here could be used
as cutoffs for clinical samples. Targeting ADBD in treatment by focusing on its relevance to
eating disordered individuals, its impact on feelings about their body, and its impact on self
concept may allow women with eating disorders to begin to moderate the effects of these
discrepancies. The impact of ADBD found in this study continue to lend importance to the
notion that the internalization of culturally sanctioned ideals of thinness (Striegel-Moore, et

al., 1998) are corrosive to women=s body and self esteem (McKinley, 1998).
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Chapter VIII
Integrating Personality and

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

University of Kentucky
Abstract
Heritability studies provide a general framework for understanding risk for bulimia
nervosa (BN): liability is a function of both genetic and environmental factors. The
authors propose a specific model that integrates identified heritable and environmental
risk factors for BN. Trait urgency, the tendency to act rashly in response to distress, is a
heritable risk factor that increases the likelihood that one will engage in some form of
rash, maladaptive behavior pattern (such as BN). The specific form of one’s maladaptive
behavior is a function of learned experiences from one’s environment. Individuals who
learn to expect alleviation of negative mood from eating, and overgeneralized life
improvement from thinness, are more likely to engage in bulimic behaviors. Thus, the
general, heritable risk from high levels of urgency is likely to become expressed as BN
when one learns to expect benefits from eating when distressed and extreme benefits
from thinness. The proposed process is empirically supported and consistent with
findings from heritability research.
Introduction
An important recent advance in understanding bulimia nervosa (BN) has been the
recognition that both genetic and environmental factors appear to play roles in the emergence
of BN. That perspective, of course, is very general: there are many ways in which genes and
environment might combine in the risk process. Our intent in this chapter is to propose a
specific theory of this process, by describing key heritable causes of BN, key environmental
160 Sarah Fischer, Gregory T. Smith and Melissa A. Cyders
causes of BN, and mechanisms by which they combine. We propose that the heritable trait of
urgency, which is the tendency to act rashly when distressed, is a general risk factor for
addictive/risky behaviors. The combination of trait urgency and certain kinds of psychosocial
learning (indexed as expectancies for the consequences of eating and of dieting), lead to
substantially increased risk for BN. We argue here that urgency reflects an important part of
the heritable component of risk, and that psychosocial learning reflects an important part of
the impact of environmental risk. To make this argument, we will briefly review general
evidence for the heritability of BN and for environmental causes of BN. We will then
describe our specific model, illustrate how it fits within a gene-environment framework, and
review the empirical evidence supporting it.
Heritability of BN and Binge Eating
The concept of heritability refers to the proportion of population variance on an attribute

that overlaps with genetic variance (Keel and Klump, 2003). Typical heritability studies
compare monozygotic twins reared together to those reared apart, and monozygotic twins to
dyzygotic twins. Adoption studies are also employed. Behavioral genetic methods allow
researchers to partition the population variance on an attribute three ways: that due to genetic
influences; that due to environmental influences shared among study participants; and that
due to environmental events unique to individuals. Recent studies of the heritability of BN
seem to converge on the finding that risk for the disorder has large genetic influences, large
non-shared environmental influences, and very few to no shared environmental influences
(Bulik, Sullivan, and Wade, 2000). Thus, causes of BN appear to include a genetic
preparedness along with unique aspects of an individual’s learning history, but not
environmental events which one shares with one’s siblings.
According to a meta analysis of these findings, estimates of genetic effects for the
disorder range from .28 to .83 (Bulik et al., 2000). In their study using the Virginia Twin
Registry, Kendler, MacLean, Neale, et al. (1991) concluded that approximately 50% of the
variability in BN diagnosis is due to additive genetic effects. Specific evidence to that effect
is (a) concordance of diagnosis in monozygotic twins was significantly greater than that in
dizygotic twins, and (b) if a member of a monozygotic twin pair was diagnosed with BN, the
co-twin was eight times as likely as a member of the general population to also be diagnosed
with BN (Kendler et al., 1991). These effects were not explained by shared environmental
features or current contact with the co-twin. Various other studies using the Virginia Twin
Registry have found similar results for partial syndrome BN, for diagnoses of BN that adhere
to strict diagnostic criteria, and for binge eating behavior (Bulik, Sullivan, and Kendler,
2003; Bulik et al., 2000).
Findings from two other twin registries are consistent with those from the Virginia Twin
Registry. Work with the Minnesota Twin Registry found that a large portion of variability in
BN is heritable (Klump, McGue, and Iacono, 2000, 2002), and findings from the Australian
Twin Registry showed moderate heritability for BN (Wade, Neale, Lake, and Martin, 1999).
Interestingly, Wade et al. (1999) differed from the other reports in also finding moderate
effects of common environmental influences.
Integrating Personality and Environmental Risk Factors for Bulimia Nervosa 161
In sum, several studies conducted using twin samples in the last fifteen years have
converging results: a moderate to large portion of the variance in BN is genetically
influenced, and a moderate to large portion of the variance is influenced by unique or non-
shared environmental effects. Very little of the disorder’s variance, and perhaps none, is
influenced by shared environmental factors. A comprehensive model of risk for BN must
incorporate genetic risk for the disorder.
It is also true that the rates of BN appear to have risen in Western cultures in recent
decades (Keel and Klump, 2003). To understand why varying rates of BN can exist, even
though risk for BN is heritable, it is important to understand that there are different possible
mechanisms of genetic risk. One mechanism is that there is a genetic/biological cause of
some specific behavior or dysfunction. When the cause is present, the disorder inevitably
occurs. Under such a circumstance, there is no reason to expect the rate of the disorder to
vary across time and across contexts. A different possible mechanism is that there is a genetic
risk for a more general behavioral disposition, and the general disposition can take varying
forms, depending on environmental and cultural factors. In the case of BN, the heritable risk
appears likely to be of this second form, because although there is heritable risk, the rates of
the disorder vary across time and across cultures. One obvious implication is that
environmental factors are also important influences on the liability for BN.
Evidence for the Role of Environment in the

Development of BN
The causal role of environmental and cultural factors in BN has, in fact, been much more
widely emphasized in the literature. Among the classic indicators of those factors are the
ideal female images presented in the media. Anyone with access to a television or magazines
in Western society may plausibly assume that we live in a high risk media environment for
disordered eating. Images of women in the media are much thinner than the average Western
woman, and these images are pervasive. The British Medical Association (BMA) recently
released a statement saying that the media play a large role in the development of both
anorexia nervosa (AN) and BN (BMA, 1999). This assumption is due, at least in part, to the
fact that Western media images of women seem to be getting thinner and thinner, while
average individuals in industrialized nations get bigger and bigger (Wadden, Brownell, and
Foster, 2002). The Western cultural ideal of attractiveness—the thin ideal--is quite different
from the physical reality of most adults. This appears to increase women’s body
dissatisfaction (Rodin, Silberstein, and Striegel-Moore, 1985). In fact, some researchers
suggest that dissatisfaction with one’s body is now normative among Western women (Rodin
et al., 1985). These factors, the thin ideal for women and body dissatisfaction, appear to
promote bulimic behaviors (Stice, 2002).
Stice summarized a theoretical model for cultural effects on risk for BN (Stice,1994). In
this model, pressure from society on women falls into three categories: the thin-ideal body
image for women, the importance of appearance in the female gender role, and the
reinforcement of attractiveness. He reviews evidence that the shrinking body size of women
in the media is correlated with increases in dieting articles in women’s magazines (Stice,
1994). Therefore, it is hypothesized that the ideal image of women in Western society is very
thin.
This ideal seems to be associated with gender roles for women. Thin body shapes are
rated as more feminine, endorsing traditional female gender roles is associated with
endorsement of the thin ideal, and women who eat less food are rated as more feminine
(Stice, 1994). So, thinness is associated with attractiveness and femininity. In addition, there
is evidence that attractive people are perceived more positively and receive more
reinforcement than do unattractive people. Attractive people are rated as more intelligent,
socially skilled, honest, and better qualified for jobs than unattractive people (Feingold,
1992). If being thin is considered attractive for women, and level of attractiveness has real
consequences in social and work settings, then it seems there is extreme pressure for women
to try to be thin in our society (Stice, 1994).
The internalization of this pressure has come to be described as thin-ideal internalization
(Stice, 2002; Thompson, van den Berg, Roehrig, Guarda, and Heinberg, 2004).
Internalization is defined as “the incorporation of specific values to the point that they
become guiding principles” (Thompson et al., 2004). Thin-ideal internalization is considered
a risk factor for body dissatisfaction, dieting, and bulimic symptoms themselves. The
evidence for the relationship of dieting, body dissatisfaction, and thin-ideal internalization to
bulimic symptoms can be construed as evidence that environmental factors influence the
development of the disorder. Polivy and Herman (2002) stated in a recent review that “the
influence of sociocultural factors in the context of eating disorders can be summarized
succinctly as the idealization of thinness.”
A recent meta-analysis by Stice (2002) summarizes findings of prospective longitudinal
studies and experimental studies of risk factors for BN, including thin-ideal internalization.
He found that thin-ideal internalization led to increases in bulimic symptoms, with a
significant effect size of .08 (Stice, 2002). A subscription to a teen magazine featuring thin
models led to increased bulimic symptoms among girls with low social support (Stice,
Spangler, and Agras, 2001). Additionally, bulimic women endorse the thin ideal more than
women without bulimia (Thompson et al., 2004). There is also evidence that thin-ideal
internalization is present in girls as young as age nine (Sands and Wardle, 2003).
Body dissatisfaction may mediate the influence of thin-ideal internalization on bulimic
symptoms (Stice, 1994). Body dissatisfaction is defined as negative subjective evaluation of
physical attributes (Stice and Shaw, 2002). This risk factor for bulimia (Stice, 2002) is
thought to be primarily transmitted through media influences. Body dissatisfaction likely
results from social comparison, in which women look at media images and compare
themselves unfavorably to those images. This relationship has been confirmed in the
laboratory many times. The basic paradigm is that women are asked to rate their body
dissatisfaction and negative affect both before and after viewing images of thin models. The
majority of studies find that after viewing thin models, women experience an increase in
negative affect and body dissatisfaction. Halliwell and Ditmar (2004) expanded on this model
by assessing level of internalization of the thin ideal and how this affected body
dissatisfaction in the experimental paradigm. Women with higher internalization reported
greater anxiety after viewing thin model slides.
Body dissatisfaction is an important risk factor for BN because it is hypothesized to lead

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

Environmental Perspectives
From the foregoing, we know there is an inherited risk for BN, and we know that
environmental risk factors increase risk for the disorder. Bulik et al. (2000) provide a general
integration of the two types of causes in their liability threshold risk model. The notion is that
liability for BN reflects the combination of several genetic and environmental effects, each of
which likely has a small individual effect. This liability has a normal distribution in the
population and is only expressed as the disorder if one’s liability is greater than a particular
critical threshold. In the case of BN, there may be several genetic and environmental effects
that contribute to the expression of the disorder, but BN appears only in that small percentage
of individuals with enough of the factors to cross the critical threshold. Thus, the incidence
rate of BN is roughly 2.5% (APA, 1994; Bulik et al., 2000).
Bulik et al. (2000) go on to argue that a genotype by environment interaction is an
important mechanism in increasing risk beyond the threshold. Thus, individuals who are
genetically liable for the disorder will be the ones to develop the disorder, but will do so only
in a high risk environment. Therefore, the effect of the environment on an individual depends
on the genotype of that person (Klump, Wonderlich, Lehoux, Lilenfeld, and Bulik, 2002).
Several authors note that this genotype by environment interaction may be an important
direction of study for risk for BN (Bulik et al., 2000; Kaye et al., 2004; Keel and Klump,
2003; Klump et al., 2002). An interaction of this type would reconcile the perception that the
Western environment is high risk with the awareness that only a small percentage of women
develop BN: the environment may be high-risk for a BN diagnosis only among women with
high liability, even if it is high-risk for subclinical eating and dieting problems for women in
general.
This framework of risk is very general. We propose one specific inherited risk factor
(trait urgency) and a set of specific psychosocial learning risk factors (measured as
expectancies for reinforcement from eating and from dieting) that, we believe, operate as risk
factors in the way that Bulik et al.’s (2000) model describes. We make the argument as
follows. First, we present a theoretical rationale for the consideration of urgency as a risk
factor. We then demonstrate that urgency is distinct from other impulsivity-related constructs
and heritable, and we review evidence for its role in relation to BN and binge eating. Next,
we present a theoretical rationale for focusing on learned expectancies to capture individual
differences in environmental risk. We follow that with empirical evidence for eating and
dieting expectancy theory. Finally, we present a theoretical integration of urgency and
learned expectancies (which includes interaction effects), and we summarize empirical
evidence for that integration.
Urgency as a Risk Factor for BN
One of the most common ways researchers have tried to explain rash, maladaptive action,
such as binge eating and purging, is through use of the broad construct of impulsivity. A
number of studies have attempted to relate impulsivity to BN and binge eating, but the
findings have been inconclusive and the effect sizes small (Stice, 2002). There is growing
evidence that these inconsistent findings occur because the broad construct of impulsivity
actually includes several more specific constructs, which themselves are only moderately
related to each other and which account for different phenomena (Evendon, 1999; Petry,
1999; Whiteside and Lynam, 2001). Impulsivity has often, but not always, been described as
acting without thinking. Descriptions of impulsivity in the DSM-IV include acting without
thinking, the inability to concentrate, and the tendency to become easily distracted. In
addition, specific acts, such as binge eating and substance abuse, are described as impulsive
(APA, 1994).
Whiteside and Lynam (2001) conducted a factor analysis of several different major self-
report measures of impulsivity and found four factors or impulsivity-related constructs.
Sensation seeking is the tendency to seek out novel and thrilling experiences. A lack of
deliberation is the tendency to act without thinking. A lack of persistence is the inability to
remain focused on a task. Urgency is the tendency to act rashly when faced with distress.
They developed a self-report inventory to assess these four impulsivity- related constructs
(UPPS-R: Whiteside and Lynam, 2001). The measure was designed to assess each trait
uncontaminated by items measuring similar constructs. For example, the sensation seeking
scale was designed without items measuring a lack of planning. They found that the four
scales were only modestly intercorrelated. Prior to their work, impulsivity measures tended to
include items reflecting some, or all, of the four constructs, and the proportional
representation of different constructs varied from scale to scale. Since scales included four
different constructs, to varying degrees, there was built-in inconsistency in measurement
(Smith, Fischer, and Fister, 2003).
Among those four impulsivity-like constructs, we believe trait urgency--the tendency to
act rashly when distressed—is the construct that best captures the nature of binge eating and
bulimic behavior. Binge behavior does not reflect lack of persistence, nor does it primarily
reflect pursuit of new and novel sensations. Although there may be a lack of planning
component to some binge eating, we contend that the propensity to act rashly or
maladaptively, in response to distress, best reflects what clinicians mean when they refer to
the impulsivity of binge eating and BN clients. We also favor trait urgency because of its
specificity: rather than referring to general impulsive tendencies, the idea is that if one has a
propensity to act rashly when distressed, then one is at increased risk for binge eating and BN
problems.
There is considerable evidence that stress, distress, and negative mood often precede
binge eating episodes. Experimental studies indicate that binge eating provides immediate, if
fleeting, relief of negative affect (Deaver, Miltenberger, Smyth, Meidinger, and Crosby,
2003; Kaye, Gwirtzman, George, Weiss, and Jimerson, 1986; Sanftner and Crowther, 1998;
Steinberg, Tobin, and Johnson, 1989; but see Davis, Freeman, and Solyom, 1985), perhaps
by facilitating escape from self-awareness (Heatherton and Baumeister, 1991). Laboratory
induced negative affect leads to increases in eating (Stice, 2002). Motives for eating include
comforting oneself and distracting oneself from negative emotion (Jackson, Cooper, Mintz,
and Albino, 2003). Binge eating has been tied to the avoidance of emotions and the use of
distraction (Freeman and Gil, 2004). Stress is associated with binge eating on the day that the
stress occurred (Crowther, Sanftner, Bonifazi, and Shephard, 2001; Freeman and Gil, 2004).
As we have noted elsewhere, negative affectivity is an obvious precursor to urgency: among
those experiencing negative affect, those women high in urgency are most likely to act rashly
to relieve their distress (Fischer, Smith, Spillane, and Cyders, in press). It therefore seems
quite possible that urgency may be the impulsivity-like construct most relevant to binge
eating and BN.
The Distinctiveness and Heritability of Urgency
Urgency is actually represented as distinct from the other three impulsivity-related

constructs in the predominant, integrative personality trait model: the five factor model of
personality. The five factors include neuroticism, extraversion, agreeableness,
conscientiousness, and openness to experience. In Costa and McCrae’s (1992) self-report
measure of the five factor model, the NEO-PI-R, urgency is represented as the impulsivity
facet of the broader domain of neuroticism. They have described this facet as a “craving”
factor, indicating a dyscontrolled impulse to eat, drink, etc. in response to distress (Costa and
McCrae, 1992). This facet of the neuroticism domain of the NEO-PI-R loaded highly onto the
urgency factor in Whiteside and Lynam’s (2001) factor analysis of impulsivity measures. The
other impulsivity-related constructs are represented elsewhere among the five factors
(sensation seeking is a facet of extraversion, lack of deliberation is a facet of
conscientiousness, and lack of persistence is also a facet of conscientiousness).
There are several studies documenting the heritability, stability, and correlates of this
facet (Costa and McCrae, 1992; McCrae et al., 2000; Paunonen and Ashton, 2001). In a
multi-national twin study of the domains and facets of the NEO-PI-R, urgency correlated
higher among monozygotic twins than among dizygotic twins (Jang et al., 1998). Jang and
colleagues examined the heritability of the specific variance unique to urgency (i.e., that
variance not shared by the other facets of neuroticism). They found that, controlling for error
variance, the heritability estimate for the impulsivity/urgency facet in their two samples was
.49 (Jang et al., 1998). McCrae and Costa (1994) found long-term stability of the facet.
Correlates of the urgency/impulsivity facet include, for example, greater tobacco
consumption, greater alcohol consumption, more obesity, and less religiosity (Paunonen and
Ashton, 2001). Castellani and Rugle (1995) found that cocaine and alcohol abusers scored
higher on the urgency/impulsivity facet than a control sample. Miller, Flory, Lynam, and
Leukefeld (2003) found that the urgency/impulsivity facet was positively related to risky
sexual behavior, problems with alcohol use, and a composite measure of eating disorders
symptoms. In short, there is consistent evidence that the urgency/impulsivity facet of the
NEO-PI-R correlates with negative mood (Costa and McCrae, 1992) and with rash,
maladaptive actions, including excessive eating and drinking.
We have also recently examined Whiteside and Lynam’s (2001) measure of urgency. We
first sought to replicate the four-factor structure for impulsivity-related constructs that has
been operationalized in their UPPS-R (Whiteside and Lynam, 2001). The structure replicated
successfully in three different undergraduate samples (with sample sizes ranging from 156 to
1,200). Evidence for the discriminant validity of urgency from sensation seeking, lack of
planning, and lack of perseverance was also present. For example, in the sample of 1,200,
urgency’s correlations with the other constructs were .39 with lack of planning, .30 with lack
of persistence, and .11 with sensation seeking (Fischer, Smith, Cyders, and McCarthy,
2004a).
We also conducted a multitrait, multimethod (MTMM) study of urgency and the other
three impulsivity-related constructs. We developed a semi-structured interview based on the
UPPS-R, in order to examine the potential role of method variance in the assessment of
urgency and in its relations with other constructs (Campbell and Fiske, 1959). A total of 156
undergraduates completed the semi-structured interview of the UPPS-R, the self-report
version of the UPPS-R, and self-report measures of various criterion variables, such as
problem drinking, binge eating, gambling, and school performance (Fischer et al., 2004a).
Results of that study supported the convergent and discriminant validity of each construct,
including urgency. Correlations between the same construct measured in the two different
ways were much higher than were correlations of different constructs measured in the same
way. For example, interview-assessed urgency correlated with self-report urgency at r = .75,
p <.001, while the correlations between interview-assessed urgency and the other constructs,
also assessed by interview, were .21 for lack of persistence, .29 for lack of deliberation, and
.03 for sensation seeking (Fischer et al., 2004a).
Additionally, both interview and self-report assessed urgency had similar relationships to
criterion variables. For example, self-report assessed urgency was positively correlated with a
self-report measure of pathological gambling behavior (r = .27, p <.01). No other self-report
assessed impulsivity construct was associated with pathological gambling. And, interview
assessed urgency was correlated with self-report pathological gambling (r = .25, p <.01). No
other interview assessed impulsivity-related constructs were associated with pathological
gambling (Fischer et al., 2004a). Different means of measuring urgency agree, urgency is
distinct from other impulsivity-related constructs regardless of method of assessment, and

urgency predicts outcome variables consistently, regardless of means of measurement.
One possibility is that urgency may be an interaction of neuroticism and lack of planning
impulsivity, or a combination of these two traits, instead of a personality construct in its own
right. In a recent sample (n =130 women), we found that although urgency related to the
combination of neuroticism and lack of planning, there was considerable systematic variance
in urgency unexplained by those constructs. In addition, urgency accounted for an additional
6.5% of the variance in bulimic symptoms, beyond that explained by the other constructs.
The beta weight of urgency was .34 (p <.05), the largest beta weight of all predictors in the
model. The trait of urgency does not seem to be reducible to a combination of neuroticism
and lack of planning.
Cross-cultural evidence also supports the validity of the construct of urgency. As noted
above, urgency/impulsivity as measured by the NEO-PI-R appears to be comparably heritable
in different cultures. There is also evidence that both broad personality traits and specific
facets such as impulsivity tend to have the same external correlates in different cultures
(Church, 2000; Saucier and Ostendorf, 1999). While cross cultural studies have been
conducted using the facets of the NEO-PI-R, they have not yet been done with the UPPS-R.
However, Spillane and Smith (2003) conducted a study of individual difference variables that
affect Native American drinking on a reservation where high rates of alcohol abuse are
observed. While environmental factors appeared to affect drinking levels to a large extent,
they also found that urgency was positively associated with alcohol use and problem
drinking, just as it is in Caucasian samples.
To summarize, there is evidence that the unique variance associated with urgency is
heritable, that urgency can be measured with either self-report or interview methods, that
urgency correlates with various measure of negative affectivity and maladaptive behavior,
that urgency is not simply the sum or product of neuroticism and lack of planning, and that
urgency appears to operate similarly across cultures. This body of evidence is crucial for the
claim we make that urgency reflects an important part of the heritable liability for BN.
Urgency’s Relation to Binge Eating and BN
We have begun to examine urgency’s relation to binge eating and BN, and we have
compared its role to that of the other impulsivity-like constructs. In each of four samples of
college women, urgency correlated highly with binge eating behavior (Fischer, Anderson,
and Smith, 2004b; Fischer and Smith, 2004a; Fischer, Smith, and Anderson, 2003; Fischer,
Smith, and Lander, 2004). None of the other four impulsivity-related constructs correlated
meaningfully with binge eating. Most recently, a meta-analysis of impulsivity-related
constructs found the following magnitudes of relation to bulimic symptoms: urgency (r =
.43), sensation seeking (r = .18), lack of perseverance (r = .02), and lack of planning (r = .18)
(Fischer and Smith, 2004b). One limitation of the meta analysis was that many studies did not
use measures designed specifically to differentiate among the four constructs. Therefore, for
instance, lack of planning measures may have included some urgency content, and vice versa.
In other words, the effect size comparisons likely underestimate the true differences in
effects. Nonetheless, the findings clearly point to the primary importance of urgency, among
impulsivity-like constructs, in accounting for binge eating behavior.
It is important to note that these findings come from cross-sectional research. Therefore,
although they clarify the likelihood that urgency is the one impulsivity-like construct relevant
to BN, they do not show a prospective or causal relation between the trait and the disorder.
For the promise of this perspective to be realized, prospective and experimental designs that
clarify urgency’s possible causal role are essential.
Of course, the trait of urgency does not directly produce binge eating behavior and BN.
Rather, urgency reflects a general tendency to act rashly in response to distress. We believe
that urgency is best considered a general, distal risk factor for a variety of “acting out”
behaviors. We suggest that the particular form of “acting out” behavior that results from high
urgency is a function of psychosocial learning. Some individuals may learn that drinking
alleviates distress, others may learn that gambling does so, and some may learn that bulimic
symptoms can play that role. Therefore, to understand when urgency is likely to lead to
bulimic symptoms, it is necessary to consider psychosocial learning. We have adopted
expectancy theory for this purpose.
Expectancy Theory: Psychosocial Learning
In the early part of the 20th century, psychology was captivated by the power of learning
models in explaining behavior. Contingencies of reinforcement and punishment clearly exert
a powerful influence on behavior (Skinner, 1953; Watson, 1930), and so to explain behavior,
researchers focused on the learning of behavioral contingencies. During this time, Tolman
(1932) advanced learning theory by demonstrating that the content of learning may be more
cognitive than strictly behavioral in nature. After teaching rats to run mazes, he found that
rats could just as successfully swim or ride a trolley car through the maze. He concluded that
rats, instead of just learning a series of motor behaviors in response to reinforcement, actually
developed cognitive maps of the maze itself. Essentially, as a result of learning, they knew
how the maze was laid out so that they could get to the end by any number of motoric acts. In
a nutshell, Tolman (1932) argued that rats form expectancies about the maze, based on their
experiences with it. This finding of the cognitive nature of learning helped pave the way for
future cognitive and social learning theories.
Tolman, along with many other researchers to follow (Bolles, 1972; MacCorquodale and
Meehl, 1952; Rotter, 1954), described two basic kinds of expectancies: Stimulus-stimulus
expectancies and response-outcome expectancies. Stimulus-stimulus expectancies are
described as expectations that a given circumstance will be followed by some other specific
circumstance. Response-outcome expectancies are expectancies that a given behavior will
result in a given outcome. Thus, the mechanism of learning is that, as a result of one’s
learning history, one forms response-outcome and stimulus-stimulus expectancies, and those
expectancies then influence one’s future behavioral choices. In other words, one’s
expectancies summarize one’s learning history, and so are the cognitive mechanism by which
prior learning leads to subsequent behavior.
Expectancy theory has become an important construct in many areas of psychology,

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

of Sociocultural nfluence from the
Standpoint of Expectancy Theory
Many existing measures of sociocultural influences on dieting, thinness, and eating can
be though of from the perspective of expectancy theory and thus can be incorporated into this
theoretical framework. We offer a representative, though not comprehensive, list of models to
demonstrate this fact: the Perceived Sociocultural Pressure Scale (PSPS; Stice, 2001), the
Sociocultural Attitudes Toward Appearance Questionnaire (SATAQ; Heinberg, Thompson,
and Stormer, 1995), and the body dissatisfaction and drive for thinness subscales from the
Eating Disorder Inventory-2 (Garner, 1991). We chose these measures because each has
proved a reliable, valid predictor of eating disorder symptom endorsement, many of them in
longitudinal designs (Stice, 2002).
Items from the PSPS include: “I’ve noticed a strong message from my friends to have a
thin body” and “I’ve felt pressure from people I’ve dated to lose weight.” From a learning
theory perspective, these items appear to ask women to record a learning experience, or
summarize a set of learning experiences. If one has felt pressure to lose weight, or to be thin,
one has had a learning experience that will contribute to the expectancies one forms about the
benefits of dieting and thinness. Thus, in a sense, the PSPS appears to measure precursors to
thinness and dieting expectancies. In other words, the scale measures individual differences
in one of the causes of expectancy formation. From an expectancy theory perspective, that is
why scores on the PSPS predict subsequent onset of symptomatology: they contribute to the
formation of expectancies, which then influence subsequent behavior. In a practical way, they
serve as markers of likely expectancy endorsement.
The social pressure awareness subscale of the SATAQ can also be thought of under the
expectancy theory rubric. Items such as “People think that the thinner you are, the better you
look,” and “Attractiveness is very important if you want to get ahead in our culture,” seems to
reflect exposure to social learning about the benefits of thinness and attractiveness. The items
measure the individual’s recognition and endorsement of the social learning message. The
more women recognize that message, the more likely they will form expectancies for
reinforcement from thinness. These expectancies are then likely to influence their behavior.
Thus, SATAQ Awareness scale items also seem to reflect precursors to expectancy
formation.
Consider next items reflecting internalization of the thin ideal. Examples include Stice’s
(2001) “Slender women are more attractive” and the SATAQ Internalization scale’s
“Photographs of thin women make me wish that I were thin.” These items are different from
the preceding ones, in the sense that they appear to reflect conclusions on the part of the
respondent, not simply exposure to learning situations. Women who endorse these items
strongly apparently feel more strongly about the value of thinness. The Stice item refers to
one specific expectancy for thinness: thinness is more attractive. The SATAQ item’s
reference to a wish to be thinner may reflect the same expectancy (thinness is attractive), but
may also or instead reflect a more global expectancy for the benefits of thinness. Conclusions
of this kind are, essentially, endorsements of expectancies that should play a role in
influencing subsequent behavior.
Items on the Drive for Thinness scale of the EDI-2 are indicative of motivations to be
thin. Example items include “I am preoccupied with the desire to be thinner,” and “I
exaggerate or magnify the importance of my weight.” From an expectancy theory standpoint,
expectancies for reinforcement from dieting and thinness could lead to this kind of
preoccupation with one’s weight. Thus, the Drive for Thinness subscale appears to reflect
consequences of expectancy formation and endorsement of these items may serve as markers
of one’s expectancies.
The Body Dissatisfaction subscale of the EDI-2, which includes items such as “I think
that my thighs are too large” and “I think my hips are too big,” are conclusions one might
draw, and they may reflect the influence of dieting/thinness expectancies. If one endorses
expectancies for reinforcement from dieting and from thinness more strongly than the
average woman, one would likewise be more inclined to value a thinner body, and hence be
dissatisfied with one’s own body. In this sense, body dissatisfaction can be understood as a
consequence of one’s learning history, as crystallized in one’s expectancies for dieting and
thinness.
In sum, the above examples represent different stages in the psychosocial learning
process concerning eating, dieting, and thinness. We believe these constructs should be
organized from a learning theory perspective, because psychosocial learning has been shown
to be a very powerful and important tool in explaining behavior. By organizing them in this
way, they can be seen to be parts of a coherent whole, rather than as individual instruments,
each proceeding from a slightly different stage in the psychosocial learning process.
Understanding the place of each of these constructs within expectancy learning theory both
clarifies their connections with each other and produces an integrated theory of symptom
acquisition that can be readily understood with the same theoretical tools used for many other
psychological phenomena.
The Direct Measurement of Expectancies for

Reinforcement from Eating and from
Dieting/Thinness
Hohlstein et al. (1998) developed measures of expectancies for reinforcement from

eating and from dieting/thinness within the framework of the expectancy theory. To do this,
they interviewed both clinical and non-clinical women about their expectancies. After a series
of test development steps, they identified five scales to the 34-item Eating Expectancy
Inventory (EEI) and one, global scale to the 44-item Thinness and Restricting Expectancy
Inventory (TREI). The five-factor structure of the EEI and the one-factor structure of the
TREI have been replicated in nine samples (four early adolescent female samples:
MacBrayer, Smith, McCarthy, Demos, and Simmons, 2001; Simmons, Smith, and Hill, 2002;
one late adolescent sample: Simmons et al., 2002; one college female Caucasian sample and
one college female African American sample: Atlas, Smith, Hohlstein, McCarthy, and Kroll,
2002; and two more college samples, one female and one male: Boerner, Spillane, Anderson,
and Smith, 2004).
The five-factor structure of the EEI is made up of two positive reinforcement scales
(“Eating is pleasurable and useful as a reward” and “Eating enhances cognitive
competence”), two negative reinforcement scales (“Eating helps manage negative affect” and
“Eating alleviates boredom”), and one scale assessing the expectancy that “Eating leads to
feeling out of control.” The five-factor structure provided the best goodness-of-fit as
compared to alternative factor structures (CFI=.95, rmsea=.04)
The TREI’s one factor solution fit the data well (CFI = .99, rmsea = .01), and, although
multifactor solutions also fit well, intercorrelations among putative subscales were all greater
than .80, suggesting the merit of describing one, overall factor (“Thinness and restricting
food intake lead to overgeneralized self-improvement”). Important content domains included
in the TREI are reflected in these sample items: “I feel like I could conquer things more
easily if I were thin,” “I would feel more capable and confident if I were thin,” “I would cope
better with failures at work or school if I were thin,” and “I would be more attractive if I were
thin.”
There is considerable evidence for the validity of these measures of eating and
dieting/thinness expectancies. In early adolescent, late adolescent, and college samples (the
latter including men, women, Caucasians, and African Americans), expectancies that eating
helps manage negative affect, alleviate boredom, and leads to feeling out of control, along
with the expectancy that thinness/dieting leads to overgeneralized self-improvement,
consistently account for substantial variance in Bulimia Test scores, Restraint Scale scores,
and Three Factor Eating Questionnaire scores. In these analyses, correlations generally
ranged from r = .40 to r = .62 (Atlas et al., 2002; Boerner et al., 2004; Hohlstein et al., 1998;
MacBrayer et al., 2001; Simmons et al., 2002).
Eating and Thinness expectancy profiles discriminated among anorexic patients, bulimic
patients, psychiatric controls, and normal controls. There were no differences between
psychiatric and normal controls, and classification accuracy among the three groups of
anorexics, bulimics, and controls was 96% (94% if one does not use the expectancy that
eating leads to feeling out of control, which is almost identical to a bulimia nervosa
symptom). Bulimic patients simultaneously held expectancies that eating helps alleviate
negative affect and boredom, and that thinness leads to overgeneralized self-improvement.
Anorexic patients held strong expectancies for the benefits of thinness, and unusually low
expectancies for the benefits of eating. Simmons et al. (2002) found that expectancies
accounted for different symptom variance from that explained by EDI-2 personality risk
factors (perfectionism, interpersonal distrust, and ineffectiveness). MacBrayer et al. (2001)
found cross-sectional evidence consistent with the hypothesis that various expectancy scales
mediate the influences of (a) negative maternal modeling regarding eating, and (b) family
teasing about weight, on bulimic symptoms.
The next step in testing eating and dieting expectancy theory was to conduct a
longitudinal study of expectancy and symptom endorsement. We focused on early
adolescence, by following a sample of U.S. middle school children from grade 7 through
grade 9 (Smith et al., in press). We examined three expectancy scales (eating helps manage
negative affect, eating alleviates boredom, and thinness/dieting leads to overgeneralized self-
improvement) and one symptom measure, the Bulimia Test-Revised (BULIT-R).
First, we examined the cross-sectional, multiple regression correlations between the three
expectancy scales and the BULIT-R scores, which ranged from .60 to .69 across three years.
The uncontrolled, time-lagged analyses indicated that expectancies correlated with
subsequent BUILT-R scores in the .40 to .50 range. However, because these correlations did
not control for prior BULIT-R scores, they could be a product of the high cross-sectional
relationships and stable variable scores.
In order to control for prior BULIT-R scores, we utilized structural equation modeling to
examine a series of models. The model that best fit the data was one that specified reciprocal
influences: expectancies at time 1 influenced symptom level at time 2, and symptom level at
each time influenced expectancy scores at the subsequent time. The overall fit of the model
was quite good (Comparative Fit Index = .96).
Reciprocal influences between expectancies and symptom level are consistent with
expectancy theory. Learned expectancies should predict subsequent changes in symptoms,
and symptom level itself brings learning experience, and so should predict subsequent
changes in expectancies. It is interesting to note that the nature of the predictions was of the
positive feedback loop variety. Greater endorsement of expectancies for reinforcement from
both dieting and thinness predicted greater bulimic behavior, which in turn predicted yet
greater expectancies for reinforcement from both eating and dieting/thinness (Smith et al., in
press). The mechanism by which this progression operates is not yet known, but it is worth
noting that the same kind of positive feedback, reciprocal influence phenomenon was
observed with early adolescent drinking behavior (Smith et al., 1995). Thus, these
longitudinal data provide evidence supporting the application of expectancy theory to eating
disorder symptomatology.
Taken together, the early empirical work testing eating disorder expectancy theory
clearly suggests that eating and dieting expectancies operate in accord with basic expectancy
learning theory and very similarly to how expectancies operate in other applied areas. These
findings speak to the value of integrating the many measures of sociocultural influence under
an expectancy learning theory umbrella. When one considers the documented, successful
prospective, predictive role of expectancy-related constructs (perceived sociocultural
pressure, thin-ideal internalization, and so on: Stice, 2002), there currently exists evidence
that precursors to expectancy formation, global expectancies, specific expectancies, and
consequences of expectancies all predict the subsequent onset of bulimic symptomatology.
More specifically, bulimic women appear to simultaneously hold unrealistic expectancies for
reinforcement from both eating and from dieting/thinness (Hohlstein et al., 1998). Analogous
to that which has been documented in other areas of psychology, unusually strong learned
expectations for reinforcement from eating and from dieting/thinness predict bulimic
symptom endorsement.
A Heritable Trait Combines with

Psychosocial Learning: Integration
of Urgency and Expectancy Risk Models
As we noted at the beginning of the chapter, one general advance in understanding risk
for BN is the recognition that both heritable and environmental factors contribute to liability.
Our aim is to make this general advance more specific, by identifying one specific heritable
risk factor and one specific set of environmental risk factors. We have argued that urgency
(the tendency to act rashly or maladaptively when distressed) is one important heritable trait
that increases liability for BN. We have also argued that individual differences in
environmental risk can be captured using the expectancy construct. Expectancies for
reinforcement from eating and from dieting/thinness are thought to summarize one’s relevant
learning history, and so reflect a wide range of learned inputs into one’s eating and dieting
predilections. In this section, we attempt to integrate these two risk factors. Doing so has two
advantages. First, it provides substance to the general argument that genetic and
environmental factors are both involved. Second, it suggests a more general integration of
dispositional and learning risk factors that may have value beyond the eating disorder field.
We emphasize two key dimensions to the urgency-expectancy integration. First, trait
urgency is a general risk factor, in the sense that it increases one’s likelihood of developing
some form of rash/maladaptive action in response to one’s distress. Examples of rash action
patterns one might develop include binge eating, BN, alcohol use, and gambling behavior.
Which of those action patterns a highly urgent person engages in is a function of the person’s
learning history. Through modeling and experience, some individuals form expectancies for
distress relief from drinking, others from gambling, and others from binge eating. They share
the general, heritable liability of trait urgency, but their different learning histories cause
them to form different expectancies, resulting in different characteristic forms of rash action
(there are, no doubt, other forms of rash action beyond those listed, perhaps including risky
sex or dyscontrolled shopping). This notion of a general, heritable liability that can be
instantiated in various ways is consistent with what we know about risk for BN. Since BN
rates vary across time and culture, the heritable risk for BN cannot be specific to BN
symptomatology: it must involve more general dispositions that can lead to BN under the
right environmental circumstances. If this model is accurate, one should be able to show that
urgency correlates with each of those action patterns, and that what distinguishes among
people with the different action patterns is their different expectancies.
We have demonstrated this process in two recent, cross-sectional studies. Fischer et al.
(2004b) showed that urgency correlated with both alcohol use and binge eating, that alcohol
expectancies correlated with drinking levels but not with binge eating, and that eating
expectancies correlated with binge eating but not with drinking. Fischer and Smith (2004a)
extended the earlier findings by including gambling behavior. Here, too, urgency correlated
with problem drinking, binge eating, and problem gambling, but the three types of
expectancies (for alcohol, for eating, and for gambling) were behavior-specific. For instance,
problem gamblers shared trait urgency with binge eaters, but problem gamblers had strong
gambling expectancies and weak eating expectancies, whereas binge eaters had strong eating
expectancies and weak gambling expectancies.
Although there are limitations to these findings (their cross-sectional nature and the
failure to include identified clinical cases), their potential implications are clear. It seems
possible that high levels of trait urgency place one at risk for some form of “acting out”
behavior, and that one’s learning history, represented as expectancies, shapes the direction
and nature of one’s “acting out.” Moreover, the notion of dispositional tendencies being
shaped into specific behavioral predilections as a result of one’s particular learning
experience may well have importance beyond the field of eating disorders.
A second dimension to the urgency-expectancy integration is that, in the case of binge
eating, disposition and learning interact. In a series of studies, we have shown that among
individuals high in trait urgency, those who expect eating to alleviate negative affect are
much more likely to binge eat than are others (Fischer, Smith, Anderson, and Flory, 2003;
Fischer et al., 2004b; in press). Among individuals low in trait urgency, there is virtually no
relation between the eating expectancy and binge eating. The presence of this interaction is
quite consistent with the nature of each construct: eating to alleviate negative affect should be
much more likely among urgent individuals than among others, and it is.
What we are describing is not a comprehensive model of risk for BN, but it is one
integrated component of such a model. We have offered a specific theory of the integration of
genetic and learned risk, and we have provided empirical support for the theory. Evidence is
consistent with the possibility that trait urgency is an important part of the heritable liability
for BN. We have also shown that individual differences in learning can be understood using
the expectancy concept, and we have demonstrated that expectancies differentiate BN
patients from others and that expectancies predict the onset of BN symptomatology
prospectively among adolescents. We have shown that urgency is a general risk factor for
maladaptive behavior patterns, and that learned expectancies influence the particular form of
rash action one chooses.
There are, no doubt, other aspects to the heritable risk for BN. One likely possibility is
negative affectivity. For urgency (rash action in response to subjective distress) to be active,
there must be negative affect (Fischer et al., in press). Negative affectivity appears to be a
necessary precursor to high levels of urgency, and so heritable dispositions toward negative
affectivity are another part of the heritable liability for BN. Of course, the role of negative
affectivity is different, because it likely influences many more syndromes than does urgency.
Individuals experiencing negative affect, but who are not urgent, likely tend toward
internalizing disorders, such as depression and anxiety. Other individuals experiencing
negative affect tend toward externalizing disorders or rash, maladaptive actions (Krueger et
al., 2002; Krueger, McGue, and Iacono, 2001): they are likely the ones high in urgency
(Fischer et al., in press). So, negative affectivity may be one part of the risk process, but the
risk for BN is increased when urgency is present as well.
In sum, important advances in risk for BN are being made. Evidence from heritability
studies indicating the presence of both genetic and environmental risk factors dovetails nicely
with empirical demonstrations of the roles of heritable urgency and learned expectancies.
Several avenues of investigation may build on this knowledge. What is the precise role of
negative affectivity in this process? What other risk factors are also relevant? For instance, is
it possible that individuals vary in the extent to which endorphins are released via food
consumption, and hence form different expectancies for the mood effects of eating for
biological (rather than environmental) reasons? If the urgency-expectancy integration is
valid, how should one then approach prevention and intervention? Can expectancies be
modified successfully, as appears to be the case with respect to drinking (Darkes and
Goldman, 1993)? Should individuals high in urgency be targeted early for multi-component
prevention programs? On another plane, are any of the same risk factors relevant for anorexia
nervosa (AN), or is AN actually a straightforward genetic disorder not caused by learning (as
suggested by Keel and Klump, 2003)? Are learning factors, such as expectancies, causal for
BN but artifacts of a genetic process for AN? Despite the progress in understanding risk for
BN, there are, clearly, many unanswered questions that require further investigation. The
prospect of addressing them is exciting.
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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 under-
investigated and ignored as health care professionals focus on the general medical,
dietary and psychiatric/psychological needs of patients. Disordered eating and chaotic
lifestyle may affect patterns of caries (decay) and gum disease. Oral microbial flora,
either in dental plaque or saliva, could theoretically differ to normal flora as a
consequence of repeatedly low intra-oral pH secondary to self-induced vomiting (SIV).
Parotid salivary gland enlargement and altered salivary composition have been described.
The presence of gastric acid in the mouth can result in acid erosion, with disfiguring
consequences to the dentition. The impact of anomalous behaviours such as chaotic
eating and self-induced vomiting upon the dental health of eating disordered subjects
may not be apparent to the subjects themselves or their carers, be they physicians,
psychiatrists, psychologists, nurses or relatives. Nonetheless, the effects upon the teeth
can be significant such that it has been postulated that the dentist may be the first health
care professional to suspect an eating disorder in an otherwise healthy individual. The
mouth is the first part of the digestive system and commonly exhibits signs of disease
occurring elsewhere. This chapter reviews the literature and illustrates the clinical
problems faced by real cases. Prevention will also be discussed.
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. Fewer still are the reports in the literature describing oral
lesions related to anorexic or bulimic behaviour.
Vitamin B2 (Riboflavin) deficiency is associated with inflammatory and degenerative
changes in the mucous membranes of the lips and tongue. Angular stomatitis also termed
cheilosis, consisting of red, sore fissures at the angles of the mouth and shiny reddened
mucous membranes are characteristic. The inflamed and sore tongue is termed glossitis
[Cawson, 1991]. There are no recorded cases of this in the eating disorders.
The well described swollen bleeding gums present in Vitamin C deficiency or scurvy are
a very late stage of the disease and have not been described in the eating disorders.
Glossitis and stomatitis are sometimes early changes in nicotinamide deficiency
(pellagra). The tongue tip and lateral borders become reddened, swollen and occasionally
deeply fissured as can the gum margins [Cawson, 1991]. No reports of this in the eating
disorders have been made.
A tongue abscess was described in a 30-year-old female with anorexia who presented
with submandibular tenderness and difficulty swallowing (dysphagia). This was associated
with angular stomatitis, minor apthous ulceration of the lips and tongue depapillation.
Cervical lymphadenopathy was not present but proteinuria was. Blood chemistry revealed a
severe anaemia with a Haemoglobin concentration of 7.0g/dL (normal range 11.5-16.5 g/dL)
and a decreased total plasma protein concentration of 55 g/L (normal range 62-80g/L) [Keith
and Flint, 1989]. Although the abscess was of dental origin, it was an unusual presentation
and the authors believed secondary immuno-deficiency was a predisposing factor. Treatment
included an extraction, intravenous antibiotics and a 5-day course of oral penicillin with anti-
fungal cream for the lip commisures [Keith and Flint, 1989].
Contrary to an anecdotal report, the potential chronic irritation to the oral mucosa from
long term vomiting has not resulted in any reported case of malignant change [Brady, 1980].
Saliva
Saliva has several important functions in the maintenance of oral health. Its proteins have
protective antibacterial, digestive and lubricative actions and, with respect to the mineral
content of teeth, saliva can be supersaturated with calcium and phosphate and thus promote
remineralisation. Furthermore, all the soft tissue membranes such as cheeks and tongue are
covered by protective mucous and the teeth themselves are coated by the acquired salivary
pellicle. The pellicle has a significant role in protecting the tooth from caries and erosion.
The salivary functions of lubrication and neutralization of intra-oral acids also termed
buffering capacity are probably most important during bouts of self-induced vomiting (SIV).
The Impact of Anorexia and Bulimia Nervosa on Oral and Dental Health 187
Initial case reports described salivary parotid gland enlargement in cases of bulimia
[Levin et.al., 1980; Hasler, 1982; Burke, 1986; Taylor and Sneddon, 1987]. Most studies
have investigated function (see below) rather than structure, probably because needle
aspiration biopsy and sialography are invasive procedures. The parotid gland sialogram on an
18-year-old female showed a hypertrophic “leafless tree” pattern and the aspiration biopsy
demonstrated packed acini with few ducts [Hasler, 1982]. Other sialograms performed on a
19-year-old female student [Levin et.al., 1980], the 20-year-old female reported by Burke
(1986) and on the 26-year-old female reported by Taylor and Sneddon (1987) found no
structural abnormality of the gland. It seems that parotid gland enlargement is not a consistent
feature, is usually asymptomatic, although some have noted discomfort and can resolve
spontaneously and is thus episodic in nature. The histological appearance of parotids in
malnourished South Africans was of cellular hypertrophy with accumulation of secretory
granules, nuclear displacement and cellular distention [du Plessis, 1956]. Nutritional mumps
was used to describe the parotid swelling seen in starvation and malnutrition [Batsakis and
McWhirter, 1972]. The mechanism for gland enlargement remains unclear although humoral
transmission between the pancreas and parotid was postulated with changes in serum amylase
[Kakizaki et.al, 1978]. Salivary amylase accounts for 55% of the total serum amylase and the
rest is of pancreatic origin [Gillard et.al., 1983]. Raised salivary amylase in anorexia and
bulimia has been reported [Humphries et.al.,1987; Kronval and Theander 1987; Hempen et
al., 1989]. The severity of abnormal eating behaviours, measured as binge frequency and
SIV, was not correlated with salivary amylase concentration although significant reductions
in amylase levels were found in patients with good treatment outcome but not in those with
poor treatment outcome [Kronvall et.at., 1992]. Stimulated and unstimulated salivary
concentrations of potassium, chloride, calcium, urea nitrogen and albumin were reported to
be within normal values although unstimulated salivary values were measured in only one
subject [Tylenda et.al., 1991].
Although resting salivary flow rates were originally investigated, stimulated salivary
flow is more relevant as salivary flow increases dramatically before vomiting because the
medullary centre that controls vomiting is connected to salivary nuclei [Edgar, 1992]. Any
nausea caused by esophageal and stomach distention after a binge eating episode will further
stimulate salivation. Little is known about the influence of general metabolic disturbance in
eating disordered subjects upon salivary function. Chronic malnutrition in Indian children
reduced stimulated salivary secretion and buffering capacity and the authors speculated that
the low protein diet coupled with low fat favoured reduced salivary buffering capacity
[Johansson et.al., 1992].Others assessed the influence of personality traits on salivary flow
but concluded that psychological factors appeared to have no predictive power on salivation
despite the evidence to show that depression and anxiety can affect salivation [Millar et.al.,
1993].
Flow rate, buffering capacity and pH were assessed in both resting and paraffin-
stimulated saliva in anorexia nervosa [Hellstrom, 1977]. Although a very low resting saliva
rate was reported, this was not statistically significant nor would it be clinically significant as
stimulated saliva is of greater interest. Stimulated flow rates between anorexics, bulimics and
controls were not statistically different, but the mean salivary pH in both eating disorder
188 Alex Milosevic
groups was significantly lower than the control subjects [Liew et.al., 1991;Touyz et.al.,
1993].
Bulimics with and without pathological dental erosion had significantly lower (p<0.01)
mean stimulated saliva flow rates compared to the control group [Milosevic and Dawson,
1996]. Salivary pH was within the normal range whereas the mean bicarbonate concentration
was significantly lower (p<0.01) in the two bulimic groups compared to the control group.
Bulimics with pathological or unacceptable dental erosion had significantly more viscous
saliva compared to bulimics without pathological erosion and the controls see Table 1.
Table 1. Mean whole salivary viscosity measured in Centipoise (cP) according to the
presence or absence of pathological erosion
Group Salivary viscosity, cP

Bulimics with pathological erosion (N=9) 7.39 (3.56)
Bulimics without pathological erosion (N=8) 4.46 (0.43)
Controls (N=10) 4.12 (0.54)
Reduced parotid gland function in bulimia could result in a less watery or serous output
and reduced bicarbonate contribution to whole saliva. Furthermore, a significant reduction in
parotid secretion could result in an increased salivary viscosity because of a proportional
increase in submandibular and sublingual salivary gland secretion which are more viscous
[Milosevic and Dawson, 1996].
A subjective feeling of dry mouth or xerostomia was more frequent among the bulimic
group (34%) than controls (10%) despite there being no difference in stimulated flow rates
[Rytőmaa et.al., 1998].
Overall, salivary function is altered in the eating disorders. There are, however, few
reported cases of significant difficulties associated with this. It seems likely that parotid gland
hypertrophy is episodic but the clinical picture is very varied with some cases of altered
salivary output which is not associated with parotid enlargement.
Periodontal Disease
The supporting structures of the teeth include the bony socket, the cementum layer of the
root and the intervening ligament which, with the overlying gum, are collectively termed the
periodontium. The first stage of periodontal disease is inflammation of the superficial tissues,
the gums or gingivae, manifest as swollen, bleeding gums and called gingivitis. This is
caused by ineffective oral hygiene or plaque control. Chronic gingivitis can be followed by
progress of the inflammatory response to deeper tissues such that bone resorption (loss of
attachment) takes place but in certain resistant individuals gingivitis does not lead to
periodontitis. The inflammation and subsequent loss of attachment is in response to the
microbial flora or dental plaque which may be characterised by specific species or particular
virulence factors such that its chronic progressive nature results in tooth loosening and
eventual tooth loss. Smoking is a co-factor. Hence the importance of correct and effective
oral hygiene procedures which includes tooth brushing ideally with fluoridated toothpaste,
flossing and use of mouth rinses.
The evidence that periodontitis is worse in the eating disorders is conflicting. The initial
studies found unremarkable levels of plaque, gingivitis and periodontitis. Inflammation was
significantly more common in the non-vomiting group than in the vomiting or regurgitating
anorexics [Hurst et.al., 1977]. The presence of plaque and gingivitis was similar in the
vomiters and non-vomiters although periodontal bone loss was not assessed [Hellstrom,
1977; Roberts and Li, 1987]. The approximal plaque index and sulcus bleeding index were
significantly higher in the healthy controls compared to the anorexia and bulimia study
groups but calibration and the degree of reproducibility of the examiners was not stated
although the authors did state that “patients had no loss of attachment” [Philipp et.al., 1991].
One study found that controls had more surfaces with a plaque score of 0 but the anorexics
had significantly more lingual/facial sites with plaque scores of 1 and scores of 2 were similar
between the two groups [Liew et.al., 1991]. The clinical significance of differences in plaque
score and gingivitis around the dental arch is not apparent and probably not important. More
recent results consistently failed to find any difference between plaque, gingivitis and
periodontal disease between eating disordered subjects and controls [Milosevic and Slade,
1989; Altshuler et.al., 1990].
Dental Erosion
Dental erosion is the acid dissolution of tooth substance. It differs to dental caries (decay)
in that it does not involve bacterial or plaque acids but does involve dietary or gastric acids
having a direct effect upon enamel and dentine. Carbonated beverages such as cola drinks,
fresh fruit juices, herbal teas and white wines have been associated with erosion as have fresh
fruit and pickled foods. The increased consumption of these food stuffs increases the risk of
erosion although the epidemiological evidence for this is limited. Gastric acid enters the
mouth secondary to gastro-oesophageal reflux disease (GORD) or during vomiting. Self-
induced vomiting (SIV) is a common purging behaviour in the eating disorders and may
produce a similar pattern of erosion as in subjects with GORD or excessive dietary intake of
acids.
The impact of eating disorders upon oral health was initially reported by Hellstrom
(1977) and Hurst et al. (1977). In of a sample of 39 anorexics, severe lingual-occlusal erosion
was reported in 27 subjects (Hellstrom, 1977) although no attempt was made to correlate
vomiting variables with the outcome of erosion. Furthermore, buccal erosion due to a high
consumption of acid fruits and drinks to relieve thirst was more frequent in vomiting than
non-vomiting subjects. Fresh fruit was eaten in order to induce diarrhoea. The presence or
absence of erosion was related to the duration of vomiting [Simmons et.al., 1986]. Of the 66
females in study sample, 25 (38%) had significant erosion. Eroded teeth occurred in a third of
cases sampled by Roberts and Li (1987) despite the observation that only 65% of the
anorexics vomited compared to all the bulimics.
The strength of association between vomiting variables and the outcome of dental
erosion has been investigated more recently. In 58 subjects with an eating disorder, compared
190 Alex Milosevic
to 50 age-matched controls, significant differences were found between the observed

frequencies in the absence or presence of pathological tooth wear within the various groups,
see Table 2 [Milosevic and Slade, 1989].
Table 2. Number of cases within groups showing

presence or absence of pathological tooth wear
Group 1 Group 2 Group 3 Group 4 Row

Bulimics with SIV Bulimics without SIV Anorexics Controls Totals
Pathological erosion/tooth 14 (42%) 2 (28%) 6 (33%) 3 (6%) 25
wear present
Pathological erosion/tooth 19 (58%) 5 (72%) 12 (67%) 47(94%) 83
wear absent
Column Totals 33 7 18 50 108
It is clear from Table 2 that far more erosion/tooth wear is present in the eating disorder
groups compared to the control group. The within group proportion with erosion was highest
in the vomiting bulimics (group 1) which was also reported in a South African case-control
study published in the same year [Jones and Cleaton-Jones, 1989]. Bulimic patients were also
found to have more severe erosion compared to anorexics although neither the method used
to measure erosion nor the comparison test were stated [Philipp et.al., 1991]. In the study by
Milosevic and Slade, the frequency of SIV, its duration and the product of these two
variables, the total number of vomiting episodes, were not linearly associated (Pearson
correlation coefficient) with dental erosion. Similarly, the severity of erosion was no different
between those who vomited more frequently compared to those that vomited less frequently
[Robb et.at., 1995]. This result was counter intuitive as it would be expected that more
vomiting episodes would lead to increased severity or presence of eroded teeth. Other factors,
therefore, must be involved in determining whether or not erosion occurs.
Table 3. Presence or absence of dental erosion/tooth wear in vomiting bulimics

according to total number of vomiting episodes
Total number of vomiting episodes

<1100 >1100
Pathological tooth wear present 3 11 14
Pathological tooth wear absent 15 4 19
Column total 18 15 33
Chi square = 8.56, p= 0.003; Relative Risk 3.73
Further analysis of the 14 cases in Group 1 found that 11 had 1100 or more vomiting
episodes which forms the basis for Table 3. From the data in Table 3, the Relative Risk is
3.73 (95% CI 1.5, 9.3) for the occurrence of dental erosion if subjects have vomited more
than 1100 times. Similar results were reported by Altshuler et al. [1990]. Vomiting duration
was only moderately associated with the number of eroded teeth (r=0.46, p=0.01) but the
frequency of SIV was not significantly related to dental erosion (r=0.11, ns). The authors did
comment that after six months of SIV most bulimics exhibited one or more eroded tooth
surfaces and that after five years all subjects exhibited some erosion.
The greater severity of erosion in bulimics compared to anorexics was confirmed in a
sample of Australian cases who had six-fold the number of eroded surfaces [Touyz et.al.,
1993].
Both the prevalence and severity of dental erosion were greater in Finnish bulimic
subjects compared to controls [Rytőmaa et al., 1998]. Interestingly, over half the bulimics
had discovered erosion themselves (12 out of 22) and in a quarter of cases the erosion was
diagnosed for the first time by the examiners.
The Distribution of Acid Eroded Teeth
In any one mouth, all the teeth are at risk of erosion, although most workers have
assessed its surface or site distribution and compared it to controls groups [Jones and
Cleaton-Jones, 1989; Milosevic and Slade, 1989; Robb et.al., 1995; Rytőmaa et al., 1998].
The most commonly eroded teeth are the upper incisors. The commonest surfaces to be
severely affected by erosion in subjects with an eating disorder are the palatal (upper inner
sites) and occlusal (the biting top surfaces of bicuspids and molars). These sites are also
eroded in subjects who drink excessive amounts of fruit juice or carbonated beverages and
therefore it can be difficult to determine the relative contributions from intrinsic gastric acid
and extrinsic dietary acid. Mean palatal and labial (front facing sites) exhibited significantly
greater erosion in vomiting anorexics and bulimics compared to abstaining anorexics and
controls [Robb et.al., 1995]. The authors also reported that abstaining and vomiting anorexics
exhibited more lower posterior erosion on buccal (cheek facing surfaces) and occlusal
surfaces than controls. The reason why non-vomiting anorexics had buccal and occlusal
erosion is not clear although Scheutzel [1996] believed that extrinsic acids affected the
buccal and labial surfaces whereas gastric acid from SIV attacked the palatal and occlusal
surfaces. This hypothesis has not been proven and others reported that the etiology of the
erosion could not be ascertained from its location or distribution [Jarvinen et.al., 1992].
Dentine Hypersensitivity
Severe enamel erosion may result in exposed dentine. This can be sensitive to
temperature change and normal activities like tooth brushing and drinking become painful.
Dentine sensitivity may be presenting feature. Its management is discussed later.
Dental Caries (Decay) and Its Difference to Dental Erosion
Dental decay or caries is caused by the bacterial breakdown of fermentable

carbohydrates, most notably sucrose, resulting in acidic metabolic by-products which attack a
susceptible site on a tooth surface. Bacterial plaque acids mainly implicated in the carious
process are lactic, acetic and propionic acids. This is a different process to acid erosion as the
192 Alex Milosevic
teeth become cavitated and require fillings. Erosion by contrast occurs when dietary acids
“bathe” the whole tooth with resultant thinning of the surface rather than a small area of
demineralisation beneath the plaque. Enamel is the initial dental tissue to be involved as it
forms the “cap” or covering of the tooth. A further distinguishing feature of dental decay is
that enamel caries is a sub-surface phenomenon with the body of the lesion having greater
porosity (5-25%) than the surface zone (approximately 1%). Erosion, by contrast, is a surface
development with loss of the original surface tooth substance and porosity or softening of the
remaining surface see Figures 2 and 5. This new surface is more readily worn away by tooth
grinding habits (bruxism), tooth brushing (abrasive processes) and chewing hard foods.
The evidence that dental caries is worse in eating disordered individuals than the normal
population is slightly conflicting. Although caries experience was not different in the 27
vomiters compared to the twelve non-vomiters [Hellstrom, 1977)], others reported non-
vomiters to have less caries experience [Hurst et al., 1977]. The latter authors discussed diet
and recognised that the abnormal eating pattern including bouts of high carbohydrate
consumption would increase the risk of caries. Neither study benefited with a control group
and measures for caries and erosion were not validated. The standard measures for decay,
DMFT (Decayed, Missing and Filled Teeth) and DMFS (Decayed, Missing and Filled
Surfaces) were used by Roberts and Li (1987) who concluded that caries experience between
anorexics and bulimics was no different and believed neither group were more or less
susceptible to dental caries than healthy people. “Clinically detectable” caries occurred in
only two cases out of 66 bulimics examined by Simmons et.al., 1986. The mean DMFS
scores for a bulimic group and age and sex-matched controls were 27.9 and 19.1 respectively,
which was not statistically significant (Jones and Cleaton-Jones, 1989). No difference in
DMFS between eating disorder groups and controls was reported by Milosevic and Slade
(1989), Altshuler et. al. (1990) and Rytömaa et.al. (1998) and for DMFT by Touyz et.al.
(1993). Bulimic individuals had significantly greater DMF-“value” compared to anorexics
and controls, although whether the index related to surfaces or teeth is unclear (Philipp et.al,
1991).
Overall, the literature indicates that dental decay is no worse in eating disordered
subjects compared to controls. This is despite the greater theoretical risk associated with
haphazard eating habits and increased intake of carbohydrates. Perfectionist tendencies or
obsessive-compulsive traits are common in the eating disorders which may manifest as good
oral hygiene practices so reducing the risk of caries.
Microbiology
As discussed in the previous section, dental caries involves microbial plaque acids
attacking the tooth surface. Repeatedly low intra-oral pH from SIV could in theory manifest
as an altered oral microbial flora to more aciduric species [Bretz et.al., 1989]. Streptococcus
mutans and Lactobacilli are cariogenic because they are able to produce acid rapidly from
fermentable carbohydrates. They thrive under acid conditions and adhere tenaciously to tooth
surfaces because not only do they produce acids but very sticky extracellular
polysacchharides [Kidd and Joyston-Bechal, 1987].
The selective serotonin re-uptake inhibitor, fluoxetine or Prozac, has been used to reduce
binge-eating and vomiting. In a double-blind placebo-controlled trial, fluoxetine was
effective in reducing the frequency of bingeing and purging and salivary levels of
Streptococcus sobrinus [Bretz et.al., 1993]. The authors demonstrated that Streptococcus
sobrinus was capable of producing acid at low pH values, whereas other streptococci ceased
acid production. It was believed that Streptococcus sobrinus could be a marker of emetic
activity and therefore instruct carers on compliance with treatment.
Neither Streptococcus mutans nor Lactobacillus counts were any different between
anorexics, bulimics and controls although the authors failed to state whether they cultured
dental plaque or saliva [Touyz et.al., 1993]. Salivary bacterial counts of Streptococcus
sobrinus were statistically higher in the eating disorder group than in the healthy controls
[Bretz et.al., 1989]. Furthermore, salivary levels of Streptococcus mutans, Lactobacilli and
yeast were increased but this was not reflected in greater decay as the DMFS (see above) in
the eating disorder group was actually lower than a high risk caries comparison group [Bretz
et.al., 1989]. These authors offered several explanations for this contradictory result,
including an alteration of microbial virulence secondary to vomiting, reduced risk of decay
because of the older age of onset of bulimia and a protective effect from greater consumption
of dietary fat which protects for decay. None of these possible reasons have been
investigated.
Temporo-Mandibular Joint Function and Tooth Grinding (Bruxism)
Mouth opening, closing and lateral movements are enabled by the jaw joint, termed the
temporo-mandibular joint (TMJ). The TMJ is principally between the articular inferior
surface of the squamous temporal bone and the mandibular condyle. Between the cranially
convex glenoid fossa and the condylar head is an intra-articular collagenous fibrous disc of
variable thickness that completely divides the jaw joint into upper and lower joint
compartments [McKay et.al., 1992]. Detailed description of the TMJ is beyond the scope of
this chapter, but joint dysfunction is a common and well-recognised problem. It is associated
with parafunctional tooth clenching and grinding known by dentists as bruxism. Bruxism is
believed to be a stress relieving mechanism that occurs during sleep in the early hours of the
morning. The extremely high loads imposed across the teeth and the jaw joint result in tooth
wear (attrition) and a clicking joint. If muscle spasm is present, pain can also co-exist with
limited mouth opening. Masseter muscle hypertrophy is a feature of long standing bruxism.
None of the studies on the oral and dental sequelae to the eating disorders have described
TMJ dysfunction as a finding despite the hypothetical risk to the joint from frequent wide
opening of the mouth during bouts of SIV and stress related bruxism. Perhaps acid erosion of
teeth has overshadowed any assessment of dental attrition, which would be difficult to see if
erosion was present.
194 Alex Milosevic
Table 4. The facial, oral and dental problems possibly associated with eating disorders
Non-specific Specific
Dental caries Erosion (secondary to SIV)
Gingivitis Altered oral microbial flora
Chronic Periodontitis Altered salivary function
Temporo-mandibular joint dysfunction including parotid hypertrophy
Bruxism
The Inter-Relationship of Psychological Wellbeing

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

Aspects of Eating Disorders
The bulk of the dental literature regarding anorexia and bulimia focuses on issues of
management whereas few papers discuss the added difficulty of history taking in these cases.
History Taking and Ethical Considerations
Knowledge of eating disorders by dentists was thought to be important as they may be

the first to health care professional to suspect an eating disorder because of the characteristic
oral presentation [Burke et.al., 1996]. Unfortunately in a survey of 100 dentists working in
the county of Kent, England, the general level of knowledge regarding the oral signs of
bulimia was very low [Harwood and Newton, 1995]. This was despite 29% having provided
dental treatment for a sufferer. Moreover, patients diagnosed in dental clinics are often
younger than those seen in eating disorder clinics and hence have a better prognosis for
treatment [Brown and Bonifazi, 1993].
The dental management of patients with anorexia and bulimia can be broadly divided
into intervention and non-intervention. Whichever approach is adopted it must be
sympathetic and non-judgmental [Kidd and Smith, 1993]. A further and potentially more
difficult problem to solve concerns issues of confidentiality and consent [Crossley et.al.,
2001]. Should the dentist suspect an eating disorder and question the patient regarding this, is
it ethical to refer to a medical practitioner? If the patient is an adolescent is it ethical to
inform the child’s parents or guardians that he/she has admitted to an eating disorder? In the
latter situation, if the child is deemed competent a breach of confidentiality would be
unethical, despite the morbidity and mortality associated with the disorder. Referral to
another health care professional would be less of a breach of confidentiality as there is an
understanding of implied consent for any information disclosed during examination which
can be passed on to professional colleagues in order to benefit the patient. Many eating
disorder patients are highly secretive or are too embarrassed to admit they have a problem
and thus disclosure is not forthcoming [Milosevic, 1999]. However, direct communication
with the patient and involvement in all aspects of decision making and treatment planning is
very important otherwise feelings of lack of control may become exacerbated [Crossley et.al.,
2001]. Treatment is unlikely to succeed in a non-compliant and poorly motivated patient.
Another contentious issue for the eating disordered patient is the provision of care in relation
to their disorder. Some have advocated that treatment is withheld or at least the advanced
“comprehensive” procedures are not undertaken until the individual is cured or significant
improvement in vomiting behaviour has been achieved [Faine, 2003]. The ethics of a dentist
withholding treatment for a dental problem are uncertain. Finally, taking a relevant medical
196 Alex Milosevic
history is mandatory and this may identify other medical conditions unassociated with the
eating disorder.
The Examination
Extra-orally, the parotid glands, facial muscles and jaw joint function are checked.
The oral and dental examination should follow a standard protocol for all patients
irrespective of the eating disorder. Soft tissues and gums (gingivae) should be examined prior
to the teeth, lest problems with teeth disrupt a thorough examination of all the mouth. Plaque
and gingivitis should be measured with recognised indices and examiners should be
calibrated for diagnostic accuracy of scoring criteria. Dental erosion and caries are assessed
with the aid of good lighting and dry teeth. Radiographs are usually also required, certainly at
the initial presentation.
Once the dentist has gained all the information, the patient is informed about the oral
condition and discussion can ensue as how best to proceed with treatment.
Non-Interventionist Dental Management
The dentist can make several recommendations to minimise the effect of dietary acid and
vomitus harming the mouth, see Table 5.
If erosion is present, the patient needs to be informed about the causes and given
appropriate advice as to how to reduce its effects. Unless the eroded surfaces are visible,
patients do not usually complain about them. Therefore, once explanation of the causes of
dental erosion are made, its progress can be monitored by way of study casts which require
an impression, photographs or a putty index. A review one year after initial presentation and
comparison with the previously mentioned techniques will help determine if the erosion has
progressed.
Dental decay can be controlled by correct oral hygiene techniques and dietary advice.
Naturally occurring sugars in milk and fruit are virtually non-cariogenic, whereas sucrose,
glucose, fructose and maltose have all been associated with dental decay. Both the frequency
and quantity of sugar intake should be reduced to lessen the risk of decay [Rugg-Gunn,
1996]. The mean intake of diet soda was more than three litres per day in a group of bulimics
resident in an inpatient unit [Hetherington et .al., 1994]. Such drinking patterns and chaotic
eating habits will only serve to increase risk of decay and possibly erosion. Hygienist phase
therapy to professionally remove deposits and instruct on effective plaque control will help
lessen the risk of both periodontal health and caries. Diet sheets are helpful in identifying the
time and pattern of food consumption, but it is unlikely that eating disordered patients would
comply with a request percieved to be too intrusive.
Table 5 Advice to minimise dental problems in eating disorders
Raise awareness of the role of plaque and diet in dental caries:
• The importance of effective plaque control

• Reduction in frequency of intake of sweet foods, snacks etc but balance this with
any programme to improve weight
• Maintain close liaison with dietitician/nutritionist
Raise awareness of acidic sources in the diet:
• Reduce intake of acidic drinks, such as carbonated colas and fresh fruit juice
(low calorie drinks are still potentially erosive)
• Increase consumption of water (carbonated or fizzy water has low erosive
potential)
• Use of a straw will reduce fluid contact with tooth surfaces
• Monitor intake of fresh fruit and especially acidic fruits such as citrus, sour
apples
• Alcohol eg white wine, cider, mixers (tonic and colas)
• Vinegar dressing, pickled foods
Post-vomiting methods to increase pH and improve oral milieu:
• After self-induced vomiting (SIV), chew gum, rinse mouth with water or milk
• Gentle tooth brushing with a small amount of desensitising or bicarbonate tooth
paste after SIV may be safe
Check that medication does not provoke dry mouth or nausea

For salivary hypofunction/dry mouth
• Prescribe neutral artificial saliva or sialogogue pastilles
Toothbrushing after vomiting is generally regarded as inadvisable as the softened,

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

solution whereas greater durability will be achieved by sealing and impregnating the dentine
198 Alex Milosevic
surface with a commercially available un-filled resin. This can only be done in the dental
office.
Placement of Dental Composite Filled Resin
One of the most effective methods of replacing worn/eroded surfaces is by way of

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

teeth getting thinner and shorter, a gap between the upper and lower teeth does not
automatically occur as there is a tendency for teeth to re-establish contact and physically
erupt to maintain contact with opposing teeth. It appears that in some cases the rate of wear
and eruption are equal, although in some individuals it may not occur. This dento-alveolar
compensation causes difficulty when patients wish to regain longer teeth as there is no space
to do so. Space can be gained by the interim use of a Dahl appliance or an anterior bite
platform, which intrudes the anterior teeth and allows eruption of the posterior teeth. This
may take several months and depends on the skeletal and incisal relationships and degree of
space needed for build up of the eroded front teeth.
Case 1
This male, aged 28 years at initial presentation in 1990, was referred to the dental
hospital as he complained of pain and having lost fillings. He was diagnosed with gingivitis,
caries (decay) and erosion although the latter was attributed to acidic drinks. His treatment
included an extraction, both amalgam and tooth coloured restorations as well as hygienist
phase therapy and palatal veneers to the upper four incisors. It was only after this treatment
had been completed that he volunteered he had “psychiatric” problems and had taken an
overdose resulting in hospitalisation. Furthermore, the patient stated he had “regurgitated” for
the previous six years although he had only received treatment for this for six months. His
then medication was Amitryptilline 10mg daily. He attended for review over several years
and at one stage presented with bilaterally enlarged parotid salivary glands which was worse
on the right. During this time the dental erosion progressed, other teeth became carious and at
least one bicuspid became abscessed requiring root canal therapy. By 1996, his medication
changed to Fluoxetine, Chlorpromazine Hydrochloride and Propranolol with cessation of the
Amitryptilline. Unfortunately, he continued to engage in occasional SIV, his oral hygiene
was not well maintained and his dietary intake of sugary food continued. Consequently, teeth
became carious around the existing restorations resulting in larger restorations and the
erosion progressed. The parotid enlargement is illustrated in figure 1 and the appearance of
his teeth is shown in figure 2.
Fig 1. Facial view of bilateral enlarged parotid glands in the male described in Case 1.
200 Alex Milosevic
Fig 2. Intra-oral view of eroded upper teeth in Case 1. Note the proud amalgam restoration indicating that
tooth substance has dissolved from around the amalgam.
Fig 3. The palate appears to have a hematoma probably caused by the fingers traumatising the soft tissues
during bouts of SIV. Female aged 26 years.
Case 2
This patient, a female nurse, was aged 26 years when first seen by the specialist. She was
not taking any medication although she admitted to SIV over a ten year period. Her main
complaint was of the poor dental appearance and inability to incise food because of the
significant erosion to the front teeth, which is shown in figures 4 and 5. She was worried that
the teeth would disappear. On examination, she had good plaque control and a generally
caries free dentition. The upper teeth were very eroded whereas the lower teeth less so.
Indeed, the upper teeth exhibited deeper dentine and the pulps were visible on several teeth,
see figure 5. Despite the significant erosion, dento-alveolar compensation had not occurred,
and it can be seen from figure 4 that space is available to lengthen the short upper incisors.
Fig 4. Front view of Case 2 showing the severely eroded front teeth and the inability of the incisors to meet.
Fig 5. Case 2, palatal view of the upper teeth, showing the pulpal area of the teeth. Sensitivity is likely once
most of the dentine has been eroded away.
It was decided to restore the upper teeth with resin bonded crowns and use a
commercially available kit. This was carried out in stages, with restoration of the upper six
anterior teeth followed by the posterior teeth. Space was not available on three teeth and so
these were left untouched. The patient was delighted with the result and the crowns, although
somewhat experimental at the time of placement, have proven a valuable method of restoring
severely eroded teeth. Follow up several years later revealed the crowns had functioned well,
although the margins had stained as the early bonding resin was permeable to food dyes eg
tea, coffee, red wine etc.
202 Alex Milosevic
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Index
African American women, 177

African Americans, 173
A
age, 6, 9, 10, 14, 28, 42, 45, 46, 53, 92, 93, 98, 99,
acceptance, 8, 12, 45, 48, 49, 52, 54, 55, 56, 135 101, 109, 114, 152, 162, 190, 192, 193
access, 51, 53, 102, 161, 163 aggression, 97, 98, 100
accommodation, 54 aggressive behavior, 9, 95, 96, 100
accountability, 58 aging, 72, 85
accounting, 46, 151, 169 agonist, 76
acculturation, 50 albumin, 79, 187
accumulation, 187 alcohol, 5, 6, 7, 10, 11, 13, 14, 96, 100, 101, 167,
accuracy, 156, 173, 196 168, 170, 175, 177, 178, 179, 181, 182, 183
achievement, 15 alcohol abuse, 7, 10, 11, 14, 101, 167, 168, 170
acid, xi, 73, 78, 79, 83, 85, 185, 189, 191, 192, 193, alcohol consumption, 96, 167, 183
196, 198 alcohol problems, 182
activation, 65, 73, 76, 79, 182 alcohol use, 167, 168, 175, 177
adaptation, 12, 26, 31, 124, 141 alcoholics, 178
adenosine, 78, 89 alienation, 5
adhesion, 198 alternative, 32, 48, 49, 173
adipose, 75 amalgam, 199, 200
adiposity, 69 ambivalence, 99
adjustment, 12, 15 ambivalent, 14
adolescence, 9, 12, 15, 21, 22, 92, 173, 182, 194 amenorrhea, 92
adolescent drinking, 174 American Psychiatric Association, 136, 156, 177
adolescent female, 156, 157, 172, 180 American Psychological Association, 157, 177
adolescents, 5, 7, 8, 12, 13, 14, 18, 20, 22, 23, 24, amino acids, 79, 83, 89, 142
26, 92, 93, 94, 95, 96, 100, 102, 103, 107, 137, amylase, 187, 202, 203
140, 176, 182 anemia, 83
adulthood, 12, 22, 114, 194 anger, 11, 16, 98
adults, 2, 13, 85, 89, 146, 158, 161, 204 animals, 74, 76, 177, 183
advertisements, 183 annihilation, 2
advertising, 179, 183 anorexia, vii, viii, ix, 1, 3, 4, 5, 6, 7, 8, 9, 10, 13, 15,
aesthetics, 194, 198 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29,
affect, xi, 6, 24, 50, 87, 93, 94, 95, 157, 162, 163, 31, 32, 33, 34, 37, 38, 39, 41, 42, 43, 44, 45, 46,
166, 168, 170, 173, 174, 176, 177, 178, 182, 183, 47, 50, 51, 52, 53, 54, 55, 57, 58, 59, 61, 63, 64,
185, 187, 194 65, 66, 67, 68, 69, 71, 72, 73, 74, 75, 76, 77, 78,
affective disorder, 3, 26 79, 80, 82, 83, 85, 86, 87, 89, 90, 91, 92, 93, 94,
206 Index
96, 101, 102, 103, 107, 113, 136, 137, 138, 139, 95, 96, 97, 98, 100, 106, 108, 109, 110, 111, 112,
140, 142, 156, 161, 177, 186, 187, 189, 194, 195, 113, 115, 116, 120, 122, 123, 124, 125, 127, 133,
202, 203, 204 134, 135, 136, 137, 138, 139, 140, 142, 143, 159,
ANOVA, 113 160, 161, 166, 167, 168, 169, 170, 171, 172, 174,
antagonism, 76 175, 176, 177, 178, 179, 180, 181, 183
antidepressant, 3, 17, 24 behavior modification, 177
antisocial behavior, 8, 180 behavior therapy, x, 95, 106, 139, 178
antisocial personality, 8, 181 behavioral aspects, 37
anxiety, 3, 6, 16, 18, 34, 35, 101, 134, 162, 170, 176, behavioral change, 134
179, 187 behavioral sciences, 156
anxiety disorder, 6, 18 beneficial effect, 65
apoptosis, 78, 88 benign, 67
appetite, 31, 32, 64, 66, 67, 68, 69, 72, 78, 81, 82, beverages, 189, 191
83, 84, 88, 89, 92, 93, 97, 115, 117, 133 bias, 37, 132
appraisals, 141 bicarbonate, 188, 197
argument, 160, 165, 175 bicuspid, 199
arson, 100 binding, 79, 84
Asia, 42 bingeing, 180, 193
aspiration, 187 biological responses, 75
assessment, 33, 34, 36, 37, 66, 68, 84, 132, 133, 134, biopsy, 187
136, 142, 149, 155, 156, 157, 167, 168, 193 blame, 102
association, 7, 15, 151, 152, 163, 189 bleeding, 186, 188, 189
asthenia, 89 blocks, 97
asymptomatic, 127 blood, 71, 79
ATP, 78, 89 blood-brain barrier, 79
attachment, 95, 102, 188, 189 BMA, 161, 178
attacks, 94 BMI, vi, vii, x, 1, 92, 101, 110, 113, 114, 128, 129,
attention, 52, 56, 68, 71, 73, 77, 100, 135, 146 145, 147, 149, 151, 152, 154
attitudes, viii, ix, 5, 8, 23, 41, 54, 56, 105, 106, 109, body, vii, viii, ix, x, 1, 3, 4, 7, 9, 11, 12, 15, 17, 23,
112, 113, 122, 125, 127, 132, 134, 135, 136, 137, 25, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 41,
180, 183 42, 50, 56, 57, 70, 75, 77, 78, 80, 85, 91, 92, 93,
attractiveness, 161, 162, 171, 204 94, 97, 98, 99, 110, 111, 112, 113, 116, 123, 125,
Australia, 41, 47, 58 127, 128, 129, 132, 134, 135, 136, 141, 142, 143,
authority, viii, 41, 49, 53, 56, 57, 58 145, 146, 147, 148, 149, 151, 152, 153, 154, 155,
autonomy, 12, 15, 99, 102 157, 158, 161, 162, 163, 164, 168, 171, 172, 177,
autopsy, 20 178, 179, 181, 183, 184, 192, 194
availability, 57, 65, 71, 76, 79, 86 body dissatisfaction, x, 123, 127, 132, 145, 146, 147,
avoidance, 92, 101, 166 148, 151, 152, 153, 154, 155, 157, 161, 162, 163,
awareness, 12, 42, 97, 114, 164, 171, 179, 197 164, 171, 172, 183, 184
body fat, 70, 80, 155
body image, vii, viii, ix, 5, 9, 25, 27, 28, 29, 30, 31,
B
32, 33, 35, 36, 37, 42, 91, 92, 93, 110, 111, 112,
123, 125, 127, 128, 129, 135, 136, 141, 142, 143,
Barbados, 136
157, 161, 178, 194
bargaining, 44, 47, 60, 61
body mass index, vii, 1, 7, 129
barriers, 111
body shape, 4, 28, 34, 116, 146, 147, 155, 162, 181
barter, 44
body size, 123, 127, 145, 148, 161, 179
basic research, 140
body weight, 28, 35, 75, 77, 78, 85, 92, 123, 128,
Beck Depression Inventory, 30, 32, 38
145, 146, 148, 149, 153, 155, 177
behavior, vii, x, 1, 2, 3, 5, 6, 8, 9, 10, 11, 12, 13, 14,
bonding, 23, 198, 201
15, 18, 19, 20, 21, 22, 24, 25, 35, 37, 92, 93, 94,
Index 207
bonds, 93, 99 classroom, 139

borderline personality disorder, 4, 5, 8, 10, 19, 23, cleavage, 72
25, 153, 156 clients, 166
boredom, 170, 173, 174 clinical assessment, 142, 145
bowel, 82 clinical disorders, 102
boys, ix, 14, 15, 91, 92, 93, 94, 99, 101, 103, 194 clinical judgment, 22
bradycardia, 92 clinical presentation, 39
brain, 64, 70, 71, 73, 75, 76, 79, 80, 86, 87, 90, 140 clinical psychology, 25
Brazil, ix, 105, 106, 107, 114 clinical trials, 17, 68, 77, 81
breakdown, 191 cluster, 3, 7
breathlessness, 67 cluster analysis, 4
bulimia, vii, viii, ix, x, 1, 3, 4, 7, 9, 10, 11, 13, 15, cocaine, 70, 74, 167, 178
17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, coding, 132
31, 32, 33, 34, 37, 38, 39, 61, 91, 93, 94, 95, 102, coenzyme, 73, 85
105, 107, 109, 130, 136, 137, 138, 139, 140, 141, coercion, 44, 45, 46, 50, 57
142, 143, 156, 157, 159, 162, 173, 179, 180, 182, cognitive biases, 24
183, 187, 188, 189, 193, 194, 195, 202, 203, 204 cognitive map, 169
cohort, 6, 67, 89
collaboration, 13, 97
C
combination therapy, 88
commercials, 163
cachexia, 68, 72, 74, 78, 80, 87, 88, 89, 90
common symptoms, 66
calcium, 112, 120, 186, 187
communication, 12, 13, 16, 47, 85, 195
calibration, 189
community, 2, 14, 21, 38, 44, 48, 49, 51, 52, 54, 59,
caloric intake, 72, 79, 89, 163
148, 149, 157
calorie, 65, 72, 79, 92, 197
comorbidity, 3, 10, 18, 21, 22, 23, 25, 39, 94, 137,
Canada, 11, 60, 88
158
cancer, viii, 63, 64, 65, 66, 67, 68, 69, 71, 72, 74, 75,
Comparative Fit Index, 174
76, 77, 78, 79, 81, 82, 83, 84, 86, 87, 88, 89
compatibility, 36
cancer cells, 82
compensation, 198, 201
candidates, 79
competitive sport, ix, 91
cannabinoids, 77
complexity, 69, 73, 134
carbohydrate, 72, 119, 142, 192
compliance, 22, 44, 49, 56, 60, 193
case study, 45
complications, 6, 46, 139, 203, 204
cell, 82, 89, 90
components, 13, 37, 79, 108, 133, 151, 154
central nervous system, 66, 82
composition, xi, 72, 111, 117, 185
ceramic, 198, 204
comprehension, 3
CFI, 173
compulsion, 35, 97
chemotherapy, 83
compulsive behavior, 37, 98
childhood, 7, 93, 101
concentration, 4, 80, 84, 186, 187, 188
children, 12, 13, 14, 23, 24, 26, 93, 96, 98, 99, 101,
conceptual model, 60
102, 107, 142, 163, 173, 177, 179, 183, 187, 194,
conceptualization, 151
202, 203
concordance, 160
cholesterol, 142
conduct, 4, 6, 8, 9, 16, 50, 173
chronic irritation, 186
conduct disorder, 8
chronic obstructive pulmonary disease, 64
confidence, 17, 107, 124, 154, 155
chronic renal failure, 71, 75, 76
confidence interval, 107, 154, 155
chronic stress situations, 93
confidentiality, 195
cirrhosis, 64, 83
configuration, 150, 151
civil liberties, 56
conflict, 93, 94, 98, 99, 101, 102
classification, 36, 101, 113, 127, 173
208 Index
conflict avoidance, 93, 94 decision making, viii, 2, 195

conformity, 60 decisions, 43, 46, 54, 94, 102
confrontation, 138 defense, 82, 97
consciousness, 157 deficit, 117
consensus, 36, 147 definition, 2, 42, 65, 109, 116
consent, viii, 41, 46, 47, 48, 57, 195 delusion, 35, 36
conspiracy, 54 delusions, 28, 36, 39
consumers, 50, 107, 164 demographic change, 106
consumption, 106, 108, 110, 112, 113, 116, 117, demographic data, 148
119, 120, 132, 134, 163, 167, 177, 179, 189, 192, denial, ix, 12, 28, 51, 55, 91, 93, 125
193, 196, 197 Denmark, 8, 19, 139
consumption patterns, 106 density, 99, 142
context, 35, 36, 42, 49, 53, 146, 162, 163, 164, 179 dental caries, 189, 192, 203
continuity, 14 dental plaque, xi, 185, 188, 193
control, vii, viii, 1, 4, 5, 6, 16, 18, 20, 22, 32, 33, 34, dentist, xi, 185, 195, 196
38, 41, 43, 49, 50, 51, 52, 53, 56, 57, 58, 66, 73, Department of Health and Human Services, 23
76, 80, 84, 99, 102, 117, 120, 123, 124, 128, 133, dependent variable, 150, 151
141, 149, 150, 163, 167, 173, 174, 178, 188, 190, depolarization, 76
192, 194, 196, 197, 200 depression, 3, 8, 9, 10, 12, 15, 22, 24, 37, 46, 66, 93,
control group, 120, 188, 192 94, 95, 176, 187, 194
controlled trials, 17, 81 depressive symptoms, 4, 9, 18
convergence, 54, 163 deprivation, 101, 177
conversion, 60 derivatives, 78
conviction, 31, 36, 37 desire, 54, 65, 114, 123, 172
COPD, 65, 67 detention, 50
coping, viii, 2, 12, 94, 134, 179 developed countries, vii, 13, 107, 108, 109, 114
correlation, 113, 128, 129, 146, 152, 153, 155, 190 developed nations, ix, 105
correlation coefficient, 113 deviation, 150, 154
corticosteroids, 77, 78 diabetes, 71
corticotropin, 74 diabetic patients, 82
costs, 94 Diagnostic and Statistical Manual of Mental
counseling, 111, 135, 139 Disorders, viii, 27, 28, 110, 136, 177
covering, 192 diagnostic criteria, viii, 6, 27, 28, 93, 116, 133, 148
crisis management, viii, 2 dialysis, 71, 84, 86
critical period, 181 diet, ix, 34, 35, 79, 105, 106, 108, 111, 112, 115,
criticism, 94 117, 120, 122, 123, 125, 128, 134, 137, 163, 164,
cross-sectional study, 119 187, 192, 196, 197, 203
CSF, 76, 86, 87 dietary fat, 193
culture, 134, 163, 164, 171, 175, 180, 184 dietary habits, ix, 64
currency, 51 dietary intake, 189, 199
cycling, 96, 114 dieting, 39, 114, 115, 123, 133, 156, 160, 161, 162,
cytokines, ix, 63, 75, 76, 77, 78, 84 163, 164, 165, 170, 171, 172, 173, 174, 175, 179,
180, 182, 184, 204
differentiation, 61, 112
D
digestion, 65, 68, 71
direct measure, 147
data analysis, 151
disabilities, 101
death, vii, viii, 1, 2, 4, 5, 9, 10, 13, 14, 15, 16, 19,
disability, 101
25, 41, 42, 64, 67, 69, 80, 84, 88, 99
disaster, 19
death rate, viii, 41
discipline, 96
decay, xi, 185, 189, 191, 192, 193, 196, 199
Index 209
disclosure, 195
E
discomfort, 35, 125, 153, 187
disorder, ix, x, xi, 3, 6, 7, 8, 9, 10, 14, 16, 17, 18, 20,
eating, vii, viii, ix, x, xi, 1, 2, 3, 6, 7, 8, 9, 10, 11, 14,
21, 22, 23, 25, 26, 29, 37, 38, 39, 45, 51, 53, 57,
15, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28,
86, 91, 92, 93, 94, 96, 97, 99, 100, 101, 102, 107,
29, 30, 32, 34, 39, 41, 42, 45, 51, 53, 56, 57, 65,
108, 109, 113, 114, 116, 120, 128, 131, 134, 135,
67, 68, 69, 71, 91, 92, 93, 94, 95, 97, 100, 101,
136, 137, 138, 141, 143, 145, 146, 147, 148, 153,
102, 103, 105, 106, 107, 108, 109, 110, 111, 112,
155, 156, 157, 158, 160, 161, 162, 163, 164, 169,
113, 114, 115, 116, 117, 120, 122, 123, 124, 125,
171, 174, 175, 177, 178, 181, 183, 185, 187, 189,
127, 128, 130, 131, 132, 133, 134, 135, 136, 137,
190, 191, 192, 193, 194, 195, 196
138, 139, 140, 141, 142, 143, 145, 146, 147, 148,
displacement, 187
150, 153, 154, 155, 156, 157, 158, 159, 160, 161,
disposition, 161, 176
162, 163, 164, 165, 166, 167, 168, 169, 170, 171,
dissatisfaction, x, 4, 12, 28, 127, 128, 137, 145, 146,
172, 173, 174, 175, 176, 177, 178, 179, 180, 181,
147, 148, 150, 153, 154, 155, 161, 162, 163, 164
182, 183, 184, 185, 186, 187, 188, 189, 190, 191,
dissociation, 74, 195
192, 193, 194, 195, 196, 197, 202, 203, 204
distress, x, 2, 3, 7, 32, 33, 58, 102, 133, 147, 153,
eating disorders, vii, viii, ix, 1, 2, 3, 7, 8, 10, 11, 14,
155, 159, 165, 166, 169, 175, 176, 179
15, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28,
distribution, 31, 119, 125, 126, 191, 204
29, 30, 39, 42, 91, 92, 93, 94, 95, 97, 101, 102,
diuretic, 133
103, 107, 109, 114, 134, 135, 136, 137, 138, 139,
diversity, 44
140, 141, 143, 145, 146, 147, 148, 153, 155, 156,
divorce, 9, 47, 60
157, 158, 162, 167, 170, 176, 177, 179, 180, 181,
dizygotic, 160, 166
186, 188, 189, 192, 193, 194, 195, 197, 202, 203,
dizygotic twins, 160, 166
204
DMF, 192
ego, 94
docosahexaenoic acid, 78
eicosapentaenoic acid, 78, 88
doctors, 45, 53, 54
elderly, 79, 83
domain, 166, 178
electrolyte, 92
domestic violence, 100
emergence, 53, 102, 156, 159
dopamine, ix, 63, 81, 87
emotion, 2, 166
dosage, 6, 81
emotional disorder, 100
down-regulation, 78
emotional distress, 147
dream, 123, 124
emotional state, 4, 93
drinking pattern, 178, 196
emotions, ix, 2, 91, 97, 111, 166
drinking patterns, 178, 196
empathy, 16
drug abuse, 6
employment, 11
drug therapy, ix, 64, 69
encouragement, 163
drugs, 3, 6, 14, 80, 81, 107, 130, 140
endocrine, 89, 92
DSM, viii, x, 7, 20, 23, 25, 26, 27, 28, 29, 42, 92, 93,
endorphins, 177
106, 110, 115, 148, 149, 150, 156, 165, 180
endorsements, 172
DSM-II, 7, 20, 23, 25, 26, 29
energy consumption, 108, 117, 131
DSM-III, 7, 20, 23, 25, 26, 29
England, 22, 60, 178, 195
DSM-IV, viii, x, 25, 27, 28, 29, 93, 106, 110, 115,
enlargement, xi, 185, 187, 188, 199, 202, 203
148, 149, 150, 156, 165
entanglements, 102
duodenum, 71
enthusiasm, 99
durability, 197
environment, x, 14, 16, 45, 49, 56, 57, 77, 95, 99,
duration, 7, 45, 53, 80, 111, 116, 135, 140, 189, 190
159, 161, 163, 164, 180, 202
dysphagia, 66
environmental effects, 161, 164
environmental factors, x, 2, 159, 161, 162, 164, 168,
175
environmental impact, 16
210 Index
environmental influences, 160, 180 feedback, 71, 75

enzymes, 71 feelings, 4, 5, 12, 16, 55, 94, 99, 101, 108, 109, 112,
epidemic, vii 122, 123, 124, 125, 132, 133, 134, 135, 155, 195
epidemiology, 139, 180, 183 females, 5, 6, 31, 107, 189
erosion, xi, 185, 186, 188, 189, 190, 191, 192, 193, femininity, 162
196, 197, 198, 199, 200, 203, 204 fermentable carbohydrates, 191, 192
ethics, 57, 195 fibers, 71
ethnicity, 179, 184 filler particles, 198
etiology, 145, 157, 179, 180, 191 Finland, 7
Euro, 202 fish, 88
Europe, 2, 24, 42, 65 fish oil, 88
everyday life, 56 fixation, 194
evidence, viii, 5, 9, 15, 17, 34, 36, 60, 63, 71, 73, 74, flora, xi, 185, 188, 192, 194
75, 81, 82, 85, 136, 160, 161, 162, 163, 164, 165, fluctuations, 117, 123
166, 167, 168, 173, 174, 178, 182, 187, 189, 192 fluid, 76, 78, 197
evolution, 67, 113, 126, 127 fluoxetine, 17, 20, 24, 193, 202
examinations, 93 focusing, 155, 165
excitation, 87 food, vii, viii, ix, 30, 52, 53, 63, 64, 65, 66, 67, 68,
exclusion, 37, 80 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 80, 81, 84,
exercise, 42, 49, 50, 92 85, 86, 87, 88, 92, 93, 95, 98, 101, 105, 106, 108,
experimental design, 169 110, 111, 112, 113, 117, 122, 123, 124, 125, 128,
experts, 50 131, 132, 133, 134, 135, 137, 138, 139, 141, 142,
exposure, 13, 15, 171 162, 163, 164, 170, 173, 177, 178, 179, 189, 196,
expression, ix, 12, 35, 43, 49, 50, 51, 56, 64, 74, 98, 199, 200, 201
100, 102, 124, 164 food intake, viii, x, 63, 64, 65, 66, 67, 68, 69, 70, 71,
externalization, 180 72, 73, 74, 75, 76, 77, 78, 80, 81, 84, 85, 86, 87,
externalizing disorders, 176 106, 108, 110, 111, 117, 131, 132, 133, 134, 138,
extraction, 186, 199 173
extraversion, 166 food products, 163
freedom, 50
friends, 44, 48, 49, 55, 100, 171
F
friendship, 68
fructose, 196
facial expression, 97
fuel, 85
facial muscles, 196
fulfillment, 99
factor analysis, 151, 165, 166
failure, viii, 6, 15, 32, 52, 63, 64, 65, 68, 74, 76, 79,
81, 83, 84, 86, 87, 147, 156, 176 G
family, 2, 9, 12, 13, 16, 23, 24, 34, 36, 42, 43, 44,
48, 49, 53, 54, 55, 83, 93, 94, 96, 97, 98, 99, 100, gambling, 167, 169, 170, 175, 179, 181, 183
101, 102, 148, 173, 179 gastrointestinal tract, 72, 75
family conflict, 93 GATT, 61
family environment, 12 gender, vii, 1, 92, 94, 102, 136, 141, 161, 162, 181
family members, 36, 48, 49, 83, 99 gender identity, 136
family therapy, 96, 97, 98, 99, 102 gene, 72, 160
fast food, 120, 163 genes, 159
fasting, 28, 30, 34, 35, 37, 42, 92, 115, 123, 130 genotype, 164
fat, 4, 30, 32, 33, 35, 36, 72, 73, 77, 85, 93, 98, 122, Germany, 8
123, 124, 142, 163, 187 gestures, 2, 8
fatty acids, 142 gingivitis, 188, 189, 196
fear, 4, 16, 30, 36, 92, 94, 97, 98, 99, 108, 123
Index 211
girls, ix, 3, 14, 15, 58, 64, 91, 92, 94, 101, 135, 146, Hong Kong, 139
153, 162, 181, 183, 194 hopelessness, 15
gland, xi, 185, 187, 188 hormone, 69, 72, 74, 81, 89
globalization, 106 hospice, 69, 84
glossitis, 186 hospitalization, 68, 101
glucose, 82 host, 65, 82
goals, 111, 117 human subjects, 83
governance, viii, 42, 50, 57 hyperglycemia, 82, 89
grades, 15 hypertrophy, 187, 188, 193
granules, 187 hypothalamus, ix, 64, 69, 70, 71, 72, 74, 75, 76, 81,
group therapy, 97, 143 86, 87
groups, viii, x, 4, 5, 6, 28, 29, 30, 31, 32, 33, 34, 36, hypothesis, 10, 69, 70, 72, 79, 81, 86, 148, 153, 173,
37, 49, 50, 56, 75, 80, 90, 107, 133, 136, 145, 183, 191
148, 151, 152, 153, 154, 155, 157, 173, 188, 189,
190, 191, 192, 194, 197, 202
I
growth, 82, 89, 93, 183
growth hormone, 89
iatrogenic, 16
guidance, 111
ICD-, 92, 93, 100
guidelines, 111, 125
idealization, 162
guiding principles, 162
ideas, 35, 36, 39, 111
guilt, 3, 15, 94, 99, 101, 120, 181
identification, 7, 51, 55, 170
guilty, x, 95, 99, 106, 120, 122, 132, 133
identity, viii, ix, 11, 42, 43, 49, 54, 55, 56, 57, 59,
gut, 73, 85
91, 94, 102, 150, 152, 153
idiosyncratic, 36
H IL-6, ix, 63
imagery, 53
hands, 95 immune response, 78
harm, 4, 6, 13, 97 immune system, 65
hate, 5, 108, 124 immunomodulatory, 78
HE, 86, 88 implementation, 111, 157
healing, 15 impulsive, 10, 18, 20, 165, 166, 179
health, xi, 2, 12, 13, 14, 18, 26, 43, 44, 45, 46, 49, impulsiveness, 10, 181
50, 51, 54, 59, 60, 68, 80, 106, 114, 135, 138, impulsivity, 6, 10, 11, 23, 26, 165, 166, 167, 168,
177, 183, 185, 186, 189, 195, 196, 202, 203 179, 181
health care, xi, 2, 26, 44, 50, 68, 114, 185, 195, 202 in vitro, 79, 88
health care professionals, xi, 50, 68, 185 incidence, 9, 10, 89, 94, 95, 107, 164
health problems, 186 independence, 12, 101, 102
health psychology, 60 independent variable, 113
health services, 14 indication, 45, 94
health status, 135, 203 indicators, 8, 11, 15, 161
heat, 65 indices, 80, 196
heat loss, 65 individual differences, 163, 165, 170, 171, 175, 176
height, 149 induction, 13
hematoma, 200 infants, 202
hemodialysis, 67, 68, 79, 83, 85, 87 inflammation, 71, 83, 84, 88, 188
heritability, xi, 159, 160, 166, 176, 181 influence, 15, 28, 47, 52, 68, 69, 71, 73, 75, 76, 79,
high fat, 72 82, 84, 85, 116, 162, 169, 171, 172, 174, 176,
high school, 107 177, 179, 187, 194, 204
hip, 16 informed consent, 56, 110
homeostasis, 12, 73 ingestion, 72
212 Index
inhibition, 4, 70, 73, 75, 77, 78, 182 judgment, 14, 117
inhibitor, 22, 74, 90, 193 jurisdiction, 45
initiation, 15 justification, 59
injury, 11
input, 75, 135
K
insecurity, 93
insight, 31, 35, 36, 43, 46, 49, 52, 53, 65
kindergarten, 93, 96
instability, 4, 152, 153
knowledge, 17, 127, 134, 141, 154, 176, 195
institutions, 57
instruments, 29, 30, 43, 110, 172
insulation, 54 L
insulin, 71, 82, 84, 85, 89
integration, 37, 164, 165, 175, 176, 177 lack of control, 5, 28, 109, 134, 195
intensity, 97 language, 55, 56, 57, 181
intent, 10, 159 Latin America, 140
intentions, 94 laws, 43, 45
interaction, 2, 34, 49, 55, 100, 164, 165, 168, 176, lawyers, 48, 56
203 laxatives, 9, 120
interaction effect, 165 lead, 12, 54, 56, 68, 69, 78, 81, 133, 147, 160, 163,
interaction effects, 165 164, 169, 170, 172, 173, 175, 188, 190, 194
interactions, viii, 41, 51, 56, 57, 75 lean body mass, 80, 84
interdependence, 65 learning, viii, 14, 41, 56, 101, 160, 165, 169, 170,
interest, 12, 13, 65, 72, 81, 92, 108, 109, 110, 146, 171, 172, 174, 175, 176, 177, 182
187 learning process, 172
interface, 28 legislation, 43, 57
internalised, 54, 56 lens, 55, 59
internalization, 147, 156, 162, 163, 164, 171, 174, leptin, ix, 63, 69, 70, 71, 73, 84, 85, 86
179, 180 lesions, 186
internalizing, 176 liability, x, 159, 161, 164, 168, 175, 176
interpersonal processes, 170 libido, 101
interpersonal relations, 16 life course, 52
interpretation, viii, 41, 57, 58, 154 life span, 19, 181
interval, 130, 131 lifestyle, xi, 53, 54, 185
intervention, viii, 6, 17, 24, 41, 51, 56, 57, 96, 109, lifetime, ix, 4, 6, 9, 10, 13, 29, 39, 91
110, 127, 133, 134, 136, 137, 177, 182, 195 ligament, 188
interview, 29, 52, 110, 167, 168 likelihood, x, 159, 169, 175
intimacy, 102 limitation, 80, 168
intravenous antibiotics, 186 linkage, 198
invading organisms, 65 links, 23
Iran, 140 lipids, 88, 108, 117
Ireland, 20 liquids, 95
iron, 112, 120 listening, 16
isolation, 2 liver, viii, 63, 64, 65, 67, 71, 76, 79, 80, 85, 87, 88
Israel, 18, 58 liver cirrhosis, 64, 65, 67, 76, 79, 87
Italy, 1, 9, 11 liver damage, 88
liver disease, 71, 85
liver failure, 67
J liver function tests, 80
location, 191
Japan, 7, 23
loneliness, 15
jobs, 162
longitudinal study, 173, 202
Index 213
loss of appetite, 64 menstruation, 42

loyalty, 100 mental disorder, 8, 20, 21, 22, 37, 156, 180
lumen, 71 mental health, 5, 43, 44, 45, 46, 53, 57, 58, 59
lung cancer, 67, 83, 85, 89 mental health professionals, 5
lung disease, 67 messenger RNA, 86
lying, 9, 50 meta analysis, 160, 168
lymph, 186 metabolism, 68, 73, 82, 85, 89
lymphadenopathy, 186 methodology, 31, 157
microinjection, 75
Middle East, 42
M
milk, 100, 196, 197
minority, 65
magazines, 111, 161
misconceptions, 112, 123, 133
magnesium, 112, 120
modeling, 56, 170, 173, 175, 183
major depression, vii, 1, 4, 18
models, 20, 73, 74, 75, 76, 90, 111, 162, 164, 169,
malaise, 2
171, 174
males, 2, 102, 170
moderators, 115
malnutrition, viii, 36, 63, 64, 67, 68, 106, 187, 202,
mold, 50
203
molecules, 17, 78
malocclusion, 194
monitoring, 13, 18, 203
maltose, 196
monozygotic twins, 160, 166
management, viii, 16, 26, 41, 43, 44, 45, 47, 48, 49,
mood, 3, 6, 17, 18, 98, 155, 177, 180, 183
50, 51, 52, 54, 56, 59, 63, 65, 68, 88, 89, 141,
mood disorder, 3, 6, 17
142, 191, 195, 202, 203
morale, 16
manipulation, 44
morbidity, viii, 42, 63, 68, 69, 82, 139, 195
mapping, 45
mortality, viii, 5, 19, 23, 42, 63, 65, 68, 69, 82, 89,
marijuana, 78
195
mass, 15, 73
mortality rate, 65
mass media, 15
motivation, 13, 82, 123, 141, 181
matrix, 151, 178
motor behavior, 169
meals, x, 77, 93, 101, 106, 109, 111, 112, 113, 116,
moulding, 55
117, 118, 119, 120, 121, 122, 125, 126, 130, 131,
movement, 2, 101
132, 134, 138
movement disorders, 101
meanings, 36, 111, 134
mRNA, 74, 75
measurement, 110, 111, 130, 142, 165, 168
MTMM, 167
measures, 43, 44, 45, 56, 57, 84, 110, 112, 129, 133,
mucosa, 186
134, 138, 148, 150, 152, 153, 163, 165, 166, 167,
mucous membrane, 186
168, 171, 172, 173, 174, 178, 180, 182, 192
mucous membranes, 186
meat, 66
multidimensional, 2, 103, 138
media, 15, 24, 161, 162, 163, 183
multiple regression, 174
media messages, 163
multiple sclerosis, 96
median, 112, 114, 115, 116, 117, 118, 121, 127, 133
mumps, 187
medical expertise, viii, 41, 57
mutual respect, 55
medication, 17, 98, 183, 197, 199, 200
melanocyte stimulating hormone, 74
melt, 123 N
melts, 122
membranes, 186 narcissistic personality disorder, 22
memory, 179, 183 National Research Council, 140
men, ix, 7, 85, 91, 92, 93, 94, 101, 103, 141, 146, nausea, 68, 81, 100, 187
155, 173, 178, 183
214 Index
needs, xi, 15, 68, 71, 74, 83, 93, 94, 102, 116, 125, orientation, 12, 93, 94, 101
135, 142, 185, 196, 198 oscillation, 114
negative affectivity, 166, 168, 176, 182 outliers, 150
negative consequences, 44 output, 188
negative mood, x, 155, 159, 166, 167, 179 overweight, 129, 146, 163
negative reinforcement, 173 oxidation, 73, 85
negotiation, 47
nerve, 72
P
nervous system, 71, 72, 84
nervousness, 134
Pacific, 25
network, 55, 75, 178, 183
pain, 2, 15, 193, 199
neurons, 71, 73, 74, 76, 87
palliative, 65, 82, 83, 84
neuropeptides, ix, 63, 75, 87
pancreas, 72, 187, 203
neuroticism, 166, 167, 168
parameter, 113, 151
neurotransmitter, 71, 75
parental authority, 12
neurotransmitters, ix, 63, 75
parental involvement, 20
New South Wales, 45, 47
parenting, 13, 18
New Zealand, 18, 58, 59, 61
parents, ix, 13, 15, 24, 26, 42, 91, 95, 96, 97, 98, 99,
newspapers, 64
100, 101, 102, 195
nicotinamide, 186
parotid, 187, 188, 194, 196, 199, 202, 203
nicotine, 101
parotid gland, 187, 188, 203
nitric oxide, 75, 82, 90
partition, 160
nitric oxide synthase, 82, 90
passive, 71
nitrogen, 187
pathogenesis, 69, 71, 73, 74, 76, 80, 82
norepinephrine, 87
pathology, x, 4, 25, 93, 98, 99, 102, 138, 145, 146,
normal distribution, 164
148, 153, 182, 183
North America, 202
pathways, ix, 55, 64, 69, 71, 72, 73, 74, 76, 82, 87
novelty, 4
patient rights, 57
nuclei, 75, 86, 187
Pearson correlations, 151
nucleus, 69, 70, 73, 74, 76, 82, 86, 87
peers, 12, 56
nurses, xi, 50, 69, 96, 185
pellicle, 186
nursing, 16, 50, 54, 59
penicillin, 186
nutrients, ix, 65, 68, 71, 75, 105, 111
peptides, 71, 72, 75
nutrition, x, 83, 106, 107, 108, 110, 111, 112, 113,
perceptions, 54, 123, 133, 147
135, 137, 140, 141, 142, 177, 203
perfectionism, 173
nutritional deficiencies, 111
periodontal, 188, 189, 196
periodontal disease, 188, 189
O periodontitis, 189
peripheral blood, 71, 88
obesity, 4, 18, 23, 25, 36, 71, 76, 94, 106, 107, 140, peripheral blood mononuclear cell, 71, 88
143, 157, 163, 167, 177, 178, 181, 184 perseverance, 167, 168
observations, 79, 87 personal identity, 56
obsessive-compulsive disorder, 29 personality, vii, 1, 3, 7, 10, 11, 16, 18, 20, 21, 22, 23,
occlusion, 202 25, 26, 35, 36, 101, 157, 166, 168, 173, 178, 179,
OCD, 29, 35 180, 181, 183, 187, 203
olanzapine, 17 personality characteristics, 10
openness, 166 personality dimensions, 4, 21
organ, 3, 89 personality disorder, 4, 7, 10, 22, 157
organism, 65 personality factors, 181
organization, ix, 64 personality traits, 11, 18, 101, 168, 187
Index 215
perspective, 18, 19, 42, 43, 50, 56, 59, 60, 66, 103, prognosis, viii, 25, 63, 64, 65, 130, 134, 195
157, 159, 169, 171, 172 program, 45, 97, 111, 128, 133, 135, 136, 151
persuasion, 44 projective test, 97
pH, xi, 185, 187, 188, 192, 193, 197 prostate, 75, 86
pharmacological treatment, viii, 2, 17 protective role, 20
pharmacotherapy, x, 15, 17, 106 proteins, 117, 186
phenomenology, 36 proteinuria, 186
photographs, 196 protocol, 196
physical abuse, 7 Prozac, 193
physical activity, ix, 91, 115, 177 psychiatric disorders, vii, 1, 3, 7, 20
physical education, 113 psychiatric illness, 3
physical health, 12 psychiatric patients, 8
placebo, 17, 20, 21, 22, 24, 26, 79, 81, 88, 89, 138, psychiatrist, 30, 31, 43, 55, 110, 149
193 psychological health, 194
planning, 165, 166, 167, 168, 182, 195, 202 psychological pain, 16
plasma, 72, 76, 79, 82, 85, 86, 186 psychological phenomena, 172
plasma levels, 79, 86 psychological problems, 146
pleasure, 4, 12, 122, 133, 134 psychological value, 69
PM, 22 psychological variables, 146, 155
polyunsaturated fatty acids, 78 psychologist, 149
poor, 3, 6, 9, 14, 15, 68, 79, 80, 96, 116, 128, 130, psychology, 93, 97, 110, 111, 141, 169, 170, 174,
135, 187, 194, 200 178, 202
population, vii, 1, 6, 7, 13, 79, 106, 107, 112, 129, psychometric properties, 150
140, 146, 154, 155, 157, 160, 164, 192 psychopathology, vii, x, 2, 3, 4, 5, 9, 16, 23, 37, 38,
porosity, 192 128, 145, 147, 148, 153, 156, 170, 181
positive correlation, 128, 129, 130 psychoses, 38
positive feedback, 174 psychosis, 29
positive reinforcement, 173 psychosocial stress, 101
potassium, 112, 120, 187 psychotherapy, viii, 2, 13, 15, 20, 97, 139
power, 15, 42, 43, 45, 47, 49, 50, 51, 52, 56, 57, 58, psychotic symptomatology, 29
69, 155, 156, 169, 187 psychotic symptoms, 29
power relations, 50 pubertal development, 92
prediction, 137, 139, 140, 181 puberty, 42, 93, 100, 179
predictive validity, 142 public health, 2
predictors, 23, 109, 123, 136, 168 punishment, 11, 169
preference, 43, 85
pregnancy, 96, 101
Q
premature death, 6, 13
preparation, 123, 198
quality of life, 65, 69, 77, 78, 80, 81, 84
preparedness, 160, 177, 182
quartz, 198
pressure, 13, 93, 97, 161, 162, 171, 174, 194
questioning, 71
prevention, vii, 2, 14, 15, 17, 80, 81, 135, 139, 177,
183
primary school, 93 R
principle, 72
probability, 4, 14, 34, 154 range, ix, 6, 44, 91, 92, 94, 108, 113, 117, 119, 133,
problem behavior, 13 135, 155, 160, 174, 175, 186, 188, 194
problem drinking, 167, 168, 170, 175, 179, 182 rash, x, 159, 165, 167, 175, 176
production, 71, 75, 78, 81, 82, 88, 193 rating scale, 138
professions, 113 reading, 4, 125
reality, 11, 36, 37, 161
216 Index
reasoning, 44
S
recall, 150
receptors, 71, 74, 80, 81, 86, 87
sacrifice, 42, 94
recognition, 3, 10, 14, 159, 171, 175
safety, 46
reconcile, vii, 2, 164
saliva, xi, 185, 186, 187, 188, 193, 197
reconstruction, 54
salivary glands, 199
recovery, 23, 53, 55, 56, 65, 109, 116, 134, 141
sample, x, 4, 5, 6, 7, 8, 9, 10, 11, 18, 24, 31, 45, 46,
recurrence, 109, 128, 130, 133, 134, 139
107, 112, 114, 123, 137, 138, 140, 145, 146, 148,
reduction, 66, 74, 79, 111, 119, 120, 123, 124, 125,
153, 154, 155, 157, 167, 168, 172, 173, 180, 189,
163, 178, 188, 198
191, 194
reflexes, 72
sampling, 183
regression, 12
satisfaction, 4, 13, 127, 194, 202
regulators, 49
schizophrenia, 6, 29, 38
rehabilitation, 108, 110
school, viii, 2, 5, 14, 26, 44, 53, 93, 96, 100, 101,
reinforcement, 161, 162, 165, 169, 170, 171, 172,
107, 139, 142, 167, 173
174, 175, 178
school performance, 167
reinforcers, 170
schooling, 31
relapses, x, 17, 106
scientific knowledge, 15
relationship, ix, 5, 12, 16, 20, 29, 39, 45, 50, 51, 53,
scores, viii, 6, 13, 28, 30, 36, 38, 107, 109, 113, 125,
55, 86, 96, 97, 98, 100, 101, 102, 105, 106, 108,
127, 128, 129, 130, 131, 132, 133, 150, 151, 152,
109, 110, 112, 113, 123, 124, 125, 132, 133, 134,
154, 171, 173, 174, 189, 192, 194
135, 137, 146, 151, 152, 153, 155, 162
scurvy, 186
relationships, 12, 22, 49, 51, 54, 55, 93, 167, 174,
search, 65
180, 199
secondary school students, 138
relatives, 26, 44, 69
secretion, 70, 71, 89, 93, 187, 188
relevance, 65, 68, 79, 155, 203
security, 50, 100
reliability, 38, 66, 69, 83
selective serotonin reuptake inhibitor, 21
religiosity, 167
selectivity, 81
religious beliefs, 38
self, viii, x, xi, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13,
remission, 3, 109
14, 19, 20, 21, 22, 25, 28, 30, 31, 41, 42, 49, 50,
replacement, 12
53, 54, 55, 56, 57, 58, 64, 68, 92, 99, 100, 109,
repression, 12
111, 132, 138, 142, 143, 145, 146, 147, 148, 150,
reputation, 55
151, 152, 153, 154, 155, 156, 157, 165, 166, 167,
resins, 198
168, 173, 174, 179, 181, 183, 185, 186, 194, 197,
resistance, 33, 35, 36, 42, 50, 54, 56, 72, 97
203
resolution, 52, 94
self esteem, 42, 147, 148, 150, 152, 153, 154, 156
resources, 2
self-awareness, 166
respiratory, 83
self-concept, 203
responsibility, 44, 101
self-consciousness, 8
rhythm, 92
self-destruction, 4, 19
right to life, 57
self-destructive behavior, 5, 11, 12, 14, 100
risk, vii, x, 1, 3, 6, 7, 8, 9, 10, 11, 12, 13, 14, 16, 17,
self-discrepancy, 157
18, 19, 22, 24, 26, 34, 35, 42, 53, 82, 92, 93, 101,
self-efficacy, 143
103, 107, 130, 142, 146, 147, 155, 159, 160, 161,
self-esteem, viii, 2, 3, 8, 9, 20, 93, 156, 157, 181,
162, 163, 164, 165, 166, 169, 170, 173, 175, 176,
194
177, 178, 182, 189, 191, 192, 193, 196
self-image, viii, 5, 41, 50, 54, 56, 194
risk factors, x, 8, 16, 26, 34, 93, 142, 159, 162, 163,
self-monitoring, 111
164, 165, 173, 175, 176, 177, 178, 182
self-mutilation, 2, 6, 10, 11, 19
risk-taking, 9, 13, 14
self-regulation, 50
routines, viii, 41, 56
semantics, 58
Index 217
sensation, x, 5, 71, 106, 165, 166, 167, 168, 178 sodium, 112, 120
sensation seeking, 165, 166, 167, 168, 178 software, 111, 112, 132, 141
sensations, 166 solid tumors, 90
sensing, 73, 97 somatization, 97
sensitivity, 191, 198 species, 188, 192
separation, 9, 93, 94, 95, 99, 100, 102 specificity, 166
sepsis, 65 spectrum, 13, 14, 93, 95, 102, 180
series, 42, 69, 75, 127, 169, 172, 174, 176 speech, 96, 97, 100, 101
serotonin, ix, 63, 71, 75, 76, 79, 80, 81, 82, 86, 87, SPSS, 151
88, 90, 193 stability, 150, 154, 166, 181
sertraline, 17 stages, 54, 68, 92, 156, 172, 201
serum, 71, 84, 85, 140, 187, 202, 203 standard deviation, 112, 115, 118, 121, 127
services, 15, 44, 49, 107, 114 standards, 146, 147, 155, 157
severity, 4, 11, 19, 37, 68, 112, 126, 128, 129, 130, starvation, 7, 38, 58, 69, 187
131, 146, 187, 190, 191 statistics, x, 2, 6, 106
sexual behavior, 167 stigma, 13, 49, 56
sexual contact, 93 stimulus, 71, 169
sexual orientation, 101 stomach, 89, 93, 100, 187
sexuality, 102 stomatitis, 186
shame, ix, 3, 15, 91, 95, 132, 146, 181 strategies, vii, 2, 11, 56, 77, 89, 132, 135, 142
shape, 4, 11, 28, 57, 64, 112, 116, 127, 136, 137, strength, 31, 78, 102, 189
150, 153, 170 streptococci, 193
shaping, 42, 57 stress, 3, 5, 12, 93, 94, 128, 166, 179, 193
shares, 35, 160 stressors, 150
sharing, 68, 122 striae, 31
shyness, 8 structural equation modeling, 174
sialogram, 187 students, 147
sialography, 187 subjective experience, 54
sibling, 98 substance abuse, 22, 165
siblings, 160 substance use, 9, 10, 12
side effects, 78 sucrose, 183, 191, 196
sign, 66, 67, 202 sugar, 163, 196
signalling, ix, 63, 69, 71, 73, 75 suicidal behavior, vii, 1, 2, 3, 5, 6, 7, 10, 11, 12, 15,
signalling pathways, ix, 63, 69, 73 16, 18, 23
signals, ix, 64, 69, 70, 71, 72, 73, 74, 85, 97, 98 suicidal ideation, 2, 7, 9, 13, 15, 17, 23
significance level, 31 suicidal wishes, 14
sites, 49, 84, 189, 191, 197 suicide, vii, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 13, 14, 15,
skeletal muscle, 68 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 96, 97,
skills, viii, 2, 12, 14 98, 99
small intestine, 72 suicide attempters, 7, 13
smoking, 12 suicide attempts, 4, 6, 7, 8, 9, 10, 11, 13, 15, 18, 19,
social behavior, 100 22, 25, 26
social class, 140 suicide rate, 17
social comparison, 162, 164, 183 summaries, 170
social context, 52 Sun, 89
social control, 43, 44, 56, 58 supervision, 48
social environment, 43, 52 suppression, 12, 65, 75, 84
social events, 111, 133 surveillance, viii, 41, 56
social learning, 169, 171 survival, 68, 69, 84, 90, 182
social support, 162 swelling, 187, 204
218 Index
symptom, viii, 11, 27, 28, 32, 33, 35, 36, 37, 65, 67, tissue, 75, 186, 192
83, 116, 120, 125, 128, 129, 130, 133, 137, 148, TNF, ix, 63, 77, 86, 87, 88
163, 171, 172, 173, 174, 178 TNF-alpha, 86
symptoms, vii, ix, x, 1, 8, 11, 17, 19, 29, 30, 31, 33, tobacco, 167
37, 42, 64, 65, 66, 67, 68, 69, 77, 88, 91, 92, 93, tonic, 197
102, 105, 106, 109, 110, 112, 115, 116, 125, 128, total energy, 117, 118
129, 130, 131, 133, 134, 137, 145, 146, 147, 148, toxicity, 66, 78
150, 151, 153, 154, 155, 162, 163, 164, 167, 168, tracking, 47, 83
169, 173, 174, 177, 179 training, 66, 100, 132, 134, 139, 141
syndrome, 64, 65, 82, 87, 88, 89, 134, 156, 160 traits, 8, 168, 180, 181, 192, 194
synthesis, 70, 71, 73, 76, 77, 78, 79, 136, 183 trajectory, 54
systems, ix, 64, 75, 83, 87 transactions, 43, 47
transduction, 69
transference, 16, 97
T
transformation, 36, 43
transition, 12, 54, 55, 99, 106, 140
target organs, 72
transition to adulthood, 12
targets, viii, 41, 81
transitions, 16, 43, 54, 106, 141
taxonomy, 13, 36
transmission, 187
teachers, 96, 139
transport, 35, 79
teaching, 45, 169
trauma, 55
technology, 198
traumatic experiences, 7
teenagers, 2, 12
treatment methods, 95, 137
teeth, xi, 185, 186, 188, 189, 190, 191, 192, 193,
trend, 4, 119, 125, 153
194, 196, 198, 199, 200, 201
trial, 18, 19, 20, 21, 22, 24, 25, 47, 60, 79, 83, 89,
television, 100, 161, 163, 177, 179, 181
138, 181, 183, 193
television advertisements, 179
tricyclic antidepressant, 87
television viewing, 181
triggers, ix, 32, 71, 91, 94
temperature, 77, 191
trust, 13
tension, 2, 11, 52, 55
tryptophan, 76, 79, 83, 86, 87
terminally ill, 67, 68, 83, 84
tumor, 81, 83, 86, 87, 90, 100
test scores, 125, 127
tumor cells, 86
testosterone, 93
tumor growth, 90
theory, 19, 146, 153, 155, 157, 159, 169, 170, 171,
tumour growth, 72, 73, 74, 82
172, 173, 174, 176, 180, 182, 192
twins, 160, 180
therapeutic approaches, ix, 16, 91
therapeutic encounter, 16
therapeutic goal, 68 U
therapeutic interventions, 50
therapeutic relationship, 98, 99 UK, 8, 45, 59, 185
therapists, 16, 55, 57 umbilical cord, 101
therapy, 16, 19, 22, 50, 60, 65, 77, 80, 85, 95, 96, 97, UN, 86
98, 102, 110, 136, 139, 140, 141, 142, 196, 199 uncertainty, 56, 109
thinking, 16, 30, 123, 133, 165 undernutrition, 140
threat, viii, 4, 41, 56, 57, 97 uniform, 97
threats, 44, 46, 49 United Kingdom, 89
threshold, 164 United States, 2, 13
time, viii, 10, 12, 13, 15, 16, 18, 29, 35, 41, 48, 49, university students, 24
53, 55, 56, 57, 58, 65, 95, 96, 98, 114, 116, 117, urea, 187
123, 124, 125, 132, 135, 149, 161, 169, 174, 175,
191, 196, 199, 201
Index 219
weight control, 24, 36, 108, 124, 140, 141, 183

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

water, 88, 197 young men, 22, 92
wear, 190, 193, 197, 198, 204 young women, 8, 22, 26, 47, 61, 107, 112, 114, 117,
web, 49, 53, 178 120, 121, 135, 147, 155

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ANOREXIA NERVOSA AND BULIMIA

NERVOSA: NEW RESEARCH

Nova Science Publishers, Inc.

NOTICE TO THE READER

Library of Congress Cataloging-in-Publication Data

Published by Nova Science Publishers, Inc. New York

Chapter VII Actual - Desired BMI Discrepancy, Body

treatments, psychotherapy and school-based interventions involving crisis management, self-

Suicide in Anorexia Nervosa

Maurizio Pompili1, Paolo Girardi,

Suicide and Attempted Suicide

Table I – Suicides among various cohorts of patients

Study Sample Follow-up Suicides

Study Sample Follow-up A.S

Suicide and Attempted Suicide in Bulimia Nervosa

Study sample follow-up A.S.

Risk Taking Behavior as Part of Suicide in

Suicide is a leading cause of death in developed countries; lifetime prevalence of

Prediction and Prevention of Suicide Among

Psychotherapy with Suicidal

Pharmacotherapy and Suicididality in

Andriola J. A note on the possible iatrogenesis of suicide. Psychiatry 1973;36:213-218.

Corcos M, Taieb O, Benoit-Lamy S, Paterniti S, Jeammet P, Flament MF. Suicide attempts in

Favaro A, Santonastaso P. Suicidality in eating disorders: clinical and pscyhological

Russell G. Bulimia nervosa: an ominus variant of anorexia nervosa. Psychol Med

Vandereychen W, Pierloot R. The significance of subclassification in anorexia nervosa: a

Simone Mancini Castilho

The analysis of the psychopathological differences of ‘Body Image Disturbance’ in

Review of the Literature

This study aimed at:

1. Assessing obsessive, compulsive or delusional features of body image disturbance in

1. Free anamnesis. It included a description of body image disturbance.

Body Image Questionnaire

This self-reporting questionnaire, developed by Cooper et al. (1987), provides a measure

Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), Developed by

Delusional Features Assessment Scale

Using an adaptation of an instrument developed by Lelliot et al. (1988), we assessed the

Beck Depression Inventory (Beck et al., 1961)

Body Image Questionnaire

Obsessive Features According to the Y-BOCS

Compulsive Features According to the Y-BOCS

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

A complex interaction of physiological and psychological factors, cultural pressures and

American Psychiatry Association (1980). Diagnostic and statistical manual of mental

Meyer, B.C.; Weinroth, L.A. (1957). Observations on psychological aspects of anorexia

Terry Carney, Mim Ingvarson and David Tait

Clinicians sometimes turn to law for assistance in compelling hospitalisation of people

Diverse Clinical Configurations of Management

A Gradient of Forms of Suasion/coercion.

Among clinicians, a frequent next step up the compliance ladder is to encourage

Use of Formal ‘Control’ in a Typical Specialist Anorexia Unit.

a. Legally-backed coercion is the exception

b. Coercion is most likely to be considered for chronic cases

Number and coercion status of admissions.

Status Number of Admissions (%age of total by coercion status)

c. Guardianship is seldom used on its own, but mental health committal is

d. Mental health committal is also commonly used in conjunction with/after

Tracing ‘Strategic’ (or Shadow of Law) Uses of Formal Coercion

a. Guardianship is lightly used

Guardianship (GO) Applications 1994-2003.

STATUS OF Year Total

b. Strategic withdrawals are not always the end of the story

C. Disseminated Power and Control: Towards self-management/control?