Professional Documents
Culture Documents
Medical Psychiatry
Series Editor Emeritus
William A.Frosch, M.D.
Weill Medical College of Cornell University
New York, New York, U.S.A.
Advisory Board
Jonathan E.Alpert, M.D., Ph.D.
Massachusetts General Hospital and
Harvard University School of Medicine
Boston, Massachusetts, U.S.A.
Timothy D.Brewerton
Medical University of South Carolina Charleston, South
Carolina, U.S.A.
It is surprising that the literature on eating disorders has taken a very long time
to blossom. The original descriptions of anorexia nervosa by Gull and Lasègue date
back to 1874 and 1873 respectively, but there were long delays before its
recognition as a diagnostic entity. In its early editions, DSM merely labelled
anorexia nervosa as a gastrointestinal reaction or a feeding disturbance. It was
only in 1980, in DSM-III, that the “eating disorders” category was created and
the diagnostic criteria originally formulated by clinicians in the early 1970s
given a seal of approval. Bulimia nervosa was first described in 1979 and correctly
accorded this term in DSM-IIIR in 1987. Proposals for the recognition of a new
disorder, binge eating disorder, were put forward in the early 1990s, and
accorded grudging recognition in an appendix of DSM-IV in 1994.
The expansion of our field of study owes a great deal to the assiduous
research carried out by clinicians and scientists during the past 40 years, but
there is an additional reason not sufficiently recognised. This is the fact that
anorexia nervosa is an illness which has undergone profound changes over time.
It is not clear when this transformation began but the key socio-cultural changes
made an impact during the 1960s or even earlier. The actual increase in the
incidence of anorexia nervosa may have been fairly modest, but there has been
an outburst of eating disorders as a whole. Since the first description of the
syndrome of bulimia nervosa in 1979, its incidence has reached twice that of
anorexia nervosa. There has been an even larger number of patients with less
specified eating disorders. This proliferation explains in part why our subject
matter has become more varied and complex, and has given rise to a growing
clinical and scientific literature.
An important causative factor for the transformation of anorexia nervosa into
related disorders, is the cult of thinness which has pervaded modern westernised
and industrial societies. The components of the cult of thinness and its impact
have aroused much interest. In 1988, the social historian Joan Jacobs Brumberg
expressed deep concern about the social pressures promoting anorexia
nervosa and other eating disorders. She listed among the culprits magazines
FOREWORD ix
disseminating weight reducing diets, the fashion industry catering for the
slimmer figure, and television attributing sexual allure and professional success
to the possession of a svelte figure. These concerns seem at face value to be
entirely justified. She went further, however, in describing how Americans are
competitive even about a disease and regretted what she called “an army of
health professionals and a deluge of publications and conferences since the
1970s.” Presumably these observations were made tongue in cheek and have
fortunately not deterred Professor Brewerton and his team of contributors from
producing this new handbook much needed to do justice to the growth of our
subject.
The handbook aims at providing an integrated approach. The first feature of
integration that immediately strikes the reader is the full cover given to the well-
established disorders—not only anorexia and bulimia nervosa, but binge eating
disorder (BED) as well, and sometimes obesity is thrown in for good measure.
This has led the authors sometimes having to concede that there are only slender
research findings available, especially in BED. For example, there are no
randomised controlled trials for the evaluation of the psychological treatments
and very few on pharmacological agents in this disorder. Yet this negative
statement is useful because it demonstrates the gaps that remain to be filled.
Similarly, the chapter on Risk Factors in the various eating disorders frankly
admits that the number of studies into BED are very small, owing to the recency
of defining its research criteria.
Also important in the editor’s mission of integration is the convergence of the
main avenues of investigation—the psychosocial, the biomedical and the study of
personality. This handbook adheres therefore to the multidimensional
perspective first put forward in 1982 by Garfinkel and Garner. The significance
of this commitment should not be under-estimated. For example, Campbell in
1995 boldly asserted that the term “multifactorial,” although popular in
psychiatry, has little explanatory power and may simply serve as a cloak to
conceal our ignorance. His plea was to insist on research seeking a unitary and
necessary causal element as has been possible in many physical illnesses.
Unfortunately this worthwhile goal remains just as elusive now as it was in
1995. It remains important practically to examine risk factors in the various
fields of endeavour—sociocultural, psychological, and biomedical—because
this approach ensures that no field of study is neglected. What is particularly
striking in this handbook is the breadth and erudition of the chapters devoted to
the biomedical approach which range from genetics and molecular biology to
neuroendocrine, neuropeptide, and neurotransmitter disturbances, and finally
opens the hopeful prospects of brain imaging in patients with eating disorders.
A striking feature of the handbook is a strict objectivity in assessing the
relevant literature. In the overview of risk factors for each of the eating
x FOREWORD
REFERENCES
Brumberg JJ. Fasting Girls: The Emergence of Anorexia Nervosa as a Modern Disease.
Cambridge, Mass: Harvard University Press, 1988.
Campbell PG. What would a causal explanation of the eating disorders look like? In:
Szmukler G, Dare C, Treasure J, eds. Handbook of Eating Disorder: Theory,
Treatment and Research. Chichester: Wiley, 1995:49–64.
Garfinkel PE, Garner DM. Anorexia Nervosa: A Multidimensional Perspective. New
York: Brunner Mazel, 1982.
Lee S, Ho TP, Hsu LKG. Fat-phobic and non-fat phobic anorexia nervosa: a comparative
study of 70 Chinese patients in Hong Kong. Psychological Medicine 1993; 23:
999–1017.
Preface
Eating is a basic drive that is taken for granted by most people. However,
disorders of human eating behavior, including eating and feeding disorders, have
been of increasing interest and importance to clinicians over the last several
decades. This has been in part due to their increasing prevalence and the realization
that they are associated with marked degrees of an array of medical and
psychiatric comorbidities, as well as significant mortality. Parallel to other areas
in medicine, psychiatry, and psychology, progress has been swift (although
never fast enough), and this book attempts to present a concise, integrated and
up-to-date overview of the scientific advancement to date in this knowledge
base. This perspective is designed to be of particular interest and relevance to
the clinical practitioner, but it also has potential appeal for students, scholars
and researchers alike. Areas covered in this book include diagnosis and
assessment, developmental perspectives, epidemiology, course of illness,
etiology, specific and nonspecific risk factors, medical and psychiatric
comorbidity, and various treatment approaches and perspectives, including
speculations about future directions in the field. These topics are organized into
4 basic sections: (I) Diagnosis, Epidemiology, and Course (Chapters 1–5); (II)
Risk Factors, Etiology, and Comorbidity (Chapters 6–10); (III) Psychobiology
(Chapters11–14); and (IV) Treatment (Chapters 15–23).
In Chapter 1, Dr. Blake Woodside and Richelle Twose provide a modern
overview of the diagnosis and assessment of the eating disorders, not only from
the perspective of an evolving DSM, which has had its limitations, but also from
the perspective of selective populations, such as men, the very young, and the
very old, who have eating disorders. Furthermore, the authors propose and
explain the rationale for a new classification scheme for anorexia nervosa (AN)
that is “culture-independent.” In this chapter the authors underscore the fact
that accurate diagnosis is the foundation of effective treatment interventions. In
an Appendix to this chapter a very helpful outline of a sample clinical diagnostic
interview that is suitable for distinguishing between AN, bulimia nervosa (BN)
and binge eating disorder (BED) is provided.
PREFACE xiii
In Chapter 7, using a wealth of twin and family studies, Dr. Cindy Bulik
explores an exploding area of research and its profound clinical ramifications in
a chapter on the role of genetics in the eating disorders. These data underscore
the importance of biological factors in the development of all types of eating
disorders. However, because genetic factors do not explain 100% of the
variance, they also point out the limitations of genetics as an explanatory
paradigm and lend credence to the impact of important psychosocial forces in
shaping these disorders, perhaps by triggering and interacting with underlying
genetic and biological mechanisms.
In Chapter 8, Dr. Lisa Lilenfeld provides a comprehensive overview of axis I
psychiatric comorbidity that can be associated with AN, BN and BED.
Relationships with mood, anxiety, substance use, impulse control, psychotic,
dissociative, somatoform, attention-deficit, and disruptive behavior disorders
are all described, although the emphasis is on the most common co-occurring
conditions—mood, anxiety, and substance use disorders.
In Chapter 9, Drs. Howard Steiger and Kenneth Bruce look at the
increasingly recognized role of premorbid personality traits in the development
and perpetuation of the eating disorders. In addition, comorbid axis II
personality disorders that are typically associated with the eating disorders are
examined in depth. The implications of these data for the etiology and
treatment of eating disorders is a major focus of discussion in this chapter.
In Chapter 10, Drs. Pauline Powers and Yvonne Bannon examine in detail
the spectrum of medical (axis III) comorbidities associated with the various
eating disorders. Eating disorders are known to adversely affect literally every
organ system in the body, and it behooves the clinician to be informed of these
potentially irreversible and life-threatening problems. The importance of
working with a team of specialists, including a primary care physician who
understands and can treat these associated medical conditions is emphasized.
In Chapter 11, Dr. Howard Steiger and myself discuss neurotransmitter
dysregulation in the eating disorders. Primary focus is on the monoamines
(serotonin, norepinephrine, and dopamine), with special reference to
serotonin, which has been repeatedly found to be intimately involved in the
pathophysiology as well as the neuropsychopharmacology of the eating
disorders. A table that links various phenomenological aspects associated with
the eating disorders to each of these three neurotransmitter systems provides a
helpful perspective. Just as there is no one cause of the eating disorders, there is
also not just one neurotransmitter or neurochemical system involved in these
complex conditions.
Likewise, in Chapter 12, Drs. Ursula Bailer and Walter Kaye review the
fundamental areas of neuroendocrine and neuropeptide dysregulation in the
PREFACE xv
In Chapter 18, Dr. Deb Marcontell Michel and Susan Willard, M.S.W.
provide an overview of family evaluation and therapy for AN, BN and BED.
Basic concepts and principles of family therapy are described, as is the history of
its application in the management of eating disorders. The family characteristics
of individuals with eating disorders are appraised, and the components of a
family evaluation are illustrated. In addition, common approaches and issues
seen in the treatment of eating disorders are discussed.
In Chapter 19, Drs. Joy Jacobs, J.D., Robinson Welch, and Denise Wilfley
instruct us on the principles of Interpersonal Psychotherapy (IPT) for AN, BN
and BED. Originally developed for the treatment of depression, IPT has been
successfully adapted to the treatment of BN and BED and has been empirically
validated for these conditions. The authors review the theoretical foundations of
IPT and discuss the role of interpersonal functioning in the eating disorders. The
basic concepts of IPT in the treatment of eating disorders are explained, as well
as its treatment structure, therapeutic stance and typical phases of evolution.
Finally, the authors review data to date on outcome studies of the use of IPT in
the treatment of eating disorders.
In Chapter 20, Drs. Marsha Marcus and Michele Levine bring us up to speed
on the powerful principles and techniques of Dialectical Behavior Therapy
(DBT) as applied to the treatment of eating disorders. The authors review the
philosophy and assumptions underlying DBT and discuss the modes of
treatment used in this approach. The authors also provide a DBT diary card
adapted for use in patients with eating disorders.
In Chapter 21, Drs. Joanna Steinglass and Timothy Walsh update the reader
on the role of psychopharmacology in the treatment of AN, BN and BED. Unlike
some psychiatric disorders, psychopharmacologic treatment alone is neither
sufficient nor optimal for the treatment of any of the eating disorders, so it
should be ideally conceived as an adjunct to appropriate psychotherapeutic
approaches. This is especially true for AN for reasons that are elucidated. In this
chapter current and realistic guidelines and limitations for using
psychopharmacologic agents appropriate for these and related conditions are
provided.
In Chapter 22, I review the recent literature on the role of victimization in
eating disorders and related psychiatric comorbidity. A host of controlled studies
now clearly implicate victimization experiences, especially childhood sexual
abuse and subsequent post-traumatic stress disorder (PTSD) or symptoms, as
important risk factors in the development of BN, and perhaps AN, binge-purge
type, BED, and severe obesity (but not AN, restricting type). In addition,
victimization experiences are associated with a host of commonly seen
comorbid psychiatric disorders, including mood, anxiety, substance use,
dissociative, somatoform, impulse control, disruptive behavior, and personality
PREFACE xvii
disorders. The implications of these data for the understanding of the etiology
of eating disorders and associated psychiatric comorbidity, as well as for their
treatment in clinical practice, are highlighted. Specific principles or guidelines
used to approach the comorbid eating disordered patient are provided.
In Chapter 23, Dr. Joel Yager relies on his extensive experience, knowledge
and creative vision to speculate about future directions in the management of
eating disorders. Dr. Yager explores several areas, including future directions in
diagnosis, epidemiology, molecular genetic research, other biological
investigations, biological interventions, psychosocial interventions, and systems
of care. In addition, the impact of computers and information technology on
eating disorders management is explored.
I would like to earnestly thank all of these outstanding contributors. It is my
sincerest wish that the knowledge imparted to the reader will ultimately lead to
more lives saved, enhanced recovery from these formidable conditions, and less
suffering by patients and their loved ones. In addition, may it inspire continued
research and further advances in this field, without which this book would not
have been feasible.
Timothy D.Brewerton, M.D., D.F.A.P.A., F.A.E.D.
Contents
Index 571
Contributors
Diagnostic issues have always been important in the field of eating disorders,
whether debating the role of gender in these conditions or examining possible
etiologic factors. With recent advances in areas as diverse as culture and
genetics, reexamining thinking about diagnosis in anorexia nervosa, bulimia
nervosa, and binge eating disorder becomes increasingly important.
This chapter will review some of the historical issues in the diagnosis of
eating disorders and examine diagnostic schemas for special populations. A final
section will address some thoughts about possible revisions to the diagnostic
criteria in the light of recent developments in the field. A sample clinical
diagnostic interview schedule is attached as an appendix.
DIAGNOSTIC CRITERIA
Anorexia Nervosa
The essential diagnostic criteria for anorexia nervosa has undergone more
gradual and subtle shifts over time relative to bulimia nervosa. The Diag nostic
and Statistical Manual of Psychiatric Disorders (DSM) criteria (Table 1) are largely
reflective of Russell’s 1970 description of three essential factors: (a) purposeful
loss of body weight, (b) amenorrhea in females, and (c) psychopathology
expressed as an intense fear of becoming fat (1,2). Many of the successive
alterations are merely semantic in nature.
2 WOODSIDE AND TWOSE
The weight loss threshold for diagnosis of anorexia nervosa has become less
strict and severe with each revision of the DSM. In the DSM-III, a loss of 25%
of original body weight (or loss of original body weight plus projected weight
gain if an adolescent) is required (3). In subsequent versions, this threshold falls
to 15% and becomes only a “rough” guideline. In fact, the relevant text in the
DSM-IIIR (Table 2) states that weighing 85% of that expected is merely an
“arbitrary but useful guide” (4).
In contrast, the evolution of the requirement for amenorrhea has become
increasingly stringent over time. Contrary to Russell’s description (1970), the
DSM-III does not list amenorrhea as part of the diagnostic criteria but merely
mentions it in the relevant text on the section (3). In later versions, this aspect
of the disorder becomes mandatory for diagnosis, and the nature of amenorrhea
itself is further specified (4,5). However, the presence of this criterion continues
to spark controversy among experts in the field, since in approximately 15% of
cases menstruation ceases prior to weight loss, and in some individuals
amenorrhea persists for a period of time following restorative weight gain (1).
One group (6) compared women who meet all DSMIIIR criteria for anorexia
nervosa to women who met all criteria except amenorrhea and found no
significant differences on a wide variety of clinical and psychometric variables.
The final issue that is relevant is the increasingly common use of oral
contraceptives in this population, either for contraception or as a treatment for
osteoporosis. Most experts suggest that in the presence of oral contraceptive use
this criterion should be waived.
While the usefulness of this feature appears to be less and less important, it may
be some time before it is abandoned.
Successive versions of the DSM have increasingly emphasized the
psychopathological aspects of the illness. For example, criterion C in the
DSM-IV, (Table 3) was expanded to include a description of three different
DIAGNOSTIC ISSUES 3
change in the way this was handled, allowing a diagnosis of anorexia nervosa to
“trump” a diagnosis of bulimia nervosa. In DSM-IV, anorexia is subclassified into
the restricting and binge-purge subtypes. This distinction remains somewhat
controversial, particularly in the light of some of the recent genetic findings in
anorexia and bulimia, which will be reviewed below. It remains to be seen as to
whether this is the optimal way in which to proceed with this area of
comorbidity.
Bulimia Nervosa
Bulimia was not recognized as a mental disorder in the DSM until the
publication of the third edition in 1980 (Table 4) (3). This followed its
identifi cation by Russell during the previous year (7). The original diagnostic
criteria in DSM-III were overinclusive and led to some confusion among
clinicians and researchers. The publication of the DSM-IIIR and, later, the
DSM-IV addressed many of the original version’s shortcomings (4,5).
Bulimia, or “ox-like eating,” the original term for the illness itself, paints an
incomplete picture of the syndrome it is meant to characterize. It does not
depict the patient’s characteristic psychopathology regarding her intense fear
of fatness and obsession with body shape and weight, nor the presence of
compensatory behaviors that are so important in the illness. The renaming of
DIAGNOSTIC ISSUES 5
the condition as bulimia nervosa in DSM-IV helped to clarify that the illness
included important psychopathological features as well as abnormal eating.
The DSM-III criteria for bulimia is composed of both “monothetic and
polythetic criteria,” i.e., both essential and optional symptoms, respectively,
which complicates diagnosis of this disorder (8). The subsequent elimination of
the optional indicators in the DSM-IIIR (Table 5) functioned to create a more
homogeneous description (and thus a homogeneous group to research/study)
and greatly simplified the task of diagnosing this disorder.
The original description of binge eating in DSM-III, “the consumption of a
large amount of food in a discrete period of time” (3), was insufficient to
characterize this phenomenon. DSM-IIIR added the requirement for lack
of control, differentiating bingeing qualitatively from normal eating (4).
Provisions governing the time restrictions defining a binge have also evolved
over time. Originally, a binge was temporally restricted to “usually under two
hours” (3). The DSM-IIIR, on the other hand, abandoned the requirement of a
time limit, favoring a less restrictive “discrete period of time” to define the
binge event (4). The most recent criteria (5) simply provide a 2-hour period as
a useful guideline. More importantly, the criterion defines the context in which
a binge would occur. It is characterized as an amount of food that is “definitely
larger than most people would eat during a similar period of time under similar
circumstances” (5). The use of this specification distinguishes binge eating from
instances in which non-disordered individuals may overeat (i.e., at a holiday
party).
6 WOODSIDE AND TWOSE
eating (4). The proposed criteria for binge eating disorder are reminiscent of the
original characterization of bulimia in the DSM-III (3,11). This is likely a
reflection of the need for further study and characterization of this illness, in
order to create a more uniform list of criteria and thus describe/encompass a
less heterogeneous set of individuals.
The characteristics of binge eating in binge eating disorder are virtually
identical to those described in bulimia nervosa, with the exception of the
frequency and duration with which they occur. The time threshold for a binge is
lengthened, defined in terms of entire days rather than discrete 2-hour
episodes. In addition, the research criteria for binge eating disorder must be
met for 6 consecutive months, rather than 3, as required for bulimia nervosa.
Individuals who qualify for diagnosis of binge eating disorder may still
occasionally engage in inappropriate compensatory behaviors, but these
behaviors are not regularly used to counteract weight gain from a binge (5).
More research is necessary to determine the frequency/upper threshold with
which these individuals may purge and still maintain the essential features of this
disorder as distinct from bulimia nervosa. Perhaps the only major difference
between bulimia nervosa and binge eating disorder is the presence or absence of
weight consciousness (8).
DIAGNOSTIC ISSUES 9
Often the patient will not have eaten or drunk anything by mouth for a number
of years and will require extensive desensitization in order to be able to eat
normally again.
SPECIAL POPULATIONS
Males
Men have been identified as suffering from eating disorders from the beginning
of the English language literature, where Morton (12) presented both a male
and a female case of anorexia nervosa. More recent comprehensive
examinations (13–15) have demonstrated that the illnesses, when occurring in
men, are essentially indistinguishable from cases occurring in women.
Diagnostic criteria for bulimia nervosa and binge eating disorder are identical
in men and women. The requirement for amennorrhea must obviously be
waived in men; while some authors have suggested replacing this with various
substitutes (14), such as diminished sexual drive, these suggestions have not
generally been adopted. At the present time it is acceptable to diagnose
anorexia nervosa in a man if he meets all the other diagnostic criteria for the
condition.
between the restricting form of the illness and high perfectionism to a site on
chromsome 1. The addition of increasing levels of bingeing or purging symptoms
reduces the magnitude of the finding, suggesting that on a genetic basis, the
restricting form of the illness has some characteristics distinct from the binge-
purge form. The report of a significant finding for a separate area of the genome
(chromosome 10) adds to the evidence that there may be distinct genetic
liabilities for the type of dietary restriction associated with anorexia nervosa and
the purging of bulimia nervosa.
DIAGNOSTIC ISSUES 15
Further work in this area may lead to a totally new diagnostic schema that is
related to the genetic etiology of the conditions.
CONCLUSION
The field of diagnosis in eating disorders faces many challenges in the next few
years. These relate primarily to the presentation of novel data concerning
the cultural and genetic determinants of the conditions. These data have the
potential to dramatically alter the way in which we view the nature qf the
psychiatric diagnostic labels for these conditions.
It seems likely that the next revision of DSM will include formal diagnostic
criteria for binge eating disorder. However, the relationship between this
condition and the other eating disorders remains unclear. As well, the ED-NOS
classification could benefit from some clarification, possibly along the lines of
“AN-like” and “BN-like.”
Such changes, while difficult to adapt to, will in the long run allow for a
greater understanding of the nature of the illnesses.
APPENDIX 1
Sample Clinical Interview Format
• safe foods
• diet products
4. Bingeing
• carefully define and distinguish from overeating
• onset, frequency, initiating and ameliorating factors
• specific details of a typical binge
• usual response
• nocturnal binges, odd binges, stealing
5. Purging
For all of: vomiting, laxatives, diuretics, diet pills, thyroid, exercise:
• onset, frequency, initiating and ameliorating factors
• ipecac
• surgery
• consumption of inedible items
6. Complications of starvation/bingeing and purging
• endocrine (menses)
• metabolic (K+, Hgb, ECG)
• Dermatological (skin, hair, nails)
• Gastrointestinal (bloating, early satiety, parotid swelling, dental caries,
hematemesis, hematochezia, bowel function)
• cardiac (palpitations, edema)
• psychological
sleep pattern
concentration
food preoccupation
mood
7. Medical history
• significant illnesses
• current medications
8. Past treatment history
9. Past psychiatric history
• Axis I screen
10. Family history
• includes family/genetic history
11. Personal and developmental history
• includes screen for sexual abuse
12. Relationship history
DIAGNOSTIC ISSUES 17
REFERENCES
1. Fairburn CG, Garner DM. Diagnostic criteria for anorexia nervosa and bulimia
nervosa: the importance of attitudes to shape and weight. In: Garner DM, Garfinkel
PE, eds. Diagnostic Issues in Anorexia Nervosa and Bulimia Nervosa. New York:
Brunner/Mazel, 1988.
2. Russell GFM. Premenarchal anorexia nervosa and its sequelae. J Psychiat Res
1985; 19:363–369.
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 3rd ed. Washington, DC.
4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 3rd ed. Revised. Washington, DC.
5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC.
6. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom D, Kennedy S, Kaplan
A, Woodside DB. Purging and non-purging forms of bulimia nervosa in a
community sample. Int J Eating Disord 1996; 20:23–231.
7. Russell GFM. Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol
Med 1979; 9:429–448.
8. Pope HG Jr, Hudson JI, Spitzer RL, Williams JBW. Revisions in DSM-III criteria
for bulimia nervosa. In: Garner DM, Garfinkel PE, eds. Diagnostic Issues in
Anorexia Nervosa and Bulimia Nervosa. New York: Brunner/Mazel, 1988:80–111.
9. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom D, Kennedy S, Kaplan A,
Woodside DB. Bulimia nervosa in a Canadian community sample. Am J Psychiatry
1995; 152:1052–1058.
10. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom D, Kennedy S, Kaplan A,
Woodside DB. Is amenorrhea necessary for the diagnosis of anorexia nervosa?
Br J Psychiatry 1996; 168:500–506.
11. Keys A, Brozek J, Henschel A, Mickelsen O, Taylor HL. The Biology of Human
Starvation, Vol. 1. Minneapolis: University of Minnesota Press, 1950.
12. Morton R. Phthisologica: Or a Treatise of Consumption. London: S Smith and
B Walford, 1694.
13. Woodside DB, Garfinkel PE, Lin E, Goering P, Kaplan AS, Goldbloom DS,
Kennedy SH. Men with full and partial syndrome eating disorders: community
comparisons with non-eating disordered men and eating disordered women. Am J
Psychiatry 2001; 158:570–574.
14. Crisp AH, Burns T. Primary anorexia nervosa in the male and female: a comparison
of clinical features and prognosis. In: Andersen AA, ed. Males with Eating
Disorders. New York: Brunner/Mazel, 1990:77–99.
15. Andersen A. Males with Eating Disorders. New York: Brunner/Mazel, 1990.
16. Treasure J, Thompson P. Anorexia nervosa in childhood. Br J Hosp Med 1988;
40:362–369.
17. Pobee, Kodwo A, LaPalio, Lawrence R. Anorexia nervosa in the elderly: a
multidisciplinary diagnosis. Clin Gerontologist 1996; 16:3–9.
18 WOODSIDE AND TWOSE
18. Lee S, Ho TP, Hsu LKG. Fat phobic and non-fat phobic anorexia nervosa: a
comparative study of 70 Chinese patients in Hong Kong. Psychol Med 1993; 23:
999–1017.
19. Lee S. How abnormal is the desire for slimness? A survey of eating attitudes and
behaviour among Chinese undergraduates in Hong Kong. Psychol Med 1993;
23(2):437–451.
20. Lee S, Ho TP, Hsu LKG. Fat phobic and non-fat phobic anorexia nervosa—a
comparative study of 70 Chinese patients in Hong Kong. Psychol Med 1993; 23:
999–1004.
21. Hsu, George L, Lee, Sing. Is weight phobia always necessary for a diagnosis of
anorexia nervosa? Am J Psychiatry 1993; 150:1466–1471.
22. Grice DE, Halmi KA, Fichter MM, Strober M, Woodside DB, Treasure JT, Kaplan
AS, Magistretti PJ, Goldman D, Kaye WH, Bulik CM, Berrettini WH. Evidence
for a susceptibility gene for restricting anorexia nervosa on chromosome 1. Am J
Hum Genet 2002; 70:787–792.
23. Bulik CM, Devlin B, Bacanu SA, Thornton L, Klump KL, Fichter MM, Halmi KA,
Kaplan AS, Strober M, Woodside DB, Bergen AW, Ganjei K, Crow S, Mitchell J,
Rotondo A, Mauri M, Cassano G, Keel P, Berrettini WH, Kaye WH. Significant
linkage on chromosome 10p in families with bulimia nervosa. Am J Hum Genet
2003; 72:200–207.
2
Psychometric Assessment of Eating Disorders
Jacqueline C.Carter, Traci L.McFarlane, and Marion
P.Oimsted
University of Toronto
Toronto, Ontario, Canada
SPECIFIC PSYCHOPATHOLOGY
Specific psychopathology refers to features that are distinctive to eating
disorders. The clinical features of the two recognized eating disorders, anorexia
nervosa (AN) and bulimia nervosa (BN), overlap significantly. The central
features of BN are binge eating and inappropriate compensatory behaviors to
prevent weight gain. In the fourth edition of the Diagnostic and Statistical Manual
of Mental Disorders (DSM-IV; 7), binge eating has two defining characteristics:
(a) the consumption of a large amount of food given the circumstances; and
(b) a sense of loss of control. Compensatory behaviors are divided into two
categories: purging and nonpurging. Purging techniques include self-induced
vomiting and laxative or diuretic misuse. Nonpurging compensatory behaviors
include strict dieting, fasting, and excessive exercise. The central features of AN
are extreme food restriction and a refusal to maintain body weight at or above a
minimally normal weight for age and height (i.e., body mass index ≤ 17.5).
Approximately half of those presenting with AN also report binge eating and/or
purging. Undue influence of body shape and weight on self-evaluation is
common to both disorders. Binge eating disorder, a provisional diagnostic
category in the DSM-IV, is characterized by recurrent binge eating in the
absence of compensatory behaviors.
Structured Interviews
Structured interviews have the advantage of affording a more detailed
examination of symptoms as compared with self-report inventories as they allow
the opportunity for probing and clarification. On the other hand, interviews
rely on the subject’s self-report and the results may therefore still be influenced
by recall bias, denial, or minimization of symptoms (8). A number of structured
interviews to measure eating disorder symptoms have been developed.
Examples include the Clinical Eating Disorder Rating Instrument (9) and the
PSYCHOMETRIC ASSESSMENT 21
Self-Report Instruments
Self-report instruments offer a number of advantages over structured interview
measures. They are completely standardized, require little or no formal training
to administer, are economical, and may be completed in a group format. On the
other hand, Wilson (16) identified a number of shortcomings shared by most
self-report measures of eating disorder features, including the lack of a specific
time frame and the failure to ask directly about the frequency of key eating
disorder behaviors. In addition, most fail to define key terms such as “binge
eating.”
Numerous measures of certain aspects of eating disorder psychopathology are
available, e.g., the Restraint Scale (22), the Three Factor Eating Questionnaire
which primarily measures restraint and disinhibition (23), and the Binge
Eating Scale (24). For the purposes of this chapter, we will concentrate on
comprehensive measures that cover a broad range of the core cognitive and
behavioral features of eating disorders. Selected measures of specific constructs
(e.g., motivation to change, body image) will also be discussed. The following
self-report measures may be used as screening instruments in nonclinical
samples or as measures of eating disorder symptom severity for clinical or
research purposes. None are intended to be the sole basis for making a
diagnosis, although they may be a useful adjunct to a diagnostic interview.
derived through factor analysis (EAT-26; 26). Each item is rated on a 6point
Likert scale ranging from “never” to “always.” The most symptomatic answer
receives a score of 3, the next adjacent response a score of 2, and so on. The
three least symptomatic responses receive a score of 0. No specific time frame is
given. In addition to a total score, the EAT-26 yields three subscales: Dieting,
Bulimia/Food Preoccupation, and Oral Control. The EAT-26 total score is highly
correlated with the EAT-40 total score and the 14 eliminated items were found
to be redundant (26). A children’s version of the EAT-26 intended for use with
those younger than 16 years has been developed (ChEAT; 28).
The EAT has been widely employed as a screening instrument in
epidemiological research to identify suspected cases of eating disorders. For
screening purposes, a total score above 20 on the EAT-26 is the recommended
cutoff. On average, most studies have found the EAT-26 to have a relatively low
positive predictive value (e.g., 29,30). That is, a significant proportion of those
scoring above 20 do not have clinical eating disorders upon diagnostic
interview. Regarding the rate of false negatives, one study reported that 1 % of
low scorers (i.e., <20) were subsequently identified as cases.
Carter and Moss (31) reported the test-retest reliability of the EAT-40 over a
2- to 3-week period to be 0.84. Both the EAT and EAT-26 have been found to
correlate moderately to highly with other measures of eatingdisordered
attitudes and behavior (e.g., 32–35). Gross et al. (32) found that the EAT-40
differentiated BN subjects from normal controls. However, it has not been
found to differentiate between AN and BN (36). The test-retest reliability
coefficient for the 26-item children’s version of the EAT following a 3-week
interval has been found to be 0.81 and it has been shown to have good internal
consistency (28). Scores on the 26-item ChEAT have been shown to correlate
significantly with measures of weight management behavior and body
dissatisfaction among middle-school girls (37).
responding to the items. Raw subscale scores are plotted on profile forms to
allow comparison with norms for eating disorder patients (N = 889) and a
female college student control group (N = 205). The EDI is ssuitable for those
12 years and older. Criterion-related and construct validity for the eight
original EDI subscales have been well documented (e.g., 32, 38–40). Wear
and Pratz (41) obtained 3-week test-retest reliability coefficients above
0.80 for all of the original subscales except Maturity Fears. A cutoff score of 14
on the Drive for Thinness subscale has been recommended for screening
purposes (27). However, this measure is most useful as a measure of eating
disorder symptom severity for clinical or research purposes.
was found to be 0.78 over a 2-month interval for the original version and the
coefficient a was 0.90 for the revised version. The test-retest reliability of the
revised scale has not been studied. A number of studies support the concurrent
and discriminant validity of the MACS, and it has been shown to be sensitive to
change with treatment (57). This measure may be useful for elucidating eating
disorder cognitions and measuring cognitive change with treatment.
Motivation to Change
As previously mentioned, individuals with eating disorders are typically
ambivalent about recovery. This is related to the ego-syntonic nature of certain
feature of eating disorders (e.g., dietary restriction and weight con trol). The
PSYCHOMETRIC ASSESSMENT 27
GENERAL PSYCHOPATHOLOGY
General psychopathology refers to features that are shared with other
psychiatric conditions. In eating disorders, commonly associated
psychopathology includes depression, anxiety, low self-esteem, interpersonal
problems, and personality disturbance. In addition, features of obsessive-
compulsive disorder, substance abuse, posttraumatic stress disorder, and
dissociative disorder may be present. Such concerns may represent premorbid
conditions, or may indeed be caused or exacerbated by the eating disorder
itself. Many of these symptoms have been shown to improve with successful
management of the eating disorder. Patients who are severely depressed or
severely anxious may need to be stabilized before undertaking a specialized
symptom-focused eating disorder treatment program. Many comorbid concerns
are entangled with the eating disorder and will need to be addressed during the
eating disorder treatment (e.g., obsessive-compulsive disorder), while
longstanding interpersonal and personality disturbances may require additional
treatment after the eating disorder has been resolved. Numerous well-
established measures of general psychopathology exist, and it is beyond the scope
of this chapter to review them all. We will describe the instruments that we
recommend for clinical and research purposes.
PSYCHOMETRIC ASSESSMENT 29
Structured Interviews
There are separate subtotals for the severity of obsessions (items 1–5) and
compulsions (items 6–10). Symptoms are assessed in terms of how much of the
respondent’s time they occupy, the extent to which they interfere with normal
functioning, the degree of subjective distress they cause, and the extent to
which they are actively resisted by the patient and can be controlled by the
patient. The YBOCS has been documented to have strong psychometric
properties. It shows good internal consistency (76,78), excellent interrater
reliability (76,78), and acceptable test-retest reliability (78). Evidence for its
convergent validity has been established in studies that compared the Y-BOCS
total score with other standard self-report and behavioral measures of obsessive-
compulsive disorder (77–79). A self-report version of the Y-BOCS has been
developed and has been shown to be highly correlated with the YBOCS
interview (80,81). There is also a children’s version of the Y-BOCS that has
been shown to be reliable and valid (82).
SELF-REPORT QUESTIONNAIRES
Depression
Anxiety
phobias, the Panic Disorder Severity Scale (94) to assess panic disorder severity
in patients already diagnosed with panic disorder, the Penn State Worry
Questionnaire (95) to measure the tendency to worry excessively indicative of
generalized anxiety disorder, the Social Phobia Inventory (96) to measure the
fear, avoidance, and physiological arousal associated with social phobia, and the
Yale-Brown Obsessive-Compulsive Scale (81). For more information about
these and other scales, the reader is referred to Antony et al. (97) for a
comprehensive review of anxietyrelated assessment measures.
Self-Esteem
Substance Abuse
people” (e.g., join in on groups, confront people with problems that come up);
the other section begins with “The following are things that you do too much”
(e.g., I am overly generous to other people, I argue with other people too
much). Response options range from “not at all” to “extremely.” Both the IIP-64
and the IIP-32 have moderate to high internal consistency for the total scales
corresponding to 0.96 and 0.93, respectively, and both have test-retest
reliability after a 1-week interval of 0.78 in a nonclinical sample. Test-retest
reliability is higher in clinical samples. Normative information is based on adults
aged 18–89 (127,128).
Family Functioning
Disturbances in family functioning are common in the eating disorders, and
family therapy has been found to be helpful, particularly for younger
patients (134). Therefore, it can be useful to include a measure of family
functioning in the assessment battery. For a detailed discussion of self-report
instruments for family assessment, see Skinner (135). We recommend using
one of the following measures.
REFERENCES
1. Vitousek K, Daly J, Heiser C. Reconstructing the internal world of the
eatingdisordered individual: overcoming denial and distortion in self-report. Int J Eat
Disord 1991; 10:647–666.
2. Crowther JH, Sherwood NE. Assessment. In: Garner DM, Garfinkel PE, eds.
Handbook of Treatment for Eating Disorders. New York: Guilford Press, 1997:
34–39.
3. Miller WR, Rollnick S. Motivational Interviewing. 2d ed. New York: Guilford
Press, 2002.
4. Allison DB. Handbook of Assessment Methods for Eating Behaviors and Weight-
Related Problems—Measures, Theory and Research. Thousand Oaks,CA: Sage
Publications, 1995.
5. Groth-Marnat G. Handbook of Psychological Assessment. 3d ed. New York: John
Wiley and Sons, 1996.
6. American Psychiatric Association. Practice guidelines for the treatment of patients
with eating disorders. Am J Psychiatry 2000; 157:1–39.
7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC, 1994.
8. Pike KM, Loeb K, Walsh BT. Binge eating and purging. In: Allison DB,
ed. Handbook of Assessment Methods for Eating Behaviors and Weight-Related
Problems: Measures, Theory and Research. Thousand Oaks, CA: Sage
Publications, 1995:303–346.
9. Palmer R, Christie M, Cordle C, Davies D, et al. The Clinical Eating Disorder
Rating Instrument (CEDRI): a preliminary description. Int J Eat Disord 1987; 6:
9–16.
10. Fichter MM, Elton M, Engel K, Meyer A-E, et al. Structured Interview for Anorexia
and Bulimia Nervosa (SIAB): development of a new instrument for the assessment
of eating disorders. Int J Eat Disord 1991; 10:571–592.
38 CARTER ET AL.
11. Fairburn CG, Cooper Z. The Eating Disorder Examination. In: Fairburn CG,
Wilson GT, eds. Binge Eating: Nature, Assessment and Treatment. 12th ed. New
York: Guilford Press, 1993:317–360.
12. Mazure CM, Halmi KA, Sunday SR, Romano SJ, Einhorn AM. The YaleBrown-
Cornell Eating Disorder Scale: development, use, reliability and validation.
J Psychosom Res 1994; 28:425–445.
13. Sunday SR, Halmi KA, Einhorn A. The Yale-Brown-Cornell Eating Disorder Scale:
a new scale to assess eating disorder symptomatology. Int J Eat Disord 1995; 18:
237–245.
14. First MB, Gibbon M, Spitzer RL, Williams JB. User’s Guide for the Structured
Clinical Interview for DSM-IV Axis I Disorders. New York: Biometrics Research,
1996.
15. First MB, Gibbon M, Spitzer RL, Williams JB, Benjamin LS. User’s Guide for the
Structured Clinical Interview for DSM-IV Axis II Personality Disorders.
Washington, DC: American Psychiatric Press, 1997.
16. Wilson GT. Assessment of binge eating. In: Fairburn CG, Wilson GT, eds. Binge
Eating: Nature, Assessment and Treatment. New York: Guilford Press, 1993:
317–360.
17. Cooper Z, Cooper PJ, Fairburn CG. The validity of the Eating Disorder
Examination and its subscales. Br J Psychiatry 1989; 154:807–812.
18. Rosen JC, Vara L, Wendt S, Leitenberg H. Validity studies of the Eating Disorder
Examination. Int J Eat Disord 1990; 9:519–528.
19. Wilson GT, Smith D. Assessment of bulimia nervosa: an evaluation of the Eating
Disorder Examination. Int J Eat Disord 1989; 8:173–179.
20. Rizvi SL, Peterson CB, Crow SJ, Agras WS. Test-retest reliability of the Eating
Disorder Examination. Int J Eat Disord 2000; 28:311–316.
21. Bryant-Waugh RJ, Cooper PJ, Taylor CL, Lask BD. The use of the Eating Disorder
Examination with children: a pilot study. Int J Eat Disord 1996; 19: 391–397.
22. Herman CP, Polivy J. Restrained eating. In: Stunkard AJ, ed. Obesity.
Philadelphia: W.B. Saunders, 1980:208–225.
23. Stunkard AJ, Messick S. The three factor eating questionnaire to measure dietary
restraint, disinhibition and hunger. J Psychosom Res 1985; 29:71–81.
24. Gormally J, Black S, Daston S, Rardin D. The assessement of binge eating severity
among obese persons. Addict Behav 1982; 7:47–55.
25. Garner DM, Garfinkel PE. The Eating Attitudes Test: an index of the symptoms of
anorexia nervosa. Psychol Med 1979; 9:273–279.
26. Garner DM, Olmsted MP, Bohr Y, Garfinkel PE. The Eating Attitudes Test:
psychometric features and clinical correlates. Psychol Med 1982; 12:871–878.
27. Garner DM. Eating Disorder Inventory-2 professional manual. Odessa, FL:
Psychological Assessment Resources, 1991.
28. Maloney M, McGuire J, Daniels S. Reliability testing of a children’s version of the
Eating Attitudes Test. J Am Acad Child Adol Psychiatry 1988; 5:541–543.
PSYCHOMETRIC ASSESSMENT 39
47. Fairburn CG, Beglin SJ. Assessment of eating disorders: interview or self-report
questionnaire. Int J Eat Disord 1994; 16:363–370.
48. Luce KH, Crowther JH. The reliability of the Eating Disorder Examination—Self-
Report Questionnaire Version (EDE-Q). Int J Eat Disord 1999; 25:349–351.
49. Black CMD, Wilson GT. Assessment of eating disorders: Interview versus
questionnaire. Int J Eat Disord 1996; 20:43–50.
50. Carter JC, Aime A, Mills J. Assessment of bulimia nervosa: a comparison of
interview and self-report questionnaire methods. Int J Eat Disord 2001; 30:
187–192.
51. Grilo CM, Masheb RM, Wilson GT. A comparison of different methods for
assessing the features of eating disorders in patients with binge eating disorder.
J Consult Clin Psychol 2001; 69:317–322.
52. Wilfley DE, Schwartz MB, Spurrel EB, Fairburn CG. Assessing the specific
psychopathology of binge eating disorder: interview or self-report? Behav Res Ther
1997; 35:1151–1159.
53. Wilson GT, Nonas CA, Rosenblum GD. Assessment of binge eating in obese
patients. Int J Eat Disord 1993; 8:173–179.
54. Carter JC, Stewart DA, Fairburn CG. Eating Disorder Examination Questionnaire:
norms for young adolescent girls. Behav Res Ther 2001; 39:625–632.
55. Mizes JS, Christiano B, Madison J, Post G, Seime R, Varnado P. Development of
the Mizes Anorectic Cognitions Questionnaire-Revised: psychometric properties
and factor structure in a large sample of eating disorders patients. Int J Eat Disord
2000; 28:415–421.
56. Mizes JS. Construct validity and factor stability of the Anorectic Cognitions
Questionnaire. Addict Behav 1991; 16:89–93.
57. Mizes JS. Validity of the Mizes Anorectic Cognitions Scale: a comparison between
anorectics, bulimics and psychiatric controls. Addict Behav 1992; 17:283–289.
58. Geller J, Johnson C, Madsen K. The role of shape and weight in self-concept: the
shape and weight based self-esteem inventory. Cog Ther Res 1997; 21:5–24.
59. Cooper Z, Fairburn CG. Confusion over the core psychopathology of bulimia
nervosa. Int J Eat Disord 1993; 13:385–389.
60. Fairburn CG, Peveler RC, Jones R, Hope RA, Doll HA. Predictors of 12month
outcome in bulimia nervosa and the influence of attitudes to shape and weight.
J Consult Clin Psychol 1993; 61:696–698.
61. Geller J, Srikameswaran S, Cockell S, Zaitsoff Z. Assessment of shape- and weight-
based self-esteem in adolescents. Int J Eat Disord 2000; 28:339–345.
62. Geller J, Johnson C, Madsen K, Goldner EM, Remick RA, Birmingham CL. Shape
and weight-based self-esteem and the eating disorders. Int J Eat Disord 1998; 24:
285–298.
63. McConnaughy EA, DiClemente CC, Prochaska JO, Velicer WF. Stages of change
in psychotherapy: a follow-up report. Psychotherapy 1983; 26:494–503.
64. McConnaughy EA, Prochaska JO, Velicer WF. Stages of change in psychotherapy:
measurement and sample profiles. Psychotherapy 1983; 20:368–375.
PSYCHOMETRIC ASSESSMENT 41
99. Rosenberg M. Conceiving the Self. New York: Basic Books, 1979.
100. Demo DH. The measurement of self-esteem: refining our methods. J Personality
Social Psychol 1985; 48:1490–1502.
101. Wylie RC. Measures of Self-concept. Lincoln: University of Nebraska Press, 1989.
102. Fairburn CG, Kirk J, O’Connor M, Anastasiades P, Cooper PJ. Prognostic factors
in bulimia nervosa. Br J Clin Psychol 1987; 26:223–224.
103. McFarlane T, McCabe RE, Jarry J, Olmsted MP, Polivy J. Weight-related and
shape-related self-evaluation in eating-disordered and non-eating-disordered
women. Int J Eat Disord 2001; 29:328–335.
104. Selzer ML. The Michigan Alcoholism Screening Test: the quest for a new
diagnostic instrument. Am J Psychiatry 1971; 127:1653–1658.
105. Brady JP, Foulks EF, Childress AR, Pertschuk M. The Michigan Alcoholism
Screening Tests as a survey instrument. J Oper Psychiatry 1982; 13:27–31.
106. Thurber S, Snow M, Lewis D, Hodgson JM. Item characteristics of the Michigan
Alcoholism Screening Test. J Clin Psychol 2001; 57:139–144.
107. Hedlund JL, Vieweg BW. The Michigan Alcoholism Screening Test (MAST): a
comprehensive review. J Oper Psychiatry 1984; 15:55–65.
108. Harrell AV, Wirtz PW. The Adolescent Drinking Index Professional Manual.
Odessa, FL: Psychological Assessment Resources, 1985.
109. Harrell AV, Wirtz PW. Screening for adolescent problem drinking: validation of a
multidimensional instrument for case identification. Psychol Assess 1989; 1:61–63.
110. Skinner HA. The Drug Abuse Screening Test. Addict Behav 1982; 7:363–371.
111. Gavin DR, Ross HE, Skinner HA. Diagnostic validity of the Drug Abuse Screening
Test in the assessment of DSM-III drug disorders. Br J Addict 1989; 84:301–307.
112. Martino S, Grilo CM, Fehon DC. Development of the Drug Abuse Screening Test
for Adolescents (DAST-A). Addict Behav 2000; 25:57–70.
113. Bernstein EM, Putnam FW. Development, reliability, and validity of a dissociation
scale. J Ner Men Dis 1986; 174:727–735.
114. Carlson EB, Putnam FW. An update of the Dissociative Experiences Scale.
Dissociation: Progr Dissoc Disord 1993; 6:16–27.
115. Dubester KA, Braun BG. Psychometric properties of the Dissociative Experiences
Scale. J Nerv Ment Dis 1995; 183:231–235.
116. van Ijzendoorn MH, Schuengel C. The measurement of dissociation in normal and
clinical populations: meta-analytic validation of the Dissociative Experiences Scale
(DES). Clin Psychol Rev 1996; 16:365–382.
117. Draijer N, Boon S. The validation of the Dissociative Experiences Scale against the
criterion of the SDIC-D, using receiver operating characteristics (ROC) analysis.
Dissociation: Progr Dissoc Disord 1993; 6:28–37.
118. Armstrong JG, Putnam FW, Carlson EB, Libero DZ, Smith SR. Development and
validation of a measure of adolescent dissociation: the Adolescent Dissociative
Experiences Scale. J Nerv Men Dis 1997; 185:491–497.
119. Farrington A, Waller G, Smerden J, Faupel AW. The Adolescent Dissociative
Experiences Scale: psychometric properties and difference in scores across age
groups. J Nerv Ment Dis 2001; 189:722–727.
44 CARTER ET AL.
120. Smith SR, Carlson EB. Reliability and validity of the Adolescent Dissociative
Experiences Scale. Dissociation: Progr Dissoc Disord 1996; 9:125–129.
121. Derogatis LR. Brief Symptom Inventory: Administration, Scoring and Procedures
Manual. 3d ed. Minneapolis: National Computer Systems, 1993.
122. Derogatis LR. Symptom Checklist 90-R: Administration, Scoring and Procedures
Manual. Minneapolis: National Computer Systems, 1994.
123. Croog SH, Levine S, Testa MA, Brown B, Bulpitt CJ, Jenkins CD, Klerman GL,
Williams CH. The effects of antihypertensive therapy on quality of life. N Engl J
Med 1986; 314:1657–1664.
124. Derogatis LR. BSI Bibliography. Minneapolis: National Computer Systems, 1993.
125. Foa EB, Riggs DS, Dancu CV, Rothbaum BO. Reliability and validity of a brief
instrument for assessing post-traumatic stress disorder. J Traum Stress 1993; 6:
459–473.
126. Coffey SF, Dansky BS, Falsetti SA, Saladin ME, Brady KT. Screening for PTSD in a
substance abuse sample: psychometric properties of a modified version of the PTSD
Symptom Scale Self-Report. J Traum Stress 1998; 11:393–399.
127. Horowitz LM, Alden LE, Wiggins JS, Pincus AL. Inventory of Interpersonal
Problems Manual. United States: The Psychological Corporation, 2000.
128. Horowitz LM, Rosenberg SE, Baer BA, Ureno G, Villasenor VS. Inventory of
Interpersonal Problems: psychometric properties and clinical applications.
J Consult Clin Psychol 1988; 56:885–892.
129. Livesley WJ, Jackson DW, Schroeder ML. Dimensions of personality pathology.
Can J Psychiatry 1991; 36:557–562.
130. Clark LA, Livesley WJ, Schroeder ML, Irish S. The structure of maladaptive
personality traits: convergent validity between two systems. Psychol Assess 1996;
8:294–303.
131. Schroeder ML, Wormworth JA, Livesley WJ. Dimensions of personality disorder
and their relationship to the big five dimensions of personality. Psychol Assess 1992;
4:47–53.
132. Goldner EM, Srikameswaran S, Schhroeder ML, Livesley WJ, Birmingham CL.
Dimensional assessment of personality pathology in patients with eating disorders.
Psychiatry Res 1999; 85:151–159.
133. Clark LA, Harrison JA. Assessment Instruments. In: Livesley, WJ ed. Handbook of
Personality Disorders. New York: Guilford Press, 2001.
134. Eisler I, Dare C, Russell GFM, Szmukler G, le Grange D, Dodge E. Family
and individual therapy in anorexia nervosa: A 5-year follow-up. Arch Gen
Psychiatry 1997; 54:1025–1030.
135. Skinner HA. Self-report instruments for family assessment. In: Jacob T ed. Family
Interaction and Psychopathology. New York: Plenum Publishers Co, 1987.
136. Moos R, Moos B. Family Environment Scale Manual. Palo Alto, CA: Consulting
Psychologists Press, 1981.
137. Grotevant HD, Carlson CI. Family Assessment: A Guide to Methods and
Measures. New York: Guilford Press, 1989.
PSYCHOMETRIC ASSESSMENT 45
This chapter examines the range of feeding problems from birth to early
childhood from a theoretical and clinical perspective. Feeding problems are
usually understood as being part of a relationship and never simply located
within the child. Feeding problems are usually defined as starting before the age
of 6 years and are rarely, if ever, defined in terms of subjective anxieties of the
child but usually in terms of observed behavior or adults’ descriptions. A
feeding difficulty becomes a problem when it is associated with additional
developmental, medical, or emotional problems. The boundary between a
feeding problem, often parent defined, and a disorder, often professionally
defined, is indistinct. Most cases presenting to a hospital setting have a
multifactorial cause and maintenance involving medical, developmental, social,
and psychological factors; and in these cases it is unlikely that the children will
simply grow out of the problem without help. The difficulty of negotiating
issues of independence and control with their caregivers can result in conflict,
and these problems are often labeled as behavioral. This chapter will give an
overview of issues relating to diagnosis and classification, control and
responsibility, and assessment, with reference to texts from which further
information can be sought.
Pica
Pica describes the persistent eating of nonnutritive substances over an extended
period of time (more than a month) (see Table 1 for diagnostic criteria). It is
usually only diagnosed separately if of such severity that specific intervention is
48 NICHOLLS
Rumination
Rumination is a syndrome characterized by the effortless regurgitation of
recently ingested food (see Table 2 for diagnostic criteria). It has been linked to
severe medical and psychosocial conditions, including malnutrition, aspiration
pneumonia, and complete social withdrawal, and is seen in three distinct
populations: infants; individuals with psychiatric and neurological disorders,
particularly developmental disabilities; and adults who do not have overt
psychiatric or neurological disorders (3). The hallmark of rumination, which
separates it from other disorders of the upper gastrointestinal tract (such as
gastroesophageal reflux disease), is that in rumination the stomach contents
appear in the mouth without retching or nausea. The subject appears to make a
conscious decision on how to handle the regurgitated food, and the experience
seems to be pleasurable. It usually occurs very soon after a meal and tends to
last for 1–2 hours.
FEEDING DISORDERS IN INFANCY AND EARLY CHILDHOOD 49
classified under the generic diagnosis of “feeding disorders of infancy and early
childhood” (see Table 3 for diagnostic criteria). The classification of feeding
disorders has been hampered by a lack of knowledge about feeding behaviors in
healthy, typically developing children, thus making the boundaries between
normal, problem, and disordered feeding hard to identify. In addition, reported
feeding problems are common. More than 50% of parents report one problem
feeding behavior and more than 20% report multiple problems (5) in children
aged 9 months to 7 years. Trying to get children to eat food during structured
mealtimes appears to provide the most tension for parents. Problem feeding is
more likely to be reported among the children of parents using strategies such
as coaxing, threatening, making multiple meals, and force feeding (5). In this
study, psychosocial variables such as marital status, socioeconomic status, or the
child’s birth order were not significantly associated with reported frequency and
number of feeding problems.
Bax [quoted in (6)] has suggested that the fact that feeding and feeding
problems are covered so extensively in the child rearing literature in part
explains the relative neglect of scientific research in the area. For example,
information about typical length of mealtimes in infants and toddlers has only
recently been established, from which a definition of slow eating was
derived (7). In this study more than 30 minutes was considered slow. The
relative paucity of knowledge about the range of normal feeding behaviors has
led to an overreliance on parental report of feeding as problematic in order to
define disorder. An exception is the work of Dahl and colleagues in Sweden,
who studied a sample of infants aged 3–12 months (8) and published follow-up
findings up to primary school age. Problem feeding was defined on the basis of
parent and nurse reports, had to be present for more than 1 month, and had to
have responded to medical and psychological advice and treatment. She
identified 50 infants fulfilling these criteria (a prevalence of 1.4%). The majority
(82%) were underweight for their age. Three main problem categories were
FEEDING DISORDERS IN INFANCY AND EARLY CHILDHOOD 51
distinguished: refusal to eat (56%), colic (18%), and vomiting (16%), with 10%
miscellaneous others.
pragmatic approach, simply identifying two types of food refusal that may occur
separately or together, i.e., refusal to take in sufficient calories and refusal to
ingest a sufficient range of foods.
From a psychodynamic perspective, Chatoor and colleagues have described a
number of feeding problems based on attachment-separation theory, the best
characterized of which are infantile anorexia (15) and posttraumatic feeding
disorder of infancy (PTFD) (16). This approach emphasizes the difficulties
infants have distinguishing somatic sensations such as hunger and satiety from
emotional feelings such as sadness, anger, and frustration. The term infantile
anorexia derives from Bruch’s early descriptions of patients with anorexia
nervosa, and relates to the interpersonal nature of the infant’s struggle to have his
or her needs met. Infant-mother relationships in this group of infants have been
characterized by a lack of reciprocity, conflict, and a struggle for control in
which food refusal is central (see below). In PTFD, children are distinguished by
showing increased resistance during feeding interactions and a marked resistance
to swallowing food. This may be an infantile precursor to what had been termed
“functional dysphagia” (17), in which children identify a specific fear of
swallowing, often associated with a history of choking.
Finally, attempts have been made to classify parental responses to feeding in
recognition of the role that managing the “balance of power” (18) has in feeding
problems. Birch and colleagues identified three types of parenting styles
applicable to feeding: highly controlling, laissez-faire, and responsive. Highly
controlling and laissez-faire parenting may interfere with self-regulation of
children’s feeding behaviors. Perhaps most importantly in this context is the
association between highly controlling parenting and maternal eating
disorders (19), and the link to feeding problems in their offspring (20,21).
Maternal feeding practices and perceptions of their child’s eating have also been
linked subsequent overweight (22).
One study of classification is particularly noteworthy in terms of its research
methodology. Crist et al. (5), used a feeding screening questionnaire, the
Behavioral Pediatrics Feeding Assessment Scale (BPFAS), to empirically derive
subtypes of feeding problem from a sample of 96 control and 249 clinically
referred subjects. Using a principal-components analysis, they identified the
following factors, which accounted for 55% of the total variance for the
combined clinical and normative groups.
years, to the more severe end of the spectrum where children have narrowed
their food selection to the extent that they are consuming insufficient amounts of
key vitamins and minerals. Reau et al. (7) found an association between picky
eating and length of meal times and speculated that lengthened meal times
might reflect underlying oral-motor dysfunction in some cases. Recently Jacobi
et al. (23) aimed to clarify and validate the nature of picky eating by examining
the relationship between parental report of picky eating and objective
behavioral measures, and also looked at both parent and child precursors of
picky eating. This study is important because it attempts to clarify the relationship
between parent-reported problem feeding and observed disorder. Of 29 cases
classified as “picky” on the basis of parent report, objective measures confirmed
a lower number and variety of foods consumed, predominantly the avoidance of
vegetables. These authors found no association between picky eating and slow
eating. Picky eating, sometimes to quite an extreme degree, is commonly found
in children with autistic spectrum disorders. This type of feeding pattern has
also been termed selective eating (24) or perseverative feeding disorder (14), both of
which convey the extreme selectivity in preferred foods and resistance to trying
new foods [food neophobia (25)]. Overall caloric intake is often adequate for
these children, and growth and development are usually normal (26).
Rydell et al. (27) found that at primary school age choosiness was not related to
gender, social class, or ethnic background. The choosy children had modestly
elevated levels of externalizing, hyperactive, and internalizing behavior. More
pronounced choosiness was found in those with a history of refusal to eat in
infancy or at preschool age. These children had more problem behaviors in
other areas than less choosy children.
Factor 5: Stallers
This factor was not as well defined as others. The authors assigned the term
“stallers” because the feature of “letting food sit in the mouth without
swallowing it” was common to all cases. It was associated with a preference for
fluids over food (e.g., would rather drink than eat; drinks milk). This feeding
pattern may be similar to restrictive eating, a term that Bryant-Waugh and
Lask (28) have used to describe children with a constitutionally small appetite,
who show limited interest in food, don’t eat much, and who grow and develop
normally in the lower centiles for weight and height. This type of feeding
pattern could therefore be considered a normal variant. Clinical presentation is
often due to anxiety about growth, and there may be a long history of attempts
to feed the child more that he or she can manage. Indeed, feeding practices such
FEEDING DISORDERS IN INFANCY AND EARLY CHILDHOOD 55
as coercion to eat, excessive anxiety about weight gain, and conflict over food
can precipitate food refusal, vomiting, and failure to thrive.
None of the five groups outlined above would seem to identify a single factor
reflecting the more serious condition of failure to thrive, which describes a
pattern of faltering development as a result of poor weight gain. It may be that
failure to thrive can result from any of the feeding problems described above, if
sufficiently severe, and/or other factors contribute to exacerbation of feeding
problems, such as the use of coercion or other negative parent-child
interactions. Although malnutrition is the end point, disentangling the complex
contributions of child, parent, and their interactions is not always
straightforward. For example, the dichotomy of organic versus nonorganic
failure to thrive is used less often since the contribution of subtle differences in
sucking, chewing, and swallowing were noted in a group of children identified
as having nonorganic failure to thrive (29). Nonetheless, failure to thrive can
be, but is not always, associated with other evidence of neglect and deprivation.
This way of grouping feeding problems is not dissimilar to other attempts at
classification but has the advantage of being empirically derived. However,
there are a number of limitations. First, only 55% of the variance was accounted
for by these five factors. Second, larger sample sizes would be needed to
determine whether any of these patterns of feeding behavior were more
common for specific medical conditions than for others. Perhaps surprisingly,
only one prospective study has examined the role of early feeding problems in
the development of subsequent onset of eating disorders (30), although feeding
problems have been identified as a risk factor from retrospective studies (31,32)
and there is increasing interest in developmental precursors of subsequent
problem eating. In Marchi and Cohen’s study, 659 children and their mothers
were interviewed three times between 1 and 21 years of age. Picky eating in early
childhood was found to predict symptoms of anorexia nervosa in later
adolescence (30). The authors defined picky eating by the presence of three of
the following (maternally reported) behaviors of the child: “does not eat enough,”
“is often or very often choosy about food,” “usually eats slowly,” “is usually not
interested in food.” This concept of picky eating is therefore broader than that
defined above, in which only choosiness is a feature. Disinterest in food is a
characteristic most often associated with restrictive eating, classifiable in the
“stallers” group above.
What evidence there is suggests that the nature of feeding problems found in
children with and without medical conditions do not differ signifi cantly in type
but only in frequency or intensity (5,33). For a review of diagnosis and
treatment of feeding difficulties in children with developmental difficulties see
Schwarz et al. (34), and for feeding difficulties associated with illness see Harris
et al. (35).
56 NICHOLLS
Enteral Feeding
Increasingly children presenting to clinical services have been started on enteral
feeding for any of a number of reasons and are having difficulty making the
transition from tube feeding to oral feeding. Enteral feeding is a passive
experience for the child. Problems created by enteral feeding include reduction
of appetite and thirst leading to lack of recognition of hunger and thirst drive;
absence of normal response to the sight or smell of food, e.g., salivation, lack of
pleasure; reduction of opportunities to practice routine and skills required for
oral feeding, such as the use of cutlery; and fear and revulsion at certain
textures, tastes, and smells. Each of these difficulties may be present to a
greater or lesser degree. It is unrealistic to expect a child to start oral feeding
simply by withdrawing enteral feeds. Psychological approaches may consider a
program of desensitization to anxiety-provoking textures and foods, as well as
the establishment of normal mealtime behaviors in order to expose the child to
food and to encourage feeding. Play with food must be modeled by caregivers in
a relaxed, nonpressurizing manner. Self-feeding by mouthing, kissing, and
licking food should be encouraged. Reduction of enteral feeds should be
attempted once feeding skills have been established and a small but measured
amount of food or drink is taken by mouth on a daily basis. A window of hunger
and thirst may be created by tube feeding the child overnight or spacing bolus
feeds. Enteral feeds should be reduced slowly and gradually under the
supervision of a dietitian, in conjunction with the child’s medical care and with
regular weight checks. To prevent feeding problems developing while on
enteral feeding, children should be encouraged to maintain feeding skills,
engage in textured/messy food play, and maintain patterns of feeding and social
aspects of feeding, such as sitting at the table for regular mealtimes with others.
Although mothers with eating disorders may be at the extreme end of the
spectrum, the link between parental eating concern and reported childhood
feeding problem is evident from a number of studies as well as from clinical
experience. For example, in a community sample of 397 children whose
parents were questioned when their child was 13 months and 5 years of age,
problematical or maladaptive eating habits of the children were found to be
connected to those of their parents (40). The mother’s poor ability to enjoy
eating and high tendency to snack regardless of hunger, as well as the father’s
difficulty in weight regulation, significantly predicted persistent poor eating in
their children.
While there is increasing recognition of the association between parental
eating behavior and child eating behavior, far less is known about the longterm
course of feeding disorders and later problems both in eating and in other
aspects of control and self-regulation. We are increasingly aware from clinical
experience that a number of feeding problems can persist into later life.
Examples are children who are tube fed, in whom increased survival may also
be a factor in some patient groups; children with selective (picky) eating, which
can persist into adolescence (26) and even adulthood; and food phobias.
The mechanism by which feeding problems may be linked to eating disorders
or other types of eating problem in adolescence or adulthood is at this time
somewhat speculative. Issues of control and of the development of specific
cognitions relating to beliefs about self and others may play a part. Our capacity
to distinguish eating disorder cognitions in younger children may enhance our
understanding in this area. True eating disorders can be understood as disorders
characterized by grossly disordered or chaotic eating behavior associated with
morbid preoccupation with body weight and shape. In children as young as 7,
true eating disorders have been described and can be distinguished from
children of comparable age with other types of food avoidance. For these
disorders, anorexia nervosa and bulimia nervosa, the overall clinical
presentation is similar to that in adults, with some important distinctions that
reflect developmental and gender-based differences in expression rather than
differences in the disorder per se (41). Using the childhood version of the Eating
Disorders Examination (EDE) (42,43), Cooper et al. (38) have shown that
early-onset patients with anorexia nervosa had comparable scores to later-onset
patients on all subscales apart from Eating Concern, but that AN patients were
clearly distinguishable from those with other types of eating problems. It is
these other types of eating problems presenting in childhood, not classifiable as
eating disorders, that are of un certain nosological status (44). In particular, a
few of the subjects in the Cooper et al. study were difficult to classify and what
at first appeared to be an atypical feeding/eating problem later become more
characteristic of anorexia nervosa. A few may be diagnosed as “eating disorder
60 NICHOLLS
not otherwise specified,” and a proportion whose food avoidance dates back to
younger than 6 years would meet criteria for “feeding disorder of infancy and
early childhood.” There remain a number of children who present clinically
with disordered eating who do not fit into any of the current classification
systems. This heterogeneous group of patients need further systematic
investigation. Food avoidance emotional disorder (45), psychogenic vomiting,
food phobias, and functional dysphagia are just some of the terms that have been
used to describe problem eating behaviors in this age group (41). We have
suggested that these can be usefully thought about in relation to associated
psychopathology. For example, children with food avoidance emotional
disorder or psychogenic vomiting often have other medically unexplained
symptoms, and their parents may attribute weight loss to an undiagnosed
physical disorder. As such, classification as a somatization disorder may be
appropriate. Some children develop specific circumscribed fears in relation to
food, which are associated with specific cognitions. Generalized anxiety,
unrelated to food, may also be present. In these cases anxiety management
techniques in combination with family work can be effective once nutritional
intake has been reestablished, and hence classification as anxiety disorder, a
specific phobia, or obsessive-compulsive disorder may be appropriate depending
on clinical presentation. What each of these problems has in common with
feeding and eating disorders is a need to specifically address the nutritional as
well as the emotional needs of the child.
FIGURE 1 Conceptual model for the maintenance of “vicious cycles” within feeding
problems. Assessment aims to identify the relative contributions of physical, emotional,
behavioral, and cognitive contributions to the maintenance of the feeding problem within
a developmental and systemic framework.
Physical Assessment
In addition to aiding diagnosis and management decisions, information obtained
from physical assessments can be a powerful tool for both sufferers and parents/
caregivers. Furthermore, medical concerns are often the main cause for concern
or the reason that the problem has been taken seriously. The commonest causes
for concern are significant weight loss or weight gain, failure to gain weight or
height appropriately for age and stage of development, or a single low or high
BMI or other weight-to-height ratio index measurement (outside 3rd or 97th
centile for age). The potentially irreversible effects of malnutrition on physical,
psychological, and emotional growth and development in infants and children
are well described. Monitoring of growth and development should continue until
the child is growing and developing along appropriate centiles. Weight and
height charts are of more value for monitoring change than for assessing the
significance of a single measurement. More importantly, growth charts
emphasize the rate of expected weight gain for a child. Over the past few years
many countries have published BMI centiles for children, e.g., (47–49), which
will enable nutritional status to be more conveniently and routinely assessed.
It is important that the presence of unidentified and untreated or partially
treated physical symptoms, such as esophageal reflux or problems with
swallowing as a result of oromotor dyscontrol, be assessed.
the eating difficulty, we would routinely ask all members of the family how they
understand it and how it affects them. Finally, we ask parents what they have
tried in terms of managing the problem and who or what they have found
helpful in the past. This will also allow a picture of help seeking and professional
networks to be identified.
their own ability to achieve change, and to assess their understanding of the
process by which change can be achieved.
Other professionals may be needed in the assessment process, e.g., other
physicians, nurse specialists, speech and language therapists, dietitians,
occupational therapists, social workers, and play specialists. Liaison with the
child’s professional network outside the hospital will give an indication of
previous treatment strategies that have been tried and of the extent to which
professional concerns play a part in the context of the problem.
The assessment process allows more than a diagnosis to be established. It
encompasses a risk assessment in terms of physical compromise, vulnerability to
abuse or neglect, and risk of aggression/violence to others. Itenables
determination of the impact of the feeding problem on the child’s development
and general functioning as well as on the family. Expectations of treatment are
ascertained, together with some provisional information about level of
motivation and readiness to change. A formulation can be made within the
framework outlines and this formulation shared with the family as a starting
point for a collaborative approach to the problem.
OUTCOME
Remarkably little is known of the outcome of feeding disorders in the Western
world, although the effects of malnutrition are well documented from studies in
developing countries. In one of very few studies, the developmental sequelae of
infant failure to thrive were examined in 42 unreferred 6-year-olds with a
history of severe failure to thrive at age 1 year. At 6 years, children with a
history of failure to thrive were considerably smaller than matched comparisons
in terms of body mass index and height and weight centiles. Failureto-thrive
patients had more limited quantitative and memory skills than controls, but
there were no significant differences in general cognitive functioning once
maternal IQ was taken into consideration (53). In this small series, therefore,
there was little evidence of adverse effects of early malnutrition on cognitive
functioning by school age. The most comprehensive follow-up study to date has
been that of Dahl and colleagues, who followed 25 of their sample of infant
problem eaters. At primary school age, those who had initial refusal to eat
continued to present more eating problems both at home and at school than
controls but were otherwise no different on measures of general behavior,
somatic health, or growth. Whether these problem eating behaviors persisted into
66 NICHOLLS
SUMMARY
A developmental framework encompassing the range of feeding and eating
problems from childhood to adulthood is needed, as increasing evidence of
continuities between feeding and eating problems are found. A small but
expanding literature is emerging identifying relationships between early feeding
difficulties and later eating concerns, and in the mechanisms for systemic and
transgenerational influence of food-related beliefs and cognitions. Central to
this are issues of control and the development of selfregulation, concepts that go
far beyond the feeding behavior in terms of their importance and impact on
child development.
There are still many areas where knowledge is lacking, in terms of both
theoretical understanding and treatment approaches. In particular, issues of
classification remain far from resolved, nor is it clear in which conceptual
framework feeding problems are best classified and understood. This hampers
many aspects of further research. The relationship between parent-defined
feeding problems from primary care and community samples and cases of
feeding “disorder” presenting clinically needs further consideration. Treatment
and outcome studies are needed.
ACKNOWLEDGMENT
My thanks to Catherine Dendy for her comments and conceptual framework.
REFERENCES
1. Stein MA, Mendelsohn J, Obermeyer WH, Amromin J, Benca R. Sleep and
behavior problems in school-aged children. Pediatrics 2001; 107(4):E60.
2. Stein DJ, Bouwer C, Van Heerden B. Pica and the obsessive-compulsive spectrum
disorders. S Afr Med J 1996; 86(suppl 12): 1582–1586.
FEEDING DISORDERS IN INFANCY AND EARLY CHILDHOOD 67
infants. A study of women with maternal eating disorder, postnatal depression and
a healthy comparison group. Br J Psychiatry 2001; 179:157–162.
20. Whelan E, Cooper PJ. The association between childhood feeding problems and
maternal eating disorder: a community study. Psychol Med 2000; 30(l):69–77.
21. McCann JB, Stein A, Fairburn CG, Dunger DB. Eating habits and attitudes of
mothers of children with non-organic failure to thrive. Arch Dis Child 1994; 70(3):
234–236.
22. Birch LL, Fisher JO. Mothers’ child-feeding practices influence daughters’ eating
and weight. Am J Clin Nutr 2000; 71(5):1054–1061.
23. Jacobi C, Agras WS, Hammer L. Predicting children’s reported eating disturbances
at 8 years of age. J Am Acad Child Adolesc Psychiatry 2001; 40(3):364–372.
24. Bryant-Waugh R. Overview of the eating disorders. In: Lask B, Bryant-Waugh R,
eds. Anorexia nervosa and related eating disorders in childhood and adolescence.
Hove, East Sussex: Psychology Press, 2000:27–40.
25. Pliner P, Loewen ER. Temperament and food neophobia in children and their
mothers. Appetite 1997; 28:239–254.
26. Nicholls D, Christie D, Randall L, Lask B. Selective eating: symptom, disorder or
normal variant? Clin Child Psychol Psychiatry 2001; 6(2):257–270.
27. Rydell AM, Dahl M, Sundelin C. Characteristics of school children who are choosy
eaters. J Genet Psychol 1995; 156(2):217–229.
28. Bryant-Waugh R, Lask B. Eating disorders in children. J Child Psychol Psychiatry
1995; 36(2): 191–202.
29. Reilly SM, Skuse DH, Wolke D, Stevenson J. Oral-motor dysfunction in children
who fail to thrive: organic or non-organic? Dev Med Child Neurol 1999; 41 (2):
115–122.
30. Marchi M, Cohen P. Early childhood eating behaviors and adolescent eating
disorders. J Am Acad Child Adol Psychiatry 1990; 29(1):112–117.
31. Rastam M. Anorexia nervosa in 51 Swedish adolescents: premorbid problems and
comorbidity. J Am Acad Child Adol Psychiatry 1992; 31(5):819–829.
32. Jacobs BW, Isaacs S. Pre-pubertal anorexia nervosa: a retrospective controlled
study. J Child Psychol Psychiatry 1986; 27(2):237–250.
33. Stark LJ, Jelalian E, Powers SW, Mulvihill MM, Opipari LC, Bowen A, et al.
Parent and child mealtime behavior in families of children with cystic fibrosis.
J Pediatr 2000; 136(2): 195–200.
34. Schwarz SM, Corredor J, Fisher-Medina J, Cohen J, Rabinowitz S. Diagnosis and
treatment of feeding disorders in children with developmental disabilities.
Pediatrics 2001; 108(3):671–676.
35. Harris G, Blissett J, Johnson R. Food refusal associated with illness. Child Psychol
Psychiatry Rev 2000; 5(4): 148–156.
36. Birch LL, Fisher JO. Development of eating behaviors among children and
adolescents. Pediatrics 1998; 101(3 Pt 2):539–549.
37. Patel P, Wheatcroft R, Park RJ, Stein A. The children of mothers with eating
disorders. Clin Child Fam Psychol Rev 2002; 5(1):1–19.
FEEDING DISORDERS IN INFANCY AND EARLY CHILDHOOD 69
38. Cooper PJ, Watkins B, Bryant-Waugh R, Lask B. The nosological status of early onset
anorexia nervosa. Psychol Med 2002; 32(5):873–880.
39. Agras S, Hammer L, McNicholas F. A prospective study of the influence of eating-
disordered mothers on their children. Int J Eat Disord 1999; 25(3):253–262.
40. Saarilehto S, Keskinen S, Lapinleimu H, Helenius H, Simell O. Connections
between parental eating attitudes and children’s meagre eating: questionnaire
findings. Acta Paediatr 2001; 90(3):333–338.
41. Nicholls D, Bryant-Waugh R. Children and young adolescents. In: Treasure J,
Schmidt U, van Furth E, eds. Handbook of Eating Disorders. Chichester: John
Wiley and Sons, 2003:415–433.
42. Fairburn CG, Cooper Z. The eating disorders examination. 12th ed. In: Fairburn
CG, Wilson GT, eds. Binge Eating: Nature, Assessment and Treatment. New
York: Guilford Press, 1993:317–332.
43. Bryant-Waugh R, Cooper P, Taylor C, Lask B. The use of the Eating Disorder
Examination with children: a pilot study. Int J Eat Disord 1996; 19(4):391–397.
44. Nicholls D, Chater R, Lask B. Children into DSM IV don’t go: a comparison of
classification systems for eating disorders in childhood and early adolescence. Int J
Eat Disord 2000; 28(3):317–324.
45. Higgs JF, Goodyer IM, Birch J. Anorexia nervosa and food avoidance emotional
disorder. Arch Dis Child 1989; 64:346–351.
46. Birch LL, Fisher JO, Grimm-Thomas K, Markey CN, Sawyer R, Johnson SL.
Confirmatory factor analysis of the Child Feeding Questionnaire: a measure of
parental attitudes, beliefs and practices about child feeding and obesity proneness.
Appetite 2001; 36(3):201–210.
47. Cole TJ, Freeman JV, Preece MA. Body mass index reference curves for the UK,
1990. Arch Dis Child 1995; 73(l):25–29.
48. Williams S. Body Mass Index reference curves derived from a New Zealand birth
cohort. N Z Med J 2000; 113(1114):308–311.
49. Luciano A, Bressan F, Zoppi G. Body mass index reference curves for children aged
3–19 years from Verona, Italy. Eur J Clin Nut 1997; 51(1):6–10.
50. Southall A, Schwartz A. Feeding Problems in Children: A Practical Guide.
Abingdon, Oxford: Radcliffe Medical Press, 2000.
51. Bithoney WG, McJunkin J, Michalek J, Snyder J, Egan H, Epstein D. The effect of
a multidisciplinary team approach on weight gain in nonorganic failure-tothrive
children. J Dev Behav Pediatr 1991; 12(4):254–258.
52. Steinhausen HC. Outcome of anorexia nervosa in the younger patient. J Child
Psychol Psychiatry 1997; 38(3):271–276.
53. Boddy J, Skuse D, Andrews B. The developmental sequelae of nonorganic failure to
thrive. J Child Psychol Psychiatry Nov 2000; 41(8): 1003–1014.
70 NICHOLLS
4
Epidemiology of Eating Disorders and
Disordered Eating: A Deveiopmental
Overview
Maria Råstam
Göteborg University, Göteborg, Sweden
Christopher Gillberg
Göteborg University, Göteborg, Sweden, and St. George’s
Hospital Medical School,
London, England
Daphne van Hoeken
Parnassia, The Hague, The Netherlands
Hans Wijbrand Hoek
Parnassia, The Hague, The Netherlands, and Mailman School of
Public Health, Columbia University,
New York, New York, U.S.A.
How common are the eating disorders? The social and economic burden for the
individual and the society makes the epidemiology of eating disorders an
important issue. Furthermore, studies of representative samples of eating
disorders are the soundest base for the examination of etiologic factors and
outcome. The most consistent finding across time and studies seems to be that
anorexia nervosa predominantly affects adolescent girls.
How do the eating disorders develop over time? Do they belong to a
spectrum with disordered eating at one end and anorexia and bulimia nervosa at
the other, with the partial syndromes of anorexia and bulimia nervosa in the
middle? How often does disordered eating develop into a (partial) eating
disorder? Most individuals with anorexia nervosa develop bulimia nervosa or a
partial syndrome of anorexia or bulimia nervosa in the course of their
recovery (1). There are no data as to how often those subjects with a diagnosis
of Eating Disorders-Not Otherwise Specified (ED-NOS) progress to the full
syndrome of anorexia or bulimia nervosa.
72 RÅSTAM ET AL.
EATING DISORDERS
Classification
In the sections on anorexia nervosa and bulimia nervosa only studies using strict
definitions of these eating disorders (meeting Russell, DSM, or ICD criteria) are
discussed. Another category, the ED-NOS, is a mixed category. It includes
heterogeneity of patients who do not meet all criteria for anorexia nervosa or
bulimia nervosa but who have symptoms severe enough to qualify them as
EPIDEMIOLOGY 73
Disordered Eating
Dieting is very common among young women and is considered a major risk factor
for disordered eating and the development of eating disorders (10,11). Fairburn
and colleagues compared subjects with bulimia nervosa (12), BED (13), and
anorexia nervosa (14) with each other, with healthy control subjects without an
eating disorder (general risk factors), and with subjects with other psychiatric
disorders (specific risk factors), recruited from general practices in
Oxfordshire, England. After screening with self-report questionnaires, a
retrospective risk factor interview was carried out that addressed the premorbid
period. The results suggest that both bulimia nervosa and BED are most likely to
develop in dieters who are at risk of obesity and psychiatric disorder in
general (12,13). Disordered eating in teenagers may be an important future
health risk. In a community-based longitudinal investigation in New York State,
10% of girls and 1% of boys (out of 717 individuals, 51% female) were
diagnosed with DSM-IV eating disorder diagnosis in adolescence. Compared to
those without an eating disorder diagnosis, they had significantly more physical
problems and anxiety and depressive disorders during early adolescence.
Furthermore, data indicated that problems with eating or weight during
adolescence may be associated with physical and mental health problems during
early adulthood, regardless of whether the full syndrome of an eating disorder
had been present or not (15).
In Sweden in 1880, a health survey of schools for girls (from the upper
classes) showed that 35% of 3000 adolescent girls had “chlorosis,” defined as
being pale, weak, and anemic with no or irregular menstruations. The cause
was ascribed to the half starvation recommended for girls of that social standing.
The illness was reported occasionally to be epidemic in higher school grades (16).
Nowadays even young children have grasped the ideal of a thin female body. In
a British study, one of five 9-year-old girls was dieting, and, although more
common in heavier girls, dieting was not restricted to that group (17). In a
study of 318 girls and boys aged 9 12 years (18), 45% wanted to lose weight,
significantly more girls than boys. Dieting occurred in 37% (Table 1), and 6.9%
had high scores on the Children’s Eating Attitudes Test (ChEAT), indicating
disordered eating. Trying to replicate the Maloney study on children in the
74 RÅSTAM ET AL.
same age range in Israel, Sasson and coworkers (19) found 8.8% high scorers on
the ChEAT.
In a cross-sectional self-report study of eating attitudes and behaviors in girls
attending junior high and high schools in Toronto, Ottawa, and Hamilton (20),
one in five girls were dieting (Table 1). Bingeing and purging at a frequency
consistent with a diagnosis of DSM-IV bulimia nervosa occurred in 4.9%.
Disordered eating attitudes and behaviors tended to increase gradually
throughout adolescence, especially in heavier teenagers (20). Table 1
summarizes one-stage (or the first stage of two) surveys of disordered eating in
children and adolescents with a participation rate of at least 70%.
In a questionnaire study (28), 35% out of 1241 Swedish schoolgirls aged
14–18 years were dieting. A follow-up of 130 females with dieting plus mental
problems gave an accumulated prevalence of 1.2% of anorexia nervosa for the
whole female population (29). In South Carolina (22), 3129 middle school
students (out of 4282) completed a self-report questionnaire, the Kids’ Eating
Disorders Survey (KEDS). Dieting and disordered eating was found to be fairly
common in 9-to 16-year-olds (Table 1). In a second stage, designed to validate
the screening tool, altogether 165 subjects, a mixture of high scorers on the
KEDS and randomly selected students, were personally interviewed. One
subject fulfilled criteria for DSM-IIIR anorexia nervosa and 22 for ED-NOS.
With the new male body ideal in the media, young men have become
increasingly engaged in body building and the use of anabolic steroids (30, 31).
Many of these young men are reminiscent of young females with anorexia nervosa
in their compulsive pursuit of more training and a specific body image. Still,
generally, teenage girls diet because they feel fat whereas most boys who diet
are fat (32).
In a representative sample of 4746 adolescents from 31 Minnesota public
schools, about 6% were self-reported vegetarians (33). The vegetarians were
more likely than nonvegetarians to be female and to be involved in weight
control behaviors, including some with an eating disorder. Some individuals
may use vegetarianism as a disguise for dieting. In a communitybased
study on teenage-onset anorexia nervosa, 25% introduced their diet as
vegetarianism (34), and during a 10 year follow-up period altogether 41 % had
a vegetarian phase (1). One cannot exclude the possibility that for some
individuals a drastic change of diet per se might be a risk for the development of
an eating disorder.
TABLE 1 Surveys of Disordered Eating in School Years
For Tables 1–4 ANIS, Anorexia Nervosa Inventory Scale; BCDS, Bulimic Cognitive Distortions Scale; ChEAT, Childrens Eating Attitudes Test-26;
DIS, Diagnostic Interview Schedule; DSED, Diagnostic Survey for Eating Disorders; EAT-26, Eating Attitudes Test-26; EDE, Eating Disorder
Examination; EDE-Q, Eating Disorder Examination-Questionnaire; EDE-S, Eating Disorder Examination-Screening Version; EDI, Eating Disorder
Inventory; KEDS, Kids’ Eating Disorders Survey. a first stage of two-stage study.
EPIDEMIOLOGY 75
76 RÅSTAM ET AL.
Anorexia Nervosa
Prevalence
The current standard for prevalence studies of eating disorders are studies
employing a two-stage selection of cases. Table 2 summarizes the two-stage
surveys of anorexia nervosa in young females. All researchers have succeeded in
obtaining high response rates of 85% or more, except Meadows et al. (38), who
obtained a response rate of 70%. Those two-stage surveys that identified cases
found a prevalence rate of strictly defined anorexia nervosa of between 0.2%
and 0.8% of young females, with an average prevalence of 0.3%. These rates
are possibly minimal estimates. Most studies found much higher prevalence
rates for partial syndromes of anorexia nervosa. One twostage study (23)
screened 607 14- to 17-year-olds with a wide battery of questionnaires. The
surveys was completed by 583 participants. The first stage reported on eating
behaviors in teenagers (Table 1). In a second stage, 399 parents of screen-
positive and control subjects were interviewed. The adolescents were not
examined. At the first screening a clinical eating disorder was suspected in two
cases, one a girl with anorexia and the other a girl with bulimia nervosa, and this
was confirmed in parents’ interviews. No more clinically significant eating
disorders were found.
Two other studies give prevalence figures for the entire population. In a
general-practice study in the Netherlands, Hoek (46) found a raw point
prevalence rate of 18.4 per 100,000 of the total population (95% CI
12.7–26.8) on January 1, 1985. Lucas et al. (47) used a very extensive case finding
method. It included all medical records of health care providers, general
practitioners, and specialists in Rochester, Minnesota. They also screened
records mentioning related diagnostic terms for possible undetected cases. They
found an overall sex-and age-adjusted point prevalence of 149.5 per 100,000
(95% CI 119.3–179.7) on January 1, 1985. A main explanation for this
difference can be found in the inclusion of probable and possible cases by Lucas
et al. Definite cases constituted only 39% (82 of 208) of all incident cases
identified in the period 1935–1989 (48). Applying this rate to the point
prevalence of 149.5 gives an estimated point prevalence of 58.9 per 100,000
for definite cases in Rochester, Minnesota on January 1, 1985. The remaining
difference with the point prevalence reported by Hoek (46) could be explained
by the greater variety of medical sources searched by Lucas et al. (47).
TABLE 2 Two-Stage Surveys of Prevalence of Anorexia Nervosa in Young Females
a
EPIDEMIOLOGY 77
Incidence
Incidence rate differences between groups are better clues to etiology than
prevalence rate differences because they refer to recently started disease (49). The
incidence studies of anorexia nervosa have used psychiatric case registers,
medical records of hospitals in a circumscribed area, registrations by general
practitioners, or medical records of health care providers in a community.
Table 3 summarizes the results of the studies on the incidence of anorexia nervosa
that report overall rates for a general population sample. The overall rates vary
considerably, ranging from 0.10 in a hospital-recordsbased study in Sweden in
the 1930’s to 12.0 in a medical-records-based study in the USA in the 1980’s,
both per 100,000 population per year.
Incidence rates derived from general practices on average represent more
recently started eating disorders than those based on other medical records.
There were two studies of this type. In the study by Hoek and colleagues (58),
general practitioners using DSM-IIIR criteria have recorded the rate of eating
disordersin a large (1985:7V=151,781), representative sample (l.l%) of the
Dutch population. The incidence rate of anorexia nervosa was 8.1 per 100,000
person years (95% CI 6.1–10.2) during 1985–1989. During the study period
63% of the incident cases were referred to mental health care, accounting for an
incidence rate of anorexia nervosa in mental health care of 5.1 per year per
100,000 population. Turnbull et al. (59) searched the UK General Practice
Research Database (GPRD), covering 550 general practitioners and 4 million
patients, for first diagnoses of anorexia in the period 1988–1993. A randomly
selected subset of cases was checked with DSM-IV criteria, from which
estimates for adjusted incidence rates were made. For anorexia nervosa they
found an age-and sex-adjusted incidence rate of 4.2 (95% CI 3.4–5.0) per
100,000 population in 1993.
Lucas et al. (47,48) used the most extensive case finding method (see the
section on prevalence). Over the period 1935–1989, they report an overall age-
and sex-adjusted incidence rate of anorexia nervosa of 8.3 per 100,000 person-
years (95% CI 7.1–9.4).
earlier (64). Incidence rates of anorexia nervosa are highest for females 15–19
years old. These constitute approximately 40% of all identified cases and 60%
of female cases. For example, Lucas et al. (48) report an incidence rate of 73.9
per 100,000 person-years for 15- to 19-year-old women during the period
1935–1989, with a continual rise since the 1930s to a top rate of 135.7 for the
period 1980–1989. On an overall female rate of 15.0 per 100,000 population
per year, Lucas et al. (48) report a rate of 9.5 for 30- to 39year-old women, 5.9
for 40- to 49-year-old women, 1.8 for 50- to 59-year-old women, and 0.0 for
women 60 years and older.
The majority of male incidence rates reported were below 0.5 per
100,000 population per year, e.g., Turnbull et al. (59). In those studies where
it is reported, the female-to-male ratio usually is around 11:1, e.g., Hoek
et al. (58).
80 RÅSTAM ET AL.
Time Trends
In spite of some reports of an increased rate of anorexia nervosa from the
mid-1960s to the mid-1980s in certain regions (48), there is no consensus
that anorexia nervosa prevalence generally has increased over the corresponding
time period. Case register studies prior to the 1980s show at most a slight
increase over time of incident anorexia nervosa cases (3). The studies done in the
1980s show widely diverging incidence rates. Most likely there is a
methodological explanation for these differences. The main problem lies in the
need for long study periods. This results in a sensitivity of these studies to minor
changes in absolute incidence numbers and in methods, e.g., variations in
registration policy, demographic differences between populations, faulty
inclusion of readmissions, the particular method of detection used, or the
availability of services (65–67).
From the studies that have used long study periods, it may now be concluded
that there is an upward trend in the incidence of anorexia nervosa since the
1950s. The increase is most substantial in females 15–24 years of age. Lucas
et al. (48) found that the age-adjusted incidence rates of anorexia nervosa in
females 15–24 years old showed a highly significant linear increasing trend from
1935 to 1989, with an estimated rate of increase of 1.03 per 100,000 person-
years per calendar year. In 10- to 14-year-old girls a rise in incidence was
observed for each decade since the 1950s. The rates for men and for women 25
and older remained relatively low.
All record-based studies will grossly underestimate the true incidence
because not all patients will be referred to mental health care or become
hospitalized (68). The increase in incidence rates of registered cases implies at
least that there is an increased demand for health care facilities for anorexia
nervosa.
Bulimia Nervosa
Prevalence
In 1990 Fairburn and Beglin gave a review of the prevalence studies on bulimia
nervosa (6). This landmark review yielded the generally accepted prevalence
rate of 1 % of young females with bulimia nervosa according to DSM criteria.
Table 4 summarizes two-stage surveys of bulimia nervosa in young females that
have been published since the review by Fairburn and Beglin. Despite the
different classifications used—DSM-III (72) versus DSM-IIIR (73)—and
different types of prevalence rates provided [lifetime prevalence, e.g.,
sgfsdfdsdgfsdfs
TABLE 4 Two-Stage Surveys of Prevalence of Bulimia Nervosa in Young Females
EPIDEMIOLOGY 81
82 RÅSTAM ET AL.
Bushnell et al. (69), versus point prevalence, e.g., Rathner and Messner (43)],
the aggregated prevalence rate according to DSM criteria remains 1%. The
prevalence of subclinical eating disorders is substantially higher than that of full-
syndrome bulimia nervosa, e.g., Whitehouse et al. (42): 1.5% for fullsyndrome
and 5.4% for partial-syndrome bulimia nervosa.
The results of three studies not using a two-stage procedure for case finding
are reported here as well because they are likely to represent the entire
population of women. Garfinkel et al. (74) assessed eating disorders in a ran
dom, stratified, nonclinical community sample, using a structured interview for
the whole sample. They reported a lifetime prevalence for bulimia nervosa of
1.1 % in women and of 0.1 % in men aged 15–65, using DSM-IIIR criteria.
This is a study of a representative sample of women in the United States and
provides a good estimate of the lifetime prevalence of bulimia nervosa in the
United States. Another study from the United States designed for examining the
relationship among assault, bulimia nervosa, and BED (DSM-IV criteria) by
interviewing by telephone a national representative sample of 3006 women
yielded a prevalence for bulimia nervosa of 2.4% (75). In a study by Soundy
et al. (76), no attempt was made to determine prevalence rates for bulimia
nervosa because they considered the information about how long symptoms had
persisted and the long duration (mean 39.8 months) of symptoms before
diagnosis to be too unreliable.
Incidence
There have been few incidence studies of bulimia nervosa. The most obvious
reason is the lack of criteria for bulimia nervosa in the past. Most case registers
use the International Classification of Diseases, currently ICD-10 (77). The
ICD-9 (78) and previous versions did not provide a separate code for bulimia
nervosa. Bulimia nervosa has been distinguished as a separate disorder by
Russell in 1979 (79) and DSM-III in 1980 (72). Before 1980 the term “bulimia”
in medical records designated symptoms of heterogeneous conditions
manifested by overeating, but not the syndrome as it is known today.
Therefore, it is difficult to examine trends in the incidence of bulimia nervosa
or a possible shift from anorexia nervosa to bulimia nervosa, which might have
influenced the previously described incidence rates of anorexia nervosa.
Three studies are of main interest: those of Soundy et al. (76), Hoek
et al. (58), and Turnbull et al. (59). Soundy and colleagues used methodology
similar to that in the long-term anorexia nervosa study by Lucas et al. (47)
screening all medical records of health care providers, general practitioners, and
specialists in Rochester, Minnesota over the period 1980–1990 for a clinical
diagnosis of bulimia nervosa as well as for related symptoms (76). Hoek and
EPIDEMIOLOGY 83
colleagues studied the incidence rate of bulimia nervosa using DSM-IIIR criteria
in a large general-practice study representative of the Dutch population,
covering the period 1985–1989 (58). Turnbull and colleagues screened the
General Practice Research Database (GPRD), covering a large, representative
sample of the English and Welsh population, for first diagnoses of anorexia
nervosa and bulimia nervosa in 1993 (59). The three studies all report an annual
incidence of bulimia nervosa around 12 per 100,000 population: 13.5 for
Soundy et al., 11.5 for Hoek et al., and 12.2 for Turnbull et al.
Another general-population study of a relatively small population (lower than
50,000 inhabitants) is of some interest because it was based on a homogeneous
population from a small Danish island (80). The Danish Psychiatric Case
Register and the local records of in-and outpatients were screened, psychiatrists
and physicians in primary care were interviewed, as were all school medical
officers. In the period 1985–1989, the average annual incidence of bulimia
nervosa was 6.8 per 100,000 population.
Time Trends
Soundy et al. (76) found yearly incidence rates to rise sharply from 7.4 per
100,000 females in 1980 to 49.7 in 1983, and then remain relatively constant at
around 30 per 100,000 females. This would seem to be related to the
publication, and following implementation in the field, of DSM-III in
1980 (72), introducing bulimia nervosa as an official diagnostic category. Hoek
et al. (58) report a nonsignificant trend for the incidence rates of bulimia
nervosa to increase by 15% each year in the period 1985–1989. Turnbull
et al. (59) noted a highly significant, threefold increase in bulimia nervosa
incidence rates for women aged 10–39 in the period 1988–1993, increasing
from 14.6 in 1988 to 51.7 in 1993. These incidence rates of bulimia nervosa can
only serve as minimal estimates of the true incidence rate. The reasons are the
84 RÅSTAM ET AL.
lack of data, the greater taboo surrounding bulimia nervosa, and its smaller
perceptibility in comparison with anorexia nervosa.
of 0.2%. The low rate may be due to the relatively young age of the investigated
population. Also, the sample size is rather small for a low-frequency disorder.
In a telephone survey, Dansky et al. (75) found DSM-IV BED to be present in
1% of 3006 adult females. Hay (85) conducted interviews to determine the
prevalence of bulimic-type eating disorders on all subjects in a large general-
population sample (3001 interviews). The mean age of the cases was 35.2 years.
Using DSM-IV criteria, a point prevalence for BED of 1 % was found. Using a
broader definition by Fairburn and Cooper (86), the prevalence was estimated at
2.5%. A weakness of the study was that diagnoses were based on a very limited
number of questions (two gating questions and three additional probes). No
information was given regarding the sensitivity and specificity of the
instrument.
Time Trends
To study the prevalence of binge eating and weight control practices in West
Germany over time, 2130 adult subjects were examined in 1997 and compared
with 1773 adults in 1990 (87). Participation was almost 70%. The same self-
report questionnaire was used in 1990 and in 1997 (complemented with a
personal interview for a subsample in 1997). The prevalence for BED dropped
from 1.5% in 1990 to 0.7% in 1997 in women and from 2.4% to 1.5% in men.
The prevalence for bulimia nervosa dropped from 2.4% to 1.1% in women and
from 2.0% to 1.1 % in men. None of the differences were statistically significant.
Social Class
Most psychiatric disorders show a higher prevalence in the lower socioeconomic
classes. It is difficult to determine whether this is the result of the social
selection process or whether it is caused by social factors (88).
For anorexia nervosa, there has been a traditional belief of an upper social
class preponderance. In reviewing the evidence, Gard and Freeman (89)
concluded that the relationship between anorexia nervosa and high socioeconomic
status is unproven, due to data collection biases including sample size, clinical
status, and referral patterns. A recent study on a large comprehensive clinical
database, covering 692 referrals to a U.K. national specialist center in 33 years’
time, challenges this conclusion: McLelland and Crisp (90) found referrals for
anorexia nervosa from the two highest social classes to be almost twice as high
as expected. They present evidence that their findings are unrelated to
86 RÅSTAM ET AL.
Level of Industrialization
It is commonly thought that anorexia nervosa is a Western illness: there
appears to be a developmental gradient across countries, with a predominance
in industrialized, developed countries, linking the disorder to an affluent
society (3). This gradient has been hypothesized to be connected with the
sociocultural theory. This theory holds that eating disorders are promoted by a
“Western” culture favoring slimness as a beauty ideal for females.
By consequence eating disorders would be less prevalent in underdeveloped,
nonWestern cultures. Unfortunately, to date few developing countries have the
facilities and means to arrive at reliable epidemiological data.
According to a recent extensive review of studies from the Far East (92),
body dissatisfaction and dieting rates were similar to those in the West. Dieting
occurred in more than 60% of females in Japan; prevalence rates were around
0.03% for anorexia nervosa and ranged from 1.9% to 2.9% for bulimia
nervosa. Community studies in China found the anorexia nervosa prevalence to
be 0.01 %, and bulimia nervosa rates ranged from 0.5% to 1.3%. The very low
rate of anorexia nervosa in the Far East may seem surprising. It could be due to
a slightly different behavioral phenotype of the syndrome, including cases
masquerading as bulimia nervosa. Reports from Eastern Europe are very scant.
In Hungary and Poland two-stage studies have been conducted; see Tables 2 and
4 (44,70). A questionnaire lifestyle study of 453 medical students between 1995
and 1999 in Slovakia showed excessive underweight (BMI=17.5 or lower)
in 1.0% of men and 2.8% of women (93), suggesting a possible eating disorder.
In Iran, Nobakht and Dezhkam (25) examined disordered eating with EAT-26 in
3100 female students, with no attrition (Table 1). Of 749 high scorers, 99.8%
completed another selfreport questionnaire to assess DMS-IV eating disorder
diagnoses. Accumulated prevalence for full-syndrome anorexia nervosa
was 0.9%, for the partial syndrome 1.84%, and for full-syndrome bulimia
nervosa 3.23%, for the partial syndrome 4.79%. Comparing 59 Iranian female
students living in Tehran to 45 female students of Iranian descent living in Los
Angeles, Abdollahi and Mann (94) found similar amounts of self-reported
disordered eating in the two samples. In a population of 351 secondary school
EPIDEMIOLOGY 87
girls in Cairo, Egypt, 11.4% scored positively on the Eating Attitude Test
(EAT) Questionnaire and were subsequently interviewed (95). Three cases
fulfilled Russell’s criteria for a diagnosis of bulimia nervosa (1.2%), and an
additional 12 individuals (3.4%) were deemed to have a partial syndrome of
bulimia nervosa.
Girls and women born in countries with a low prevalence of anorexia
nervosa seem to have an increased risk of developing the disorder after moving
to a high-frequency region (96,97). Some recent publications cast doubts on the
validity of the sociocultural theory, at least for anorexia nervosa (98,99). For
example, Hoek et al. (100) found an incidence of anorexia nervosa on the
Caribbean island of Curaçao within the lower range of rates reported in
Western countries.
Level of Urbanization
Hoek et al. (58) report that the incidence of bulimia nervosa is three to five
times higher in urbanized areas and cities than in rural areas, whereas ano rexia
nervosa is found with almost equal frequency in areas with different degrees of
urbanization. The drift hypothesis, relating urbanization differences to migration
for educational reasons, is rejected because the differences remain after
adjusting for age. Other social factors involved might be an increased pressure
to be slender and decreased social control in urbanized areas. If these hold true,
this would imply that anorexia nervosa is less sensitive to social factors than
bulimia nervosa, has a more biological origin, and is more driven by other
factors such as a tendency toward asceticism and compulsive behavior.
Occupation
Some occupations appear to be linked to an increased risk of the development
of an eating disorder (101). Typical examples are professions in the world of
fashion (102) and ballet (2). We do not know whether this is a causal factor or
rather the result of disturbed attitudes around body and shape. In other words,
are preanorectics attracted by the ballet world, or are the requirements of the
profession conducive to the development of anorexia nervosa?
According to a meta-analysis of 34 studies, elite athletes had a higher risk of
eating disorders than nonathletes. On the other hand, nonelite athletes were
more satisfied with their bodies than controls, and they seemed to have a
reduced risk of eating disorders (103). In a recent study of 181 elite women
runners in the United Kingdom (104), 7 (4%) had anorexia nervosa, 2
individuals (1%) had bulimia nervosa, and 20 (11%) females had an EDNOS.
88 RÅSTAM ET AL.
CONCLUSIONS
For anorexia nervosa an average prevalence rate of 0.3% was found for young
girls. Although Soundy et al. (76) caution for the possibility of unreliable
information, figures of an average prevalence rate of bulimia nervosa of 1 % in
women and of 0.1 % in men seem accurate. A tentative conclusion is that the
prevalence of BED is more likely to be 1 % than 4% or more.
Assuming that even the studies with the most complete case finding methods
yield an underestimate of the true incidence, as state of the art we conclude that
the overall incidence of anorexia nervosa is at least 8 per 100,000 population
per year and the incidence of bulimia nervosa is at least 12 per 100,000
population per year. The incidence rate of anorexia nervosa has increased
during the past 50 years, particularly in females aged 10–24 years. The
registered incidence of bulimia nervosa has increased, at least during the first
5 years after bulimia nervosa was added to the DSM-III (72). For BED not
enough incidence information is available to summarize.
Little is known about how many people with or without (a combination of)
known risk factors develop an eating disorder over time. Dieting seems a
general nonspecific risk factor, increasing the risk of developing an eating
disorder by about fivefold.
COMMENTS
The value of epidemiology lies in its particular methodology that gives rise to
population-based disease rates and ratios. When properly established, these
rates and ratios provide a scientific basis on the community level for treatment
planning and etiological model building. Epidemiological information is needed
to examine and extend on clinical observations.
The basic epidemiological measures are incidence and prevalence rates. For
the purpose of treatment planning, there is an ongoing need for prevalence
information at the local level. For reasons of time and cost efficiency, this is best
done by monitoring existing health care consumption registers. Attention must
be paid to the interpretation of changing consumption rates in relation to
changes in health care recruitment and admission policy. When the adequacy or
accuracy of case definition and registration is questioned, efforts are needed to
improve registration.
For the purpose of etiological model building, the mere determination of
prevalence and incidence rates is not enough. Although more is becoming
known on general and specific risk factors for the onset of an eating disorder
there still is an impressive gap. Furthermore, the developmental mechanisms of
these factors are largely unknown. The general conclusion is that dieting
EPIDEMIOLOGY 89
SUMMARY
The average prevalence rate for young girls is 0.3% for anorexia nervosa and 1%
for bulimia nervosa. The overall incidence is at least 8 per 100,000 person-years
for anorexia nervosa and 12 per 100,000 person-years for bulimia nervosa.
The incidence rate of anorexia nervosa has increased during the past
50 years, particularly in females 10–24 years old. The registered incidence of
bulimia nervosa has increased, at least during the first 5 years after bulimia
nervosa was introduced in the DSM-III.
There is a need for prospective, follow-up designs using initially healthy
subjects at high risk for developing an eating disorder. Depending on the
question to be answered, these could be matched on sex, age, and
socioeconomic status with initially healthy intermediate-and low-risk groups.
Detailed and reliable registration of case definition, demographic, and other
characteristics of the patient, symptoms, and concomitants of the dis ease or
disorder remain of the utmost importance to advance evidence-based treatment
and prevention.
REFERENCES
1. Wentz E, Gillberg C, Gillberg IC, Råstam M. Ten-year follow-up of adolescent-
onset anorexia nervosa: psychiatric disorders and overall functioning scales. J Child
Psychol Psychiatry 2001; 42:613–622.
2. Szmukler GI. The epidemiology of anorexia nervosa and bulimia. J Psychiatr Res
1985; 19:143–153.
3. Hoek HW, van Hoeken D. Review of the prevalence and incidence of eating
disorders. Int J Eat Disord 2003; 34:383–396.
4. Hsu LKG. Epidemiology of the eating disorders. Psychiatric Clin North Am 1996;
19:681–700.
5. Williams P, Tarnopolsky A, Hand D. Case definition and case identification in
psychiatric epidemiology: review and assessment. Psychol Med 1980; 10:101–114.
6. Fairburn CG, Beglin SJ. Studies of the epidemiology of bulimia nervosa. Am J
Psychiatry 1990; 147:401–408.
7. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC, 1994.
8. van Hoeken D, Lucas AR, Hoek HW. Epidemiology. In: Hoek HW, Treasure JL,
Katzman MA, eds. Neurobiology in the Treatment of Eating Disorders.
Chichester: John Wiley and Sons, 1998:97–126.
9. Hoek HW, van Hoeken D, Katzman MA. Epidemiology and cultural aspects of
eating disorders: a review. In: Maj M, Halmi K, Lopez-Ibor JJ, Sartorius N, eds.
Eating Disorders. Vol. 6. Chichester: John Wiley and Sons, 2003:75–104.
EPIDEMIOLOGY 91
10. Patton GC, Johnson-Sabine E, Wood K, Mann AH, Wakeling A. Abnormal eating
attitudes in London schoolgirls—a prospective epidemiological study: outcome at
twelve month follow-up. Psychol Med 1990; 20:383–394.
11. Patton GC, Selzer R, Coffey C, Carlin JB, Wolfe R. Onset of adolescent eating
disorders: population based cohort study over 3 years. BMJ 1999; 318:765–768.
12. Fairburn CG, Welch SL, Doll HA, Davies BA, O’Connor ME. Risk factors for
bulimia nervosa: a community-based case-control study. Arch Gen Psychiatry 1997;
54:509–517.
13. Fairburn CG, Doll HA, Welch SL, Hay PJ, Davies BA, O’Connor ME. Risk factors
for binge eating disorder: a community-based case-control study. Arch Gen
Psychiatry 1998; 55:425–432.
14. Fairburn CG, Cooper Z, Doll HA, Welch SL. Risk factors for anorexia nervosa:
three integrated case-control comparisons. Arch Gen Psychiatry 1999; 56:
468–476.
15. Johnson JG, Cohen P, Kasen S, Brook JS. Eating disorders during adolescence and
the risk for physical and mental disorders during early adulthood. Arch Gen
Psychiatry 2002; 59:545–552.
16. Johannisson K. The Dark Continent. Stockholm: Nordstedts Förlag, 1994: 131.
17. Hill AJ, Draper E, Stack J. A weight on children’s minds: body shape
dissatisfactions at 9-years old. Int J Obes Relat Metab Disord 1994; 18:383–389.
18. Maloney MJ, McGuire J, Daniels SR, Specker B. Dieting behavior and eating
attitudes in children. Pediatrics 1989; 84:482–489.
19. Sasson A, Lewin C, Roth D. Dieting behavior and eating attitudes in Israeli
children. Int J Eat Disord 1995; 17:67–72.
20. Jones JM, Bennett S, Olmsted MP, Lawson ML, Rodin G. Disordered eating
attitudes and behaviours in teenaged girls: a school-based study. CMAJ 2001; 165:
547–552.
21. Whitaker A, Davies M, Shaffer D, Johnson J, Abrams S, Walsh BT, Kalikow K.
The struggle to be thin: a survey of anorexic and bulimic symptoms in a non-
referred adolescent population. Psychol Med 1989; 19:143–163.
22. Childress AC, Brewerton TD, Hodges EL, Jarrell MP. The Kids’ Eating Disorders
Survey (KEDS): a study of middle school students. J Am Acad Child Adol
Psychiatry 1993; 32:843–850.
23. Steinhausen HC, Winkler C, Meier M. Eating disorders in adolescence in a Swiss
epidemiological study. Int J Eat Disord 1997; 22:147–151.
24. Nakamura K, Hoshino Y, Watanabe A, Honda K, Niwa S, Tominaga K, Shimai S,
Yamamoto M. Eating problems in female Japanese high school students: a
prevalence study. Int J Eat Disord 1999; 26:91–95.
25. Nobakht M, Dezhkam M. An epidemiological study of eating disorders in Iran. Int
J Eat Disord 2000; 28:265–271.
26. Koskelainen M, Sourander A, Helenius H. Dieting and weight concerns among
Finnish adolescents. Nord J Psychiatry 2001; 55:427–431.
27. Carter JC, Stewart DA, Fairburn CG. Eating disorder examination questionnaire:
norms for young adolescent girls. Behav Res Ther 2001; 39:625–632.
92 RÅSTAM ET AL.
28. Nylander I. The feeling of being fat and dieting in a school population. An
epidemiologic interview investigation. Acta Sociomed Scand 1971; 3:17–26.
29. Schleimer K. Dieting in teenage schoolgirls. A longitudinal prospective study. Acta
Paediatr Scand Suppl 1983; 312:1–54.
30. Irving LM, Wall M, Neumark-Sztainer D, Story M. Steroid use among adolescents:
findings from Project EAT. J Adol Health 2002; 30:243–252.
31. Labre MP. Adolescent boys and the muscular male body ideal. J Adol Health 2002;
30:233–242.
32. Lau B, Alsaker FD. Dieting behavior in Norwegian adolescents. Scand J Psychol
2001; 42:25–32.
33. Perry CL, McGuire MT, Neumark-Sztainer D, Story M. Characteristics of
vegetarian adolescents in a multiethnic urban population. J Adol Health 2001; 29:
406–416.
34. Råstam M. Anorexia nervosa in 51 Swedish adolescents: premorbid problems and
comorbidity. J Am Acad Child Adol Psychiatry 1992; 31:819–829.
35. Button EJ, Whitehouse A. Subclinical anorexia nervosa. Psychol Med 1981; 11:
509–516.
36. Szmukler GI. Weight and Food Preoccupation in a Population of English
Schoolgirls. Columbus, Ohio: Ross, 1983.
37. King MB. Eating disorders in a general practice population. Prevalence,
characteristics and follow-up at 12 to 18 months. Psychol Med Monogr Suppl
1989; 14:1–34.
38. Meadows GN, Palmer RL, Newball EUM, Kenrick JMT. Eating attitudes and
disorder in young women: a general practice based survey. Psychol Med 1986; 16:
351–357.
39. Johnson-Sabine E, Wood K, Patton G, Mann A, Wakeling A. Abnormal eating
attitudes in London schoolgirls—a prospective epidemiological study: factors
associated with abnormal response on screening questionnaires. Psychol Med 1988;
18:615–622.
40. Råstam M, Gillberg C, Garton M. Anorexia nervosa in a Swedish urban region. A
population-based study. Br J Psychiatry 1989; 155:642–646.
41. Whitaker A, Johnson J, Shaffer D, Rapoport JL, Kalikow K, Walsh BT, Davies M,
Braiman S, Dolinsky A. Uncommon troubles in young people: prevalence
estimates of selected psychiatric disorders in a nonreferred adolescent population.
Arch Gen Psychiatry 1990; 47:487–496.
42. Whitehouse AM, Cooper PJ, Vize CV, Hill C, Vogel L. Prevalence of eating
disorders in three Cambridge general practices: hidden and conspicuous morbidity.
Br J Gen Pract 1992; 42:57–60.
43. Rathner G, Messner K. Detection of eating disorders in a small rural town: an
epidemiological study. Psychol Med 1993; 23:175–184.
44. Wlodarçzyk-Bisaga K, Dolan B. A two-stage epidemiological study of abnormal
eating attitudes and their prospective risk factors in Polish schoolgirls. Psychol Med
1996; 26:1021–1032.
EPIDEMIOLOGY 93
63. Young JK. Estrogen and the etiology of anorexia nervosa. Neurosci Biobehav Rev
1991; 15:327–331.
64. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, Herman-Giddens ME. Earlier
onset of puberty in girls: relation to increased body mass index and race. Pediatrics
2001; 108:347–353.
65. Wakeling A. Epidemiology of anorexia nervosa. Psychiatry Res 1996; 62:3–9.
66. Williams P, King M. The “epidemic” of anorexia nervosa: another medical myth?
Lancet 1987; 1:205–207.
67. Fombonne E. Anorexia nervosa. No evidence of an increase. Br J Psychiatry 1995;
166:462–471.
68. Gillberg C, Råstam M, Gillberg IC. Anorexia nervosa: who sees the patients and
who do the patients see? Acta Paediatrica 1994; 83:967–971.
69. Bushnell JA, Wells JE, Hornblow AR, Oakley-Browne MA, Joyce P. Prevalence of
three bulimia syndromes in the general population. Psychol Med 1990; 20:
671–680.
70. Szabo P, Tury F. The prevalence of bulimia nervosa in a Hungarian college and
secondary school population. Psychother Psychosom 1991; 56:43–47.
71. Santonastaso P, Zanetti T, Sala A, Favaretto G, Vidotto G, Favaro A. Prevalence of
eating disorders in Italy: a survey on a sample of 16-year-old female students.
Psychother Psychosom 1996; 65:158–162.
72. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 3d ed. Washington, DC,1980.
73. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 3d ed. revised. Washington, DC, 1987.
74. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom DS, Kennedy S, Kaplan AS,
Woodside DB. Bulimia nervosa in a Canadian community sample: prevalence and
comparison of subgroups. Am J Psychiatry 1995; 152:1052–1058.
75. Dansky BS, Brewerton TD, Kilpatrick DG, O’Neil PM. The National Women’s
Study: relationship of victimization and posttraumatic stress disorder to bulimia
nervosa. Int J Eat Disord 1997; 21:213–228.
76. Soundy TJ, Lucas AR, Suman VJ, Melton LJ III. Bulimia nervosa in Rochester,
Minnesota from 1980 to 1990. Psychol Med 1995; 25:1065–1071.
77. World Health Organization. The ICD-10 Classification of Mental and Behavioural
Disorders: Clinial Descriptions and Diagnostic Guidelines. Geneva, 1992.
78. World Health Organization. The ICD-9 Classification of Mental and Behavioral
Disorders. Clinical Descriptions and Diagnostic Guidelines. Geneva, 1979.
79. Russell G. Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol Med
1979; 9:429–448.
80. Pagsberg AK, Wang AR. Epidemiology of anorexia nervosa and bulimia nervosa in
Bornholm County, Denmark, 1970–1989. Acta Psychiatr Scand 1994; 90:
259–265.
81. Schwitzer AM, Rodriguez LE, Thomas C, Salimi L. The eating disorders NOS
diagnostic profile among college women. J Am Coll Health 2001; 49:157–166.
EPIDEMIOLOGY 95
82. Striegel-Moore RH, Cachelin FM, Dohm FA, Pike KM, Wilfley DE, Fairburn CG.
Comparisonof binge eating disorder and bulimia nervosa in a community sample.
Int J Eat Disord 2001; 29:157–165.
83. Hay P, Fairburn C. The validity of the DSM-IV scheme for classifying bulimic
eating disorders. Int J Eat Disord 1998; 23:7–15.
84. Cotrufo P, Barretta V, Monteleone P, Maj M. Full-syndrome, partialsyndrome and
subclinical eating disorders: an epidemiological study of female students in
Southern Italy. Acta Psychiatr Scand 1998; 98:112–115.
85. Hay P. The epidemiology of eating disorder behaviors: an Australian community-
based survey. Int J Eat Disord 1998; 23:371–382.
86. Fairburn CG, Cooper Z. The Eating Disorder Examination. 12th ed. In: Fairburn
CG, Wilson GT, eds. Binge Eating: Nature, Assessment and Treatment. New
York: Guilford Press, 1993:317–360.
87. Westenhoefer J. Prevalence of eating disorders and weight control practices in
Germany in 1990 and 1997. Int J Eat Disord 2001; 29:477–481.
88. Dohrenwend BP, Levav I, Shrout PE, Schwartz S, Naveh G, Link BG, Skodol AE,
Stueve A. Socioeconomic status and psychiatric disorders: the causationselection
issue. Science 1992; 255:946–952.
89. Gard MCE, Freeman CP. The dismantling of a myth: a review of eating disorders
and socioeconomic status. Int J Eat Disord 1996; 20:1–12.
90. McClelland L, Crisp A. Anorexia nervosa and social class. Int J Eat Disord 2001;
29:150–156.
91. Råstam M, Gillberg C. The family background in anorexia nervosa: a population-
based study. J Am Acad Child Adol Psychiatry 1991; 30:283–289.
92. Tsai G. Eating disorders in the Far East. Eat Weight Disord 2000; 5:183–197.
93. Baska T, Straka S, Madar R. Smoking and some life-style changes in medical
students—Slovakia, 1995–1999. Cent Eur J Public Health 2001; 9:147–149.
94. Abdollahi P, Mann T. Eating disorder symptoms and body image concerns in Iran:
comparisons between Iranian women in Iran and in America. Int J Eat Disord
2001; 30:259–268.
95. Nasser M. Screening for abnormal eating attitudes in a population of Egyptian
secondary school girls. Soc Psychiatry Psychiatr Epidemiol 1994; 29:25–30.
96. Nasser M. Comparative study of the prevalence of abnormal eating attitudes among
Arab female students of both London and Cairo Universities. Psychol Med 1986;
16:621–625.
97. Dolan B, Lacey JH, Evans C. Eating behaviour and attitudes to weight and shape in
British women from three ethnic groups. Br J Psychiatry 1990; 157:523–528.
98. Nasser M. Culture and Weight Consciousness. London: Routledge, 1997.
99. Nasser M, Katzman MA, Gordon RA, eds. Eating disorders and cultures in
transition. London: Routledge, 2001.
100. Hoek HW, van Harten PN, van Hoeken D, Susser E. Lack of relation between
culture and anorexia nervosa: results of an incidence study on Curaçao. N Engl J
Med 1998; 338:1231–1232.
96 RÅSTAM ET AL.
101. Vandereycken W, Hoek HW. Are eating disorders culture-bound syndromes? In:
Halmi KA, ed. Psychobiology and Treatment of Anorexia Nervosa and Bulimia
Nervosa. Washington, DC: American Psychiatric Press, 1993:19–36.
102. Santonastaso P, Mondini S, Favaro A. Are fashion models a group at risk for eating
disorders and substance abuse? Psychother Psychosom 2002; 71:168–172.
103. Smolak L, Murnen SK, Ruble AE. Female athletes and eating problems: a meta-
analysis. Int J Eat Disord 2000; 27:371–380.
104. Hulley AJ, Hill AJ. Eating disorders and health in elite women distance runners.
Int J Eat Disord 2001; 30:312–317.
5
Long-Term Outcome, Course of Illness and
Mortality in Anorexia Nervosa, Bulimia
Nervosa, and Binge Eating Disorder
Pamela K.Keel
Harvard University
Cambridge, Massachusetts, U.S.A.
David B.Herzog
Massachusetts General Hospital
Boston, Massachusetts, U.S.A.
ANOREXIA NERVOSA
Mortality
Anorexia nervosa has been associated with one of the highest risks of premature
death among psychiatric disorders (1). Estimates of crude mortality rates across
outcome studies suggest that 5–5.9% of patients diagnosed with anorexia
nervosa will suffer a fatal outcome (2,3), with a 5.6% crude mortality rate per
decade (4). Standardized mortality ratios (representing the ratio of the observed
number of deaths to the expected number of deaths in a matched population)
have ranged from 1.32 (4b) to 12.82 (4c) with most studies reporting
significantly elevated risk of premature death. Earlier studies tended to report
starvation as the cause of death; conversely, more recent studies have reported
suicide as a leading cause of death in anorexia nervosa (5). This shift may reflect
several coinciding secular trends. First, the diagnostic criteria for anorexia
nervosa shifted from requiring a loss of 25% of prior body weight to weight 15%
below that expected for age and height. For most individuals who develop
anorexia nervosa during adolescence, the shift effectively decreased the weight
loss required to be diagnosed with anorexia nervosa. Similarly, epidemiological
data have demonstrated that weight of patients presenting for treatment of
anorexia nervosa has increased over time (6), reflecting both the change in
diagnostic criteria and the possibility of earlier intervention. Finally, there may
have been secular improvements in techniques employed to refeed
undernourished patients. Few predictors of fatal outcome have been revealed.
These have included low weight (7,8), poor psychosocial function (9,10),
longer duration of follow-up (2,10), and severity of alcohol use disorders (10).
Recovery
Although longer duration of follow-up has been associated with increased risk of
death, it is also associated with higher rates of recovery (2,11). Prospective,
longitudinal analyses of anorexia nervosa course suggest that recovery increases
at a slow and steady rate, with continued recovery occurring years after
intake (11) or treatment (12). Collapsing recovery rates across studies of
varying durations of follow-up, Steinhausen (2) reported that approximately
46% of patients recover, 33% improve (but remain symptomatic), and 20%
remain chronically ill.
LONG-TERM OUTCOME 99
Relapse
Unlike mortality and recovery, which can be investigated in outcome studies,
relapse can only be assessed by studies of eating disorder course. Thus, fewer
studies have elucidated this important variable. Morgan and Russell (13)
reported that 51 % of patients hospitalized for anorexia nervosa required
readmission over the course of follow-up. Herzog and colleagues (11) reported
that 40% of women with anorexia nervosa who achieve full recovery later
relapsed. Finally, Strober et al. (12) reported that approximately 30% of
women who had achieved weight recovery during hospitalization relapsed after
discharge, and they recorded even lower rates of relapse among women
considered partially recovered (9.8%) or fully recovered (0%) over follow-up.
These latter data indicate that the definition of recovery (or remission) has a
significant effect on the likelihood of relapse. A common pattern among patients
with anorexia nervosa is to experience improvement in weight (a sign of
recovery) as a consequence of the development of binge eating episodes (a sign
of cross-over).
Cross-over
A recent report from a prospective longitudinal study of eating disorders
indicated that the majority of women with the restricting subtype of anorexia
nervosa develop symptoms of binge eating and purging over time (14). These
findings are consistent with the restraint hypothesis (15), which posits that
dietary restriction increases susceptibility to develop binge eating episodes. For
some patients with anorexia nervosa, binge eating and purging occur at low
weight and the person continues to suffer from anorexia nervosa. For others,
binge eating results in weight gain and the binge-purge behaviors are maintained
at normal weight representing cross-over from anorexia nervosa to bulimia
nervosa. Across follow-up studies, approximately 10–15% of individuals
presenting with anorexia nervosa cross over and develop bulimia nervosa(16).
Prognostic Factors
Table 1 presents prognostic factors adapted from a recent review of outcome in
anorexia nervosa (2). As can be seen from Table 1, no prognostic factor has
been unambiguously associated with prognosis in anorexia nervosa. However,
there is a clear trend in the nature of the contradictory results. Studies finding a
specific direction of association are most often contradicted by studies finding
no significant association rather than an equal number of studies finding an
association in the opposite direction. For example, 12 studies have suggested
100 KEEL AND HERZOG
Note: Data are adapted from Steinhausen (2) to allow comparison with data from Keel
and Mitchell (19) updated in Table 2.
Treatment Utilization
In Germany, Fichter and colleagues (17) reported that 63% of women received
further inpatient treatment following baseline inpatient care for anorexia
nervosa. Levels of outpatient care were also high, with approximately 89% of
women receiving some form of outpatient care during follow-up (among a
subset of women for whom data were available). This treatment comprised an
average of 69.3 individuals sessions, 5.0 group sessions, and 0.4 family session.
In the United States, Striegel-Moore et al. (18) reported that female patients
with anorexia nervosa utilized an average of 26.0 days of inpatient care and
LONG-TERM OUTCOME 101
17.0 days of outpatient care during one year. Male patients utilized an average of
15.6 and 9.2 days of inpatient and outpatient care per year, respectively.
BULIMIA NERVOSA
Mortality
A crude mortality rate of 0.3% has been reported across follow-up studies of
bulimia nervosa (19). However, this value might represent an underestimate
given the relatively short duration of follow-up across studies and the low
ascertainment rates for several studies. Few studies have calculated standardized
mortality ratios for bulimia nervosa, and no original report has found a
standardized mortality ratio that differed significantly from 1. In a recent meta-
analysis of mortality in eating disorders, Nielsen (4) reported a significantly
elevated SMR for bulimia nervosa. However, this analysis included studies
reporting mortality among “bulimic patients” comprising both normal-weight
bulimia nervosa and the binge-purge subtype of anorexia nervosa. In a recent
examination of mortality in eating disorders, Keel et al. (10) found that
mortality was similarly elevated for both the restricting and binge-purge
subtypes of anorexia nervosa but was not elevated in bulimia nervosa. As the
ascertainment methods and duration of follow-up were uniform across
diagnostic categories, this study provides the strongest evidence that bulimia
nervosa is not associated with increased risk of premature death. Causes of
premature death have primarily included suicide and automobile accidents (19).
Because risk of death does not appear to be elevated in bulimia nervosa, no
predictors of fatal outcome have been revealed.
Recovery
Prospective, longitudinal analyses of bulimia nervosa course (11,20) suggest
that the majority of patients recover from their eating disorder at some point
during the course of follow-up. Combining results across outcome studies of
varying durations of follow-up, Keel and Mitchell (19) reported that
approximately 50% of individuals presenting with bulimia nervosa recover and
maintain their recovery, 30% are improved but maintain partial syndromes, and
20% continue to meet full criteria for bulimia nervosa. Follow-up studies of
longer duration (21,22) suggest that rates of full bulimia nervosa drop to 10%
by 10 years follow-up.
102 KEEL AND HERZOG
Relapse
Rates of relapse have ranged from 26% to 50% across follow-up studies of
bulimia nervosa (19,23,24), with definitions of “recovery” explaining the
majority of variance in these estimates. Similar to the patterns observed with
anorexia nervosa, more stringent definitions of recovery are associated with lower
relapse rates than less stringent definitions (25,26). This pattern raises the
question of whether studies are assessing relapse or simple symptom
fluctuation. Despite considerable differences in methodology across studies,
relapse rates converge around 30% (19), suggesting that approximately onethird
of women who initially recover from their eating disorder suffer a resurgence of
their bulimic symptoms.
Crossover
Across follow-up studies, between 0% and 7% crossover from bulimia nervosa
to anorexia nervosa (19,24). However, it remains unclear whether these
represent new-onset cases of anorexia nervosa or relapse from previous
episodes of anorexia nervosa that had crossed over to bulimia nervosa.
Crossover to binge eating disorder also seems low, ranging from 0% to
1.1% (19,21,24). A recent paper concerning the predictive validity of bulimia
nervosa as a diagnostic category (27) reported that over time women with bulimia
nervosa were more likely to continue to suffer from bulimia nervosa than the
other recognized eating disorders of the DSM. Although approximately 10%
reported a brief history of binge eating in the absence of inappropriate
compensatory behavior, all but one of these women experienced full remission
of her eating disorder, suggesting that this symptom pattern represented a phase
of recovery rather than development of a distinct eating disorder. Conversely,
approximately 10% of women suffered from a purging disorder, characterized
by recurrent purging in the absence of objectively large binge episodes at normal
weight. The likelihood of suffering from a purging disorder did not differ
significantly from the likelihood of suffering from bulimia nervosa at long-term
follow-up and was significantly more likely than suffering from binge eating
disorder (27). Thus, to the extent that cross-over occurs in bulimia nervosa, it
seems to involve crossing over to a purging disorder.
Prognostic Factors
Table 2 presents prognostic factors updated from a recent review of outcome in
bulimia nervosa (19). As can be seen from the Table 2, few prognostic factors
have been replicated across studies. Similar to the pattern observed in Table 1,
LONG-TERM OUTCOME 103
Note: Data are updated from Keel and Mitchell (19) with findings from studies of follow-
up duration 5 years (21,24,43).
most often findings diverge along the lines of a significant association in one
direction versus no significant association. For example, six studies reported that
longer duration of symptoms prior to presentation was associated with poor
prognosis in bulimia nervosa, and three studies found no significant association.
However, no studies reported that a longer duration of symptoms was
associated with favorable prognosis in bulimia nervosa. Similarly, six studies
suggested that personality disturbance was associated with poor prognosis, and
four studies found no significant association, but no studies reported that
personality disturbances were associated with favorable outcome. Despite this
pattern for duration of symptoms and personality disturbance, the number of
studies suggesting no significant associations is greater than the number of
studies suggesting significant associations for the remaining variables, including
the impact of treatment. However, a recent investigation (20) has demonstrated
an association between baseline treatment and long-term course in bulimia
nervosa, suggesting that cognitive behavioral therapy may speed recovery (28).
Treatment Utilization
Although most women who suffer from bulimia nervosa may never seek
treatment (23,29), treatment utilization is high among those who do. In
Germany, Fichter et al. (24) reported that 67% of women received further
inpatient treatment following baseline inpatient care for bulimia nervosa. Levels
of outpatient care were also high, with approximately 83% of women receiving
some form of outpatient care during follow-up (among a subset of women for
whom data were available). This treatment comprised an average of 59.2
individuals sessions, 10.9 group sessions, and 0.7 family session (24). In the
United States, Striegel-Moore et al. (18) reported that female patients with
bulimia nervosa utilized an average of 14.7 days of inpatient care and 15.6 days
104 KEEL AND HERZOG
of outpatient care during one year. Male patients utilized an average of 21.7 and
9.1 days of inpatient and outpatient care per year, respectively. Although
inpatient care did not differ between female and male patients, women received
significantly more outpatient care (18).
bulimia nervosa is not. Suicide has been noted as a common cause of death for
both disorders. Interestingly, rates and lethality of suicide attempts have not
differed between women with anorexia nervosa versus bulimia nervosa (38).
Thus, suicide attempts appear to be more likely to result in death among
women suffering from anorexia nervosa. One possible explanation for this
difference is that starvation compromises the health of individuals with anorexia
nervosa, leaving them less likely to survive a suicide attempt.
Within studies (11,17), anorexia nervosa has been associated with both lower
and slower rates of recovery in comparison with bulimia nervosa. However,
collapsing results across studies suggests a similar distribution of recovery,
improvement, and chronicity across syndromes (2,19). However, this latter
comparison is flawed because follow-up studies for anorexia nervosa have a
significantly longer duration of follow-up in comparison with follow-up studies
of bulimia nervosa, and longer duration of follow-up is associated with higher rates
of recovery for both syndromes (2,21). Thus, the apparent similarity in results
between disorders across studies is likely an artifact of differences in duration of
follow-up.
Despite differing rates of recovery, relapse rates were surprisingly similar
between anorexia nervosa and bulimia nervosa within one study of longterm
course (21). However, the relationship between relapse and chronicity likely
differs between disorders. Because a higher percentage of women with bulimia
nervosa than women with anorexia nervosa recover at some point during the
course of follow-up, a higher percentage of women who are ill at follow-up in
bulimia nervosa outcome studies represent women who have recovered and
relapsed. Thus, for women with bulimia nervosa, chronicity appears to be
characterized by considerable symptom fluctuation. Conversely, a smaller
percentage of women recover from anorexia nervosa; thus, a smaller
percentage of women who remain ill are women who achieved even brief
periods of remission. Thus, chronicity within anorexia nervosa is marked by a
more steady course of illness. This difference may also be reflected in the nature
of the core features of these syndromes. For anorexia nervosa, the core
symptom represents the absence of a behavior—eating. Conversely, for bulimia
nervosa, the core symptoms represent the presence of a set of behaviors—binge
eating and purging. Thus, in order to develop anorexia nervosa an individual
must demonstrate persistence in not eating. Conversely, a woman can develop
bulimia nervosa by having relatively normal eating behaviors interrupted by
episodes of abnormal eating behaviors. For these reasons, the nature of a
chronic course may differ markedly between these disorders.
Patterns of cross-over also differ markedly between anorexia nervosa and
bulimia nervosa. Approximately 10–50% of women with anorexia nervosa
cross over and develop bulimia nervosa, and approximately 30% of women with
106 KEEL AND HERZOG
individuals with bulimia nervosa received treatment during the course of follow-
up, resulting in a total of 40% ever receiving treatment for an eating disorder.
CONCLUSIONS
In the introduction, we noted that data on long-term course and outcome could
improve our treatment, diagnosis, and understanding of eating disorders. Such
data support the predictive validity of distinguishing between anorexia nervosa
and bulimia nervosa. These disorders appear to be associated with different
rates of mortality, recovery, relapse, cross-over, and distinct sets of prognostic
indicators (including differential treatment response). While promising
treatments have been identified for bulimia nervosa, significant work remains for
anorexia nervosa. Current controlled treatment outcome studies for anorexia
nervosa should be designed to facilitate repeated follow-up assessments.
While few studies have assessed the long-term outcome of bulimia nervosa
and binge eating disorder, even fewer have examined the natural history of
these disorders at long-term follow-up. Almost all longitudinal studies of eating
disorders (including those on anorexia nervosa) are based on treatment seeking
samples, even though the majority of women with eating disorders may not seek
treatment (23,29). The reliance on treatment seeking samples introduces
certain biases in study results. For example, Fairburn et al. (29) reported higher
rates of comorbid disorders in women seeking treatment for bulimia nervosa
than in women with bulimia nervosa from the community. This is referred to as
Berkson’s bias (41) and represents the increased likelihood of comorbidity
among treatment-seeking individuals compared to individuals who do not seek
treatment. Indeed, this bias likely explains the prospective treatment utilization
was predicted by greater severity of eating disorder symptoms, comorbid mood
disorders, and comorbid personality disorders (40). Thus, follow-up studies of
treatment seeking samples may present a more dire description of outcome due
to Berkson’s bias. Furthermore, relying on treatment seeking samples prevents
LONG-TERM OUTCOME 109
REFERENCES
Note’. The following references were included in the original reports of
prognostic indicators for anorexia nervosa and bulimia nervosa presented in
Tables 1 and2: (2,11–13,17,19,22,26,42,44–124).
1. Harris EC, Barraclough B. Excess mortality in mental disorder. Brit J Psychiatry
1998; 17:11–53.
2. Steinhausen H-C. The Outcome of Anorexia Nervosa in the 20th Century. Am J
Psychiatry 2002; 159(8): 1284–1293.
3. Sullivan PF. Mortality in anorexia nervosa. Am J Psychiatry 1995; 152:1073–1074.
4a. Nielsen S. Epidemiology and mortality in eating disorders. Eating Disorders 2001;
24:201–214.
4b. Crisp AH, Callander JS, Halek C, Hsu LKG. Long-term mortality in anorexia
nervosa. Brit J Psychiatry 1992; 161:104–107.
4c. Eckert E, Halmi KA, Marchi P, Grove W, Crosby R. Ten-year follow-up study of
anorexia nervosa: clinical course and outcome. Psychol Med 1995; 25:143–156.
5. Nielsen S, Moller-Madsen S, Isager T, Jorgensen J, Pagsberg K, Theander S.
Standardized mortality in eating disorders: a quantitative summary of previously
published and new evidence. J Psychosom Res 1998; 44:413–434.
6. Eagles JM, Johnston MI, Hunter D, Lobban M, Millar HR. Increasing incidence of
anorexia nervosa in the female population of northeast Scotland. Am J Psychiatry
1995; 152:1266–1271.
7. Patton GC. Mortality in eating disorders. Psychol Med 1988; 18:947–951.
8. Herzog W, Deter HC, Fiehn W, Petzold E. Medical findings and predictors
of long-term physical outcome in anorexia nervosa: a prospective, 12-year
followup study. Psychol Med 1997; 27:269–279.
9. Engel K, Wittern M, Hentze M, Meyer AE. Long-term stability of anorexia
nervosa treatments: Follow-up study of 218 patients. Psychiatric Dev 1989; 4:
395–407.
110 KEEL AND HERZOG
10. Keel PK, Dorer DJ, Eddy KT, Franko DL, Charatan DL, Herzog DB, Predictors of
mortality in eating disorders. Arch Gen Psychiatry 2003; 60:179–183.
11. Herzog D, Dorer DJ, Keel PK, Selwyn SE, Ekeblad ER, Flores A, Greenwood
DN, Burwell RA, Keller MB. Recovery and relapse in anorexia and bulimia
nervosa: a 7.5-year follow-up study. J Am Acad Child Adol Psychiatry 1999; 38:
829–837.
12. Strober M, Freeman R, Morrell W. The long-term course of servere anorexia
nervosa in adolescents: survival analysis of recovery, relapse, and outcome
predictors over 10–15 years in a prospective study. Int J Eat Disord 1997; 22:
339–360.
13. Morgan H, Russell GFM. Value of family background and clinical features as
predictors of long-term outcome in anorexia nervosa: four-year follow-up study of
41 patients. Psychol Med 1975; 5:355–371.
14. Eddy KT, Keel PK, Dorer DJ, Delinsky SS, Franko DL, Herzog DB. Longitudinal
comparison of anorexia nervosa subtypes. Int J Eat Disord 2002; 31:191–201.
15. Polivy J, Herman CP. Dieting and binging: a causal analysis. Am Psychologist
1985; 40:193–201.
16. Herzog DB, Keller MB, Lavori PW. Outcome in anorexia nervosa and bulimia
nervosa: a review of the literature. J Nerv Ment Dis 1988; 176:131–143.
17. Fichter M, Quadlieg N. Six-year course and outcome of anorexia nervosa. Int J
Eating Disord 1999; 26:359–385.
18. Striegel-Moore RH, Leslie D, Petrill SA, Garvin V, Rosenheck RA. One-year use
and cost of inpatient and outpatient services among female and male patients with
an eating disorder: evidence from a national database of health insurance claims. Int
J Eat Disord 2000; 27:381–389.
19. Keel PK, Mitchell JE. Outcome in bulimia nervosa. Am J Psychiatry 1997; 154(3):
313–321.
20. Miller KB, Keel PK, Crow SJ, Thuras P, Mitchell JE: Treatment and treatment
response predict the long-term course of bulimia nervosa. Submitted.
21. Keel PK, Mitchell JE, Miller KB, Davis TL, Crow SJ. Long-term outcome of bulimia
nervosa. Arch Gen Psychiatry 1999; 56:63–69.
22. Collings S, King M. Ten-year follow-up of 50 patients with bulimia nervosa. Br J
Psychiatry 1994; 164:80–87.
23. Fairburn CG, Cooper Z, Doll HA, Norman P, O’Conner M. The natural course of
bulimia nervosa and binge eating disorder in young women. Arch Gen Psychiatry
2000; 57:659–665.
24. Fichter MM, Quadflieg N. Six-year course of bulimia nervosa. Int J Eat Disord
1997; 22:361–384.
25. Field AE, Herzog DB, Keller MB, West J, Nussbaum K, Colditz GA.
Distinguishing recovery from remission in a cohort of bulimic women: how should
asymptomatic periods be described? J Clin Epidemiol 1997; 50:1339–1345.
26. Olmsted M, Kaplan AS, Rockert W. Rate and prediction of relapse in bulimia
nervosa. Am J Psychiatry 1994; 151:738–743.
LONG-TERM OUTCOME 111
27. Keel PK, Mitchell JE, Miller KB, Davis TL, Crow SJ. Predictive validity of bulimia
nervosa. Am J Psychiatry 2000; 157:136–138.
28. Keel PK, Mitchell JE, Davis TL, Crow SJ. The long-term impact of treatment in
women diagnosed with bulimia nervosa. Int J Eat Disord 2002; 31:151–158.
29. Fairburn CG, Welch SL, Norman PA, O’Connor ME, Doll HA. Bias and bulimia
nervosa: how typical are clinic cases? Am J Psychiatry 1996; 153:386–391.
30. American Psychiatric Association. Diagnostic and Statistical Manual for Mental
Disorders. 4th ed. Washington, DC, 1994.
31. Cachelin FM, Striegel-Moore RH, Elder KA, Pike KM, Wilfley DE, Fairburn CG.
Natural course of a community sample of women with binge eating disorder. Int J
Eat Disord 1999; 25:45–54.
32. Agras WS, Telch CF, Arnow B, Eldredge K, Marnell M. One-year follow-up of
cognitive-behavioral therapy for obese individuals with binge eating disorder.
J Consult Clin Psychol 1997; 64:343–347.
33. Devlin MJ, Goldfein JA, Carino JS, Wolk SL. Open treatment of overweight binge
eaters with phentermine and fluoxetine as an adjunct to cognitivebehavioral
therapy. Int J Eat Disord 2000; 28:325–332.
34. Peterson CB, Mitchell JE, Engbloom S, Nugent S, Pederson MM, Crow SJ, Thuras
P. Self-help versus therapist-led group cognitive-behavioral treatment of binge
eating disorder and follow-up. Int J Eat Disord 2001; 30:363–374.
35. Ricca V, Mannucci E, Mezzani B, Moretti S, Di Bernardo M, Bertelli M, Rotella
CM, Faravelli C. Fluoxetine and fluvoxamine combined with individual cognitive-
behaviour therapy in binge eating disorder: a one-year follow-up study. Psychother
Psychosom 2001; 70:298–306.
36. Ciano R, Rocco PL, Angarano A, Biasin E, Balestrieri M. Group-analytic and
psychoeducational therapies for binge-eating disorder: an exploratory study on
efficacy and persistence of effects. Psychother Res 2002; 12:231–239.
37. Fichter MM, Quadflieg N, Gnutzman A. Binge eating disorder: treatment outcome
over a 6-year course. J Psychosom Res 1998; 44:385–405.
38. Franko DL, Keel PK, Dorer DJ, Renn R, Eddy KT, Herzog DB. Suicidality in
eating disorders: data from a 12-year longitudinal study. Submitted.
39. Peterson CB, Mitchell JE. Psychological and pharmacological treatment of eating
disorders: a review of research findings. J Clin Psychol 1999; 55:685–697.
40. Keel PK, Dorer DJ, Eddy KT, Delinsky SS, Franko DL, Blais MB, Keller MB,
Herzog DB. Predictors of treatment utilization among women with anorexia and
bulimia nervosa. Am J Psychiatry 2002; 159:140–142.
41. Berkson J. Limitations of the application of fourfold table analysis to hospital data.
Biometrics 1946; 2:47–53.
42. Fairburn C, Norman PA, Welch SL, O’Connor ME, Doll HA, Peveler RC. A
prospective study of outcome in bulimia nervosa and the long-term effects of three
psychological treatments. Arch Gen Psychiatry 1995; 52:304–312.
43. Reas D, Williamson DA, Martin CK, Zucker NL. Duration of illness predicts
outcome for bulimia nervosa: a long-term follow-up study. Int J Eat Disord 2000;
27:428–434.
112 KEEL AND HERZOG
63. Fichter MM, Quadflieg N, Rief W. Longer-term course (6-year) course of bulimia
nervosa. Neuropsychopharmacology 1994; 10:7728.
64. Fichter M, Quadfleig N, Rief W. Course of multi-impulsive bulimia. Psychol Med
1994; 24:591–604.
65. Frazier S. Anorexia nervosa. Dis Nerv Syst 1965; 26:155–159.
66. Garfinkel P, Moldofsky H, Garner DM. The outcome of anorexia nervosa:
significance of clinical features, body image and behavior modification. In: Vigersky
R, ed. Anorexia Nervosa. New York: Raven Press, 1977:315–329.
67. Giles T, Young RR, Young DE. Behavioral treatment of severe bulimia. Behav
Ther 1985; 16:393–405.
68. Goetz P, Succop RA, Reinhart JB, Miller A. Anorexia nervosa in children: a follow-
up study. Am J Orthopsychiatry 1977; 47:597–603.
69. Greenfeld D, Anyan WR, Hobart M, Quinlan DM, Plantes M. Insight into illness
and outcome in anorexia nervosa. Int J Eat Disord 1991; 10:101–109.
70. Hall A, Slim E, Hawker F, Salmond C. Anorexia nervosa—long-term outcome in
50 female patients. Br J Psychiatry 1984; 145:407–413.
71. Halmi K, Brodland G, Loney J. Prognosis in anorexia nervosa. Ann Intern Med
1973; 78:907–909.
72. Halmi K, Bordland G, Rigas C. A follow-up study of seventy-nine patients with
anorexia nervosa: an evaluation of prognostic factors and diagnostic criteria. In:
Winokur G, Roff M, Wirt RD, eds. Life History Research in Psychopathology.
Vol. 4. Minneapolis: University of Minnesota Press, 1976:290–300.
73. Hawley R. The outcome of anorexia nervosa in younger subjects. Br J Psychiatry
1985; 146:657–660.
74. Herpetz-Dahlmann B, Wewetzer C, Schulz E, Remschmidt H. Course and
outcome in adolescent anorexia nervosa. Int J Eat Disord 1996; 19:335–345.
75. Herzog D, Sacks NR, Keller MB, Lavori PW, von Ranson KB, Gray HM. Patterns
and predictors of recovery in anorexia nervosa and bulimia nervosa. J Am Acad
Child Adol Psychiatry 1993; 32:835–842.
76. Herzog T, Hartmann A, Sandholz A, Stammer H. Prognostic factors in outpatient
psychotherapy of bulimia. Psychother Psychosom 1991; 56:48–55.
77. Higgs J, Goodyer IM, Birch J. Anorexia nervosa and food avoidance emotional
disorder. Arch Dis Child 1989; 64:346–351.
78. Hsu L, Holder D. Bulimia nervosa: treatment and short-term outcome. Psychol
Med 1986; 16:65–70.
79. Hsu L, Crisp AH, Harding B. Outcome of anorexia nervosa. Lancet 1979; 1:
61–65.
80. Hudson J, Pope HG, Keck PE, McElroy SL. Treatment of bulimia nervosa with
trazodone: short-term response and long-term follow-up. Clin Neuropharmacol
1989; 12(suppl 1):S38-S46.
81. Jarman F, Rickards WS, Hudson L. Late adolescent outcome of early-onset
anorexia nervosa. J Paediatr Child Health 1991; 27:221–227.
114 KEEL AND HERZOG
In the field of eating disorders, more than 30 variables have been reported as
risk factors for the development of an eating disorder (Table 1). Among these
variables, risk has been assessed from different perspectives: reported risk
factors include social, familial, psychological, developmental, and biological
factors. For many of these factors, the question of whether they occurred prior
to the onset of the eating disorder has not yet been definitively answered.
Therefore, it is impossible to determine whether they are symptoms,
maintaining factors, consequences, or “scars” of the disorder.
The inconsistent use of the term risk factor as well as the lack of precise
definitions led Kraemer and coworkers to set out a conceptual basis for a
typology of risk factors (1,2). This theoretical framework forms the basis of our
overview on risk factors for eating disorders.
In the past, risk and etiological factors for eating disorders have either been
proposed from a specific theoretical perspective (e.g., biological, cognitive-
behavioral, psychodynamic) or from an integrative perspective (e.g.,
biopsychosocial model). Factors in these models can be based on both clinical
experience and empirical data, but the empirical foundation can vary from very
strong to very weak and can comprise a wide range of methods and definitions
for risk and etiologic factors. In contrast, the risk factor approach applied here
118 JACOBI ET AL.
for the different eating disorder syndromes, and discuss additional risk factor
characteristics (i.e., specificity, potency).
METHOD
The methodology of our approach has been described in detail in Jacobi
et al. (5). Therefore, only the most important methodological issues are
summarized here.
RISK FACTORS 121
FIGURE 2 Risk factors, fixed and variable markers, and retrospective correlates for bulimia nervosa.
RISK FACTORS 125
Gender
In both clinical and nonclinical samples, anorexia and bulimia nervosa have been
observed to occur predominantly in females (14,15,22–25): populationbased
studies estimate a female-to-male ratio of 10:1 (26,27). Since gender is an
immutable characteristic and asymmetrical gender distributions have been found
for other mental disorders, e.g., (28), female status is classifiable as a
nonspecific fixed marker for both anorexia and bulimia nervosa.
Ethnicity
Though eating disorders have been traditionally regarded as a predominantly
Caucasian issue [see review by Striegel-Moore and Smolak (29)], a literature
survey from Crago et al. (30) revealed a more complex ethnic distribution
pattern: native Americans were noted as having higher rates of eating disorders
than Caucasians, whereas equal rates were reported for Hispanics and lower
rates for Asians and blacks. The results from two further studies also point to
lower rates of anorexia and bulimia nervosa among Asians (31,32). Therefore,
non-Asian ethnicity can be classified as a fixed marker of currently unknown
specificity.
Acculturation
An association between the level of acculturation within ethnic minorities and
the presence of eating disorder symptoms has been reported in a number of
cross-sectional studies (33–35). On the basis of the assumption that
acculturation predates onset of eating disorders symptoms, it is classified as a
retrospective correlate of unknown specificity.
Age
In both clinical and population-based surveys, the peak incidence of eating
disorders has been found in the age range from adolescence to early
adulthood (36). The magnitude of the age-associated increase in risk depends on
which age groups are compared. As yet, direct comparisons of eating disorder
rates in latency age samples with later adolescent samples have not been made.
126 JACOBI ET AL.
In the Kraemer typology age is classified as a variable risk factor and, because of
its relationship to other psychiatric disorders, age is categorized as nonspecific.
Sexual Abuse
Cross-Sectional Evidence. Sexual abuse in childhood, adolescence, or adulthood
has been discussed as a risk factor for eating disorders in many studies as well as
in early (41) and more recent reviews (38). All but one study are cross-
sectional in nature. The studies included here were not restricted to childhood
abuse but included sexual abuse at a later age as well. This procedure was
elected, as a valid distinction between childhood and adolescent sexual abuse
often proved impossible due to methodological inconsistencies and divergent
definitions in the cross-sectional studies.
In general, cross-sectional studies comparing homogeneous diagnostic
groups of anorexic patients to controls are rare. The few controlled studies
primarily comprise a mixture of anorexic and bulimic clinical samples. Whereas
some studies found higher rates of sexual abuse in these mixed samples, in
others elevated rates seemed to be linked to binge eating-type anorexic
patients (42–44). However, no information was given in these studies on the onset
of the eating disorder and the first occurrence of sexual abuse.
In the study by Webster and Palmer (45), on set of eating disorders occurred
in 74% of the eating-disordered subjects after age 16 years. However, no
differences were found in the rates of sexual abuse occurring before age 16
when comparing four clinical groups [anorexia nervosa (AN), bulimia nervosa
(BN), mixed AN/BN, major depression] to a nonmorbid comparison group.
One study with clinical samples explicitly assessed the precedence of the abuse
relative to the eating disorders (46). Comparing three patient groups (AN, BN,
and depressive patients) and a control group, they found that the rates
of abuse did not differ significantly between the three patient groups
(42.9%/27.1%/40.0%), but that all of the clinical groups had significantly
higher rates of sexual abuse than the control group (6.7%).
Taken together, the evidence for the classification of sexual abuse as a
retrospective correlate of anorexia nervosa is based on one study only with
retrospective assessment. Replication studies are therefore needed urgently.
Longitudinal Evidence. To date, only one longitudinal study has addressed the
role of sexual abuse as a risk factor for eating disorders (8). Because only one
patient developed anorexia nervosa at follow-up, the results will be reported in
the respective section of risk factors for bulimia.
age 17. When compared with the nonmorbid group, patients with anorexia
nervosa showed no significant differences on any of the variables studied (e.g.,
parental indifference, control and care, antipathy, discord in family).
Shoebridge and Gowers (60) addressed overprotection or high-concern
parenting in anorexia nervosa as part of a cross-sectional case-control study.
High-concern parenting was assessed by a structured clinical interview carried
out with the mothers covering the first 5 years of the child’s life. Two or more
high-concern attitudes and behaviors were almost four times more common in
mothers of anorexic patients than in mothers of controls. In addition, infant
sleep pattern difficulties were significantly more common in anorexic patients
than in controls. In the same sample, a more than threefold higher frequency of
obstetric losses was found prior to the birth of the future anorexic patients
compared with controls. The findings concerning parenting may therefore also
reflect an adaptive parental behavior to a severe life event and may not be
generalizable to a different sample or different (e.g., adolescent) age group. The
presence of two or more variables of high-concern parenting is classified as
retrospective correlate of unclear specificity.
The community-based studies by Fairburn et al. (61–63) compared three
groups of eating-disordered patients (patients with a history of anorexia
nervosa, with bulimia nervosa, and with binge eating disorder) with general
psychiatric patients and healthy controls. A large number of putative risk factors
(including variables of parental interaction) were assessed by an interview
focusing on the period before the onset of the eating disorders. For most of the
retrospectively assessed variables of parental interaction (arguments, criticism,
high expectations, underinvolvement, minimal affection, low care, and high
overprotection) the (previously) anorexic patients showed elevated rates when
compared with normal controls (63). However, in comparison with the
psychiatric controls, none of these variables turned out to be specifically
predictive of anorexia nervosa.
These factors together with high-concern parenting are therefore classified as
nonspecific retrospective correlates.
Longitudinal Evidence. As anorexia nervosa was not included as an outcome in
any of the longitudinal studies assessing variables of family interaction, no
evidence for these variables as risk factors for anorexia nervosa exists.
Perfectionism
Cross-Sectional Evidence. From a clinical point of view it is well recognized that
anorexic patients often display rigid, stereotypical, ritualistic, or perfectionistic
behaviors. Most recently, these characteristics have been examined in a
psychobiological light, connecting perfectionistic traits with alterations in
serotonin activity in a number of cross-sectional studies. These studies found
elevated scores for perfectionism in remitted anorexic and bulimic patients,
even when using different measures of perfectionism, e.g., (66–68). Because
none of the studies addressed premorbid perfectionism, the status of the factor
perfectionism based on these studies remains a correlate.
To our knowledge, again only Fairburn et al.’s risk factor study (63) included
perfectionism in their retrospective assessment of putative risk factors. They
found that in (recovered) anorexic patients premorbid perfectionism was more
common than in psychiatric and healthy controls. Perfectionism in these studies
is therefore classified as a specific, retrospective correlate.
Longitudinal Evidence. The basis of longitudinal studies including cases of
anorexia nervosa as outcome is currently too weak to classify perfectionism as a
risk factor for anorexia nervosa. It therefore remains a correlate.
Sundgot-Borgen (79) surveyed 522 female elite athletes. 1.3% of the sample
met DSM-IIIR criteria for anorexia nervosa and 8.2% for a category defined as
“anorexia athletica.”
More conservative results were obtained from a recent national survey of
male and female student athletes (80). None of the student athletes met
stringent criteria for anorexia nervosa. Using less stringent criteria, 2.85% of
the females and none of the males were classified as having subclinical anorexia.
However, the precedence of participation in weight-related subcultures to the
eating disorders was not addressed in any of these studies.
Of all the studies examining the impact of physical activity or exercise in a
noncompetitive context on the development of eating disorders, only one
retrospectively assessed the amount of physical activity before the onset of the
eating disorder. Davis et al. (81) compared a mixed eating-disordered sample of
anorexic, previously anorexic, and bulimic patients with control subjects on the
amount of physical activity predating the eating disorder using a structured
interview. The results indicated that the eating-disordered patients were
significantly more physically active than controls from adolescence (age 13)
onward and also prior to the onset of the disorder.
On the basis of cross-sectional studies, athletic competition and participation
in a competitive weight-related subculture are classified as correlates. However,
high level of exercise is classified as a retrospective correlate.
Longitudinal Evidence. Participation in weight-related subcultures and high-
level exercise have not been addressed in longitudinal studies as yet.
Other Factors
Cross-Sectional Evidence. In addition to the specific retrospective correlates
reported above, in Fairburn et al.’s study (63) a greater level of exposure to all
three risk domains (personal, environmental, dieting) was found in the
previously anorexic patients when compared to healthy controls but not in
comparison with psychiatric controls. The exposure to the three risk domains
thus seems to be a nonspecific effect.
Body dysmorphic disorder was assessed retrospectively for a period of at
least 6 months prior to the onset of the eating disorder in samples of anorexic
and bulimic patients as well as in controls. Body dysmorphic disorder (BDD)
belongs to the somatoform disorder spectrum according to both ICD and
DSM-IV, but similarities to OCD are also stressed by some authors. Symptoms
of BDD were found to be more than three times higher in anorexic patients than
in controls and were not observed at all in bulimic patients. BDD is therefore
classified as a retrospective correlate of unclear specificity.
RISK FACTORS 135
Genetic Factors
It must be kept in mind that genes, environment, and neurobiology interact and
are inseparable. The prevailing hypothesis assumes that an accumulation of
various genes of small effect together with adverse environmental factors
increases the risk of developing an eating disorder in those carrying the greatest
genetic and environmental loading. At the moment, relevant genetic factors
must be seen as fixed markers because they precede the onset of the eating
disorder but cannot be manipulated.
Family studies provide a necessary first step in determining whether a
disorder is genetic by establishing whether it clusters among biologically related
individuals. These studies generally have found an increased rate of eating
disorders in relatives of anorexics compared with controls. However, given that
first-degree relatives share genes and environments, these studies cannot
differentiate genetic versus environmental causes for family clusters. In twin
studies, the contribution of additive genetic effects to liability has been
estimated to be between 58% and 88% for anorexia nervosa (82–17). Even
though these numbers are intriguing, the small number of studies precludes
definite conclusions. In addition, in one study (88) the concordance rates of the
dizygotic twins were higher than those of the monozygotic twins.
Researchers have begun directly examining genetic influences through
candidate genes and linkage studies. Thus far, only a few polymorphisms have
been found to be associated with anorexia nervosa. However, the literature in
this area is growing rapidly, and studies are under way that include performance
of genome-wide screenings in affected families [see (5)].
Pubertal Timing
Cross-Sectional Evidence. Pubertal timing effects (i.e., the age of occurrence of a
pubertal event) are often confounded with pubertal status effects in cross-
sectional studies limited to one age or grade. Although all girls pass through
puberty, the age at which puberty begins varies considerably. An association
between early pubertal timing and eating disorder symptoms or diagnosis has
been observed in girls in pubertal transition as well as retrospectively after
puberty completion (106,107). Whether the association between eating
disorders and early sexual maturation is a function of increasing body mass index
(BMI) or other aspects of puberty is not clear. Early pubertal timing as assessed
in the cross-sectional studies is a nonspecific fixed marker.
Longitudinal Evidence. In none of the longitudinal studies, in which pubertal
timing was addressed, did cases of anorexia nervosa emerge during the follow-
up periods.
138 JACOBI ET AL.
Sexual Abuse
Cross-Sectional Evidence. Sexual abuse, especially during childhood, has been
discussed as a risk factor for bulimia nervosa in many studies and reviews,
e.g., (41,123). The majority of the cross-sectional studies on abuse have been
conducted using clinical samples. Higher rates of childhood sexual abuse have
been found for eating-disordered subjects (mixed anorexia and bulimia) in
comparison with general-practice and nonmorbid controls (42), but not in
comparison with psychiatric controls (43). Several studies addressing bulimia
nervosa more specifically yielded similar results (44,46). In others no evidence
of elevated rates of sexual abuse before age 16 (45) or during childhood (124) was
found. In the latter study, however, higher rates of rape, sexual harassment, and
molestation after age 17 were reported. In another study, significantly elevated
rates of sexual abuse before age 13 were found only in bulimic patients with a
comorbid borderline personality disorder (125). Only one study with a clinical
sample explicitly assessed temporal precedence of abuse (46). However, in the
studies by Steiger et al. (125) and Webster and Palmer (45), it seems quite
likely that abuse predated eating disorder onset.
Three further studies investigating sexual abuse and bulimia nervosa were
conducted using community samples. Dansky et al. (126) found significantly
higher rates of rape, sexual molestation, aggravated assault, direct
victimization, and posttraumatic stress disorder in bulimic respondents than in
controls. Bulimics in a large epidemiological study were found to have
experienced childhood sexual abuse approximately three times more often than
comparison subjects (127). Sexual abuse was also found to be significantly more
common in bulimics than in nonmorbid subjects (126). However, no difference
was found between bulimics and general psychiatric patients. Though Garfinkel
et al. (127) failed to report age of first sexual abuse and age of bulimia onset,
the temporal sequence of abusive experiences predating eating disorder was
established in the studies by Dansky et al. (126) and Welch and Fairburn(128).
Taken together, strong evidence of elevated rates of sexual abuse prior to
onset of bulimia nervosa has been reported or is highly probable in five studies
(two with community samples, three with clinical samples). The studies failing
to address precedence also yield evidence of elevated rates of sexual abuse. No
differences were found when comparing bulimics with psychiatric controls. Thus,
sexual abuse is classified as a nonspecific, retrospective correlate of bulimia
nervosa.
Longitudinal Evidence. The association between childhood adversities including
sexual abuse and later eating- or weight-related problems has only been
investigated in one longitudinal study (8). In the large community-based sample
of mothers and their offspring, individuals who had experienced sexual abuse or
142 JACOBI ET AL.
physical neglect during childhood were at elevated risk for subsequent eating
disorders and eating problems. Information on sexual abuse and physical neglect
were obtained from a central registry and—for a subgroup of the sample—from
maternal interviews. Sexual abuse and physical neglect are classified as
nonspecific, variable risk factors on the basis of this study. However, additional
prospective replication studies are needed.
controls. Low self-esteem was also reported by Raffi et al. (119) to be one of
several prodromal symptoms of bulimic patients in comparison with controls.
Although low self-esteem would have to be considered a highly potent
retrospective correlate, the most potent prodromal symptom reported was
anorexia or strict dieting. It remains unclear as to how the two prodromal
symptoms were interrelated before the onset of bulimia.
Taken together, negative self-evaluation as assessed in the studies by Fairburn
et al. (61) and Raffi et al. (119) can be classified as a specific retrospective
correlate.
Longitudinal Evidence. Measures of self-concept have been included in four
longitudinal studies (7,17,18,20). In the studies by Leon et al. (20) and Calam
and Waller (19) they did not prove important in risk prediction or disordered
eating. On the other hand, low self-esteem predicted elevated EAT scores 4
years later in the study by Button et al. (17). Girls in the lowest self-esteem
range had an eightfold increased risk for a high EAT (≥20) compared to those
with high self-esteem. Similarly, Ghaderi and Scott (7) reported significantly
lower self-esteem at time 1 for the incidence group that developed an eating
disorder 2 years later. The EDI-Ineffectiveness subscale was included in four of
the studies at baseline (9,10,20,21), but turned out to be predictive of disturbed
eating patterns or caseness in only one of the multivariate analyses as part of the
latent variable negative affectivity (21). However, significant differences were
found in the univariate comparisons of the subsequent symptomatic and
asymptomatic groups (9,10).
Based on longitudinal assessment, there seems to be a slight superiority of
studies confirming the presence of a negative self-concept, low self-esteem, or
higher ineffectiveness prior to the onset of an eating disorder. Exclusion of the
two longitudinal studies with limitations (17,18) did not affect these results.
Low self-esteem and ineffectiveness are therefore classified as variable risk
factors. Based on existing studies, their specificity is unclear although it seems
reasonable to assume that they are not highly specific for eating disorders.
Replication studies are needed for further confirmation of risk factor status.
Perfectionism
Cross-Sectional Evidence. Elevated scores for perfectionism have been found in
eating-disordered patients in a number of cross-sectional studies. The results of
the studies, which warrant the classification of perfectionism as a correlate, have
been presented in full in the anorexia nervosa section. However, premorbid
perfectionism was not addressed in these studies. Only Fairburn et al.’s risk
factor study (61) included perfectionism in their retrospective assessment of
putative risk factors. Premorbid perfectionism in bulimic patients was elevated
146 JACOBI ET AL.
compared to healthy controls but did not differ from that of the psychiatric
control group. On the basis of this study, perfectionism can be classified as a
nonspecific retrospective correlate of bulimia nervosa.
Longitudinal Evidence. Perfectionism has been assessed using the corresponding
EDI subscale in four longitudinal studies (9,10,20,21). In the studies by
Killen et al. (9,10), perfectionism at time 1 was not found to be related to
subsequent eating disturbances in multivariate analyses, but differentiated
between symptomatic and asymptomatic girls at baseline in univariate
comparisons (9). In both studies by Leon et al. (20,21), perfectionism did not
turn out to be predictive in multivariate comparisons. No other measures of
perfectionism have been employed in any of the longitudinal studies. On the
basis of these results, perfectionism is classified as a correlate.
Other Factors
Cross-Sectional Studies. In addition to the specific retrospective correlates
reported above, Fairburn et al. (103) also found a greater level of exposure to
all three assessed risk domains (personal, environmental, dieting) in bulimic
patients compared with healthy controls. Exposure to the three risk domains is
therefore classified as a nonspecific retrospective correlate.
Longitudinal Evidence. Girls who later turned out to be symptomatic in the
study by Killen et al. (9) showed elevations on subscales of Aggressive and
Unpopular in a personality inventory when compared with asymptomatic girls.
In the study by Killen et al. (10), girls who developed a partial syndrome had
higher 30-day prevalence of alcohol consumption. These factors thus are
classified as nonspecific variable risk factors.
High use of escape-avoidance coping as well as low perceived social support
were found to be prospective risk factors for subsequent eating disorders
(primarily bulimia nervosa and binge eating disorder) in the study by Ghaderi
and Scott (7). Accordingly, these are classified as variable risk factors but are in
need of replication.
Genetic Factors
Similarly as in anorexia nervosa, there is an increased rate of eating disorders in
bulimia nervosa relatives compared to control relatives. In twin studies, the
contribution of additive genetic effects to liability to bulimia nervosa has been
found to vary between 28% and 83%. The remaining variance is explained mainly
by unique environmental factors. The magnitude of the contribution of shared
environment is less clear, but it appears to be less prominent than of additive
genetic factors (85). However, in one study (130), an equal environment
assumption (EEA) violation (twin resemblance) accounted for all of the variance
otherwise attributed to additive genetic effects. The EEA is central to the twin
method and assumes that monozygotic and dizygotic twins are exposed to
equivalent environmental influences of etiological importance. Only a small
number of molecular genetic studies have been conducted for bulimia nervosa,
with mostly negative results.
Pubertal Timing
Cross-Sectional Evidence. Based on evidence from the studies by Hayward
et al. (106) and Graber et al. (107), described in detail in the anorexia nervosa
section above, early pubertal timing can be regarded as a nonspecific fixed
marker of bulimia nervosa.
Longitudinal Evidence. Indicators of pubertal timing were also assessed in five
longitudinal studies, in which neither an association with subsequent eating
disturbance (9,16,19,20) nor predictive status in a structural model (21) could
be found. In the study by Graber et al. (19), timing of pubertal maturation was
related to eating disturbances present at study begin, with the girls in the “chronic”
group evidencing earliest age of menarche. Taken together, there is no
longitudinal basis for the classification of pubertal timing as a risk factor or a
correlate.
Psychosocial Factors
BED is not a distinct diagnostic category like anorexia and bulimia nervosa but
put part of eating disorders not otherwise specified (ED-NOS). Because the
research criteria have only been put forward in the latest revision of the DSM
(DSM-IV), the number of risk factor studies explicitly including the proposed
BED criteria are very small. As the outcome of the longitudinal studies is often a
mixture of bulimic or binge eating syndromes, it can be assumed that some of
the risk factors listed in the bulimia section are also relevant for BED.
Unfortunately, the majority of longitudinal studies do not permit a strict
differentiation between bulimic versus binge eating-related syndromes.
Therefore, only longitudinal and cross-sectional studies with explicit reliance on
the research criteria for BED will be covered in this section.
Cross-Sectional Evidence. Binge eating disorder has been observed to occur
predominately in females, as was also the case for anorexia and bulimia nervosa.
However, the gender distribution is not quite as asymmetrical for BED:
Preliminary estimates suggest a 2.5 female-to-male ratio (149). Accordingly,
gender is classified as a nonspecific fixed marker for BED.
Eating disorders have generally been seen as afflictions of Caucasian females
[see (29) and anorexia nervosa section]. However, though lower rates of body
dissatisfaction and weight concerns have been found among African Americans,
the rates of bingeing behavior are equal or elevated in comparison to
Caucasians (150). African American and Caucasian ethnicity can therefore be
classified as fixed markers for BED of currently unknown specificity.
150 JACOBI ET AL.
Genetic Factors
There are no twin studies on BED. However, because of the low lifetime
prevalence of eating disorders and the restricted power of the statistical
analyses, attempts have been made to quantify the contribution of genes
and environment to individual symptoms of eating disorders (e.g., binge
eating) and to continuous measures of disordered eating and related
attitudes (152–154). Studies with population-based twin samples suggest a
genetic risk for the development of binge eating (86) with heritability estimates
of 46% (155).
There are even fewer molecular genetic studies for BED than bulimia
nervosa, Burnetet al. [(156), 5-HT2C receptor] and Ricca et al. [(157), 5-HT2A
receptor] did not find a difference in genotype and allele frequencies between
subjects with BED and controls.
for a few retrospective correlates of anorexia and bulimia nervosa. The only
well-supported high-potency factors are gender and weight concerns. Because
many of the risk factors may be population specific, replication studies are
needed.
Although the majority of longitudinal studies included sample sizes of several
hundred subjects, the samples are still too small for consistent and meaninful
risk factor detection of full syndromes of eating disorders. Given the low
prevalence of eating disorders, especially of anorexia nervosa, this is not
surprising. Consequently, longitudinal evidence on risk factors is much stronger
for bulimia nervosa and binge-related syndromes, whereas our knowledge on
risk factors for anorexia nervosa is still very limited. When attrition rates of
longitudinal studies are also taken into account, one may question whether risk
factor identification for full syndromes of anorexia nervosa is possible at all.
Furthermore, because of the overlap of the syndromes, especially partial
syndromes, previous research does not permit a valid differentiation of risk
factors for bulimia nervosa versus binge eating disorder.
The majority of factors are variable risk factors, theoretically amenable to
modification. No causal factors have been found, i.e., factors preceding the
onset of eating disorders that change the probability of the risk of the outcome.
For many of the factors (e.g., dieting, perfectionism), an experimental
manipulation would seem unethical. Although randomized controlled CBT
trials for bulimia nervosa can be considered a way of manipulating a variable risk
factor, i.e., weight and shape concerns, the similar reductions in weight and
shape concerns and dieting, achieved by such divergent treatment approaches as
CBT, IPT, and pharmacotherapy, raise the question about the mechanisms of
change in general.
To date, probably the most realistic way to manipulate a potential causal
factor would be to target the most potent variable risk factors in a highrisk
group within a preventive approach and to show that by reducing exposure to
the risk factor the risk of developing the disorder can be decreased in
comparison with a low-risk group. Preliminary studies (163,164) indicate that
such targeted approaches may result in stronger effects than those found in
previous, more universal (e.g., school-based) preventive approaches. Large-
scale studies testing the causal status of variable risk factors in highrisk samples
are currently under way and will help to further clarify the status of specific
factors.
Finally, as pointed out above, some of the risk factors, such as maternal
eating disorders, parental weight, and early feeding and gastrointestinal
problems, are already present at birth or during the first years of a child’s life.
To manipulate these, preventive interventions would have to target parental
attitudes and behaviors. To our knowledge, none of the prevention programs to
154 JACOBI ET AL.
date have focused on or included parents in order to reduce the risk for their
children. However, the identification of risk factors during different
developmental periods could result in differential recommendations for
preventive intervention in the future.
REFERENCES
1. Kraemer HC, Kazdin AE, Offord DR, Kessler RC, Jensen PS, Kupfer DJ. Coming
to terms with the terms of risk. Arch Gen Psychiatry 1997; 54:337–343.
2. Kazdin AE, Kraemer HC, Kessler RC, Kupfer DJ, Offord DR. Contributions of
risk factor research to developmental psychopathology. Clin Psychol Rev 1997; 17:
375–406.
3. Kazdin AE. Research Designs in Clinical Psychology. 3d ed. Boston: Allyn and
Bacon,1998.
4. Rutter M. Beyond longitudinal data: causes, consequences, changes, and continuity.
J Consult Clin Psychol 1994; 62:928–940.
5. Jacobi C, Hayward C, de Zwaan M, Kraemer H, Agras WS. Coming to terms with
risk factors for eating disorders: application of risk terminology and suggestions for
a general taxonomy. Psychol Bull. In press.
6. Kraemer HC, Kazdin AE, Offord DR, Kessler RC, Jensen PS, Kupfer DJ.
Measuring the potency of risk factors for clinical or policy significance. Psychol
Meth 1999; 4:257–271.
7. Ghaderi A, Scott B. Prevalence, incidence and prospective risk factors for eating
disorders. Acta Psychiatrica Scand 2001; 104:122–130.
8. Johnson JG, Cohen P, Kasen S, Brook JS. Childhood adversities associated with
risk for eating disorders or weight problems during adolescence or early adulthood.
Am J Psychiatry 2002; 159:394–400.
9. Killen JD, Taylor CB, Hayward C, Wilson DM, Haydel KF, Hammer LD,
Simmonds B, Robinson TN, Litt I, Varady A, Kraemer H. Pursuit of thinness and
onset of eating disorder symptoms in a community sample of adolescent girls: a
three year prospective analysis. Int J Eat Disord 1994; 16:227–238.
10. Killen JD, Taylor CB, Hayward C, Haydel KF, Wilson DM, Hammer LD,
Kraemer HC, Blair-Greiner A, Strachowski D. Weight concerns influence the
development of eating disorders: a 4-year prospective study. J Consul Clin Psychol
1996; 64:936–940.
11. Kotler LA, Cohen P, Davis M, Pine DS, Walsh BT. Longitudinal relationships
between childhood, adolescent, and adult eating disorders. J Am Acad Child Adol
Psychiatry 2001; 40:1424–1440.
12. Marchi M, Cohen P. Early childhood eating behaviors and adolescent eating
disorders. J Am Acad Child Adol Psychiatry 1990; 29:112–117.
13. Patton GC, Johnson-Sabine E, Wood K, Mann AH, Wakeling A. Psychol Med
1990; 20:383–394.
RISK FACTORS 155
14. Patton GC, Selzer R, Coffey C, Carlin JB, Wolfe R. Onset of adolescent eating
disorders: population based cohort study over 3 years. Br Med J 1999; 318:
765–768.
15. Vollrath M, Koch R, Angst J. Binge eating and weight concerns among young
adults. Results from the Zurich Cohort Study. B J Psychiatry 1992; 160:498–503.
16. Attie I, Brooks-Gunn J. Development of eating problems in adolescent girls: a
longitudinal study. Dev Psychol 1989; 25:70–79.
17. Button EJ, Sonuga-Barke EJS, Davies J, Thompson M. A prospective study of self
esteem in the prediction of eating problems in adolescent schoolgirls: questionnaire
findings. Br J Clin Psychol 1996; 35:193–203.
18. Calam R, Waller G. Are eating and psychosocial characteristics in early teen age
years useful predictors of eating characteristics in early adulthood? A 7-year
longitudinal study. Int J Eat Disord 1998; 24:351–362.
19. Graber JA, Brooks-Gunn J, Paikoff RL, Warren MP. Prediction of eating
problems: an 8-year study of adolescent girls. Dev Psychol 1994; 30:823–834.
20. Leon GR, Fulkerson JA, Perry CL, Early-Zald MB. Prospective analysis of
personality and behavioral influences in the later development of disordered eating.
J Abnormal Psychol 1995; 104:140–149.
21. Leon GR, Fulkerson JA, Perry CL, Keel PK, Klump KL. Three to four year
prospective evaluation of personality and behavioral risk factors for later disordered
eating in adolescent girls and boys. J Youth Adol 1999; 28:181–196.
22. Lewinsohn PM, Hops H, Roberts RE, Seeley JR, Andrews JA. Adolescent
psychopathology: I. Prevalence and incidence of depression and other DSMIII-R
disorders in high school students. J Abnormal Psychol 1993; 102:133–144.
23. Nielsen S. The epidemiology of anorexia nervosa in Denmark from 1973 to 1987: a
nationwide register study of psychiatric admission. Acta Psychiatrica Scand 1990;
81:507–514.
24. Schotte DE, Stunkard AJ. Bulimia vs. bulimic behaviors on a college campus. JA
1987; 258:1213–1215.
25. Whitaker AH, Johnson J, Shaffer D, Rapoport JL, Kalikow K, Walsh BT, Davis M,
Braimann S, Dolinsky A. Uncommon troubles in young people: prevalence
estimates of selected psychiatric disorders in a nonreferred adolescent population.
Arch Gen Psychiatry 1990; 47:487–496.
26. Hsu LKG. Epidemiology of the eating disorders. Psychiatric Clin North Am 1996;
19:681–700.
27. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC, 1994.
28. Blazer DG, Kessler RC, McGonagle KA, Swartz MS. The prevalence and
distribution of major depression in a national community sample: the National
Comorbidity Survey. Am J Psychiatry 1994; 151:979–986.
29. Striegel-Moore R, Smolak L. The role of race in the development of eating
disorders. In: Smolak L, Levine MP, Striegel-Moore R, eds. The Develomental
Psychopathology of Eating Disorders. Mahwah, NJ: Lawrence Erlbaum Associates,
1996:259–284.
156 JACOBI ET AL.
30. Crago M, Shisslak CM, Estes LS. Eating disturbances among American minority
groups: a review. Int J Eat Disord 1996; 19:239–248.
31. Chen CN, Wong J, Lee N, Chan-Ho MW, Lau JT, Fung M. The Shatin
Community mental health survey in Hong Kong. II. Major findings. Arch Gen
Psychiatry 1993; 50:125–133.
32. Ohzeki T, Hanaki K, Motozumi H, Ishitani N, Matsuda-Ohtahara H, Sunaguchi M,
Shiraki K. Prevalence of obesity, leanness and anorexia nervosa in Japanese boys
and girls aged 12–14 years. Ann Nutr Metab 1990; 34:208–212.
33. Davis C, Katzman MA. Perfection as acculturation: psychological correlates of
eating problems in Chinese male and female students living in the United States. Int
J Eat Disord 1999; 25:65–70.
34. Gowen LK, Hayward C, Killen JD, Robinson TN, Taylor CB. Acculturation and
eating disorder symptoms in adolescent girls. J Res Adol 1999; 9:67–83.
35. Hooper MSH, Garner DM. Application of the eating disorders inventory to a
sample of black, white and mixed race schoolgirls in Zimbabwe. Int J Eat Disord
1986; 5:161–168.
36. Woodside DB, Garfinkel P. Age of onset in eating disorders. Int J Eat Disord 1992;
12:31–36.
37. Mitchell JE, Specker SM, de Zwaan M. Comorbidity and medical complications of
bulimia nervosa. J Clin Psychiatry 1991; 52(Suppl 10): 13–20.
38. Wonderlich SA, Mitchell JE. Eating disorders and comorbidity: Empirical,
conceptual, and clinical implications. Psychopharmacol Bull 1997; 33:381–390.
39. Rastam M. Anorexia nervosa in 51 Swedish adolescents: premorbid problems and
comorbidity. J Am Acad Child Adol Psychiatry 1992; 31:819–829.
40. Bulik CM, Sullivan PF, Fear JL, Joyce PR. Eating disorders and antecedent anxiety
disorders: a controlled study. Acta Psychiatrica Scand 1997; 96:101–107.
41. Pope HG, Hudson JI. Is childhood sexual abuse a risk factor for bulimia nervosa?
Am J Psychiatry 1992; 149:455–463.
42. Brown L, Russell J, Thornton C, Dunn S. Experiences of physical and sexual abuse
in Australian general practice attenders and an eating disordered population. Aust N
Z J Psychiatry 1997; 31:398–404.
43. Folsom V, Krahn D, Nairn K, Gold L, Demitrack MA, Silk KR. The impact of
sexual and physical abuse on eating disordered and psychiatric symptoms: a
comparison of eating disordered and psychiatric inpatients. Int J Eat Disord 1993;
13:249–257.
44. Steiger H, Zanko M. Sexual traumata among eating-disordered, psychiatric, and
normal female groups. J Interpers Viol 1990; 5:74–86.
45. Webster JJ, Palmer RL. The childhood and family background of women with
clinical eating disorders: a comparison with women with major depression and
women without psychiatric disorder. Psychol Med 2000; 30:53–60.
46. Vize CM, Cooper PJ. Sexual abuse in patients with eating disorder, patients with
depression and normal controls. A comparative study. Br J Psychiatry 1995; 167:
80–85.
RISK FACTORS 157
47. Troop NA, Treasure JL. Psychosocial factors in the onset of eating disorders:
responses to life events and difficulties. Br J Med Psychol 1997; 70:373–385.
48. Schmidt U, Tiller J, Blanchard M, Andrews B, Treasure J. Is there a specific
trauma precipitating anorexia nervosa? Psychol Med 1997; 27:523–530.
49. Rastam M, Gillberg C. Background factors in anorexia nervosa. A controlled study
of 51 teenage cases including a population sample. Eur Child Adol Psychiatry 1992;
1:54–65.
50. Horesh N, Apter A, Lepkifker E, Ratzoni G, Weizman R, Tyrano S. Life events
and severe anorexia nervosa in adolescence. Acta Psychiatrica Scand 1995; 91:5–9.
51. Horesh N, Apter A, Ishai J, Danziger Y, Miculincer M, Stein D, Lepkifker
E, Minouni M. Abnormal psychosocial situations and eating disorders in
adolescence. J Am Acad Child Adol Psychiatry 1996; 35:921–927.
52. Gowers SG, North CD, Byram V. Life event precipitants of adolescent anorexia
nervosa. J Child Psychol Psychiatry 1996; 37:469–477.
53. Minuchin S, Rosman BL, Baker L. Psychosomatic Families: Anorexia Nervosa in
Context. Cambridge, MA: Harvard University Press, 1978.
54. Bruch H. Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within.
New York: Basic Books, 1973.
55. Cole-Detke H, Kobak R. Attachment processes in eating disorder and depression.
J Consul Clin Psychol 1996; 64:282–290.
56. Friedmann MA, Wilfley DE, Welch RR, Kunce JT. Self-directed hostility and
family functioning in normal-weight bulimics and overweight binge eaters. Addict
Behav 1997; 22:367–375.
57. McNamara K, Loveman C. Differences in family functioning among bulimics,
repeat dieters, and nondieters. J Clin Psychol 1990; 46:518–523.
58. Shisslak CM, McKeon RT, Crago M. Family dysfunction in normal weight bulimic
and bulimic anorexic families. J Clin Psychol 1990; 46:185–189.
59. Strober M, Humphrey LL. Familial contributions to the etiology and course of
anorexia nervosa and bulimia. J Consult Clin Psychol 1987; 55:654–659.
60. Shoebridge P, Gowers SG. Parental high concern and adolescent-onset anorexia
nervosa. Br J Psychiatry 2000; 176:132–137.
61. Fairburn CG, Welch SL, Doll HA, Davies BA, O’Connor ME. Risk factors for
bulimia nervosa. A community-based case-control study. Arch Gen Psychiatry
1997; 54:509–517.
62. Fairburn CG, Doll HA, Welch SL, Hay PJ, Davies BA, O’Connor ME. Risk factors
for binge-eating disorder: a community-based case-control study. Arch Gen
Psychiatry 1998; 55:425–432.
63. Fairburn CG, Cooper Z, Doll HA, Welch SL. Risk factors for anorexia nervosa.
Three integrated case-control comparisons. Arch Gen Psychiatry 1999; 56:
468–476.
64. Bruch H. Perceptual and conceptual disturbances in anorexia nervosa. Psychosom
Med 1962; 14(2): 187–194.
65. Jacobi C. Zur Spezifitat und Veranderbarkeit von Beeinträchtigungen
desSelbstkonzepts bei Essstörungen. Regensburg: S. Roderer Verlag, 1999.
158 JACOBI ET AL.
66. Kaye WH, Greeno CG, Moss H, Fernstrom J, Fernstrom M, Lilenfeld LR,
Weltzin TE, Mann JJ. Alterations in serotonin activity and psychiatric symptoms
after recovery from bulimia nervosa. Arch Gen Psychiatry 1998; 55:927–935.
67. Srinivasagam NM, Kaye WH, Plotnicov KH, Greeno C, Weltzin TE, Rao R.
Persistent perfectionism, symmetry, and exactness after long-term recovery from
anorexia nervosa. Am J Psychiatry 1995; 152:1630–1634.
68. Bastiani AM, Rao R, Weltzin T, Kaye WH. Perfectionism in anorexia nervosa. Int
J Eat Disord 1995; 17:147–152.
69. Garner DM, Garfinkel PE. Sociocultural factors in anorexia nervosa. Lancet 1978;
2:674.
70. Brownell KD. Eating disorders in athletes. In: Brownell KD, Fairburn CG, eds.
Eating Disorders and Obesity. A Comprehensive Handbook. New York: Guilford
Press, 1995:191–196.
71. Putukian M. The female athlete triad. Clin Sports Med 1998; 17:675–696.
72. Davis C, Fox J, Cowles M, Hastings P, Schwass K. The functional role of exercise
in the development of weight and diet concerns in women. J Psychosom Res 1990;
34:563–574.
73. Davis C, Katzman DK, Kaptein S, Kirsh C, Brewer H, Kalmbach K, Olmstedt MP,
Woodside DB, Kaplan AS. The prevalence of high-level exercise in the eating
disorders: etiological implications. Comprehen Psychiatry 1997; 38:321–326.
74. Joseph A, Wood IK, Goldberg SC. Determining populations at risk for developing
anorexia nervosa based on selection of college major. Psychiatry Res 1982; 7:
53–58.
75. Abraham S. Eating and weight controlling behaviors of young ballet dancers.
Psychopathology 1996a; 29:218–222.
76. Abraham S. Chracteristics of eating disorders among young ballet dancers.
Psychopathology 1996b; 29:223–229.
77. Kurtzman FD, Yager J, Landsverk J, Wiesmeier E, Bodurka DC. Eating disorders
among selected female student populations at UCLA. J Am Diet Assoc 1989; 89:
45–53.
78. Braistedt JR, Mellin L, Gong EJ, Irwin CE Jr. The adolescent ballet dancer.
Nutritional practices and characteristics associated with anorexia nervosa. J Adol
Health Care 1985; 6:365–371.
79. Sundgot-Borgen J. Risk and trigger factors for the development of eating disorders
in female elite athletes. Med Sci Sports Exercise 1994; 26:414–419.
80. Johnson C, Powers PS, Dick R. Athletes and eating disorders: the National
Collegiate Athletic Association study. Int J Eat Disord 1999; 26:179–188.
81. Davis C, Kennedy SH, Ravelski E, Dionne M. The role of physical activity in the
development and maintenance of eating disorders. Psychol Med 1994; 24:957–967.
82. Holland AJ, Hall A, Murray R, Russell GFM, Crisp AH. Anorexia nervosa: a study
of 34 twin pairs and one set of triplets. Br J Psychiatry 1984; 145:414–419.
83. Holland AJ, Sicotte N, Treasure J. Anorexia nervosa: evidence for a genetic basis.
J Psychosom Res 1988; 32:561–571.
RISK FACTORS 159
99. Frank GK, Kaye WH, Weltzin TE, Perel J, Moss H, McConaha C, Pollice C.
Altered response to meta-chlorophenylpiperazine in anorexia nervosa: support for
a persistent alteration of serotonin activity after short-term weight restoration. Int
J Eat Disord 2001; 30:57–68.
100. O’Dwyer AM, Lucey JV, Russell GMF. Serotonin activity in anorexia nervosa after
long-term weight restoration: response to D-fenfluramine challenge. PsycholMed
1996; 26:353–359.
101. Kaye WH, Gwirtsman, El H, George DT, Ebert MH. Altered serotonin activity in
anorexia nervosa after long-term weight restoration. Does elevated cerebrospinal
fluid 5-hydroxyindoleacetic acid level correlate with rigid and obsessive behavior?
Arch Gen Psychiatry 1991; 48:556–562.
102. Geddes JR, Lawrie SM. Obstetric complications and schizophrenia: a metaanalysis.
Br J Psychiatry 1995; 167:86–93.
103. Foley DL, Thacker LR, Aggen SH, Neale MC, Kendler KS. Pregnancy and
perinatal complications associated with risks for common psychiatric disorders in a
population-based sample of female twins. Am J Med Genet 2001; 105:426–431.
104. Cnattingius S, Hultman CM, Dahl M, Sparén P. Very preterm birth, birth trauma,
and the risk of anorexia nervosa among girls. Arch Gen Psychiatry 1999; 56:
634–638.
105. Hultman CM, Sparén P, Takei N, Murray RM, Cnattingius S. Prenatal and
perinatal risk factors for schizophrenia, affective psychosis, and reactive psychosis
of an early onset: case control study. Br Med J 1999; 318:421–426.
106. Hayward C, Killen JD, Wilson DM, Hammer LD, Litt IF, Kraemer HC, Haydel F,
Varady A, Taylor CB. Psychiatric risk associated with early puberty in adolescent
girls. J Am Acad Child Adol Psychiatry 1997; 36:255–262.
107. Graber JA, Lewinsohn PM, Seeley JR, Brooks-Gunn J. Is psychopathology
associated with the timing of pubertal development? J Am Acad Child Adol
Psychiatry 1997; 36:1768–1776.
108. Mitchell JE, Hatsukami D, Pyle RL, Eckert ED. The bulimia syndrome: course of
the illness and associated problems. Comprehens Psychiatry 1986; 27:165–170.
109. Pyle RL, Mitchell MD, Eckert ED. Bulimia: a report of 34 cases. J Clin Psychiatry
1981; 42:60–64.
110. Russell GF. Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol Med
1979; 9:429–448.
111. Garfmkel, Modolfsky, Garner. The heterogeneity of anorexia nervosa: Bulimia as a
distinct subgroup. Arch Gen Psychiatry 1980; 37:1036–1040.
112. Brewerton TD, Dansky BS, Kilpatrick DG, O’Neil PM. Which comes first in the
pathogenensis of bulimia nervosa, dieting or bingeing ? Int J Eat Disord 2000; 28:
259–264.
113. Mussell MP, Mitchell JE, Fenna CJ, Crosby RD, Miller JP, Hoberman HM. A
comparison of onset of binge eating versus dieting in the development of bulimia
nervosa. Int J Eat Disord 1997; 21:353–360.
114. Haiman C, Devlin MJ. Binge eating before the onset of dieting: A distinct subgroup
of bulimia nervosa ? Int J Eat Disord 1999; 25:151–157.
RISK FACTORS 161
115. Keys A, Brozek J, Hentschel A, Mickelsen O, Taylor HL. The Biology of Human
Starvation. Minneapolis: University of Minnesota Press, 1950.
116. Polivy J, Herman PC. Dieting and bingeing. A causal analysis. Am Psychol 1985;
40:193–201.
117. Ruderman AJ. Dietary restraint: a theoretical and empirical review. Psychol Bull
1986; 99:247–262.
118. Tuschl RJ. From dietary restraint to binge eating: some theoretical considerations.
Appetite 1990; 14:105–109.
119. Raffi AR, Rondini M, Grandi S, Fava GA. Life events and prodromal symptoms in
bulimia nervosa. Psychol Med 2000; 30:727–731.
120. Hayward C, Killen JD, Kraemer HC, Taylor CB. Predictors of panic attacks in
adolescents. J Am Acad Child Adol Psychiatry 2000; 39:207–214.
121. Ingram RE, Price JM, Eds. Vulnerability to Psychopathology. New York:
Guildford Press, 2000.
122. Pine DS, Cohen P, Gurley D, Brook J, Ma Y. The risk for early adulthood anxiety
and depressive disorders in adolescents with anxiety and depressive disorders. Arch
Gen Psychiatry 1998; 55:56–64.
123. Wonderlich SA, Brewerton TD, Jocic Z, Dansky B, Abbott DW. Relationship of
childhood sexual abuse and eating disorders. J Am Academy of Child and
Adolescent Psychiatry 1997; 36:1107–1115.
124. Casper RC, Lubomirsky S. Individual psychopathology relative to reports of
unwanted sexual experiences as predictor of a bulimic eating pattern. Int J Eat
Disord 1997; 21:229–236.
125. Steiger H, Leonard S, Ng Ying Kin NMK, Ladouceur C, Ramdoyal D, Young SN.
Childhood abuse and platelet tritiated-paroxetine binding in bulimia nervosa:
implications of borderline personality disorder. J Clin Psychiatry 2000; 61:
428–435.
126. Dansky BS, Brewerton TD, Kilpatrick DG, O’Neal PM. The National women’s
study: Relationship of victimization and posttraumatic stress disorder to bulimia
nervosa. Int J Eat Disord 1997; 21:213–228.
127. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom DS, Kennedy S, Kaplan AS,
Woodside DB. Bulimia nervosa in a Canadian community sample: prevalence and
comparison of subgroups. Am J Psychiatry 1995; 152:1052–1058.
128. Welch SL, Fairburn CG. Sexual abuse and bulimia nervosa: three integrated case-
control comparisons. Am J Psychiatry 1994; 151:402–407.
129. Welch SL, Doll HA, Fairburn CG. Life events and the onset of bulimia nervosa: A
controlled study. Psychol Med 1997; 27:515–522.
130. Jacobi C, Paul Th, de Zwaan M, Nutzinger DO, Dahme B. Specificity of
selfconcept disturbances in eating disorders. Int J Eat Disord. In press.
131. Hettema JM, Neale MC, Kendler KS. Physical similarity and the equalenvironment
assumption in twin studies of psychiatric disorders. Behav Gene 1995; 25:
327–335.
132. Brewerton TD, Mueller EA, Lesem MD, Brandt HA, Quearry B,
George DT, Murphy DL, Jimerson DC. Neuroendocrine responses to
162 JACOBI ET AL.
148. Wolfe BE, Metzger ED, Levine JM, Finkelstein DM, Cooper TB, Jimerson DC.
Serotonin function following remission from bulimia nervosa.
Neuropsychopharmacology 2000; 22:257–263.
149. Spitzer RL, Devlin M, Walsh BT, Hasin D, Wing R, Marcus M, Stunkard A,
Wadden T, Yanovski S, Agras S, Mitchell J, Nonas C. Binge-eating disorder: A
multisite field trial of the diagnostic criteria. Int J Eat Disord 1992; 11:191–203.
150. Striegel-Moore RH, Schreiber GB, Lo A, Crawford P, Obarzanek E, Roding J.
Eating disorder symptoms in a cohort of 11 to 16-year-old black and white girls:
The NHLBI growth and health study. Int J Eat Disord 2000; 27:49–66.
151. Dominy NL, Johnson WB, Koch C. Perception of parental acceptance in women with
binge-eating disorder. J Psychol 2000; 134:23–36.
152. Rutherford J, McGuffin P, Katz RJ, Murray RM. Genetic influences on eating
attitudes in a normal female twin population. Psychol Med 1993; 23:425–436.
153. Klump KL, McGue M, Iacono WG. Age differences in genetic and environmental
influences on eating attitudes and behaviors in preadolescent and adolescent female
twins. Journal of Abnormal Psychology 2000; 109:239–251.
154. Wade T, Martin NG, Tiggemann M. Genetic and environmental risk factors for the
weight and shape concerns characteristic of bulimia nervosa. Psychological
Medicine 1998; 28:761–771.
155. Sullivan PF, Bulik CM, Kendler KS. Genetic epidemiology of binging and
vomiting. British Journal of Psychiatry 1998; 173:75–79.
156. Burnet PWJ, Smith KA, Cowen PJ, Harrison PJ. Allelic variation of the 5HT2c
receptor in bulimia nervosa and binge-eating disorder. Psychiatric Genetics 1999;
9:101–104.
157. Ricca V, Nacmias B, Cellini E, Di Bernardo M, Rotella CM, Sorbi S. 5-HT2A
receptor gene polymorphism and eating disorders. Neuroscience Letters 2002;
323:105–108.
158. Stunkard A, Berkowitz R, Tanrikut C, Reiss E, Young L. d-Fenfluramine
treatment of binge-eating disorder. Am J Psychiatry 1996; 153:1445–1449.
159. Hudson JI, McElroy SL, Raymond NC, Crow S, Keck PE, Carter WP, Mitchell JE,
Strakowski SM, Pope HG, Coleman B, Jonas JM. Fluvoxamine in the treatment of
binge-eating disorder. Am J Psychiatry 1998; 155:1756–1762.
160. McElroy SL, Casato LS, Nelson EB, Lake KA, Soutullo CA, Keck PE Jr, Hudson
JI. Placebo-controlled trial of sertraline in the treatment of binge eating disorder.
Am J Psychiatry 2000; 157:1004–1006.
161. Grilo CM, Masheb RM, Heninger G, Wilson GT. Psychotherapy and medication
for binge eating disorder, Abstract 095. International Conference on Eating
Disorders, Boston, April 25–28, 2002.
162. Devlin M. Psychotherapy and medication for binge eating disorder, Abstract
Plenary Session. International Conference on Eating Disorders, Boston,
April 25–28, 2002.
164 JACOBI ET AL.
163. Taylor CB, Altman T. Priorities in prevention research for eating disorders.
Psychopharmacol Bull 1997; 33:413–417.
164. Winzelberg AJ, Eppstein D, Eldredge KL, Wilfley D, Dasmahapatra R, Dev P,
Taylor CB. Effectiveness of an Internet-based program for reducing risk factors for
eating disorders. J Consult Clin Psychol 2000; 68:346–350.
7
Role of Genetics in Anorexia Nervosa,
Bulimia Nervosa, and Binge Eating Disorder
Cynthia M.Bulik
University of North Carolina
Chapel Hill, North Carolina, U.S.A.
Family Studies
The first step is to determine whether a trait or disorder runs in families. This
question can be addressed by the standard family study, which determines
whether there is a significantly greater lifetime risk of eating disorders in
biological relatives of individuals who have an eating disorder in comparison to
relatives of individuals without eating disorders. If risk to relatives is not
increased, then the probability of the disorder being influenced by genetic
factors is low. Family studies are limited in that they cannot tell you the extent
to which the familial aggregation is due to genes and to what extent it is due to
environment.
Adoption Studies
Two additional designs are possible that enable the disentangling of genetic and
environmental effects: adoption and twin designs. In an adoption paradigm, one
compares the degree of similarity between an adoptee and his or her biological
versus adoptive parents. A greater similarity to biological parents suggests genetic
effects whereas greater similarity to adoptive parents suggests environmental
effects. Although adoption studies are statistically powerful, adoption is rare and
many of the assumptions of the method are often not met (e.g., random
placement). Moreover, when studying relatively rare conditions such as eating
disorders, the prevalence of the disorders is often too low to allow meaningful
conclusions to be drawn from adoption studies.
Twin Studies
Twin studies are often the only practical design for teasing out the relative
contributions of genetic and environmental factors to complex traits.
Monozygotic (MZ) twins emerge from two genetically identical embryos.
ROLE OF GENETICS 167
Therefore, any differences between MZ twins provides strong evidence for the
role of environmental influences (1, pp. 171–172). Dizygotic (DZ) twins result
from the fertilization of two ova by different spermatozoa. DZ twins are no
more similar genetically than nontwin siblings and share—on average—half of
their genes identical by descent. Thus, differences between DZ twins can result
from genetic and/or environmental effects.
The classical twin study uses the similarities and differences between MZ and
DZ twin pairs to quantify and qualify genetic and environmental causes for a
particular trait. Using structural equation modeling techniques, one is able to
parse liability to a trait into three sources of variability: additive genetic
effects (a2), common or shared environmental effects (c2), and unique
environmental effects (e2).
Additive Genetic Effects (abbreviation “A”). Additive genetic effects result from
the cumulative impact of many individual genes each of small effect. The
presence of A is inferred when the correlation between MZ twins is greater than
the correlation between DZ twins. For example, the correlation between MZ
twins for Body Dissatisfaction from the Eating Disorders Inventory was 0.60 for
MZ twins and 0.13 for DZ twins in a study conducted by Klump et al. (2). The
fact that the MZ twin correlation was more than twice the DZ correlation
suggests that genes affect Body Dissatisfaction as measured by the EDI in this sample.
Common Environmental Effects (abbreviation “C”). Common environmental effects
result from etiological influences to which both members of a twin pair are
exposed regardless of zygosity. Thus, common environmental effects contribute
equally to the correlation between MZ and between DZ twins. For example, if
the correlation for body dissatisfaction had been 0.61 for MZ and 0.61 for DZ
twins, then we would infer that common environment was influencing the trait.
Individual-Specific Environmental Effects (abbreviation “E”). The second type of
environmental effect results from etiological influences to which one member
of a twin pair is exposed but not the other. Thus, individual-specific
environmental effects contribute to differences between members of a twin pair
and decrease the magnitude of the correlation between both MZ and DZ twin
pairs. In the simplest case, if the correlation between both MZ and DZ is 0, then
the trait is entirely determined by individual-specific environmental effects.
Examples include one member of a twin pair being exposed to a traumatic
experience not shared with the cotwin.
More sophisticated analyses allow one to quantify the relative contributions of
A, C, and E. The proportion of variance due to A (additive genetic effects) is a2
(also known as “heritability”). The proportion of variance due to C is c2 and the
proportion due to E is e2. The value of e2 also incorporates measurement error.
Finally, a2, c2, and e2 must add up to the total variance of 1.
168 BULIK
Each of these grossly misrepresents what the heritability estimate tells us.
Even more challenging is helping patients incorporate this information into
their schema regarding the causes of their illness. The two concepts that are
keyto understanding heritability are confidence intervals and variability in
liability. Even though the research may come up with a point estimate like 83%
heritable, it is critical to pay attention to the confidence interval that bounds the
estimate. So it is more accurate to say that between 49% and 100% of the
variance in liability to BN is due to genetic effects. The second part of the
equation is variance. We all vary in terms of our risk for developing BN. What
these results are saying is that genes play a role in determining the extent to
which an individual is likely to develop BN (or whatever the relevant trait
may be).
Another critical point is that there is not one true heritability estimate for any
given trait or disorder. It is inaccurate to say “The heritability of bulimia nervosa
is 83%.” Heritability is a statistic that varies across populations and across time.
Kendler and Pedersen (4) illustrated beautifully how heritability estimates can
change for a trait over time. They explored the pattern of twin resemblance for
regular tobacco use in a population-based sample of Swedish twins. Results for
males suggested both genetic and rearing-environmental effects, which, in the
best-fit biometrical model, accounted for 61% and 20% of the variance in
liability to regular tobacco use, respectively. For women, the pattern differed
by birth cohort. In women born before 1925, rates of regular tobacco use were
low and twin resemblance was influenced primarily by environmental factors. In
ROLE OF GENETICS 169
later cohorts, rates of regular tobacco use in women increased substantially and
heritability estimates were on par with those seen in men (63%). Thus, the
genetic influences were only detectable in females once social constraints on
female tobacco use were relaxed and smoking became more prevalent.
FIGURE 1 Bivariate twin model exploring the nature of the genetic and environmental
relation between anorexia (AN) and bulimia nervosa (BN).
to address a critical question in the field, namely, what is the nature of the
relation between anorexia and bulimia nervosa?
Saying that common environment does not influence a trait is not equivalent to
saying that “family environment” has no influence on risk for the trait. What we
casually refer to as “family environment” is composed of factors that qualify both
as common environment and as unique environmental features (58), and
research strongly suggests that children raised in the same families experience
surprisingly different environments (59).
For example, let’s assume for a moment that maternal dieting is an
environmental factor (although we will illustrate later that this may be
a fallacious assumption). Since both members of a twin pair are exposed to
maternal dieting, we could conceptualize this as a shared environmental factor.
Although the shared component is that both twins were exposed to this
behavior, the exposure may be uniquely experienced by each twin. Whereas
one twin might climb on board and adopt the behavior herself to try to lose
weight and boost her own self-esteem, the other twin might recognize the
futility and vow never to become so ruled by her weight and appearance. Thus,
what appeared to be a common environmental experience actually exerted
more influence through its unique environmental effects.
In addition, the relative absence of shared environmental effects does not
mean that the environment does not impact on liability to eating disorders at
all. Indeed, all studies have found that a substantial portion of the variance
resulted from nonshared environmental factors (57). These unique
environmental factors simply appear to be more etiologically relevant than the
shared ones.
Also, several observational and self-report studies have found differences
between the family environment of women with eating disorders and
controls (60–65). The problem with these family environment designs is that
they cannot take into account the presence of gene-environment correlations.
Many of the variables that are assumed to be “environmental” may be influenced
or elicited by features of either the child or the parent that are genetically
mediated.
Genotype-environment correlation arises when the exposure to positive or
negative environmental influences is not randomly distributed with respect to
genetic differences. For example, girls who are genetically more prone to drive
for thinness may evoke more intrusive comments about eating and dieting from
their parents (evocative gene-environment correlation) and actively seek peers
or activities that reinforce their drive to lose weight, such as, ballet or
gymnastics (active gene-environment correlation). Another type of gene-
environment correlation (“passive” correlation) reflects the fact that children
receive genotypes that are correlated with their family environment. This type
of gene-environment correlation reflects that one receives one’s genes from the
same individuals who create one’s environment. Moreover, the environment
ROLE OF GENETICS 177
that they create for you is in part determined by their genotype. Concretely,
one can imagine a mother with a history of an eating disorder who still has
lingering concerns about her own weight who has passed on this genetic
predisposition to her daughter. In addition, she contributes to an environment
in the household that is highly weight focused by only buying low-fat foods,
watching her daughter’s caloric intake, and often commenting about the size
and shape of her own body. Thus, the daughter is not only dealing with the
impact of her inherited genotype; she is also being raised in an environment that
may facilitate the expression of that genetic predisposition.
Last, shared environmental factors may be important to the etiology of eating
disorders but may only exert their influence in concert with an individual’s
genetic makeup. Thus, the independent main effect of shared environmental
factors may be small, but their effects via one of several types of gene
x-environment interactions might be profound (66).
prevented. Combined, the results of family and twin studies confirm that
offspring of women with anorexia and bulimia constitute a high-risk group for
eating disorders. Targeted prevention programs could be tested that intervene at
several different points along the continuum. The earliest intervention point
could focus on enhanced prenatal and postnatal care for women with current or
even historical eating disorders. These efforts would focus on healthy and
adequate nutrition during pregnancy, dealing with issues that arise as body size
increases with pregnancy, developing healthy feeding and parenting styles after
birth, and having realistic postdelivery expectations about the resumption of
normal body weight (67).
A second preventive option would be to develop programs for mothers with
eating disorders or food and weight issues to help them develop tools to model
healthy eating behaviors and healthy body esteem and self-esteem to their
daughters (and sons). As noted above, although at this stage little can be done to
alter the transmission of susceptibility genes to offspring of women and men
with eating disorders, we can assist in modifying the environments that these
individuals create that may contribute to the expression of those genetic
predispositions.
A third preventive option could focus on the offspring themselves. In much
the same manner that children of alcoholics are encouraged to delay the onset of
alcohol consumption, offspring of individuals with eating disorders could be
provided with assistance to avoid the pitfalls of dieting, for developing non-
body-centered self-esteem, and other ways to prevent the development of
eating disorders.
CONCLUSIONS
We have been aware for decades that family and society influence risk for eating
disorders. We have been less clear on how they exert their influence. Family
and twin studies have helped us understand the nontrivial role of genes in
influencing risk. Somewhat paradoxically, given recent advances in technology,
the study of genes has become more tractable and practical than the study of
environments. All of the twin studies to date have shown that nonshared
environment significantly influences liability to eating disorders (57). We should
not abandon research on environment simply because our tools to explore the
human genome have become more practical. The environment is amazingly
complex and no doubt exerts its influence in myriad often idiosyncratic ways.
Nonetheless, a complete understanding of pathways of risk to eating disorders will
necessarily require further research designed to identify both the specific genes
that influence risk and the specific environmental factors that evoke and inhibit
expression of those genes.
ROLE OF GENETICS 179
REFERENCES
1. Plomin R, DeFries JC, McClearn GE, Rutter M. Behavioral Genetics. 3d ed.
New York: W.H. Freeman & Co, 1994.
2. Klump KL, McGue M, Iacono WG. Genetic relationships between personality and
eating attitudes and behaviors. J Abnorm Psychol 2002; 111:380–389.
3. Allison D, Faith M. Genetic and environmental influences on human body weight:
implications for the behavior therapist. Nutrition Today 2000; 35:18–21.
4. Kendler KS, Thornton LM, Pedersen NL. Tobacco consumption in Swedish twins
reared apart and reared together. Arch Gen Psychiatry 2000; 57(9):886–892.
5. Gershon E, Schreiber J, Hamovit J, Dibble E, Kaye W, Nurnberger J, Anersen A,
Ebert M. Anorexia nervosa and major affective disorders associated in families: a
preliminary report. In: Guze SB, Earls FJ, Barrett JE, eds. Childhood
Psychopathology and Development. New York: Raven Press, 1983:279–284.
6. Hudson JI, Pope HG, Jonas JM, Yurgelun-Todd D, Frankenburg FR. A controlled
family history study of bulimia. Psychol Med 1987; 17:883–890.
7. Kassett J, Gershon E, Maxwell M, Guroff J, Kazuba D, Smith A, Brandt H,
Jimerson D. Psychiatric disorders in the first-degree relatives of probands with
bulimia nervosa. Am J Psychiatry 1989; 146:1468–1471.
8. Strober M, Lampert C, Morrell W, Burroughs J, Jacobs C. A controlled family
study of anorexia nervosa: evidence of familial aggregation and lack of shared
transmission with affective disorders. Int J Eating Disord 1990; 9:239–253.
9. Lilenfeld L, Kaye W, Greeno C, Merikangas K, Plotnikov K, Pollice C, Rao R,
Strober M, Bulik C, Nagy L. A controlled family study of restricting anorexia and
bulimia nervosa: comorbidity in probands and disorders in first-degree relatives.
Arch Gen Psychiatry 1998; 55:603–610.
10. Strober M, Freeman R, Lampert C, Diamond J, Kaye W. Controlled family study
of anorexia nervosa and bulimia nervosa: evidence of shared liability and
transmission of partial syndromes. Am J Psychiatry 2000; 157:393–401.
11. Woodside D, Field LL, Garfinkel P, Heinmaa M. Specificity of eating disorders
diagnoses in families of probands with anorexia nervosa and bulimia nervosa. Comp
Psychiatry 1998; 39:261–264.
12. Brody ML, Walsh BT, Devlin MJ. Binge eating disorder: reliability and validity of a
new diagnostic category. J Consult Clin Psychol 1994; 62(2):381–386.
13. Fowler S, Bulik C. Family environment and psychiatric history in women with
binge eating disorder and obese controls. Behav Change 1997; 14:106–112.
14. Kendell RE. Clinical validity. Br J Psychiatry 1989; 19:45–55.
15. Kendler KS. Toward a scientific psychiatric nosology. Arch Gen Psychiatry 1990;
47:969–973.
16. Robins E, Guze SB. Establishment of diagnostic validity in psychiatric illness: its
application to schizophrenia. Am J Psychiatry 1970; 126:107–111.
17. Klump KL, Holly A, Iacono WG, McGue M, Willson LE. Physical similarity and
twin resemblance for eating attitudes and behaviors: a test of the equal
environments assumption. Behav Genet 2000; 30(l):51–58.
180 BULIK
18. Bulik C, Sullivan P, Wade T, Kendler K. Twin studies of eating disorders: a review.
Int J Eat Disord 2000; 27:1–20.
19. Kendler KS, Neale MC, Kessler RC, Heath AC, Eaves LJ. A test of the equal
environment assumption in twin studies of psychiatric illness. Behav Genet 1993;
23:21–27.
20. Sullivan PF, Bulik CM, Kendler KS. The genetic epidemiology of binging and
vomiting. Br J Psychiatry 1998; 173:75–79.
21. Askevold F, Heiberg A. Anorexia nervosa: two cases in discordant MZ twins.
Psychother Psychosom 1979; 32:223–228.
22. Suematsu H, Kuboki T, Ogata E. Anorexia nervosa in monozygotic twins.
Psychother Psychosom 1986; 45:46–50.
23. Vandereycken W, Pierloot R. Anorexia nervosa in twins. Psychother Psychosom
1981; 35:55–63.
24. Nowlin N. Anorexia nervosa in twins: case report and review. J Clin Psychiatry
1983; 44:101–105.
25. Holland AJ, Hall A, Murray R, Russell GFM, Crisp AH. Anorexia nervosa: a study
of 34 twin pairs and one set of triplets. Br J Psychiatry 1984; 145:414–419.
26. Holland AJ, Sicotte N, Treasure J. Anorexia nervosa: evidence for a genetic basis.
J Psychosom Res 1988; 32(6):561–571.
27. Treasure J, Holland A. Genetic vulnerability to eating disorders: evidence from
twin and family studies. In: Remschmidt H, Schmidt M, eds. Child and Youth
Psychiatry: European Perspectives. New York: Hogrefe & Huber, 1989:59–68.
28. Klump KL, Miller KB, Keel PK, McGue M, Iacono WG. Genetic and
environmental influences on anorexia nervosa syndromes in a population-based
twin sample. Psychol Med 2001; 81(4):737–740.
29. Kortegaard LS, Hoerder K, Joergensen J, Gillberg C, Kyvik KO. A preliminary
population-based twin study of self-reported eating disorder. Psychol Med 2001;
31:361–365.
30. Wade TD, Bulik CM, Neale M, Kendler KS. Anorexia nervosa and major
depression: shared genetic and environmental risk factors. Am J Psychiatry 2000;
157:469–471.
31. Lilenfeld L, Kaye W, Strober M. Genetics and family studies of anorexia nervosa
and bulimia nervosa. In: Balliere’s Clinical Psychiatry, 1997:177–197.
32. Kaminer Y, Feingold M, Lyons K. Bulimia in a pair of monozygotic twins. J Nerv
Ment Dis 1988; 176:246–248.
33. Fichter MM, Noegel R. Concordance for bulimia nervosa in twins. Int J Eat Disord
1990; 9:255–263.
34. Hsu GLK, Chesler BE, Santhouse R. Bulimia Nervosa in eleven sets of twins: a
clinical report. Int J Eat Disord 1990; 9:275–282.
35. Kendler KS, MacLean C, Neale MC, Kessler RC, Heath AC, Eaves LJ. The genetic
epidemiology of bulimia nervosa. Am J Psychiatry 1991; 148:1627–1637.
36. Bulik CM, Sullivan PF, Kendler KS. Heritability of binge-eating and broadly
defined bulimia nervosa. Biol Psychiatry 1998; 44(12):1210–1218.
ROLE OF GENETICS 181
37. Wade T, Neale MC, Lake RIE, Martin NG. A genetic analysis of the eating and
attitudes associated with bulimia nervosa: dealing with the problem of
ascertainment. Behav Genet 1999; 29:1–10.
38. Wade TD, Martin N, Neale M, Tiggemann M, Trealor S, Heath A, Bucholz K,
Madden P. The structure of genetic and environmental risk factors for three
measures of disordered eating characteristic of bulimia nervosa. Psychol Med 1999;
29:925–934.
39. Anderson C, Bulik CM. A twin study of binge-eating disorder (in preparation).
40. Reichborn-Kjennerud T, Tambs K, Harris JR, Bulik CM. Gender differences in
binge-eating in the absence of compensatory behaviors.
41. Eckert ED, Halmi KA, Marchi P, Grove W, Crosby R. Ten-year follow-up
of anorexia nervosa: clinical course and outcome. Psychol Med 1995; 25:143–156.
42. Gillberg IC, Rastam M, Gillberg C. Anorexia nervosa outcome: six-year controlled
longitudinal study of 51 cases including a population cohort. J Am Acad Child Adol
Psychiatry 1994; 33:729–739.
43. Herpertz-Dahlman B, Wewetzer C, Schulz E, Remschmidt H. Course and
outcome in adolescent anorexia nervosa. Int J Eat Disord 1996; 19:335–345.
44. Hsu G, Crisp A, Callender J. Psychiatric diagnoses in recovered and unrecovered
anorectics 22 years after onset of illness: a pilot study. Comp Psychiatry 1992; 33:
123–127.
45. Schork EJ, Eckert ED, Halmi KA. The relationship between psychopathology,
eating disorder diagnosis, and clinical outcome at 10-year follow-up in anorexia
nervosa. Comp Psychiatry 1994; 35:113–123.
46. Smith C, Feldman S, Nasserbakht A, Steiner H. Psychological characteristics and
DSM-III-R diagnoses at 6-year follow-up of adolescent anorexia nervosa. J Am
Acad Child Adol Psychiatry 1993; 32:1237–1245.
47. van der Ham T, van Strien D, van Engeland H. A four-year prospective followup
study of 49 eating-disordered adolescents: differences in course of illness. Acta
Psych Scand 1994; 90:229–235.
48. Zipfel S, Lowe B, Reas DL, Deter HC, Herzog W. Long-term prognosis in
anorexia nervosa: lessons from a 21-year follow-up study. Lancet 2000; 355(9205):
721–722.
49. Braun DL, Sunday SR, Halmi KA. Psychiatric comorbidity in patients with eating
disorders. Psychol Med 1994; 24:859–867.
50. Fairburn CG, Cooper PJ. The clinical features of bulimia nervosa. Br J Psychiatry
1984; 144:238–246.
51. Pyle RL, Mitchell JE, Eckert ED. Bulimia: a report of 34 cases. J Clin Psychiatry
1981; 42:60–64.
52. Russell GFM. Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol
Med 1979; 9:429–448.
53. Schmidt U, Keilen M, Tiller J, Treasure J. Clinical symptomatology and etiological
factors in obese and normal weight bulimic patients: a retrospective case-control
study. J Nerv Ment Dis 1993; 181:200–202.
182 BULIK
54. Sullivan PF, Bulik CM, Carter FA, Gendall KA, Joyce PR. The significance of a
prior history of anorexia in bulimia nervosa. Int J Eat Disord 1996; 20:253–261.
55. Herzog DB, Keller MM, Sacks NR, Yeh CJ, Lavori PW. Psychiatric comorbidity in
treatment-seeking anorexics and bulimics. J Am Acad Child Adol Psychiatry 1992;
31:810–818.
56. Walters EE, Kendler KS. Anorexia nervosa and anorexic-like syndromes in a
population-based female twin sample. Am J Psychiatry 1995; 152:64–71.
57. Klump KL, Wonderlich S, Lehoux P, Lilenfeld LR, Bulik CM. Does environment
matter? A review of nonshared environment and eating disorders. Int J Eat Disord
2002; 31(2):118–135.
58. Silberg JL, Erickson MT, Meyer JM, Eaves LJ, Rutter ML, Hewitt JK.
The application of structural equation modeling to maternal ratings of twins’
behavioral and emotional problems [published erratum appears in J Consult Clin
Psychol 1994 Dec; 62(6): 1234]. J Consult Clin Psychol 1994; 62(3):510–521.
59. Dunn J, Plomin R. Separate Lives: Why Siblings Are So Different. New York:
Basic Books, 1990.
60. Fallon BA, Sadik MSW, Saoud JB, Garfinkel RS. Childhood abuse, family
environment, and outcome in bulimia nervosa. J Clin Psychiatry 1994; 55(10):
424–428.
61. Humphrey LL, Apple RF, Kirschenbaum DN. Differentiating bulimic-anorexic
from normal families using interpersonal and behavioral observational systems.
J Consult Clin Psychol 1986; 54(2): 190–195.
62. Humphrey L. Family relations in bulimic-anorexia and nondistressed families.
Int J Eat Disord 1986; 5:223–232.
63. Wonderlich S. Relationship of family and personality factors in bulimia. In:
Crowther J, Tennenbaum D, Hobfall S, Parvis S, eds. The Etiology of Bulimia
Nervosa: The Individual and Familial Context. Washington, D.C.: Hemisphere
Publishers, 1992:103–126.
64. Woodside D, Shekter-Wolfson L, Garfinkel P, Olmsted M, Kaplan A, Maddocks
S. Family interactions in bulimia nervosa: 1. Study design, comparisons to
established population norms, and changes over the course of an intensive day
hospital treatment program. Int J Eat Disord 1995; 17:105–115.
65. Woodside D, Shekter-Wolfson L, Garfinkel P, Olmsted M. Family interactions in
bulimia nervosa II: complex intrafamily comparisons and clinical significance. Int J
Eat Disord 1995; 17:117–126.
66. Kendler KS, Eaves LJ. Models for the joint effect of genotype and environment on
liability to psychiatric illness. Am J Psychiatry 1986; 143:279–289.
67. Mitchell-Gieleghem A, Mittelstaedt ME, Bulik CM. Eating disorders and
childbearing: concealment and consequences. Birth 2002; 29(3): 182–191.
8
Psychiatric Comorbidity Associated with
Anorexia Nervosa, Bulimia Nervosa, and
Binge Eating Disorder
Lisa Rachelle Riso Lilenfeld
Georgia State University
Atlanta, Georgia, U.S.A.
OVERVIEW
The term “comorbidity” was introduced in the medical literature by Feinstein
(1) to refer to patients with two co-occurring diseases. In recent years, this
concept has become well known in the field of psychiatry. Extensive
comorbidity has been documented among a number of psychiatric disorders,
not the least of which are eating disorders. Such comorbidity has several
important clinical and research implications, as reviewed by Klein and Riso (2).
First, the presence of comorbid disorders may affect the course and treatment
response of the primary disorder. Second, comorbidity can make it unclear as to
whether associations between the primary disorder and other variables are true
associations or instead correlations with a comorbid condition. Third, a great
degree of comorbidity may lead to reevaluation of the validity of a diagnostic
category. That is, it may suggest an alternative diagnostic grouping. Fourth, high
rates of comorbidity may provide important information regarding the etiology
of the primary disorder, as well as the comorbid disorders.
Klein and Riso (2) provide an in-depth review of the many reasons for which
comorbidity may exist. A brief overview of those most relevant to the field of
eating disorders will be provided here. The first, possibly least interesting, but
important reason for comorbidity that is often overlooked is simply chance.
Two disorders with high prevalences will co-occur within individuals simply on
the basis of chance due to base rates. While anorexia nervosa is a relatively
uncommon disorder with a lifetime prevalence rate of approximately 0.5–1.0%
among young females, bulimia nervosa and binge eating disorder are more
common with lifetime prevalence estimates of approximately 1–3% and 3%,
respectively, among this population (3). A second reason comorbidity may be
observed is sampling bias, often referred to as “Berkson’s bias” (4). This is
particularly relevant in the field of psychiatry, where studies using clinical
populations can produce high estimates of comorbidity. This occurs because
184 LILENFELD
individuals with multiple disorders are more likely to seek treatment than
individuals with one disorder. This bias has often led to higher comorbidity
estimates in studies where eating disorder subjects are recruited from treatment
centers as opposed to studies in which subjects are recruited from the
community. A third reason for comorbidity is population stratification. That is,
each of two disorders may be associated with distinct risk factors. If both sets of
risk factors happen to have an increased prevalence in the same subgroup of the
population (e.g., as has been proposed for bulimia nervosa and substance
abuse), the rate of comorbidity is higher than that expected by chance for the
population as a whole. A fourth reason is overlapping diagnostic criteria. For
example, one of the criteria for borderline personality disorder is potentially
dangerous impulsive behavior, among which binge eating is listed. Thus,
someone with this symptom would simultaneously partially meet one criterion
for borderline personality disorder, as well as for bulimia nervosa or binge
eating disorder, obviously increasing the likelihood of comorbidity of the
personality disorder and eating disorder. A fifth reason for comorbidity is
known as “multiformity,” referring to the fact that disorders may assume
multiple heterogeneous forms. For instance, the comorbid disorder might be an
alternative manifestation of the target disorder. For instance, some have
suggested that anorexia nervosa and obsessive-compulsive disorder (OCD) may
be alternate forms of the same underlying pathology (5).
The last two reasons for comorbidity, which the majority of eating disorder
comorbidity studies have focused on, are among the more interesting. First, one
disorder may be a risk factor for another. For instance, it has been suggested that
anxiety disorders may be a risk factor for eating disorders (6). The final reason
for comorbidity to be reviewed here is overlapping etiological processes. That
is, there may be overlapping risk factors that contribute to “pure” forms of each
disorder. Thus, the two disorders can appear in their pure forms as well as
comorbidly. For instance, low self-esteem and perfectionism may be risk factors
for both depression and eating disorders, which would contribute to their
co-occurrence. In addition, depression and eating disorders each have their own
set of unique risk factors, leading to these disorders often appearing without the
other.
As mentioned at the outset of this chapter, the different reasons for
comorbidity among eating disorders and other psychiatric disorders are
important from both a basic science and clinical perspective. Patterns of
comorbidity may help us further refine our diagnostic categories, which have
continued to evolve; however, there is general agreement that such categories
are in need of further refinement (7). Comorbidity patterns may help to identify
taxons, i.e., naturally occurring categories that exist in the world (8), such that
PSYCHIATRIC COMORBIDITY 185
our diagnostic system would reflect true relationships among different forms of
psychopathology.
Clinically, as much as comorbidity patterns may lead to a better
understanding of underlying etiological processes, this may help in our
conceptualization model of eating disorders, which may in turn lead to more
effective treatment aimed at these etiological factors. Alternatively, or
additionally, understanding comorbidity patterns may lead to better
identification of risk factors, which may ultimately aid in prevention. At the
very least, clinicians who treat eating-disordered patients must be well versed in
the most commonly observed comorbid psychiatric disorders in this population,
as these disorders should often be a focus of treatment, either separately (as
suggested by some in the case of comorbid substance abuse) or in conjunction with
the eating disorder treatment (as suggested in the case of comorbid depression).
Thus, clinicians must be sure to conduct a thorough psychiatric assessment
focused on eating disorder symptoms, as well as comorbid conditions,
particularly major depressive disorder, all anxiety disorders, substance use
disorders, and cluster B and C personality disorders. Onset patterns, i.e.,
whether the eating disorder preceded the comorbid disorder(s), may also be
relevant to treatment.
The remainder of the chapter is devoted to reviewing comorbidity among
anorexia nervosa, bulimia nervosa, and binge eating disorder, beginning with an
emphasis on general differences between subtypes in a diagnostic category.
Anorexia Nervosa
The two DSM-IV diagnostic subtypes of anorexia nervosa, restricting type and
bingeing-purging type, display somewhat different patterns of comor bidity.
Both subtypes share the same core symptoms (refusal to maintain a minimally
normal body weight, intense fear of weight gain, body image disturbance, and
amenorrhea in postmenarcheal females). The key difference between the two
subtypes is that weight loss is accomplished primarily through dieting, fasting,
or excessive exercise in restricting-type anorexia nervosa, without any regular
binge eating or purging. In the bingeing-purging type, the individual regularly
engages in bingeing and/or purging, so that weight loss may be accomplished
through misuse of laxative, diuretics, or enemas, in addition to the methods
used in the restricting type.
While some comorbid disorders are common among both types of anorexia
nervosa, such as depression and anxiety disorders, other comorbid disorders are
186 LILENFELD
Bulimia Nervosa
The two DSM-IV diagnostic subtypes of bulimia nervosa are purging type and
nonpurging type. Both share the same core symptoms of binge eating,
inappropriate compensatory methods to prevent weight gain, and selfevaluation
being unduly influenced by body shape and weight. What distinguishes the
subtypes is the compensatory methods used. Purging-type bulimia nervosa
involves regular use of self-induced vomiting or misuse of laxatives, diuretics,
or enemas. Those with nonpurging-type bulimia nervosa use fasting or exercise,
but not vomiting, laxatives, diuretics, or enemas, as compensatory methods to
prevent weight gain. Bulimic patients may also use diet pills (e.g., stimulants) to
prevent weight gain, although the DSM-IV does not specify this type of
compensatory strategy in either subtype definition. If none of the other purging
methods are used, then a patient who abuses diet pills as their compensatory
strategy of choice is usually classified as having nonpurgingtype bulimia nervosa.
Nearly all comorbidity studies of bulimia nervosa have been conducted with
individuals who have the purging subtype. Patterns of comorbidity among this
subtype of bulimia nervosa often resemble patterns seen with the bingeing-
purging subtype of anorexia nervosa. Both disorders share the symptoms of
binge eating and purging (though it may be one or the other rather than both in
bingeing-purging anorexia nervosa). Thus, it may be this (these) particular
symptom(s) that are critical in accounting for the observed comorbidity.
PSYCHIATRIC COMORBIDITY
It is well recognized that both anorexia nervosa and bulimia nervosa are often
accompanied by other psychiatric symptoms and syndromes, in particular
depression, anxiety disorders and substance use disorders. Of great importance
in recognizing and studying comorbidity and eating disorders is that these
comorbidities are likely substantially exaggerated by malnutrition and
pathological eating behaviors (9). Thus, one must always question whether the
apparent comorbid presentation of mood disturbance or high anxiety is a
function of the physiological consequences of the eating disorder itself. Even if
the comorbid disorder predates the eating disorder, it is possible that the mood
or anxiety pathology is exacerbated by, if not caused by, the consequences of
starvation in the case of anorexia nervosa or erratic consummatory behaviors in
the case of bulimia nervosa. In some patients, it is clear that the comorbidity
antedates weight loss or disordered eating, or persists after weight recovery or
abstinence from bingeing and purging (10–12), suggesting that the comorbid
problems may not simply be sequalae of malnutrition or pathological eating
behavior. Whether such comorbid pathology enhances vulnerability to the
development of eating disorders remains uncertain.
In the absence of high-risk paradigms, unraveling the precise nature of the
mechanisms underlying eating disorder comorbidities is a formidable task.
Family studies, in which patterns of comorbidity in relatives are assessed, are
probably the single most useful means of testing alternative models of
comorbidity (2). Several recent family studies (13–15) have shed light on
comorbid disorders that may share a common familial vulnerability with
eating disorders and will be briefly reviewed. The three areas of
comorbid psychopathology of greatest relevance to eating disorders are mood
disorders, anxiety disorders, and substance use disorders, all to be reviewed
below with regard to what we know about comorbidities of each with anorexia
nervosa, bulimia nervosa, and binge eating disorder. In addition, impulse
control disorders, schizophrenia and other psychotic disorders, dissociative
disorders, somatoform disorders, as well as attention deficit-hyperactivity
disorder (ADHD) and disruptive behavior disorders will also be briefly covered.
188 LILENFELD
Mood Disorders
It is well known that individuals with eating disorders often have symptoms of
depression. While the reasons for this frequent comorbidity has been a subject of
debate, the frequent presence of comorbid depression among individuals with
eating disorders has not.
As previously reviewed, there are many potential reasons for comorbidity.
First, one must ask whether the rate of depression among people with eating
disorders exceeds that expected by a chance association of these potentially
independent disorders. The nature of the population under study will have a
great effect on the answer to this question. That is, rates of depression among
those with eating disorders recruited from a clinic or other treatment sample
will nearly always be significantly higher than rates of depression among a
community sample of individuals with eating disorders. Most comorbidity
studies have been conducted with samples of convenience (i.e., treatment
samples) and are thus subject to referral bias, which results in an increased rate
of comorbid depression observed. This is likely to occur because people with
more than one disorder are more likely to seek treatment (i.e., Berkson’s bias).
In general, a clinical sample is likely to be more disturbed than an
epidemiological sample. Nonetheless, depression comorbidity rates among a
clinical sample may be of greatest interest to clinicians, as these are the patients
they are most likely to encounter! Thus, comorbidity studies using clinical
samples may be of greatest relevance to clinicians treating patients with eating
disorders, though it is important to keep in mind that this is just a subset of the
larger population of individuals with eating disorders. So, the reasons for such
comorbidity remain uncertain and are likely related to sampling.
It is agreed that the presence of depressive comorbidity is very common, but
just how common? With the aforementioned in mind, rates of comorbid
depression among individuals with eating disorders have been found to vary
markedly, again likely due to referral biases. Rates among clinical samples have
nearly always been significantly higher than rates observed in nonpsychiatric
control subjects. In addition, elevated rates of depressive dis orders, particularly
major depressive disorder, have been observed among all types of eating
disorders. Lifetime rates of major depression appear to be relatively equally
distributed across eating disorder subtypes, though there is some suggestion that
bingeing-purging anorexic and purging bulimic patients have higher rates of
depression than restricting-type anorexic patients (16). It is generally accepted
that at least half of treatment-seeking individuals with anorexia or bulimia nervosa
will meet lifetime criteria for a depressive disorder, with rates ranging from
24% to 88% (17–25).
PSYCHIATRIC COMORBIDITY 189
Rates of dysthymic disorder have not been consistently gathered in the same
way that those of major depressive disorder have, though existing data suggest
that this comorbid condition may also be elevated among those with bulimia
nervosa (26). In contrast to unipolar mood disorders, bipolar mood disorders
appear to be relatively uncommon among this population.
Seasonal affective disorder (SAD) has received quite a bit of attention in the
eating disorders field in the past decade. This is because a growing body of research
suggests seasonal variations in mood patterns and eating behaviors among
patients with eating disorders, particularly those with bulimia nervosa. Patients
diagnosed with SAD often demonstrate dysfunctional eating behaviors similar to
those found in bulimic patients. In fact, both disorders are characterized by
disturbances in eating, appetite, weight, mood, sleep, and energy. Research
conducted primarily in North America has estimated the comorbidity rates of
winter SAD to range between 27% and 42%, with lower percentages in other
seasons (27–30), based on the Seasonal Pattern Assessment Questionnaire.
While higher global seasonality scores have been reported among those with
various types of eating disorders compared to control subjects (31), most
studies have found that individuals with bulimia nervosa specifically are most
heavily influenced by seasonality (27,30,32,33). In general, patients with
anorexia nervosa show less seasonal mood and weight variation (32). Although
most of the research has been concentrated in North America, a Japanese study
also cited the greatest seasonal changes in bulimic patients specifically, albeit
less seasonal variation in mood and eating behavior than that found in North
American patients (33). Neurochemical dysregulation, such as serotonin
dysfunction, has been proposed as a possible link between these two disorders
(e.g., 34). Phototherapy has been demonstrated to be effective in decreasing
depressive and bulimic symptoms for some patients with SAD and bulimia
nervosa (35–37).
Some have proposed that depression and eating disorders share a similar
underlying diathesis, which may account for their frequent comorbidity (e.g., 38).
However, other family and twin study data refute the shared diathesis
hypothesis (14,39–41) and suggest that eating disorders are not simply an
alternate form of depressive disorder.
Indeed, there has been considerable controversy regarding the direction of
the association between depression and eating disorders. In an attempt to
unravel the nature of the association, several retrospective studies have found
that a significant proportion of individuals have depressive symptoms before the
onset of their eating disorder (19,21,25,42). However, a more recent review of
this literature suggests that it is more common for the eating disorder to
precede the onset of the depressive disorder (43). If this is the case, we must
remember the potential role of starvation and erratic consummatory patterns in
190 LILENFELD
Anxiety Disorders
As with mood disorders, most comorbidity studies of anxiety disorders and
eating disorders have been conducted with anorexia and bulimia nervosa rather
than binge eating disorder, so these findings will be reviewed first. Also similar
to that found with mood disorders, lifetime prevalence rates of
anxiety disorders vary markedly across studies. Rates of any anxiety disorder
have ranged from 23% to 66% among anorexic and 25% to 75% among bulimic
individuals (22,23,25,38,42,52–62).
When subtypes of anorexic and bulimic subjects are examined, similar to
findings with depression, bulimic symptomatology appears to be more
predictive of anxiety disorder comorbidity. Specifically, bulimic individuals
have been found to have significantly higher lifetime rates of comorbid anxiety
disorders than restricting-type anorexic subjects, whereas anorexic subjects
192 LILENFELD
studies of anorexic and bulimic individuals have found elevated rates of OCD
among their relatives (14,15,22,66), which initially seemed suggestive of a
potentially shared etiology. However, closer examination of the patterns of
cosegregation of OCD and eating disorders suggests that these two disorders are
actually independently transmitted in families (14,15). That is, OCD has been
found to be elevated primarily among the relatives of those eating-disordered
individuals who themselves have OCD. Thus, although OCD and eating
disorders frequently co-occur within individuals and within families, there is no
evidence of a shared etiological factor from family study data. However, recent
research suggests the possibility that OCD and anorexia nervosa may both be
linked to a polymorphism of the 5-HT2a receptor (67–72), although some
studies have not supported this association for either or both disorders (73,74).
In addition to OCD and social phobia, post-traumatic stress disorder (PTSD)
is an anxiety disorder of great importance to consider in individuals with eating
disorders because it coexists specifically with binge eating problems so
frequently. Lifetime prevalence rates of PTSD among bulimic individuals have
been found to range from 11% to 52% (14,75–77). Most notably, the National
Women’s Study, a very large and representative epidemiological sample,
yielded lifetime prevalence rates of 37% among women with bulimia nervosa
and 22% among women with binge eating disorder (77). Elevated rates of both
sexual and aggravated assault among women with bulimia nervosa suggests that
victimization may contribute to the development of and/or maintenance of
bulimia nervosa. Others have concluded that while PTSD is a common and
important clinical variable among women with eating disorders, it may not be
directly related to the eating disorder per se but rather to the comorbid
depressive, anxiety, and dissociative symptoms that often coexist with an eating
disorder (76).
The suggestion that there may be a meaningful etiological relationship
between anxiety disorders and eating disorders remains. Because anxiety
disorders often precede the development of the eating disorder (25,78), it
has been suggested that anxiety disorders may serve as a risk factor for the
development of anorexia nervosa or bulimia nervosa. We are currently awaiting
more data to confirm or refute this hypothesis.
Anxiety disorder comorbidity appears to be more clearly linked with
anorexia nervosa and bulimia nervosa than binge eating disorder. Lifetime
prevalence rates of any anxiety disorder in obese binge eaters have ranged from
9% to 46% (45,47,48,79–81). Only one of these studies (45) has found
significantly increased rates of anxiety disorders among obese binge eaters
compared to obese nonbinge eaters. One issue to consider in reviewing these
findings is that the diagnostic criteria used for binge eating in some earlier
studies was not DSM-IV binge eating disorder. However, again, all but one
194 LILENFELD
study (45) that did use the current definition of binge eating disorder found no
significant group differences in lifetime rates of anxiety disorders. All of these
studies utilized treatment-seeking samples. One recent comorbidity study of a
non-treatment-seeking community sample of binge eating disorder individuals
likewise suggests no significantly elevated rates of any anxiety disorders
compared with non-eating-disordered overweight women from the
community (48). The one important exception to these findings is the National
Women’s Study, which found PTSD to occur at a rate of 22% among women with
binge eating disorder in the community (77).
At present, we can conclude that anxiety disorders are common among
anorexic and bulimic patients, though we know less about those individuals with
anorexia nervosa and bulimia nervosa in the community. Thus far, the common
co-occurrence does not seem to be due to a shared etiologic factor between
eating disorders and anxiety disorders, though more family and twin study
research would aid in making a firmer conclusion. Individuals with binge eating
disorder, including both treatment-seeking as well as community samples, do
not appear to have similarly elevated rates of anxiety disorders, with the
possible exception of PTSD. However, many fewer studies of binge eating
disorder have been conducted compared to anorexia nervosa and bulimia
nervosa.
Dissociative Disorders
Nearly all studies of dissociative pathology and eating disorders have examined
dissociation as a continuous variable (110–112), as opposed to diagnosable
dissociative disorders. Specifically, the Dissociative Experiences Scale (113) is
the most commonly used measure for this purpose. Interestingly, however,
Waller and colleagues (114) successfully created a more effective categorical
measure of dissociation from this dimensional assessment instrument and used it
to classify eating disorder patients as “high” or “low” dissociators. Dissociation
198 LILENFELD
Somatoform Disorders
Very little empirical research on somatoform and eating disorder comorbidity
has been conducted. However, “somatoform dissociation” has been assessed
with the Somatoform Dissociation Questionnaire and has been found to be
characteristic of patients with dissociative disorders and a core feature in many
patients with somatoform disorders, as well as in some patients with eating
disorders (122,123). Examples of somatoform dissociation include motor
inhibitions and analgesia. It is not surprising that these symptoms are strongly
associated with a history of trauma (122).
SUMMARY
There are many reasons for the coexistence of two disorders. Reasons for the
comorbidity of eating disorders and other psychiatric disorders is under study
and much remains to be learned. We know that among clinical samples,
elevated rates of depressive disorders, particularly major depressive disorder,
have been observed among individuals with all types of eating disorders. In
addition, elevated rates of anxiety disorders, particularly social phobia and OCD,
have been found among individuals with anorexia nervosa and bulimia nervosa,
but not binge eating disorder. Substance use disorders are common among
individuals with bulimic symptomatology, in the form of bulimia nervosa or
bingeing-purging anorexia nervosa, but not binge eating disorder.
It is important to remember that most comorbidity studies have been
conducted with samples of convenience (i.e., treatment samples) and thus are
subject to referral bias, which will usually result in higher comorbidity rates
than would be found in a community sample. This is likely to occur because
people with more than one disorder are more likely to seek treatment (i.e.,
Berkson’s bias). Thus, in general, a clinical sample is likely to be more disturbed
than an epidemiological sample.
Finally, it is also important to remember that the comorbidity observed with
eating disorders (especially depressive and anxiety disorders) may be created, or
at least exacerbated, by malnutrition and pathological eating behaviors. The
extent to which such comorbid pathology actually increases the risk of
developing an eating disorder remains the focus of ongoing research.
200 LILENFELD
REFERENCES
1. Feinstein AR. The pre-therapeutic classification of co-morbidity in chronic disease.
J Chron Dis 1970; 23:455–468.
2. Klein DN, Riso LP. Psychiatric disorders: problems of boundaries and
comorbidity. In: Costello CG, ed. Basic Issues in Psychopathology. New York:
Guilford, 1993:19–66.
3. American Psychiatric Association. Diagnostic and statistical manual of mental
disorders. 4th ed. Washington, D.C., 1994.
4. Berkson J. Limitations of the application of fourfold table analysis to hospital data.
Biometrics 1946; 2:47–53.
5. Rothenberg A. Eating disorder as a modern obsessive-compulsive syndrome.
Psychiatry 1986; 49:45–52.
6. Fahy TA, Osacar A, Marks I. History of eating disorders in female patients with
obsessive-compulsive disorder. Int J Eat Disord 1993; 14:439–443.
7. Westen D. Unresolved issues in the classification, diagnosis, and comorbidity of
eating disorders. In: Maj M, Halmi K, Lopez-Ibor JJ, Sartorius N. eds. World
Psychiatric Association: Evidence and Experience in Psychiatry. Vol. 6. Eating
Disorders, New York: John Wiley and Sons, 2003:34–37.
8. Gleaves DH, Lowe MR, Snow AC. Continuity and discontinuity models of bulimia
nervosa: a taxometric investigation. J Abnorm Psychol 2000; 109:56–68.
9. Keys A, Brozek J, Henschel A, Mickelsen O, Taylor HL. The Biology of Human
Starvation. Minneapolis: University of Minnesota Press, 1950.
10. Strober M. Personality and symptomatological features in young, nonchronic
anorexia nervosa patients. J Psychosom Res 1980; 24:353–359.
11. Srinivasagan NM, Plotnicov KH, Greeno C, Weltzin TE, Rao R, Kaye WH.
Persistent perfectionism, symmetry, and exactness in anorexia nervosa after long-
term recovery. Am J Psychiatry 1995; 152:1630–1634.
12. Pollice CP, Kaye WH, Greeno CG, Weltzin TE. Relationship of depression,
anxiety, and obsessionality to state of illness in anorexia nervosa. Int J Eat Disord
1997; 21:367–376.
13. Kaye WH, Lilenfeld LR, Plotnicov K, Merikangas KR, Nagy L, Strober M, Bulik
CM, Moss H, Greeno CG. Bulimia nervosa and substance dependence. Alcohol
Clin Exp Res 1996; 20:878–881.
14. Lilenfeld LR, Kaye WH, Greeno CG, Merikangas KR, Plotnicov K, Pollice C, Rao
R, Strober M, Bulik CM, Nagy L. A controlled family study of anorexia nervosa
and bulimia nervosa: psychiatric disorders in first-degree relatives and effects of
proband comorbidity. Arch Gen Psychiatry 1998; 55:603–610.
15. M. Strober. Unpublished data, 2000.
16. Laessle RG, Wittchen HU, Fichter MM, Pirke KM. The significance of subgroups
of bulimia and anorexia nervosa: lifetime frequency of psychiatric disorders. Int J
Eat Disord 1989; 8:569–574.
17. Hatsukami D, Eckert E, Marchi P, Sampugnaro V, Apple R, Cohen J. Affective
disorders and substance abuse in women with bulimia. Psychol Med 1984; 14:
701–704.
PSYCHIATRIC COMORBIDITY 201
18. Herzog DB. Are anorexic and bulimic patients depressed? Am J Psychiatry 1984;
141:1594–1597.
19. Hudson JI, Pope HG, Jonas JM, Yurgelun-Todd D. Phenomenologic relationship
of eating disorders to major affective disorder. Psychiatry Res 1983; 9:345–354.
20. Herzog DB. Bulimia in the adolescent. Am J Dis Child 1982; 136:985–989.
21. Walsh BT, Roose SP, Glassman AH, Glades MA, Sadik C. Depression and bulimia.
Psychosom Med 1985; 47:123–131.
22. Halmi KA, Eckert E, Marchi P, Sampugnaro V, Apple R, Cohen J. Comorbidity of
psychiatric diagnoses in anorexia nervosa. Arch Gen Psychiatry 1991; 48:712–718.
23. Herzog D, Keller M, Sacks N, Yeh C, Lavori P. Psychiatric comorbidity in
treatment seeking anorexics and bulimics. J Am Acad Child Adol Psychiatry 1992;
31:810–818.
24. Bushnell JA, Wells JE, McKenzie JM, Hornblow AR, Oakley-Browne MA, Joyce
PR. Bulimia comorbidity in the general population and in the clinic. Psychol Med
1994; 24:605–611.
25. Brewerton TD, Lydiard RB, Herzog DB, Brotman AW, O’Neil PM, Ballenger JC.
Comorbidity of axis I psychiatric disorders in bulimia nervosa. J Clin Psychiatry
1995; 56:77–80.
26. Gwirtsman HE, Roy-Byrne P, Yager J, Gerner RH. Neuroendocrine abnormalities
in bulimia. Am J Psychiatry 1983; 140:559–563.
27. Blouin A, Blouin J, Aubin P, Carter J, Goldstein C, Boyer H, Perez E. Seasonal
patterns of bulimia nervosa. Am J Psychiatry 1992; 149:73–81.
28. Ghadirian AM, Marini N, Jabalpurwala S, Steiger H. Seasonal mood patterns in
eating disorders. Gen Hosp Psychiatry 1999; 21:354–359.
29. Lam RW, Solymon L, Tompkins A. Seasonal mood symptoms in bulimia nervosa
and seasonal affective disorder. Compr Psychiatry 1991; 32:552–558.
30. Lam RW, Golner EM, Grewal A. Seasonality of symptoms in anorexia and bulimia
nervosa. Int J Eat Disord 1996; 19:35–44.
31. Brewerton TD, Krahn DD, Hardin TA, Wehr TA, Rosenthal NE. Findings from
the Seasonal Pattern Assessment Questionnaire in patients with eating disorders and
control subjects: effects of diagnosis and location. Psychiatry Res 1994; 52:71–84.
32. Fornari VM, Braun DL, Sunday SR, et al. Seasonal patterns in eating disorder
subgroups. Compr Psychiatry 1994; 35:450–456.
33. Yamatsuji M, Yamashita T, Arii I, Taga C, Tatara N, Fukui K. Seasonal variations in
eating disorder subtypes in Japan. Int J Eat Disord 2003; 33:71–77.
34. Brewerton TD, Brandt HA, Lesem MD, Murphy DL, Jimerson DC. Serotonin in
eating disorders. In: Coccaro EF, Murphy DL, eds. Serotonin in Major Psychiatric
Disorders. Spiefel D, ed. Progress in Psychiatry Monograph Series. Washington,
DC: American Psychiatric Press, 1990:153–184.
35. Lam RW, Lee SK, Tam EM, Grewal A, Yatham LN. An open trial of light therapy
for women with seasonal affective disorder and comorbid bulimia nervosa. J Clin
Psychiatry 2001; 62:164–168.
202 LILENFELD
36. Braun DL, Sunday SR, Fornari VM, Halmi KA. Bright light therapy decreases
winter binge frequency in women with bulimia nervosa: a double-blind, placebo-
controlled study. Compr Psychiatry 1999; 40:442–448.
37. Blouin AG, Blouin JH, Iversen H, Carter J, Goldstein C, Goldfield G, Perez E.
Light therapy in bulimia nervosa: a double-blind placebo-controlled study.
Psychiatry Res 1996; 60:1–9.
38. Hudson JI, Pope HG, Yurgelun-Todd D, Jonas JM, Frankenburg FR. A controlled
study of lifetime prevalence of affective and other psychiatric disorders in bulimic
outpatients. Am J Psychiatry 1987; 144:1283–1287.
39. Strober M, Lampert C, Morrell W, Burroughs J, Jacobs C. A controlled family
study of anorexia nervosa: evidence of familial aggregation and lack of shared
transmission with affective disorders. Int J Eat Disord 1990; 9:239–253.
40. Biederman J, Rivinus T, Kemper K, Hamilton D, MacFayden J, Harmatz J.
Depressive disorders in relatives of anorexia nervosa patients with and without a
current episode of nonbipolar major depression. Am J Psychiatry 1985; 142:
1495–1496.
41. Kendler KS, Walters EE, Neale MC, Kessler RC, Heath AC, Eaves LJ. The structure
of the genetic and environmental risk factors for six major psychiatric disorders in
women. Arch Gen Psychiatry 1995; 52:374–383.
42. Piran N, Kennedy S, Garfinkel PE, Owens M. Affective disturbance in eating
disorders. J Nerv Ment Dis 1985; 173:395–400.
43. Cooper PJ. Eating disorders and their relationship to mood and anxiety disorders.
In: Brownell KD, Fairburn CG, eds. Eating Disorders and Obesity: A
Comprehensive Handbook. New York: Guilford Press, 1995:159–164.
44. Vitousek K, Manke F. Personality variables and disorders in anorexia nervosa and
bulimia nervosa. J Abnorm Psychol 1994; 103:137–147.
45. Yanovski SZ, Nelson JE, Dubbert BK, Spitzer RL. Association of binge eating
disorder and psychiatric comorbidity in the obese. Am J Psychiatry 1993; 150:
1472–1479.
46. Marcus MD, Wing RR, Ewing L, Kern E, Gooding W, McDermott M. Psychiatric
disorders among obese binge eaters. Int J Eat Disord 1990; 9:69–77.
47. Specker S, de Zwaan M, Raymond N, Mitchell J. Psychopathology in subgroups of
obese women with and without binge eating disorder. Compr Psychiatry 1994; 35:
185–190.
48. Telch CF, Stice E. Psychiatric comorbidity in women with binge eating disorder:
prevalence rates from a non-treatment-seeking sample. J Consult Clin Psychol
1998; 66:768–776.
49. Kendler KS, Eaves LJ, Walters EE, Neale MC, Heath AC, Kessler RC.
The identification and validation of distinct depressive syndromes in a
populationbased sample of female twins. Arch Gen Psychiatry 1996; 53:391–399.
50. Mussell MP, Mitchell JE, Weller CL, Raymond NC, Crow SJ, Crosby RD. Onset
of binge eating, dieting, obesity, and mood disorders among subjects seeking
treatment for binge eating disorder. Int J Eat Disord 1995; 17:395–401.
PSYCHIATRIC COMORBIDITY 203
51. Smith DE, Marcus MD, Lewis C, Fitzgibbon M, Schreiner P. Prevalence of binge
eating disorder, obesity and depression in a biracial cohort of young adults. Ann
Behav Med 1998; 20:227–232.
52. Fornari V, Kaplan M, Sandberg DE, Mathews M, Skolnick N, Katz JL. Depressive
and anxiety disorders in anorexia nervosa and bulimia nervosa. Int J Eat Disord
1992; 12:21–29.
53. Laessle RG, Kittl S, Fichter MM, Wittchen H, Pirke KM. Major affective disorder
in anorexia nervosa and bulimia: a descriptive diagnostic study. Br J Psychiatry
1987; 151:785–789.
54. Toner BB, Garfinkel PE, Garner DM. Affective and anxiety disorders in the long-
term follow-up of anorexia nervosa. Int J Psychiatry Med 1988; 18:357–364.
55. Schwalberg MD, Barlow DH, Alger SA, Howard LJ. Comparison of bulimics,
obese binge eaters, social phobics, and individuals with panic disorder on
comorbidity across DSM-III-R anxiety disorders. J Abnorm Psychol 1992; 101:
675–681.
56. Smith C, Feldman SS, Nasserbakht A, Steiner H. Psychological characteristics and
DSM-III-R diagnoses at 6-year follow-up of adolescent anorexia nervosa. J Am
Acad Child Adol Psychiatry 1993; 32:1237–1245.
57. Bossert-Zaudig S, Zaudig M, Junker M, Wiegand M, Krieg JC. Psychiatric
comorbidity of bulimia nervosa inpatients: relationship to clinical variables and
treatment outcome. Eur Psychiatry 1993; 8:15–23.
58. Braun DL, Sunday S, Halmi KA. Psychiatric comorbidity in patients with eating
disorders. Psychol Med 1994; 24:859–867.
59. Deep AL, Nagy LM, Weltzin TE, Rao R, Kaye WH. Premorbid onset of
psychopathology in long-term recovered anorexia nervosa. Int J Eat Disord 1995;
17:291–297.
60. Thiel A, Broocks A, Ohlmeier M, Jacoby GE, Schussler G. Obsessive-compulsive
disorder among patients with anorexia nervosa and bulimia nervosa. Am J
Psychiatry 1995; 152:72–75.
61. Garfinkel PE, Lin E, Goering P, Speff C, Goldbloom DS, Kennedy S, Kaplan AS,
Woodside DB. Bulimia nervosa in a Canadian community sample: prevalence and
comparison of subgroups. Am J Psychiatry 1995; 152:1052–1058.
62. Keck PE Jr, Pope HG Jr, Hudson JI, McElroy SL, Yurgelun-Todd D, Hundert EM.
A controlled study of phenomenology and family history in outpatients with
bulimia nervosa. Compr Psychiatry 1990; 31:275–283.
63. Thornton C, Russell J. Obsessive compulsive comorbidity in the dieting disorders.
Int J Eat Disord 1997; 21:83–87.
64. Godart NT, Flament MF, Lecrubier Y, Jeammet P. Anxiety disorders in ano rexia
nervosa and bulimia nervosa: comorbidity and chronology of appearance. Eur
Psychiatry 2000; 15:38–45.
65. Powers PS, Coovert DL, Brightwell DR, Stevens BA. Other psychiatric disorders
among bulimic patients. Compr Psychiatry 1988; 29:503–508.
66. Pasquale L, Sciuto G, Cocchi S, Ronshi P, Billodi L. A family study of obsessive
compulsive, eating, and mood disorders. Eur Psychiatry 1994; 9:33–38.
204 LILENFELD
82. Bulik CM, Sullivan PF, Epstein LH, McKee M, Kaye WH, Dahl RE, Weltzin TE.
Drug use in women with anorexia and bulimia nervosa. Int J Eat Disord 1992; 11:
213–225.
83. Holderness CC, Brooks-Gunn J, Warren WP. Co-morbidity of eating disorders
and substance abuse. Int J Eat Disord 1994; 16:1–34.
84. Krahn DD. The relationship of eating disorders and substance abuse. J Subst Abuse
1991; 3:239–253.
85. Wilson GT. The addiction model of eating disorders: a critical analysis. Adv Behav
Res Ther 1991; 13:27–72.
86. Strober M, Freeman R, Bower S, Rigali J. Binge eating in anorexia nervosa predicts
later onset of substance use disorder: a ten-year prospective, longitudinal follow-up
of 96 adolescents. J Youth Adol 1996; 25:519–532.
87. Lacey J, Evans C. The impulsivist: a multi-impulsive personality disorder. Br J Addict
1986; 81:641–649.
88. Fichter MM, Quadflieg N, Rief W. Course of multi-impulsive bulimia. Psychol
Med 1994; 24:591–604.
89. Lilenfeld LR, Kaye WH, Greeno CG, Merikangas KR, Plotnicov K, Pollice C, Rao
R, Strober M, Bulik CM, Nagy L. Psychiatric disorders in women with bulimia
nervosa and their first-degree relatives. Int J Eat Disord 1997; 22:253–264.
90. Bulik CM. Family histories of bulimic women with and without comorbid alcohol
abuse or dependence. Am J Psychiatry 1991; 148:1267–1268.
91. Mitchell JE, Hatsukami D, Pyle R, Eckert E. Bulimia with and without a family
history of drug abuse. Addict Behav 1988; 12:245–251.
92. Schuckit MA, Tipp JE, Anthenelli RM, Bucholz KK, Hesselbrock VM, Nurnberger
JI. Anorexia nervosa and bulimia nervosa in alcohol-dependent men and women
and their relatives. Am J Psychiatry 1996; 153:74–82.
93. Dansky BS, Brewerton TD, Kilpatrick DG. Comorbidity of bulimia nervosa and
alcohol use disorders: results from the National Women’s Study. Int J Eat Disord
2000; 27:180–190.
94. Brody MJ, Walsh BT, Devlin MJ. Binge eating disorder: reliability and validity of a
new diagnostic category. J Consult Clin Psychol 1994; 62:381–386.
95. Wilfley DE, Friedman MA, Dounchis JZ, Stein RI, Welch RR, Ball SA. Comorbid
psychopathology in binge eating disorder: relation to eating disorder severity at
baseline and following treatment. J Consult Clin Psychol 2000; 68: 641–649.
96. Wilson GT. Eating disorders and addictive disorders. In: Brownell KD, Fairburn
CG, eds. Eating Disorders and Obesity: A Comprehensive Handbook. New York:
Guilford Press, 1995:165–170.
97. Steiger H, Lehoux PM, Gauvin L. Impulsivity, dietary control and the urge to
binge in bulimic syndromes. Int J Eat Disord 1999; 26:261–274.
98. Favaro A, Santonastaso P. Impulsive and compulsive self-injurious behavior in
bulimia nervosa: prevalence and psychological correlates. J Nerv Ment Dis 1998;
186:157–165.
99. Lledo EP, Waller G. Bulimic psychopathology and impulsive behaviors among
nonclinical women. Int J Eat Disord 2001; 29:71–75.
206 LILENFELD
100. Bridgeman J, Slade PD. Shoplifting and eating disorders: a psychological medical-
legal perspective. Eur Eat Dis Rev 1996; 4:133–148.
101. Penas-Lledo E, Vaz FJ, Ramos MI, Waller G. Impulsive behaviors in bulimic patients:
relation to general psychopathology. Int J Eat Disord 2002; 32:98–102.
102. Agras WS, Crow SJ, Halmi KA, Mitchell JE, Wilson GT, Kraemer HC. Outcome
predictors for the cognitive behavior treatment of bulimia nervosa: data from a
multisite study. Am J Psychiatry 2000; 157:1302–1308.
103. Sohlberg S, Norring C, Holmgren S, Rosmark B. Impulsivity and long-term
prognosis of psychiatric patients with anorexia nervosa/bulimia nervosa. J Nerv
Ment Dis 1989; 177:249–258.
104. Hudson JI, Pope HG Jr, Jonas JM. Psychosis in anorexia nervosa and bulimia. Br J
Psychiatry 1984; 145:420–423.
105. Bruch H. Eating Disorders: Obesity, Anorexia Nervosa and the Person Within.
New York: Basic Books, 1973.
106. Hsu LKG, Meltzer ES, Crisp AH. Schizophrenia and anorexia nervosa. J Nerv
Ment Dis 1981; 169:273–276.
107. Salmon G. Atypical anorexia nervosa and schizophrenia: are they linked by the
5-HTlc receptor? Eur Eat Disord Rev 1996; 4:189–194.
108. Lavia MC, Gray N, Kaye WH. Case reports of olanzapine treatment of anorexia
nervosa. Int J Eat Disord 2000; 27:363–366.
109. Newman-Toker J. Risperidone in anorexia nervosa. J Am Acad Child Adol
Psychiatry 2000; 39:941–942.
110. Everill JT, Waller G, MacDonald W. Dissociation in bulimic and non-eating
disordered women. Int J Eat Disord 1995; 17:127–134.
111. Everill JT, Waller G. Dissociation and bulimia: research and theory. Eur Eat Dis
Rev 1995; 3:129–147.
112. Vanderlinden J, Vandereycken W, van Dyck R, Vertommen H. Dissociative
experiences and trauma in eating disorders. Int J Eat Disord 1993; 13:187–193.
113. Carlson EB, Putnam FW. An update on the dissociative experiences scale.
Dissociation 1993; 6:16–27.
114. Waller NG, Putnma FW, Carlson EB. Types of dissociation and dissociative types:
a taxometric analysis of dissociative experiences. Psychol Measures 1996; 1:
300–321.
115. van der Kolk BA, Pelcovitz D, Roth S, Mandel FS, McFarlane A, Herman JL.
Dissociation, somatization, and affect dysregulation: the complexity of adaptation
to trauma. Am J Psychiatry 1996; 153:83–93.
116. Shearer SL. Dissociative phenomena in women with borderline personality
disorder. Am J Psychiatry 1994; 151:1324–1328.
117. Brodsky BS, Cloitre M, Dulit RA. Relationship of dissociation to self mutilation
and childhood abuse in borderline personality disorder. Am J Psychiatry 1995; 152:
1788–1792.
118. Waller G, Ohanian V, Meyer C, Everill J, Rouse H. The utility of dimensional and
categorical approaches to understanding dissociation in the eating disorders. Br J
Clin Psychol 2001; 40:387–397.
PSYCHIATRIC COMORBIDITY 207
119. Baumeister R, Heatherton T, Tice D. Losing Control: How and Why People Fail
at Self-Regulation. London: Academic Press, 1994.
120. Suyemoto KL. The functions of self-mutilation. Clin Psychol Rev 1998; 18:
531–554.
121. Nagata T, Kiriike N, Iketani T, Kawarada Y, Tanaka H. History of childhood
sexual or physical abuse in Japanese patients with eating disorders: relationship with
dissociation and impulsive behaviors. Psychol Med 1999; 29:935–942.
122. Nijenhuis ERS. Somatoform dissociation: major symptoms of dissociative
disorders. J Trauma Dissoc 2000; 1:7–32.
123. Zerbe KJ, Giorgio C. Whose body is it anyway? Understanding and treating
psychosomatic aspects of eating disorders. Rev Psychoanal Meth Res Clin Exp
1999; 6:13–32.
124. Fleming J, Levy L. Eating disorders in women with AD/HD. In: Quinn P, Nadeau
K, eds. Gender Issues and AD/HD: Research, Diagnosis, and Treatment. Silver
Spring, MD: Advantage Books, 2002.
125. Geist R, Davis R, Heinmaa M. Binge/purge symptoms and comorbidity in
adolescents with eating disorders. Can J Psychiatry 1998; 43:507–512.
126. Thompson KM, Wonderlich SA, Crosby RD, Mitchell JE. The neglected link
between eating disturbances and aggressive behavior in girls. J Am Acad Child
Adol Psychiatry 1999; 38:1277–1284.
208 LILENFELD
9
Personality Traits and Disorders Associated
with Anorexia Nervosa, Bulimia Nervosa, and
Binge Eating Disorder
Howard Steiger and Kenneth R.Bruce
Douglas Hospital and McGill University
Montreal, Quebec, Canada
In 1689, Thomas Morton reported two cases of anorexia nervosa (AN): one
involving a “sad and anxious” girl who “poured over books,” another involving a
young boy prone to “studying too hard” (1). With these reports, Morton not
only introduced AN to the medical literature; he introduced the concept that
AN frequently co-occurs with perfectionistic or compulsive personality traits.
Likewise, 19th century observations on bulimia nervosa (BN) documented
instability of mood and behavior (2). All of this says that there is a history
behind the association between eating disorders (EDs) and problematic
personality tendencies.
The connection may not be new, but many questions remain: Is there an
ED-prone personality type? Do AN and BN coincide with different personality
characteristics? Do EDs always involve personality problems? In this chapter, we
study personality traits and disorders in AN, BN, and binge eating disorder
(BED). We examine the coaggregation of eating symptoms with personality
trait variations and evidence that such co-occurrence involves shared
developmental, familial, neurobiological, and hereditary pathways. We also
discuss the bearing of personality pathology, in the EDs, for clinical typology,
treatment needs, and prognosis.
Specific Traits
A. Perfectionism. A hypothetical link between AN and perfectionism seems to be
well-supported empirically, with restricter and binger-purger anorexics both
producing higher self-rated perfectionism scores than healthy controls (12,13)
Recent findings suggest that a connection with perfectionism may extend to
BN (14) and to BED (15). However, any such link may be stronger for BN than
for BED (16). Perfectionism appears to exist premorbidly in ED sufferers (17)
and in AN sufferers after long-term weight recovery (13), and furthermore to
be common in relatives of those who develop an ED (14,18). While such
findings all support the speculation that perfectionism may be a risk factor for
ED development, specificity of the association with EDs (versus other forms of
maladjustment) still needs to be established.
B. Impulsivity. Findings suggest remarkable capacities for nonreflectiveness or
behavioral impulsivity in “bingers-purgers.” Self-report scales show that bulimic
individuals often fail to consider consequences of their actions and often act on
impulse (19). Furthermore, various studies report bulimics to show prominent
parasuicidality or self-mutilation: Mitchell and colleagues (20) estimated that
about 20% of their bulimic cohort showed repeated suicidal gestures, self-
mutilation, or other forms of self-destructive impulsivity. Likewise, Newton
and colleagues (21) found almost half of a cohort of normal-weight bulimics to
engage in combinations of substance abuse, drug overdoses, suicidal gestures, self-
mutilation, sexual disinhibition, or shoplifting. A similar report, based on
semistructured interviewing techniques, showed nearly 40% of bulimic
individuals to display multiple forms of destructive impulsivity (22). Combined
characteristics of suicidality, selfaggression, shoplifting, substance abuse, and
sexual promiscuity compose the features of what Hubert Lacey and his
colleagues (23) some years ago dubbed “multi-impulsive” bulimia—a subtype of
BN in which binge eating represented only one instance of pervasive
dysregulation of impulse controls. The general propensity toward impulsivity
may extend, it appears, to “binger” populations in general. For example, studies
have supported the idea that binge-purge AN has a more complicated clinical
course, with greater risk for suicide than restricting AN (24). Similarly, a study
of 495 eating-disordered outpatients by Favaro and Santonastaso (25) indicated
that 13% reported a past suicide attempt and 29% reported current suicidal
212 STEIGER AND BRUCE
1. PDs are undoubtedly more common in anorexic and bulimic women than
in healthy comparison cases. Estimated PD prevalences in eating-
disordered samples vary from roughly 20% to nearly 100%, with most
commonly cited figures occupying the 50–75% range. Corroborating this
point, a recent meta-analytical review of findings from 28 available studies
finds 58% of women with an ED to have a PD, compared to 28% of
comparison women (29).
2. Restrictive AN is associated mainly with DSM Cluster C (“Anxious-
Fearful”) PD subtypes, typified by anxiousness, orderliness, and preference
for control. More rarely, AN-R coincides with Cluster A (“Odd-
Eccentric”) PDs (e.g., Schizoid PD)—having a particularly stilted quality,
but still characterized by inhibition and restricted emotionality. The PD
subtype reported to occur most frequently in AN-R is Obsessive-
Compulsive PD (with Avoidant and Dependent PDs also sometimes named
as modal diagnoses).
PERSONALITY TRAITS AND DISORDERS 213
State-Trait Debate
Since malnutrition can adversely affect personality functioning (35), apparent
personality problems seen in ED sufferers could be attributed to “state” sequelae
of an active ED. Consistent with this, various findings show EDs to exacerbate
features with a “characterological coloring” (36,37). However, in counterpoint,
retrospective findings often suggest that personality problems predate ED onset
in ED sufferers. Råstam (38) estimated that 67% of a group of 51 adolescent
anorexics had a PD prior to ED onset, the most common of which (in 35% of
cases) was obsessive-compulsive PD. Similarly, Nagata and colleagues estimated
that parasuicidality predated onset of eating symptoms in 80% of ED patients
showing such self-destructiveness (39). Suggesting a similar independence of
personality pathology from ED sequelae, many findings indicate personality
214 STEIGER AND BRUCE
Family/Developmental Characteristics
Given systematic coaggregation of personality traits with ED subtypes, data
associating family interaction patterns with eating and personality problems
present various explicative potentials. On the personality side of this question,
some principled connections emerge: There have been inconsistent indications
of a link between obsessive-compulsive personality traits and familial
overinvolvement or overcontrol (43), and between impulsive (or borderline)
personality traits and parental neglect, hostility, or inconsistency (44).
In light of the preceding, data on family interaction patterns in ED subtypes
become suggestive. Studies on anorexic restricters and their relatives have often
corroborated concepts of enmeshment, overprotection, and emotional
constraint. In contrast, studies have associated binge-purge syndromes with
relatively more overt familial discord, disengagement, and hostility (31, 45).
Data on family interaction patterns in BED are inconclusive but suggest
comparable family interactions to those found in BN. For example, Hodges and
her colleagues (46) found BED women to describe their families as less cohesive,
expressive, and independent, and more conflictual and controlling, than did
normal-control women. Reiterating this notion, Tachi (47), working in Japan,
found women with BN and BED to perceive their families as being relatively
disengaged. Similarly, obese women with BED have been found to report more
paternal rejection than do obese women without BED (48).
Several research groups have noted severity of family dysfunction to
correspond much more closely to severity of personality pathology in
eatingdisordered individuals than to severity of eating symptoms (49,50). This
raises doubts about the extent to which family interaction patterns may be
specific to ED development—and the possibility that systematic convergences
between family interaction patterns and ED subtypes might reflect indirect
(personality-mediated) effects of family-environment variables acting on
PERSONALITY TRAITS AND DISORDERS 215
Childhood Abuse
EDs, personality pathology, and especially BPD have all been associated with
childhood abuse or neglect. Studies suggest, for example, that more than 50% of
individuals suffering from BPD (51,52) and roughly 30% of those suffering from
an ED (53,54) have experienced childhood sexual abuse. Childhood abuse
experiences therefore represent one possible area of commonality underlying
convergence of eating and personality disturbances. However, assessment of
this possibility asks that various findings be properly considered:
Genetics
Findings on the molecular genetics of eating and personality disorders are in a
nascent state. Nonetheless, preliminary findings may help inform our study of
the convergence of ED subtypes and personality trait variations. In BN, data
have pointed to gene variations that may be simultaneously linked to binge
eating and impulsive potentials. For example, Nishiguchi and colleagues (72)
reported a link, in a heterogeneous anorexic-bulimic sample, between a
polymorphism in the 5-HT2A receptor gene and the presence of (a) disinhibited
eating and (b) traits (largely impulsivity). In a related vein, Devlin and
colleagues linked drive for thinness and obsessionality, in 196 patients with
AN-restrictive subtype, to specific gene loci (73). Such findings raise the
intriguing specter that genetic factors may be substrates of a link between
bulimic eating tendencies and an “impulsive/behaviorally dysregulated”
phenotype—and between restrictive eating patterns and compulsive personality
characteristics.
Symptoms
Intuitively, personality pathology might be though to confer risk for more
severe eating symptomatology. However, empirical treatments provide limited
218 STEIGER AND BRUCE
support for this idea. (Here we see the first of several instances of apparent
independence between eating and personality pathologies.) Johnson and his
colleagues (74) compared patients with and without self-reported BPD features.
Borderlines differed from nonborderlines in showing greater depression, self-
mutilation, drug abuse, and history of sexual abuse, but not greater binge/purge
frequencies or other eating-specific symptoms. In a similar study, Wonderlich
and Swift (75) examined clinical profiles in 75 eating-disordered women,
divided (according to structured interviews) into those with and without BPD.
Borderline patients displayed more suicidality, depression, anxiety, and self-
mutilation than did their nonborderline counterparts. However, except for
more frequent vomiting, borderline patients displayed negligibly more severe
eating symptoms. Our group conducted a similar multidimensional evaluation,
rating eating and general psychopathological symptoms in a sample of 91
bulimics, in whom axis II diagnoses were established with the aid of structured
interviews (76). As in the study of Wonderlich and Swift, borderlines evinced
more pronounced anomalies on diverse measures of general psychopathology
without showing more severe eating symptoms. Thus, while it is undeniably
associated with greater generalized psychopathology in BN sufferers, PD may
not have a marked connotation for severity of ED symptoms. In apparent
contrast, personality pathology has been associated with more severe binge
eating in BED (33,77).
Outcome
Comorbid personality pathology has been associated with poorer global
outcome from AN, BN, and BED.
Anorexia Nervosa
Following an extensive review (encompassing 119 studies and 5590 patients),
Steinhausen (78) concluded that obsessive-compulsive PD is associated with an
unfavorable prognosis in AN. Intriguingly, he noted hysterical personality
features (somewhat the antithesis of obsessive-compulsive features) to coincide
with favorable prognosis. Several results suggest the prognostic utility in AN of
other personality measures. A recent study reported response in 42 restricter
anorexics after 180 days of multimodal therapy (79). Categorical PD diagnoses
did not predict improvement, but dimensional measure (low novelty seeking,
and high asceticism and maturity fears) were systematically linked to poorer
response. Suggesting similar effects at long-term follow-up, Bulik and her
colleagues (36) found anorexics who remained ill after 12 years to be
characterized partly by more severe eating disturbances and partly by
PERSONALITY TRAITS AND DISORDERS 219
greater harm avoidance (i.e., anxious avoidance and overcontrol) and lower
self-directedness. In a similar 4-year prospective study for AN, lower selfesteem
and stronger maturity fears were associated with poorer outcome (80).
Bulimia Nervosa
Results for BN also seem to associate personality pathology with poorer global
treatment response: Herzog et al. (81) linked comorbid PD (diagnosed using
structured interview in 179 bulimics) with lower probability of abstinence from
BN after 9 or more months. Similarly, Rossiter et al. (82) reported that Dramatic-
Erratic personality traits predicted greater chance of persistent vomiting in BN
after one year. Other studies corroborate the same trend: One shows BN patients
with high initial Borderline Syndrome Index scores to be more likely to remain
bulimic after one year than patients with initially lower scores (83). Another
reports that bulimic patients who showed persistent “borderline features” over
the first 3 months of therapy showed poorest response of bulimic symptoms
after 6 and 12 months (84).
When finer grained outcome dimensions (rather than “global ED outcome”)
are assayed, however, subtler effects sometimes emerge. Wonderlich et al. (85)
reported that PD comorbidity predicted poorer global response, but only weak
differences on indices of bulimic symptoms, in 30 bulimics followed for
4–5 years. Our group studied progress in treatment, in function of interview-
based PD diagnoses, of bulimics after 3, 6, and then 12 and more months.
Borderline bulimics showed greater psychiatric symptoms than did
nonborderline bulimics at all points in time but limited differences on measures
reflecting the course of eating symptoms (76,86). Norring (87) reported similar
findings in heterogeneous ED cases. Patients showing a “borderline
organization” showed poorest response after 2 and 3 years—but differences
were more pronounced on comorbid symptoms than on eatingspecific ones.
Such tendencies led Grilo (27), after an excellent and comprehensive review, to
conclude that PD may be more closely associated with the longtudinal course of
general psychiatric symptoms or psychosocial functioning in ED patients than
with fluctuations in the course of eating symptoms.
It is possible that “impulsivity” measures may yield more reliable prognostic
effects. After an extensive literature review, Keel and Mitchell (88) concluded
that impulsivity was foremost among prognostic indices for BN, with PD having
inconsistent effects. In addition, isolated personality dimensions have emerged as
having prognostic value for BN: Joiner et al. (89) found “maturity fears” and
“perfectionism” to be weak long-term (10-year) predictors of bulimic
symptoms. Bulik and her colleagues (90) examined predictors of outcome one
year after completion of a randomized psychotherapy trial. PD symptoms were
220 STEIGER AND BRUCE
Treatment Usage
Personality pathology apparently has an additional clinical relevance as a
predictor of treatment usage: Several studies document more frequent
hospitalizations and medication usage in bulimics with Dramatic-Erratic or
borderline PDs than in those with lesser PD comorbidity (74,75,86). Suggesting
that this trend cuts across ED subtypes, Keel and colleagues (91) reported a link,
in 294 women treated for AN or BN, between presence of a PD and use of
psychotherapy and medication after 5 years.
WITHIN-SUBTYPE HETEROGENEITY AS TO
PERSONALITY FEATURES
The patterning of association between personality and eating symptom
variations has inspired various speculations on the “shaping” role, in ED
expression, of personality factors. Relatively circumscribed comorbidity of a
compulsive type in restrictive AN makes an obvious appeal to the idea that
obstinacy, constriction, and hypersensitivity to social approval may “power”
rigid dieting and driven pursuit of thinness. Likewise, affinities between bulimic
behaviors and tendencies toward behavioral dyscontrol encourages the view that
bingeing and purging may only be isolated instances, in affected individuals, of a
more generalized dysregulation. Although intuitively appealing, the latter view
is challenged by the reality that individuals who binge-eat display heterogeneous
personality characteristics—sometimes impulsive, sometimes compulsive.
Diversity of personality characteristics seen in bulimic syndromes has (as
discussed earlier) been thought to correspond to different etiological
paths to binge eating-sometimes reflecting a primary and rather pervasive
disruption of controls over mood, impulses, and appetite, and sometimes a
more circumscribed erosion of appetitive controls, following prolonged
dieting (5, 31,92,93). The idea that binge eating results from prolonged dietary
PERSONALITY TRAITS AND DISORDERS 221
making in this area. To illustrate how this may be so, we offer a few general
conceptual and clinical guidelines:
(1) Eating and personality disturbances are separate but interdependent entities.
There are reasons to assume that eating and personality pathologies are
independently determined. For example, one can be severe, whereas the other
is mild; one can resolve, whereas the other persists. This implies, as suggested
by available outcome literature, that eating problems can to some extent be
treated independently of associated personality characteristics. However, that
eating and personality disturbances co-occur so frequently also suggests
nonnegligible measures of causal overlap. Consider the following:
Neurobiological vulnerabilities (e.g., altered serotonin neurotransmission) may,
along with predictable effects on personality manifestations (e.g., heightened
impulsivity), confer vulnerability to impaired satiety. If so, having a particular
personality trait (like impulsivity) might increase vulnerability to a particular
disturbance in eating behavior (like binge eating) because of neurobiological
propensities that are linked to both the trait and the appetitive behavior. Given
this notion, it becomes fascinating to contemplate all of the possible sources of
influence that may act upon the neurobiological status in a given individual at a
given moment in time (e.g., heredity, nutritional state, effects of
developmental and current stressors, etc.)—and, in turn, to contemplate the
complexity of processes that determine whether or not a given personality trait
(e.g., impulsivity) or eating symptom (e.g., binge eating) is likely to come to
expression. We address such convergences elsewhere (31,60,68,70). In a
related vein, common developmental factors (e.g., childhood sexual abuse) can
be thought to impact, not only upon interpersonal expectations and
functioning, but also upon the sense of bodily integrity, control, and esteem.
Such effects might, in turn, heighten susceptibility to concurrent interpersonal
difficulties and maladaptive weight control practices or food avoidances.
(2) Eating disturbances worsen personality disturbances. The view that ED sequelae
exacerbate obsessionality, impulsivity, or other apparent personality problems
in ED sufferers has a simple wisdom. Evidence indicates that EDs can
exaggerate personality problems, and this certainly explains recent practice
preferences leaning toward symptom-focused models of therapy for the EDs. A
rationale (aside from the obvious aim of reducing presenting symptoms) is that
improving nutritional status in an ED sufferer often improves her personality
and general functioning. Consequently, we urge that it is never appropriate to
ignore eating disturbances and focus on underlying personality issues alone. At
the same time, primacy of personality disturbances, and persistence following
recovery, suggests that it is untenable to regard personality factors solely as ED
sequelae and hence (swinging to the other extreme) to ignore them in
treatment. In a closely related vein:
PERSONALITY TRAITS AND DISORDERS 223
CONCLUSIONS
Our thinking in this chapter has been structured around the concept that eating
and personality pathologies have multiple and (often) shared biological,
psychological, and social determinants. This means that personality cannot be
conceptualized as a unidimensional psychological aspect of what occurs in
people with EDs—but rather, needs to be understood as an integral part of the
ED syndrome, tightly woven into its complex of causes and symptoms, and
relevant as both an expression of, and influence on, the ED’s biopsychosocial
“mix.”
This perspective asks that we revise our thinking about psychopathological
syndromes and traits, especially as far as the idea of separating “syndromic” and
“personality” components is concerned. It may be that we can never fully
segregate “having an eating disorder” (in either phenomenological or etiological
respects) from “concurrent personality tendencies.” Rather, “personality”
phenomena (like impulsivity, compulsivity, or perfectionism) may be at least as
relevant to defining ED syndrome “variants” as any one of a number of
superficially more relevant aspects of ED phenom enology (e.g., presence of
binge eating or laxative abuse). Indeed, available data argue that the personality
variations may be the stronger predictors of clinical phenomenology,
neurobiological substrates, sexual abuse history, treatment outcome, prognosis,
and other aspects. This argues for a more central attention to personality trait
variations in the development of ED diagnostic classifications—a view that has
been advocated by several others (30,31,93).
The same concept is relevant to treatment considerations. To date, ED
specialists have succeeded in standardizing and formalizing interventions aimed
at eating disturbances. A next step, we would urge, is to be equally rigorous in
our efforts to develop, integrate, and perfect interventions aimed at personality
components in the EDs (and their inextricable consequences for the therapeutic
alliance). We are thinking here not of an “adjunctive” use of personality
concepts—treating personality features as some sort of “grease on the wheels” of
eating-focused interventions—but of a central attention to the ways in which
personality may shape expression of eating symptoms, the relational aspects of
the therapeutic experience and, in turn, the process of change.
Various theorists have argued that eating symptoms need to be contextualized
in light of comorbid personality characteristics (5,30,31,93). For example, a
symptom like vomiting may have quite a different meaning when it arises in
(a) the emotionally constricted and weight gain-phobic patient, or (b) the highly
dysregulated or posttraumatic patient. In the former, vomiting may serve as a
phobic avoidance, driven by relatively circumscribed weight gain fears-in the
latter, as a desparate response to felt emptiness, posttraumatic memories, or
PERSONALITY TRAITS AND DISORDERS 225
REFERENCES
1. Gordon RA. Anatomy of a social epidemic. Oxford: Basil Blackwell, 1990:12.
2. Ziolko H-U. Bulimia: a historical outline. Int J Eat Disord 1996; 20:345–358.
3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders 4th ed. Washington, DC: DSM-IV, 1994.
4. Sohlberg S, Strober M. Personality in anorexia nervosa: an update and a theoretical
integration. Acta Psychiatr Scand 1994; 89(Suppl 378): 1–15.
5. Vitousek K, Manke F. Personality variables and disorders in anorexia nervosa and
bulimia nervosa. J Abnorm Psychol 1994; 103:137–147.
6. Casper RC, Hedeker D, McClough JF. Personality dimensions in eating disorders
and their relevance for subtyping. J Am Acad Child Adol Psychiatry 1992; 31:
830–840.
7. Norman DK, Blais D, Herzog D. Personality characteristics of eating-disordered
patients as identified by the Millon Clinical Multiaxial inventory. J Pers Disord
1993; 7:1–9.
8. Bulik CM, Sullivan PF, Weltzin TF, Kaye WH. Temperament in eating disorders.
Int J Eat Disord 1995; 17:251–261.
9. Brewerton TD, Hand JD, Bishop EM. The Tridimensional Personality
Questionnaire in patients with eating disorders. Int J Eat Disord 1993; 14:213–218.
10. Diaz-Marsa M, Carrasco JL, Saiz J. A study of temperament and personality in
anorexia and bulimia nervosa. J Pers Disord 2000; 14:352–359.
11. Cumella EJ, Wall AD, Kerr-Almeida N. MMPI-2 in the inpatient assessment of
women with eating disorders. J Pers Assess 2000; 75:387–403.
12. Halmi KA, Sunday SR, Strober M, Kaplan A, Woodside DB, Fichter M, Treaure J,
Berrettini W, Kaye WH. Perfectionsim in anorexia nervosa: variation by clinical
subtype, obsessionality, and pathological eating behavior. Am J Psychiatry 2000;
157:1799–1805.
13. Srinivasagam NM, Kaye WH, Plotnicov KH, Greeno C, Weltzin TE, Rao R.
Persistent perfectionism, symmetry, and exactness after long-term recovery from
anorexia nervosa. Am J Psychiatry 1995; 152:1630–1634.
226 STEIGER AND BRUCE
14. Lilenfeld LR, Stein D, Bulik CM, Strober M, Plotnicov K, Pollice C, Rao R,
Merikangas KR, Nagy L, Kaye WH. Personality traits among currently eating
disordered, recovered and never ill first-degree female relatives of bulimic and
control women. Psychol Med 2000; 30:1399–1410.
15. Pratt EM, Telch CF, Labouvie EW, Wilson GT, Agras WS. Perfectionism in
women with binge eating disorder. Int J Eat Disord 2001; 29:177–186.
16. Fairburn CG, Doll HA, Welch SL, Hay PJ, Davies BA, O’Connor ME. Risk factors
for binge eating disorders: a community-based study. Arch Gen Psychiatry 1998;
55:425–432.
17. Fairburn CG, Cooper Z, Doll HA, Welch SL. Risk factors for anorexia nervosa:
three integrated case-controlled comparisons. Arch Gen Psychiatry 1999; 56:
468–476.
18. Woodside DB, Bulik CM, Halmi KA, Fichter MM, Kaplan A, Berrettini WH,
Strober M, Treasure J, Lilenfeld L, Klump K, Kaye WH. Personality,
perfectionism, and attitudes toward eating in parents of individuals with eating
disorders. Int J Eat Disord 2002; 31:290–299.
19. Wolfe BE, Jimerson DC, Levine JM. Impulsivity ratings in bulimia nervosa:
relationship to binge eating behaviours. Int J Eat Disord 1994; 15:289–292.
20. Mitchell JE, Hatsukami D, Pyle RL, Eckert ED. The bulimia syndrome: course of
the illness and associated problems. Comp Psychiatry 1986; 27:165–170.
21. Newton JR, Freeman CP, Munro J. Impulsivity and dyscontrol in bulimia nervosa:
is impulsivity an independent phenomenon or a marker of severity? Acta Psychiatr
Scand 1993; 87:389–394.
22. Crosby RD, Wonderlich SA, Redlin J, Engel SG, Simonich H, Jones-Paxton M,
Myers T, Norton M, Thompson KM, Mitchell JE. Impulsive behavior patterns in a
sample of females with bulimia nervosa. Poster presented at the annual meeting of
the Eating Disorders Research Society, Bernalillo, New Mexico, 2001.
23. Lacey JH, Evans CD. The impulsivist: a multi-impulsive personality disorder. Br J
Addict 1986; 81:641–649.
24. Herzog DB, Dorer DJ, Keel PK, Selwyn SE, Ekeblad ER, Flores AT, Greenwood
DN, Burwell RA, Keller MB. Recovery and relapse in anorexia and bulimia
nervosa: a 7.5-year follow-up study. J Am Acad Child Adol Psychiatry 1999; 38:
829–837.
25. Favaro A, Santonastaso P. Suicidality in eating disorders: clinical and psychological
correlates. Acta Psychiatr Scand 1997; 95:508–514.
26. Paul T, Schroeter K, Dahme B, Nutzinger DO. Self-injurious behavior in women
with eating disorders. Am J Psychiatry 2002; 159:408–411.
27. Grilo CM. Recent research of relationships among eating disorders and personality
disorders. Curr Psychiatry Rep 2002; 4:18–24.
28. Johnson C, Wonderlich S. Personality characteristics as a risk factor in the
development of eating disorders. In: Crowther JH, Tennenbaum DL, Hobfell SE,
Stephens MAP, eds. The Etiology of Bulimia Nervosa: The Individual and Family
Context. New York: Hemisphere Publishing, 1992.
PERSONALITY TRAITS AND DISORDERS 227
45. Wonderlich SA. Relationship of family and personality factors in bulimia. In:
Crowther JH, Tennenbaum DL, Hobfell SE, Stephens MAP, eds. The Etiology of
Bulimia Nervosa: The Individual and Family Context. New York: Hemisphere
Publishing, 1992.
46. Hodges EL, Cochrane CE, Brewerton TD. Family characteristics of binge-eating
disorder patients. Int J Eat Disord 1998; 23:145–151.
47. Tachi T. Family environment in eating disorders: a study of the familiar factors
influencing the onset and course of eating disorders. Seishin Shinkeigaku Zasshi
1999; 101:427–445.
48. Dominy NL, Johnson W-B, Koch C. Perception of parental acceptance in women
with binge-eating disorder. J Psychol 2000; 134:23–36.
49. Schmidt U, Humfress H, Treasure J. The role of general family environment and
sexual and physical abuse in the origins of eating disorders. Eur Eat Disord Rev
1997; 5:184–207.
50. Steiger H, Liquornik K, Chapman J, Hussain N. Personality and family
disturbances in eating-disorder patients: comparison of “restricters” and “bingers”
to normal controls. Int J Eat Disord 1991; 10:501–512.
51. Herman JL, Perry C, van der Kolk BA. Childhood trauma in borderline personality
disorder. Am J Psychiatry 1989; 146:490–495.
52. Paris J, Zweig-Frank H, Guzder J. Psychological risk factors for borderline
personality disorder in female patients. Compr Psyhiatry 1994; 35:301–305.
53. Everill J, Waller G. Reported sexual abuse and eating psychopathology: a review of
evidence for a causal link. Int J Eat Disord 1995; 18:1–11.
54. Wonderlich SA, Brewerton TD, Jocic Z, Dansky B, Abbott DW. Relationship
of childhood sexual abuse and eating disorders. J Am Acad Child Adolesc
Psychiatry 1997; 36:1107–1115.
55. Steiger H, Zanko M. Sexual traumata in eating-disordered, psychiatric and normal
female groups: comparison of prevalences and defense styles. J Interpers Violence
1990; 5:74–86.
56. Bushnell JA, Wells JE, Oakley-Brown MA. Long term effects of intrafamilial
sexual abuse in childhood. Acta Psychiatr Scand 1992; 85:36–142.
57. Dansky BS, Brewerton TD, Kilpatrick DG, O’Neil PM. The National Women’s
Study: relationship of victimization and posttraumatic stress disorder to bulimia
nervosa. Int J Eat Disord 1997; 21:213–228.
58. Moreno JK, Selby MJ, Neal S. Psychopathology in sexually abused and nonsexually
abused eating-disordered women. Psychother Private Pract 1998; 17:1–9.
59. Steiger H, Jabalpurwala S, Champagne J. Axis-II comorbidity and developmental
adversity in bulimia nervosa. J Nerv Ment Dis 1996; 184:555–560.
60. Steiger H, Gauvin L, Israel M, Koerner N, Ng Ying Kin NMK, Paris J, Young SN.
Association of serotonin and cortisol indices with childhood abuse in bulimia
nervosa. Arch Gen Psychiatry 2001; 58:837–843.
61. Leonard S, Steiger H, Kao A, Childhood and adulthood abuse in bulimic and
nonbulimic women: prevalence and psychological correlates. Int J Eat Disord
2003; 33:397–405.
PERSONALITY TRAITS AND DISORDERS 229
77. Stice E, Agras WS, Telch CF, Halmi KA, Mitchell JE, Wilson T. Subtyping binge
eating-disordered women along dieting and negative affect dimensions. Int J Eat
Disord 2001; 30:11–27.
78. Steinhausen HC. The outcome of anorexia nervosa in the 20th century. Am J
Psychiatry 2002; 159:1284–1293.
79. Fassino S, Abbate Dagga G, Amianto F, Leombruni P, Fornas B, Garzaro L,
D’Ambrosio G, Rovera GG. Outcome predictors in anorexic patients after 6
months of multimodal treatment. Psychother Psychosom 2001; 70:201–208.
80. Van der Ham T, van Strien DC, van England H. Personality characteristics predict
outcome of eating disorders in adolescents: a 4-year prospective study. Eur Child
Adol Psychiatry 1998; 7:79–84.
81. Herzog DB, Keller MB, Sacks NR, Yeh CJ, Lavori PW. Psychiatric comorbidity in
treatment-seeking anorexics and bulimics. J Am Acad Child Adol Psychiatry 1992;
31:810–818.
82. Rossiter EM, Agras WS, Telch CF, Schneider JA. Cluster B personality disorder
characteristics predict outcome in the treatment of bulimia nervosa. Int J Eat
Disord 1993; 13:349–357.
83. Johnson C, Tobin DL, Dennis A. Differences in treatment outcome between
borderline and nonborderline bulimics at one-year follow-up. Int J Eat Disord
1990; 9:617–627.
84. Steiger H, Stotland S, Houle L. Prognostic implications of stable versus transient
“borderline features” in bulimic patients. J Clin Psychiatry 1994; 55:206–214.
85. Wonderlich SA, Fullerton D, Swift WJ, Klein MH. Five-year outcome from eating
disorders: Relevance of personality disorders. Int J Eat Disord 1994; 15:233–244.
86. Steiger H, Stotland S. Prospective study of outcome in bulimics as a function
of axis-II comorbidity: long-term responses on eating and psychiatric symptoms.
Int J Eat Disord 1996; 20:149–161.
87. Norring C. Borderline personality organization and prognosis in eating disorders.
Psychoanal Psychol 1993; 10:551–572.
88. Keel PK, Mitchell JE. Outcome in bulimia nervosa. Am J Psychiatry 1997; 154:
313–321.
89. Joiner TE Jr, Heatherton TF, Keel PK. Ten-year stability and predictive validity of
five bulimia-related indicators. Am J Psychiatry 1997; 154:1133–1138.
90. Bulik CM, Sullivan PF, Joyce PR, Carter FA, McIntosh VV. Predictors of 1-year
treatment outcome in bulimia nervosa. Compr Psychiatry 1998; 39:206–214.
91. Keel PK, Dorer DJ, Eddy KT, Delinsky SS, Franko DL, Blais MA, Keller MB,
Herzog DB. Predictors of treatment utilization among women with anorexia and
bulimia nervosa. Am J Psychiatry 2002; 159:140–142.
92. Meyers C, Waller G, Waters A. Emotional states and bulimic psychopathology. In:
Hoek H, Treasure J, Katzman M, eds. Neurobiology in the Treatment of Eating
Disorders. New York: John Wiley and Sons, 1998:263–279.
93. Westen D, Harnden-Fischer J. Personality profiles in eating disorders: rethinking
the distinction between axis I and axis II. Am J Psychiatry 2001; 158:547–562.
PERSONALITY TRAITS AND DISORDERS 231
94. Polivy J, Herman CP. Dieting and binging: a causal analysis. Am Psychol 1985; 40:
193–201.
95. Borman Spurrell E, Wilfley DE, Tanofsky MB, Brownell KD. Age of onset for
binge eating: Are there different pathways to binge eating. Int J Eat Disord 1997;
21:55–65.
96. Steiger H, Lehoux P, Gauvin L. Impulsivity, dietary restraint, and the urge to binge
in bulimic eating syndromes. Int J Eat Disord 1999; 26:261–274.
97. Steiger H, Gauvin L, Jabalpurwala S, Séguin JR, Stotland S. Hypersensitivity to
social interactions in bulimic eating syndromes: relationship to binge-eating.
J Consult Clin Psychol 1999; 67:765–775.
98. Safran J, Segal ZV. Interpersonal Process in Cognitive Therapy. Northvale, NJ:
Aronson, 1996.
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10
Medical Comorbidity of Anorexia Nervosa,
Bulimia Nervosa, and Binge Eating Disorder
Pauiine S.Powers and Yvonne Bannon
University of South Florida
Tampa, Florida, U.S.A.
Anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED)
are the three major eating disorders, affecting between 5 million and 10 million
people in the United States (1–3). More people have eating disorders than have
Alzheimer’s disease (4), and patients typically fall ill early in their life rather
than at the end of their life. Eating disorders are more common than
schizophrenia, which affects 2.2 million people in the United States (5). The
eating disorders are expensive to treat, in part because of the multiple medical
complications associated with them. The average yearly cost of treating eating
disorders in the United States is about $6 billion (6) compared to the global cost
of antipsychotic medication, which is about $7 billion (7). AN is the least common
eating disorder but the most expensive to treat: the average annual cost of
treating a patient with AN is $6045 compared to $4824 for a patient with
schizophrenia (6). BN and BED are somewhat less expensive to treat than AN,
similar to or more expensive than the treatment of obsessive-compulsive
disorder (8).
The eating disorders have high rates of medical comorbidity. AN has the
highest premature mortality rate of any psychiatric disorder. Untreated, after
20 years, the mortality rate is 18–20% (9). Since the typical patient falls ill in
midadolescence, by age 35 one-fifth of untreated patients have
died. Approximately two-thirds of the deaths are due to cardiac or renal
complications and about one-third due to suicide. Less is known about the
mortality for BN, but after 15–20 years 5% may have died (10). The premature
mortality rate for BED is poorly understood, but since most patients are obese,
the medical risks are probably those associated with obesity. These risks include
type 2 diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease,
stroke, sleep apnea, gallbladder disease, hyperuricemia and gout, and
osteoarthritis. Although BED was described in 1959 (11), studies specific to the
complication of BED are only now being undertaken; the most work has been
done on the relationship between BED and diabetes mellitus. Although the
night eating syndrome was described by Stunkard nearly 50 years ago (12), it is
234 POWERS AND BANNON
only recently that the physiological concomitants of this condition have been
investigated.
DIAGNOSTIC ISSUES
The current diagnostic nomenclature for eating disorders includes AN, BN, and
eating disorders-not otherwise specified (ED-NOS). Under the current
system (13), BED is technically classified as an ED-NOS, along with
subsyndromal and atypical cases of AN and BN. It is likely that the next revision
of the Diagnostic and Statistical Manual (DSM) will include BED. The night eating
syndrome, often associated with obesity, is currently under study and may
eventually be classified as an eating disorder. The night eating syndrome is
usually defined as having three main features: morning anorexia, hyperphagia at
night, and insomnia (12,14). Nocturnal sleep-related eating disorder is a
condition in which night eating occurs during total or partial unconsciousness,
often during stage 3 or 4 sleep (14). One report (15) found that 60% of patients
with nocturnal sleep-related eating disorder had sleepwalking (somnambulism).
One important issue that has not been resolved is whether or not obesity
should be considered an eating disorder. Although obesity is often associated
with abnormalities in both food consumption and energy expenditure, early
studies found that there were no typical psychological symptoms associated with
obesity and therefore obesity was not considered a psychiatric disorder.
However, recent evidence documenting some of biological underpinnings of the
typical eating disorders and evidence documenting multiple psychological
problems in many individuals with obesity may result in obesity eventually
being considered an eating disorder.
Figure 1 illustrates some of the relationships between AN, BN, BED, and other
forms of obesity. As weight increases, the condition becomes more common
(e.g., AN is less common than BN, which is less common than BED, which is
less common than obesity unassociated with binge eating). With increasing
weight, more males are affected. For example, less than 10% of patients with
AN are male, about 20% of patients with BN are male, and about 30% of patients
with BED are male.
ASSESSMENT
Ideally, the initial evaluation of patients with eating disorders includes an
assessment of the common medical complications. Many of the physiological
complications are associated with signs and symptoms. For example, patients
with BN may have enlarged parotid glands on physical examination, and
laboratory testing may reveal elevated salivary amylase levels; patients with BED
MEDICAL COMORBIDITY 235
MEDICAL COMPLICATIONS
Cardiac Complications
Cardiac complications are common in patients with eating disorders and are
associated with significant mortality and morbidity. About one-third of the
deaths in patients with AN are due to cardiac complications (16), and many of
the unexpected deaths in patients with BN are probably due to cardiac
arrhythmias. BED patients have higher psychophysiological arousal levels than
controls (17), and this may increase cardiac risk. Also, since most BED patients
are overweight or obese, they have an increased risk for cardiac comorbidity,
including hypertension and atherosclerosis.
Patients with AN or BN frequently have symptoms or signs of cardiac
malfunction, although patients with BED often do not. Common symptoms
suggesting cardiac abnormalities in AN or BN include light-headedness or
MEDICAL COMORBIDITY 237
to handle the increased circulatory load during refeeding and changes in serum
levels of phosphate, potassium, and magnesium. The immediate etiologic factor
appears to be that glucose in the food causes phosphate to enter the intracellular
space leading to low phosphate, which can affect contractility of the heart and lead
to heart failure. The symptoms include swollen ankles, shortness of breath,
tiredness, and anxiety. Signs include pedal edema, rales in the lungs, elevated
jugular venous pressure, and a midsystolic click. The chest radiograph reveals an
enlarged heart and evidence of congestive heart failure. Treatment includes
correcting electrolytes, decreasing fluid and caloric intake, diuretics, and
sometimes digitalis. Patients with the refeeding syndrome usually should be in
the coronary care unit with telemetry.
The key to preventing the refeeding syndrome is conservative management
for seriously underweight patients. Caloric intake should be low initially
coupled with correction of dehydration and electrolytes. Phosphorus and
electrolytes should be obtained every other day for the first 7–10 days and then
weekly. Calories should be increased slowly by 100–200 calories once or twice
a week during the first 2 weeks.
Renal Complications
Among AN patients, kidney failure accounts for about one-third of deaths.
Herzog and colleagues (25) have shown that high serum creatinine levels and
elevated uric acid levels predict a chronic course in AN patients. Although less
well understood, a number of BN patients also develop chronic renal
abnormalities. Several factors have been implicated in the kidney abnormalities
that develop, particularly electrolyte abnormalities. Hypokalemia and
metabolic acidosis that can result from persistent vomiting or laxative abuse are
implicated in the catabolism that occurs in uremia (26). End-stage renal disease
has been reported in patients with longstanding eating disorders; hypokalemic
nephropathy has been implicated in these cases (27). Volume depletion with
repeated dehydration from either semistarvation or purging or both contributes
to elevated blood urea nitrogen and elevated creatinine levels. Many patients
with eating disorders, especially AN, have decreased creatinine clearance as
well. Elevated levels of uric acid may account for the occasional patient who
develops gout. AN associated with rhabdomyolysis has been associated with
hypophosphatemia and renal failure (28). Nephrolithiasis may be more common
in patients with AN because chronic dehydration is known to contribute to the
development of renal stones (29). One study has found a lower filtration factor
in AN as well as a decreased urinary concentration capacity following fluid
deprivation both before and after administration of vasopressin (30).
MEDICAL COMORBIDITY 239
Electrolyte Abnormalities
Electrolyte abnormalities occur with semistarvation and various types of purging
behavior, including vomiting, diuretic and laxative abuse, and ipecac abuse.
About half of AN and BN patients have electrolyte abnormalities (31); the most
common abnormality is elevated serum bicarbonate (metabolic alkalosis).
Potassium and chloride abnormalities also occur. Potassium depletion can occur
during semistarvation if there is inadequate potassium intake. During vomiting,
hydrochloric acid is vomited and there is compensatory excretion of potassium
through the kidneys, resulting in a decrease in potassium. Total body potassium
is often decreased even when serum potassium is normal (20); thus, a random
test of serum potassium may not detect abnormally low total body potassium
and the patient may still be at risk for various cardiac complications related to
hypokalemia. Abnormalities of chloride and bicarbonate may be present prior to
the detection of hypokalemia. Among patients who are dehydrated, potassium
may be in the normal range, but when hydration occurs the hypokalemia may
become apparent.
Clinical findings suggestive of electrolyte abnormalities include weakness,
constipation, dizziness, and depression. Patients with hypokalemia may develop
leg cramps. Patients with either hypomagnesemia or hypocalcemia may develop
tetany (sharp flexion of the ankle or wrist joints).
Many patients with bulimia nervosa are very secretive about use of
selfinduced vomiting, laxatives, or diuretics. Sometimes it is helpful to assess both
serum and urinary electrolytes to determine the type of purge behavior that has
occurred. Self-induced vomiting or diuretic abuse typically results in metabolic
alkalosis with decreased serum potassium and chloride and ele vated
bicarbonate, whereas laxative abuse more typically results in metabolic acidosis.
Endocrine Abnormalities
Multiple endocrine abnormalities occur in the eating disorders (32). AN is the
best studied (see Table 2), but there are similar if less pronounced abnormalities
in BN. The endocrine abnormalities seen in BED are usually those seen in
patients with obesity, including type 2 diabetes mellitus, but other endocrine
abnormalities also occur.
The key symptom reflecting abnormalities in the hypothalamic-pituitary-
gonadotropin (HPG) axis among AN patients is amenorrhea or irregular
menses. Nearly one-third of patients with AN develop amenorrhea prior to the
onset of weight loss and this finding is unexplained. It may relate to stress, but
may also indicate a vulnerability of the endocrine system in patients with anorexia
nervosa. Patients with AN have decreased gonadotropinreleasing hormone,
240 POWERS AND BANNON
Source: Chial HJ and McAlpine DE. Anorexia nervosa: Manifestations and Management
for the Gastroenterologist. Reprinted with permission from the American College of
Gastroenterology, (Am J Gastroenterol 2002; 97:225–269).
242 POWERS AND BANNON
Gastrointestinal Complications
Gastrointestinal complaints occur in more than 50% of patients with eating
disorders and include bloating, flatulence, constipation, decreased appetite,
abdominal pain, borborygmi, and nausea (41,42). Multiple complications can
occur involving the entire gastrointestinal track. The most common
complications include dental caries, enlarged parotid glands, gastroesophageal
reflux disorder, delayed gastric emptying, and delayed colonic transit.
Semistarvation and various types of purge behavior affect metabolic and
hormonal processes that influence gastrointestinal functioning. The
complications depend in part on the type and intensity of the behavior. For
example, an underweight patient who utilizes large quantities of stimulant-type
laxatives (e.g., senna) on a daily basis is likely to be at greater risk than a
normal-weight patient who utilizes bulk agents (e.g., docusate) infrequently.
Oral and dental complications are common among patients who binge eat and
purge by vomiting. A common dental problem is enamel erosion (perimolysis)
due to chronic exposure of tooth structures to hydrochloric acid from vomiting;
this is particularly pronounced on the lingual side of the teeth. Dental caries
(cavities) occur because of consumption of high-calorie binge foods and
weakened tooth structure. Hypersensitivity of the teeth to hot, cold, and sweet
foods occurs because of exposed dentin and root surfaces. Fillings and other
restorations may fail because of exposure to hydrochloric acid. Periodontitis
(gum disease) with gingival recession occurs due to nutritional deficiencies and
trauma to the mucosa. Salivary abnormalities include reduced salivary flow
(zerostomia) experienced symptomatically as a dry mouth and enlarged parotid
and submandibular glands.
Management of dental and oral problems begins with a full assessment.
The dentist may be the first health care professional to recognize the
problem (43,44). Dental care includes emergency treatment and management of
pain, basic fillings, and other routine care. If possible, restorative cosmetic
dental care should be postponed until the eating disorder is under control;
however, if this is not possible, porcelain and ceramics may be less likely to fail
than resins in patients with active BN. Educating patients who are still binge-
eating and purging can often help prevent some dental problems (45). For
example, it may help decrease dental complications if the patient uses antiacids
after vomiting and delays brushing. Application of fluoride and use of zylitol
chewing gum may also prevent some problems.
Parotid gland enlargement (sialadenosis) is common among patients with BN
and also occasionally occurs in those with restricting AN. Sialadenosis is a
noninflammatory recurrent enlargement of the salivary glands, most commonly
the parotids, which is almost always associated with an underlying systemic
MEDICAL COMORBIDITY 243
not have water intoxication, seizures can occur in about 5% of patients with
AN (76), probably due to electrolyte disturbances or hypoglycemia.
Musculoskeletal Complications
Tendons and muscles are also affected by AN. Diminished or absent tendon
reflexes may be found on physical examination. An early report (76) found that
generalized muscle weakness was present in 43% of 47 patients with AN.
Proximal muscle weakness that is associated with a selective disturbance of the
skeletal muscle metabolism is often seen. This is due to a diminished
lactate response to ischemic exercise (81) and is associated with reduced
serum carnosinase activity. This myopathy is associated with selective type
2 fiber atrophy with abnormal accumulation of glycogen within the muscle
fibers (82).
Short stature is a common finding among AN patients. One explanation has
been that if AN develops in adolescence prior to the closure of the epiphyses
there may be a potential irreversible growth retardation resulting in short
stature. However, it has also been suggested (83) that the observed short stature
seen in many AN patients may have a different etiology. Among 85 patients,
80% developed AN after menarche, but, compared to a control group, 76% of
the patients were below the 50th height percentile and nearly 15% were below
the 5th percentile.
Scoliosis may also be more common in patients with AN. Forty-four young
women with idiopathic scoliosis were found to be similar in height to controls,
MEDICAL COMORBIDITY 247
but they had significantly lower body mass indices than controls and 25% were
in the range considered to represent anorexia (84). The reasons for this finding
are unknown.
Osteoporosis or osteopenia affects up to 90% of patients with AN and many
patients with BN who have a past history of AN (85). Among obese BED
patients, osteoporosis may be less common because obesity seems to be a
relative protective factor against loss of bone mineral density. Furthermore,
osteopenia develops early in the course of AN, often within the first year. Men
are affected as well, and there is some evidence that the loss may be greater in
men than in women (86). Furthermore, the loss of bone mineral density has long-
term consequences. Among a group of 208 patients followed an average of
40 years after diagnosis, the cumulative incidence of any fracture was 57% (87).
Among a group of 19 women who had been fully recovered for a mean of 21
years, femur BMD was still significantly less than among controls (88).
Although the cause of this significant bone loss is poorly understood, it is clear
that it is different from postmenopausal osteoporosis, which affects primarily
bone resorption; the osteoporosis of AN is related to both bone formation and
bone resorption.
The World Health Organization criteria for osteoporosis (89) is based on a
system of T scores that indicate the standard deviation (SD) from the mean
derived from a young normal sex-matched reference population. Normal bone
mineral density is defined as less than 1 SD below the normal mean; osteopenia
(low bone mass) is defined as 1 SD below to 2.5 SD below normal; osteoporosis
is defined as more than 2.5 SD below the normal mean, and severe osteoporosis
is more than 2.5 SD below the mean with one or more fractures. Z scores
compare the bone density of a subject with that of an age- and sex-matched
control.
The majority of peak bone mass is achieved by age 20, although there is some
continuing accumulation until age 30. AN typically develops during adolescence
at a time when peak bone mass has not been achieved. The osteoporosis that
occurs in AN affects both trabecular bone (found mainly in the spine) and
cortical bone (found mainly in the long bones). The spine and hip seem to be
particularly vulnerable.
Bone is constantly in a state of remodeling, which involves balanced coupling
of bone formation and bone resorption. Osteoblasts are cells involved in bone
formation and osteoclasts are cells involved in boneresorption. Serum and
urinary markers of bone formation include osteocalcin, bone-specific alkaline
phosphatase, and procollagen-I carboxy terminal propeptide; bone resorption
markers include urine deoxypyridinoline and serum carboxy terminal type I
propeptide and 7V-telopeptide. In AN, there is an increase in resorption
accompanied by a decrease or no change in the rate of bone formation.
248 POWERS AND BANNON
CONCLUSIONS
Multiple medical complications are associated with the three major eating
disorders. These complications frequently require treatment by several
specialists at various points in the recovery process. It is important for the many
physicians and other care providers involved to work collaboratively to address
the problems in an organized way utilizing an agreed-upon timeline. For
example, during the initial management of AN, the cardiologist and psychiatrist
may need to work together to design a program that prevents emergence of the
refeeding syndrome. Later in the course of treatment when the patient is near
ideal body weight, the activity therapist may have to be actively involved in
designing an appropriate exercise program to reduce the impact of
osteoporosis. Once the patient has achieved ideal body weight, the gynecologist
may be needed to assess possible need for hormonal intervention if menses have
not resumed. During the entire course of treatment from initial assessment to
eventual discharge from treatment (often several years later), there needs to be
a team leader organizing the delivery of care. When this occurs, outcome is
often improved.
REFERENCES
1. Yager J, Andersen A, Devlin M, Egger H, Herzog D, Mitchell J, Powers P, Yates
A, Zerbe K. American Psychiatric Association Work Group on Eating Disorders:
practice guideline for the treatment of patients with eating disorders (revision). Am
J Psychiatry 2000; 157(suppl):l-39.
2. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom D, Kennedy S, Kaplan AS,
Woodside DB. Should amenorrhea be necessary for the diagnosis of anorexia
nervosa? Br J Psychiatry 1996; 168:500–506.
3. National Institute of Mental Health. The Numbers Count. 2002. Web Address
Http//www.nimh.nih.gov/publicat/numbers.cfm.
4. McDowell I. Alzheimer’s disease: insights from epidemiology. Aging (Milano)
2001; 13:143–162.
5. Narrow WE. One-year prevalence of mental disorders, excluding substance use
disorders, in the US: NIMH ECA prospective data. Population estimates based on
US Census estimated residential population age 18 and over on July 1, 1998.
Unpublished.
6. Striegel-Moore RH, Leslie D, Petrill SA, Garvin V, Rosenheck RA. One year use
and cost of inpatient and outpatient services among female and male patients with
an eating disorder: evidence from a national database of health insurance claims. Int
J Eat Disord 2000; 27:381–389.
7. Tamminga CA, Lieberman JA. Schizophrenia research series: from molecule to
public policy. Biol Psychiatry 1999; 46:3.
MEDICAL COMORBIDITY 251
8. Agras WS. The consequences and costs of the eating disorders. Psychiatr Clin
North Am 2001; 24:371–379.
9. Theander S. Anorexia nervosa. A psychiatric investigatio of 94 female patients.
Arch Psychiatr Scand Suppl 1970; 214:1–194.
10. Nielsen S, Moller-Madsen S, Isager T, Jorgensen J, Pagsberg K, Theander S.
Standardized morality in eating disorders—a quantitative summary of previously
published and new evidence. J Psychosom Res 1998; 44:413–434.
11. Stunkard AJ. Eating patterns and obesity. Psychiatr Q 1959; 33:284–294.
12. Stunkard AJ, Grace WJ, Wolff HG. The night-eating syndrome: a pattern of food
intake among certain obese patients. Am J Med 1955; 19:78–86.
13. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC: Text Revision (DSM-IVTR), 2000: 583–586,
785–787.
14. Stunkard AJ, Allison KC. Two forms of disordered eating in obesity: binge eating
and night eating. Obesity 2003; 27:1–12.
15. Schenck C, Mahowald MW. Review of nocturnal sleep-related eating disorders.
Int J Eat Disord 1994; 15:343–356.
16. Schocken DD, Holoway JD, Powers PS. Weight loss and the heart: effects of
anorexia nervosa and starvation. Arch Intern Med 1989; 149:877–881.
17. Vogele C, Florin I. Psychophysiological responses to food exposure: an
experimental study in binge eaters. Int J Eat Disord 1997; 21:147–157.
18. Swenne I, Larsson PT. Heart risk associated with weight loss in anorexia nervosa
and eating disorders: risk factors for QTc interval prolongation and dispersion.
Acta Paediatr 1999; 88:304–309.
19. Wolbrette D. Gender differences in the proarrhythmic potential of QT-prolonging
drugs. Curr Womens Health Rep 2002; 2:105–109.
20. Powers PS, Tyson IB, Stevens BA, Heal AV. Total body potassium and serum
potassium among eating disorder patients. Int J Eat Disord 1995; 18:269–276.
21. de Simone G, Scalfi L, Galderisi M, Celentano A, Di Biase G, Tammaro P,
Garofalo M, Mureddu GF, de Divitiis O, Contaldo F. Cardiac abnormalities in
young women with anorexia nervosa. Br Heart J 1994; 71:287–292.
22. Oka Y, Ito T, Matsumoto S, et al. Mitral valve prolapse in patients with anorexia
nervosa. Two-dimensional echocardiographic study. Jpn Heart J 1987; 28:
873–882.
23. Powers PS, Mitchell JE, Garner DM, Monson N. International eating
disorders database: preliminary findings. Presented at Academy for Eating
Disorders, 2001 International Conference on Eating Disorders, April 27, 2001,
Boston.
24. Mehler PS. Eating disorders: 1. Anorexia nervosa. Hosp Pract 1996; 31:109–113.
25. Herzog W, Deter HC, Fiehn W, Petzold E. Medical findings and predictors of
long-term physical outcome in anorexia nervosa: a prospective, 12-year followup
study. Psychol Med 1997; 27:269–279.
26. Franch HA, Mitch WE. Catabolism in uremia: the impact of metabolic acidosis.
J Am Soc Nephrol 1998; 9:878–81.
252 POWERS AND BANNON
27. Abdel-Rahman EM, Moorthy AV. End-stage renal disease (ESD+RD in patients
with eating disorders. Clin Nephrol 1997; 47:106–111.
28. Wada S, Nagase T, Koike Y, Kugai N, Nagata N. A case of anorexia nervosa with
acute renal failure induced by rhabdomyolysis: possible involvement of
hypophosphatemia or phosphate depletion. Intern Med 1992; 31:478–482.
29. Silber TJ, Kass EJ. Anorexia nervosa and nephrolithiasis. J Adol Health Care 1984;
5:50–52.
30. Aperia A, Broberger O, Fohlin L. Renal function in anorexia nervosa. Acta
Paediatr Scand 1978; 67:219–224.
31. Mitchell JE, Pyle RL, Eckert ED, Hatsukami D, Lentz R. Electrolyte and other
physiological abnormalities in patients with bulimia. Psychol Med 1983; 14:
273–278.
32. Chial HJ, McAlpine DE, Camilleri M. Anorexia nervosa: manifestations and
management for the gastroenterologist. Am J Gastroenterol 2002; 97:255–269.
33. Birketvedt GS, Sundsfjord J, Florholmen JR. Hypothalamic-pituitary-adrenal axis
in night eating syndrome. Am J Physiol Endocrinol Metab 2002; 282(2): 366–369.
34. Crow S, Kendall D, Praus B, Thuras P. Binge eating and other psychopathology in
patients with type II diabetes mellitus. Int J Eat Disord 2001; 30:222–226.
35. Goebel-fabbri AE, Fikkan JL, Connell A, Vangsness L, Anerson B. J Binge eating,
BMI, emotional distress, and health status in women with type 2 diabetes.
Presented at the Academy for Eating Disorders 2002 International Conference on
Eating Disorders and Clinical Teaching Day, Boston.
36. Birk R, Spencer ML. The prevalence of anorexia nervosa, bulimia, and induced
glycosuria in IDDM females. Diabetes Educator, 1989, 336–341.
37. Rydall A, Rodin G, Olmsted M, Devenyi R, Daneman D. A four year follow-up
study of eating disorders and medical complications in young women with insulin-
dependent diabetes mellitus [Abstr]. Psychosom Med 1994; 56:179.
38. Monteleone P, DiLieto A, Tortorella A, Longobardi N, Maj M. Circulating leptin
in patients with anorexia nervosa, bulimia nervosa or binge-eating disorder:
relationship to body weight, eating patterns, psychopathology and endocrine
changes. Psychiatry Res 2000; 94(2): 121–129.
39. Brewerton TD, Lesem MD, Kennedy A, Garvey WT. Reduced plasma leptin
concentrations in bulimia nervosa. Psychoneuroendocrinology 2000; 25:548–649.
40. Birketvedt GS, Florholmen J, Sundsfjord J, Osterud B, Dinges D, Bilker
W, Stunkard A. Behavioral and neuroendocrine characteristics of the night-eating
syndrome. JAMA 1999; 282:657–663.
41. Chami TN, Anderson AE, Crowell MD, Schuster MM, Whitehead WE.
Gastrointestional symptoms in bulimia nervosa: effects of treatment. Am J
Gastroenterology 1995; 90:88–92.
42. McClain CJ, Humphries LL, Hill KK, Nicki NJ. Gastrointestinal and nutritional
aspects of eating disorders. J Am Coll Nutr 1993; 12:466–474.
43. Steel AW, Mehler PS. Oral and dental complications. In Eating Disorders: A Guide
to Medical Care and Complications. Baltimore: Johns Hopkins University Press,
1999:144–152.
MEDICAL COMORBIDITY 253
44. Schwartz MI. Dentistry and eating disorders. In AABA Newsletter, Fall 1997.
45. Sundaram G, Bartlett D. Preventative measures for bulimic patients with dental
erosion. Eur J Prosthodont Restor Dent 2001; 9:25–29.
46. Coleman H, Altini M, Nayler S, Richards A. Sialadenosis: a presenting sign in
bulimia. Head Neck 1998; 20:758–760.
47. Metzger ED, Levine JM, McArdle CR, Wolfe BE, Jimerson DC. Salivary gland
enlargement and elevated serum amylase in bulimia nervosa. Biol Psychiatry 1999;
45:1520–1522.
48. Rigaud D, Bedig G, Merrouche M, Vulpillat M, Bonfils S, Apfelbaum M. Delayed
gastric emptying in anorexia nervosa is improved by completion of a renutrition
program. Dig Dis Sci 1988; 33:919–925.
49. Saleh JW, Lebwohl P. Metoclopramide-induced gastric emptying in patients with
anorexia nervosa. Am J Gastroenterol 1980; 74:27–32.
50. Devlin MJ, Walsh BT, Guss JL, Kissileff HR, Liddle RA, Petkova E. Postprandial
cholecystokinin release and gastric emptying in patients with bulimia nervosa. Am J
Clin Nutr 1997; 65:114–120.
51. Geliebter A, Hashim SA. Gastric capacity in normal, obese and bulimic women.
Physiol Behav 2001; 74:743–746.
52. Kiss A, Wiesnagrotski S, Abatzi TA, Meryn S, Haubenstock A, Base W. Upper
gastrointestinal endoscopy findings in patients with long-standing bulimia nervosa.
Gastrointest Endos 1989; 35:516–518.
53. Dessureault S, Coppola D, Weitzner M, Powers P, Karl RC. Barrett’s oesophagus
and squamous cell carcinoma with psychogenic vomiting. Int J Gastrointest Cancer
2002; 32:57–61.
54. Bartlett DW, Evans DF, Smith BG. The relationship between gastroesophageal
reflux disease and dental erosion. J Oral Rehabil 1996; 23:289–297.
55. Kamal N, Chami T, Andersen A, Rosell FA, Schuster MM, Whitehead WE.
Delayed gastrointestinal transit times in anorexia nervosa and bulimia nervosa.
Gastroenterology 1991; 101:1320–1324, 1991.
56. Chun AB, Sokol MS, Kaye WH, Hutson WR, Wald A. Colonic and anorectal
function in constipated patients with anorexia nervosa. Am J Gastroenterol 1997;
92:879–883.
57. Tanaka M, Naruo T, Muranaga T, Yasuhara D, Shiiya T, Nakazato M, Matsukura S,
Nozoe S. Increased fasting plasma ghrelin levels in patients with bulimia nervosa.
Eur J Endocrin 2002; 146:R1-R3.
58. Katzman DK, Zipursky RB, Lambe EK, Mikulis DJ. A longitudinal
magnetic resonance imaging study of brain changes in adolescents with anorexia
nervosa. Arch Pediatr Adolesc Med 1997; 151:793–797.
59. Eiber R, Friedman S. Correlation between eating disorders and sleep disturbances.
Encephale 2001; 27:429–434.
60. Lambe EK, Katzman DK, Mikulis DJ, Kennedy SH, Zipursky RB. Cerebral gray
matter volume deficits after weight recovery from anorexia nervosa. Arch Gen
Psychiatry 1997; 54:537–542.
254 POWERS AND BANNON
61. Katzman DK, Lambe EK, Mikulis DJ, Ridgley JN, Goldbloom DS, Zipursky RB.
Cerebral gray matter and white matter volume deficits in adolescent girls with
anorexia nervosa. J Pediatr 1996; 129:794–803.
62. di Pietralata GM. Imaging techniques in the management of anorexia and bulimia
nervosa. Eat Weight Disord 2002; 7:146–151.
63. Garner DM, Fairburn CG, Davis R. Cognitive-behavioral treatment of bulimia
nervosa. A critical appraisal. Behav Modif 1987; 11:398–431.
64. Fassino S, Piero A, Daga GA, Leombruni P, Mortara P, Rovera GG. Attentional
biases and frontal functioning in anorexia nervosa. Int J Eat Disord 2002; 31:
274–283.
65. Neumarker KJ, Bzufka WM, Dudeck U, Hein J, Neumarker U. Are there specific
disabilities of mnumber processing in adolescent patients with anorexia nervosa?
Evidence from clinical and neuropsychological data when compared to
morphometric measures from magnetic resonance imaging. Eur Child Adol
Psychiatry 2000; 9:111–121.
66. Seed JA, Dixon RA, McCluskey SE, Young AH. Basal activity of the hypothalamic-
pituitary-adrenal axis and cognitive function in anorexia nervosa. Eur Arch
Psychiatry Clin Neurosci 2000; 250:11–15.
67. Mathias JL, Kent PS. Neuropsychological consequences of extreme weight loss and
dietary restriction in patients with anorexia nervosa. J Clin Exp Neuropsychol
1998; 20:548–564.
68. Epstein J, Wiseman CV, Sunday SR, Klapper F, Alkalay L, Halmi KA.
Neurocognitive evidence favors “topdown”over “bottom up”mechanisms in the
pathogenesis of body size distortions in anorexia nervosa. Eat Weight Disord 2001;
6:140–147.
69. Lauer CJ, Gorzewski B, Gerlinghoff M, Backmund H, Zihl J. Neuropsychological
assessments before and after treatment in patients with anorexia nervosa and
bulimia nervosa. J Psychiatr Res 1999; 33:129–138.
70. Green MW, Elliman NA, Wakeling A, Rogers PJ. Cognitive functioning, weight
change and therapy in anorexia nervosa. J Psychiatr Res 1996; 30:401–410.
71. Wu JC, Hagman J, Buchsbaum MS, Blinder B, Derrfler M, Tai WY, Hazlett E,
Sicotte N. Greater left cerbral hemispheric metabolism in bulimia assessed by
positron emission tomography. Am J Psychiatry 1990; 147:309–312.
72. Delvenne V, Lostra F, Goldman S, Biver F, DeMaertelaer V, AppelboomFondu J,
Schoutens A, Bidaut LM, Luxen A, Mendelwicz J. Brain hypometabolism of
glucose in anorexia nervosa: A PET-scan study. Biol Psychiatry 1995; 37:161–169.
73. Delvenne V, Goldman S, Simon Y, De Maertelaer V, Lotstra F. Brain
hypometabolism of glucose in bulimia nervosa. Int J Eat Disord 1997; 21:313–326.
74. Troop NA, Murphy F, Bramon E, Treasure JL. Disgust sensitivity in eating
disorders: a preliminary investigation. Int J Eat Disord 2000; 27:446–451.
75. Amann B, Schafer M, Sterr A, Arnold S, Grunze H. Central pontine myelinolysis in
a patient with anorexia nervosa. Int J Eat Disord 2001; 30:462–466.
76. Patchell RA, Fellows HA, Humphries LL. Neurologic complications of anorexia
nervosa. Acta Neurol Scand 1994; 89:111–116.
MEDICAL COMORBIDITY 255
77. MacKenzie JR, LaBan MM, Sackeyfio AH. The prevalence of peripheral
neuropathy in patients with anorexia nervosa. Arch Phys Med Rehab 1989; 70:
827–830.
78. Pirke KM. Central and peripheral noradrenalin regulation in eating disorders.
Psychiatry Res 1996; 16:43–49.
79. Raymond NC, deZwaan M, Faris PL, Nugent SM, Achard DM, Crosby RD,
Mitchell JE. Pain thresholds in obese binge-eating disorder subjects. Biol Psychiatry
1995; 37:202–204.
80. Brewerton TD, Lydiara RB, Laraia MT, Shook JE, Ballenger JC. CSF
betaendorphin and dynorphin in bulimia nervosa. Am J Psychiatry 1992; 149:
1086–1090.
81. McLoughlin DM, Wassif WS, Morton J, Spargo E, Peters TJ, Russell GF.
Metabolic abnormalities associated with skeletal myopathy in severe anorexia
nervosa. Nutirtion 2000; 16:192–196.
82. McLoughlin DM, Spargo E, Wassif WS, et al. Structural and functional changes in
skeletal muscle in anorexia nervosa. Act Neuropathol 1998; 95: 632.
83. Nussbaum M, Baird D, Sonnenblick M, Cowan K, Shenker IR. Short stature in
anorexia nervosa patients. J Adol Health Care 1985; 6:453–455.
84. Smith FM, Latchford G, Hall RM, Millner PA, Dickson RA. Indications of
disordered eating behaviour in adolescent patients with idiopathic scoliosis. J Bone
Joint Surg Br 2002; 84:392–394.
85. Grinspoon S, Thomas E, Pitts S, Gross E, Mickley D, Miller K, Herzog D,
Klibanski A. Prevalence and predictive factors for regional osteopenia in women
with anorexia nervosa. Ann Intern Med 2000; 133:790–794.
86. Andersen AE, Watson T, Schlechte J. Osteoporosis and osteopenia in men with
eating disorders. Lancet 2000; 355:1967–1968.
87. Lucas AR, Melton LJIII, Crowson CS, O’Fallon WM. Long-term fracture risk
among women with anorexia nervosa: a population-based cohort study. Mayo Clin
Proc 1999; 74:972–977.
88. Hartman D, Crisp A, Rooney B, Rackow C, Atkinson R, Patel S. Bone density of
women who have recovered from anorexia nervosa. Int J Eat Disord 2000; 28:
1007–1112.
89. Kanis JAWHO Study Group. Assessment of fracture risk and its application for
screening post-menopausal osteoporosis. Osteoporos Int 1994; 4:368–381.
90. Soyka LA, Grinspoon S, Levitsky LL, Herzog DB, Klibanksi A. The effects of AN
on bone meabolism in female adolescents. J Clin Endocrinol Metab 1999; 84:
4489–4496.
91. Andersen AE, Woodward PJ, LaFrance N. Bone mineral density of eating disorder
subgroups. Int J Eat Disord 1995; 18:335–342.
92. Klibanski A, Biller BM, Schoenfeld DA, Herzog DB, Saxe VC. The effects of
estrogen administration on trabecular bone loss in young women with AN. J Clin
Endocrinol Metab 1995; 80:898–904.
256 POWERS AND BANNON
93. Karlsson MK, Weigall SJ, Duan Y, Seeman E. Bone size and volumetric density in
women with AN receiving estrogen replacement therapy and in women recovered
from AN. J Encocrinol Metab 2000; 85:3177–3182.
94. Wolfert A, Mehler PS. Osteoporosis: prevention and treatment in anorexia
nervosa. Eat Weight Disord 2002; 7:72–81.
95. Bachrach LK, Katzman DK, Litt IF, Guido D, Marcus R. Recovery from
osteopenia in adolescent girls with AN. J Clin Endocrinol Metab 1991; 72:
602–606.
96. Heer M, Mika C, Grzella I, Drummer C, Herpertz-Dahlmann B. Changes in bone
turnover in patients with anorexia nervosa during eleven weeks of inpatient dietary
treatment. Clin Chem 2002; 48:754–760.
97. Grinspoon S, Thomas L, Miller K, Herzog D. Klibanski A Effects of recombinant
human IGF-I and oral contraceptive administration on bone density in anorexia
nervosa. J Clin Endocrinol Meab 2002; 87:2883–2891.
98. Lai KY, de Bruyn R, Lask B, Bryant-Waugh R, Hankins M. Use of pelvic
ultrasound to monitor ovarian and uterine maturity in childhood onset anorexia
nervosa. Arch Dis Child 1994; 71:228–231.
99. Treasure JL, Gordon PA, King EA, Wheeler M, Russell GF. Cystic ovaries: a phase
of anorexia nervosa. Lancet 1985; 2:1379–1382.
100. Treasure JL. The ultrasonographic features in anorexia nervosa and bulimia
nervosa: a simplified method of monitoring hormonal states during weight gain.
J Psychosom Res 1988; 32:623–634.
101. Jahanafar S, Eden JA, Nguyent TV. Bulimia nervosa and polycystic ovary syndrome.
Gynecol Endocrinol 1995; 9:113–117.
102. Johnson JG, Spitzer RL, Williams JB. Health problems, impairment and illnesses
associated with bulimia nervosa and binge eating disorder among primary care and
obstetric gynaecology patients. Psychol Med 2001; 31:1455–1466.
103. Blais MA, Becker AE, Burwell RA, Flores AT, Nussbaum KM, Greenwood DN,
Ekeblad ER, Herzog DB. Pregnancy: outcome and impact on symptomatology in a
cohort of eating-disordered women. Int J Eat Disord 2000; 27: 140–149.
104. Morgan JF, Lacey JH, Sedgwick PM. Impact of pregnancy on bulimia nervosa. Br J
Psychiatry 1999; 174:278.
105. Franko DL, Blais MA, Becker AE, Delinsky SS, Greenwood DN, Flores AT,
Ekeblad ER, Eddy KT, Herzog DB. Pregnancy complications and neonatal
outcomes in women with eating disorders. Am J Psychiatry 2000; 158:1461–1466.
106. James DC. Eating disorders, fertility, and pregnancy: relationships and
complications. J Perinat Neonat Nurs 2001; 15:36–48.
107. Franko DL, Spurrell EB. Detection and management of eating disorders during
pregnancy. Obstet Gynecol 2000; 95:942–946.
108. Stein A, Woolley H, Cooper SD, Fairburn CG. An observational study of mothers
with eating disorders and their infants. J Child Psychol Psychiatry 1994; 35:
733–748.
11
Neurotransmitter Dysregulation in Anorexia
Nervosa, Bulimia Nervosa, and Binge Eating
Disorder
Timothy D.Brewerton
Medical University of South Carolina
Charleston, South Carolina, U.S.A.
Howard Steiger
Douglas Hospital
Montreal, Quebec, Canada
The current system of psychiatric diagnosis, DSM-IV (1), addresses two official
eating disorder (ED) syndromes—anorexia nervosa (AN) and bulimia nervosa
(BN)—and a third (still provisional) diagnostic entity—binge eating disorder
(BED). However, BED has all but officially been recognized as a distinct eating
syndrome. AN, BN, and BED are all polysymptomatic syndromes, defined by
maladaptive attitudes and behaviors around eating, weight, and body image, but
typically including “nonspecific” disturbances of self-image, mood, impulse
regulation, and interpersonal functioning. All three syndromes are known to be
associated with significant mortality and morbidity, both medical and
psychiatric (2,3). Despite popular beliefs, there is no convincing evidence that
cultural factors alone cause eating disorders. Indeed, during the past few years
(and especially the last decade) investigations into the role of neurotransmitters
and other neuromodulators in the eating disorders have been highly productive,
and have implicated primary neurotransmitter disturbances in the etiology of both
AN and BN. Furthermore, recent data clearly identify strong genetic factors in
AN and BN, which appear to share common genetic vulnerabilities (4,5) linked
to obsessionality, perfectionism, anxiety, and/or behavioral inhibition (6,7).
One powerful piece of evidence to support monoamine involvement in the
eating disorders is the observation that antidepressant medications can be
beneficial in controlled studies, not only in BN patients but in recovered AN
patients as well (8).
However, it is also clear that some disturbances are consequences of the
abnormal eating practices and nutritional disturbances that characterize these
disorders (9), which in turn exacerbate or perpetuate signs and symptoms (10).
258 BREWERTON AND STEIGER
MONOAMINES
The classical monoaminergic neurotransmitter systems, including serotonin
(5-hydroxytryptamine, 5-HT), norepinephrine (NE), and dopamine (DA), have
been fairly extensively studied in the eating disorders using available techniques
in biological psychiatry. Most of these studies have been conducted during the
active state of illness, during which severe nutritional compromise may
represent an important confound. Dieting and/or semistarvation clearly
depletes central monoamines and leads to altered neurotransmitter levels and
receptor sensitivity in animals and humans (11–15). To avoid this problem, a
more recent strategy has been to study “recovered” patients, i.e., AN and BN
patients who have attained normalization of eating and weight, resumption of
menses and/or normalization of gonadal hormone levels, and abatement of
typical cognitive features to subclinical levels. This strategy attempts to
minimize starvation state-related effects and to reveal potential trait-related
disturbances or vulnerabilities. However, the long-term effects of chronic
malnutrition and disordered eating behaviors on the brain (similar to substance
use disorders) should not be minimized. Studies of transmitter function in
at-risk premorbid individuals as well as nonaffected identical and fraternal
twins, siblings, and other first-degree relatives of ED patients could begin to
confirm trait-related disturbances.
Neurotransmitter function in patients with EDs have been investigated using
a variety of existing techniques and methodologies, each of which has its own
advantages and disadvantages. Studies of cerebrospinal fluid (CSF)
concentrations of the major metabolites have been a popular strategy and
include measures of 5-hydroxyindoleacetic acid (5-HIAA) for 5-HT,
3-methoxy-4hydroxyphenylglycol (MHPG) for NE, and homovanillic acid
(HVA) for DA. Some studies have also examined actual concentrations of 5-HT
NEUROTRANSMITTER DYSREGULATION 259
and NE, but not DA. Such studies measure transmitter metabolism of the whole
brain and spinal cord and lack any anatomical specificity.
Neuroendocrine and other psychobiological response measures have been
studied following acute challenges with various agents, including amino
acid precursors, e.g., L-tryptophan (L-TRP) and 5-hydroxytryptophan (5HTP)
for 5-HT, presynaptic receptor agonists, e.g., dl-fenfluramine (dl-FEN) or
d-fenfluramine (d-FEN) for 5-HT, postsynaptic receptor agonists, e.g.,
m-chlorophenylpiperazine (m-CPP) for 5-HT, and isoproterenol (ISOP) for NE.
Longer term challenges with receptor antagonists, e.g., antipsychotics for DA
and 5-HT, and antidepressants, especially the serotonin-specific reuptake
inhibitors (SSRIs), also illuminate the role of neurotransmitters in the eating
disorders. Acute amino acid precursor depletion, most notably of L-TRP
(16–19), has been another important source of information about the role of
central 5-HT function in eating and related disorders.
Platelet (PLT) and leukocyte studies are possibly reflective of central
neurotransmitter function but are always at least one step removed from
the nervous system, e.g., platelet 5-HT reuptake, 3H-imipramine binding,
3H-paroxetine binding, platelet monoamine oxidase (MAO), platelet 5-HT
NOREPINEPHRINE
There are a number of reasons to suspect NE involvement in the eating
disorders. Most notably, NE pathways at the level of the hypothalamus are
known to be involved in the initiation of feeding (20). Disturbances in these
pathways may therefore be involved in the pathophysiology of the profoundly
altered feeding behaviors classically associated with the eating disorders. In
addition, NE’s role in the modulation of mood, anxiety, neuroendocrine control,
metabolic rate, sympathetic tone, and temperature make it a likely candidate for
260 BREWERTON AND STEIGER
study (21–26). It has been recognized for some time that lowweight anorexic
patients, and to some degree bulimic patients, have reduced body temperature,
blood pressure, pulse, and metabolic rate (25,27,28). Investigations in this area
have shown that low-weight AN patients have reduced measures of plasma,
urinary, and CSF MHPG (27,29–31). In contrast, reports of plasma NE levels in
the eating disorders has been more variable (32,33), and this appears to be
linked not only to weight but to the stresses associated with the illness (25). AN
patients tend to have higher plasma NE levels at admission, which then decrease
as treatment and weight gain progresses (25,34).
When ill, BN patients demonstrate lower values of plasma NE at
baseline (21,28) and in response to abstinence (35), standing (36), test meal
challenge (37), and mental challenge (37). They also have other evidence of
blunted sympathetic activation in response to mental stress (38). However,
despite low baseline plasma NE levels, BN patients show normal responses to
exercise (39) but reduced responses to orthostasis (40).
In AN patients, depression has been found to be significantly worse in
those patients with the lowest ∆ change in plasma NE concentrations to
orthostasis (41). Reduced urinary MHPG levels have also been related to the
presence of comorbid major depression (29,42). It is therefore important in
such studies to control for psychiatric comorbidity.
Like the plasma NE studies, CSF NE levels have been reported to be no
different in AN patients than controls at low weight and after short-
term weight gain, but then significantly lower after weight recovery of at least
6 months (26,31,32). In BN patients, reduced CSF NE levels have been
reported during the active state of the illness (23,43). However, upon long-term
recovery, concentrations of CSF MHPG have been reported to normalize in
both AN and BN (7) despite earlier reports of lower levels (32). Given that CSF
NE concentrations have not yet been reported in long-term (>1 year) recovered
AN or BN patients, the extent to which adrenergic alterations seen in the eating
disorders are trait related remains unclear. Nevertheless, available evidence
suggests exquisite sensitivity of this system to malnutrition or stress.
Challenge studies using the (β-adrenergic agonist isoproterenol in
underweight anorexic patients revealed erratic secretion of plasma NE in
response to increasing doses (24). Bulimic patients demonstrated significantly
increased chronotropic responses to isoproterenol (44). Challenge studies with
adrenergic agents in recovered patients have not been reported.
The number of platelet α2 receptors has been reported to be reduced in both
AN and BN compared to controls (33,45), suggesting increased postsynaptic
receptor sensitivity that is probably secondary to dieting or semistarvation. In
summary, peripheral and central sympathetic nervous activity is reduced in both
AN and BN, although it tends to normalize with recovery. Taken together, the
NEUROTRANSMITTER DYSREGULATION 261
preponderance of the evidence so far leads to the conclusion that these changes
are a result of chronic starvation or intermittent dieting (26). However, a trait-
related disturbance of the adrenergic system cannot be ruled out at this
time (35).
Studies of adrenergic receptors on human leukocytes have been another
strategy to investigate adrenergic function in the eating disorders. Buckholtz
et al. (46) reported altered β-adrenergic receptor affinity on circulating
lymphocytes of BN patients compared to those of controls. However, in a
similar study of a mixed group of eating disorder patients, Lonati-Galligani and
Pirke (40) reported lower receptor number (Bmax) but normal affinity (Kd) in
low-weight AN patients, whereas both measures were no different from
controls in the BN patients and the weight-recovered AN patients. Gill and
colleagues (47) reported differential changes in α–and β–adrenoceptor linked
(45Ca2+) uptake in platelets from patients with AN, further documenting an
adrenergic disturbance in eating disorder patients. However, the issue of cause
versus effect remains unanswered in platelet and leukocyte studies.
DOPAMINE
DA is also suspect in the neuropathophysiology of the eating disorders given its
reported involvement in the regulation of feeding, mood, activity, perception,
sexual/social behavior, hormone and peptide release, and to some extent
aggression (48–51). Notably, DA is involved in the hedonic reward responses to
eating and its maintenance as well as to other pleasurable activities (52–54).
The majority of studies of DA metabolism in the eating disorders have
consistently shown that low-weight AN patients have reduced measures of
peripheral and central DA activity, including decreased plasma (27) and CSF
HVA (31). In BN patients, reduced CSF HVA levels also have been reported in
BN patients with frequent binge-purge episodes (23,50) but not in those less
severely ill. Furthermore, binge frequency was inversely correlated with CSF
HVA levels in one study (50). Upon long-term recovery, concentrations of CSF
HVA have been reported to normalize in BN (8), whereas a trend for decreased
CSF HVA levels persisted in six restricting AN patients compared to controls
and to bingeing and/or purging AN patients (7). This suggests a possible trait-
related disturbance specific to restricting AN, although this finding needs
replication given the small sample size. These results could also still be due to
nutritional factors given that patients in this study weighed significantly less than
those in the BN group and may still have been at the low end of the normal
weight range.
Anecdotal reports of the successful use of dopaminergic antagonists (typical
antipsychotic agents) in the treatment of AN patients (55) have been generally
262 BREWERTON AND STEIGER
SEROTONIN
Several lines of reasoning point to disturbances of 5-HT function in
the pathophysiology and neuropsychopharmacology of the EDs (8,9,63),
including serotonin’s role in feeding (64,65), satiety (66,67), dieting/
fasting (11,12), mood regulation (16), anxiety (68), obsessive-
compulsiveness/perfectionism/behavioral inhibition (69), harm
avoidance (70,71), impulsivity/aggression (72,73), motor activity (74,75),
gender (76,77), seasonality (66,78,79), body image/perception (80), and social
behavior (81–83) (see Table 1).
Reductions in a variety of 5-HT parameters have been consistently reported
in low-weight AN patients. Although no significant differences have been found
in absolute plasma L-TRP levels (84–86), the plasma L-TRP/LNAA ratio is
reduced in the low weight state (30,87,88) but normalizes upon short-term
weight recovery (22,30). In BN, Gendal and Joyce (89) reported that the
L-TRP/LNAA ratio inversely correlated with the desire to binge-eat. In
addition, symptomatic bulimic relapse or worsening of symptoms has been
reported following acute L-TRP depletion in BN (17–19).
Other significant findings include decreased CSF L-TRP levels (90) and
decreased CSF 5-HIAA levels (22,88,91) during low-weight status with
normalization of these levels with short-term weight recovery (STWR, goal
weight maintenance ≥3 weeks). Strikingly, Kaye and colleagues (69,92) have
reported abnormally elevated CSF 5-HIAA levels following long-term weight
recovery (LTWR, goal weight maintenance ≥6–12 months), and interpret these
findings as indicating that AN may correspond to a primary state of excessive
5-HT tone, which is then masked by malnutrition-induced reductions in 5-HT
activity during active illness. In other words, they propose that the
NEUROTRANSMITTER DYSREGULATION 263
although other vulnerabilities of the 5-HT system may also exist and interact
with these psychosomatic behaviors. There is only one serotonergic challenge
study reported in BED (101), which found that PRL responses following d-FEN
were no different in patients with BED than in controls. This lends support to
the idea that purging, dieting, and weight loss (rather than bingeing per se) have
greater roles in creating the serotonergic abnormalities noted above. Dieting,
bingeing, and vomiting all may affect central 5-HT synthesis (13,14,22,116,117)
and could conceivably result in down-regulation of postsynaptic 5-HT receptors
and blunted PRL responses. In addition, these behaviors may involve
activation of the HPA axis, which in turn appears to dampen 5-HT receptor
sensitivity (9,107). Despite findings linking recovery from BN to normalization
of blunted endocrine responses after 5-HT agonists (95,115), other findings
(based on PET techniques) suggest persistent reductions in postsynaptic 5-HT2a
receptor activity even in fully recovered bulimics (118). Such findings associate
BN with a stable reduction in 5-HT neurotransmission at some central sites—
and present the possibility that such tendencies exist independently of disorder
sequelae in BN patients.
In BN, platelet studies indicate reduced PLT IMI binding (119) and PLT
MAO (120). PLT 5-HT uptake has been reported to be increased in one
study (121) but not another (120). Steiger et al. (110,122) reported reduced
PLT paroxetine binding in groups of BN patients compared to healthy controls.
MAO/ISATIN
Isatin, or tribulin, is an endogenous indole associated with stress, which inhibits
MAO (165). Brewerton et al. (94) reported significantly higher CSF
concentrations of isatin in BN patients compared to healthy controls. There
was also a trend for CSF isatin concentrations to be inversely correlated
with CSF concentrations of the serotonin metabolite 5-HIAA (n = 14,
ρ = –0.51, p = 0.06), although CSF isatin levels were not significantly
correlated with CSF MHPG or HVA. The increase in isatin levels has been
hypothesized to be in response to the resultant monoamine depletion secondary
to the effects of the illness on monoaminergic function. As noted previously,
platelet MAO has been reported to be decreased in BN (120) and in AN (105).
This decrease may represent a compensatory change in response to monoamine
depletion during the active state of the disorders.
CONCLUSIONS
Taken together, available findings implicate abnormalities of all monoamine
neurotransmitter systems during the active phases of both AN and BN. Upon
270 BREWERTON AND STEIGER
REFERENCES
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders, 4th ed. Washington, DC: American Psychiatric Press, 1994.
2. Becker AE, Grinspoon SK, Klibanski A, Herzog DB. Eating disorders. N Engl J
Med 1999; 340:1092–1098.
3. Walsh BT, Devlin MJ. Eating disorders: progress and problems. Science 1998; 280:
1387–1390.
4. Lilenfeld LR, Kaye WH, Greeno CG, Merikangas KR, Plotnicov K, Pollice C,
Radhika R, Strober M, Bulik C, Nagy L. A controlled family study of anorexia
nervosa and bulimia nervosa. Arch Gen Psychiatry 1998; 55:603–610.
5. Strober M, Freeman R, Lampert C, Diamond J, Kaye WH. Controlled family
study of anorexia nervosa and bulimia nervosa: evidence of shared liability and
transmission of partial syndromes. Am J Psychiatry 2000; 157:393–401.
NEUROTRANSMITTER DYSREGULATION 271
6. Halmi KA, Sunday SR, Strober M, Kaplan A, Woodside DB, Fichter M, Treasure
J, Berrettini WH, Kaye WH. Perfectionism in anorexia nervosa: variation by
clinical subtype, obsessionality, and pathological eating behavior. Am J Psychiatry
2000; 157:1799–1805.
7. Kaye W, Strober M, Stein D, Gendall K. New directions in treatment research of
anorexia and bulimia nervosa. Biol Psychiatry 1999b; 45:1285–1292.
8. Kaye WH, Gendall KA, Strober M. Serotonin neuronal function and selective
reuptake inhibitor treatment in anorexia nervosa and bulimia nervosa. Biol
Psychiatry 1998a; 44:825–838.
9. Brewerton TD. Toward a unified theory of serotonin dysregulation in eating and
related disorders. Psychoneuroendocrinology 1995; 20:561–590.
10. Pollice C, Kaye WH, Greeno CG, Weltzin TE. Relationship of depression, anxiety,
and obsessionality to state of illness in anorexia nervosa. Int J Eat Disord 1997; 21:
367–376.
11. Cowen PJ, Clifford EM, Walsh AE, Williams C, Fairburn CG. Moderate dieting
causes 5-HT2c receptor supersensitivity. Psychol Med 1996; 26:1155–1159.
12. Cowen PJ, Smith KA. Serotonin, dieting, and bulimia nervosa. Adv Exp Med Biol
1999; 467:101–104.
13. Goodwin GM, Fairburn CG, Cowen PJ. Dieting changes serotonergic function in
women, not men: implications for the etiology of anorexia nervosa. Psychol Med
1987a; 17:839–842.
14. Goodwin GM, Fairburn CG, Cowen PJ. The effects of dieting and weight loss
upon neuroendocrine responses to tryptophan, clonidine and apomorphine in
volunteers: important implications for neuroendocrine investigations in depression.
Arch Gen Psychiatry 1987b; 44:952–957.
15. Goodwin GM, Cowen PJ, Fairburn CG, Parry-Billings M, Calder PC, Newsholme
EA. Plasma concentrations of tryptophan and dieting. Br Med J 1990; 300:
1499–1500.
16. Deldago PL, Charney DS, Price LH, Aghajanian GK, Landis H, Henninger GR.
Serotonin function and the mechanism of antidepressant action: reversal of
antidepressant-induced remission by rapid depletion of plasma tryptophan. Arch
Gen Psychiatry 1990; 47:411–418.
17. Kaye WH, Gendall KA, Fernstrom MH, Fernstrom JD, McConaha CW, Weltzin
TE. Effects of acute tryptophan depletion on mood in bulimia nervosa. Biol Psychiatry
2000; 47:151–157.
18. Smith KA, Fairburn CG, Cowen PJ. Symptomatic relapse in bulimia nervosa
following acute tryptophan depletion. Arch Gen Psychiatry 1999; 56:171–176.
19. Weltzin TE, Fernstrom MH, Fernstrom JD, Neuberger SK, Kaye WH. Acute
tryptophan depletion and increased food intake and irritability in bulimia nervosa.
Am J Psychiatry 1995; 152:1668–1671.
20. Rowland NE, Morien A, Li BH. The physiology and brain mechanisms of feeding.
Nutrition 1996; 12:626–639.
272 BREWERTON AND STEIGER
21. Jimerson DC, George DT, Kaye W, Brewerton TD, Goldstein DS.
Norepinephrine regulation in bulimia. In: Hudson JI, Pope HG, eds. Psychobiology
of Bulimia. Washington, DC: American Psychiatric Press, 1987: 145–156.
22. Kaye WH, Gwirtsman HE, George DT, Jimerson DC, Ebert MH. CSF 5HIAA
concentrations in anorexia nervosa: reduced values in underweight subjects
normalize after weight gain. Biol Psychiatry 1988b; 23:102–105.
23. Kaye WH, Ballenger JC, Lydiard RB, Stuart GW, Laraia MT, O’Neil P, Fossey
MD, Stevens V, Lesser S, Hsu G. CSF monoamine levels in normalweight bulimia:
evidence for abnormal noradrenergic activity. Am J Psychiatry 1990; 147:225–229.
24. Kaye WH, George DT, Gwirtsman HE, Jimerson DC, Goldstein DS, Ebert MH,
Lake CR. Isoproterenol infusion test in anorexia nervosa: assessment of pre- and
post-beta-noradrenergic receptor activity. Psychopharmacol Bull 1990; 26:
355–359.
25. Lesem MD, George DT, Kaye WH, Goldstein DS, Jimerson DC. State-related
changes in norepinephrine regulation in anorexia nervosa. Biol Psychiatry 1989; 25:
509–512.
26. Pirke KM. Central and peripheral noradrenalin regulation in eating disorders.
Psychiatry Res 1996; 62:43–49.
27. Gross HA, Lake CR, Ebert MH, Ziegler MG, Kopin IJ. Catecholamine metabolism
in primary anorexia nervosa. J Clin Endocrinol Metab 1979; 49:805–809.
28. Obarzanek E, Lesem MD, Goldstein DS, Jimerson DC. Reduced resting
metabolicrateinpatientswithbulimianervosa.ArchGenPsychiatryl991;48:456^t62.
29. Halmi KA, Dekirmenjian H, Dav JM, Casper R, Goldberg S. Catecholamine
metabolism in anorexia nervosa. Arch Gen Psychiatry 1978; 35:458–460.
30. Johnston JL, Leiter LA, Burrow GN, Garfinkel PE, Anderson GH. Excretion of
urinary catecholamine metabolites in anorexia nervosa: effect of body composition
and energy intake. Am J Clin Nutr 1984; 40:1001–1006.
31. Kaye WH, Ebert MH, Raleigh M, Lake CR. Abnormalities in CNS monoamine
metabolism in anorexia nervosa. Arch Gen Psychiatry 1984; 41:350–355.
32. Kaye WH, Jimerson DC, Lake CR, Ebert MH. Altered norepinephrine metabolism
following long-term weight recovery in patients with anorexia nervosa. Psychiatry
Res 1985; 14:333–342.
33. Luck P, Mikhailid DP, Dashwood MR, Barradas MA, Sever PS, Dandona P,
Wakeling A. Platelet hyperaggregability and increased alpha-adrenoceptor density
in anorexia nervosa. J Clin Endocrinol Metab 1983; 57:911–914.
34. Pahl J, Pirke KM, Schweiger U, Warnhoff M, Gerlinghoff M, Brinkmann W,
Berger M, Krieg C. Anorectic behavior, mood, and metabolic and endocrine
adaptation to starvation in anorexia nervosa during inpatient treatment. Biol
Psychiatry 1985; 20:874–887.
35. Kaye WH, Gwirtsman HE, George DT, Jimerson DC, Ebert MH, Lake CR.
Disturbances of noradrenergic systems in normal weight bulimia: relationship to
diet and menses. Biol Psychiatry 1990; 27:4–21.
NEUROTRANSMITTER DYSREGULATION 273
36. Pirke KM, Jorg P, Schweiger U, Warnhoff M. Metabolic and endocrine indices of
starvation in bulimia: a comparison with anorexia nervosa. Psychiatry Res 1985; 15:
33–39.
37. Pirke KM, Kellner M, Philipp E, Laessle R, Krieg JC, Fichter MM. Plasma
norepinephrine after a standardized test meal in acute and remitted patients with
anorexia nervosa and in healthy controls. Biol Psychiatry 1992; 31:1074–1077.
38. Koo-Loeb JH, Pedersen C, Girdler SS. Blunted cardiovascular and catecholamine
stress reactivity in women with bulimia nervosa. Psychiatry Res 1998; 80:13–27.
39. Pirke KM, Eckert M, Ofers B, Goebl G, Spyra B, Schweiger U, Tuschl RJ, Fichter
MM. Plasma norepinephrine response to exercise in bulimia, anorexia nervosa, and
controls. Biol Psychiatry 1989; 25:799–802.
40. Lonati-Galligani M, Pirke KM. Beta 2-adrenergic receptor regulation in circulating
mononuclear leukocytes in anorexia nervosa and bulimia. Psychiatry Res 1986; 19:
189–198.
41. Laessle RG, Schweiger U, Pirke KM. Mood and orthostatic norepinephrine
response in anorexia nervosa. Psychiatry Res 1988; 24:87–94.
42. Biederman J, Herzog DB, Rivinus TM, Ferber RA, Harper GP, Onsulak PJ,
Schildkrautt JJ. Urinary MHPG in anorexia nervosa patients with and without a
concomitant major depressive disorder. J Psychiatr Res 1984; 18:149–160.
43. Kaye WH, George DT, Gwirtsman HE, Jimerson DC, Goldstein DS, Ebert MH,
Lake CR. Isoproterenol infusion test in anorexia nervosa: assessment of pre- and
post-beta-noradrenergic receptor activity. Psychopharmacol Bull 1990; 26:
355–359.
44. George DT, Kaye WH, Goldstein DS, Brewerton TD, Jimerson DC. Altered
norepinephrine regulation in bulimia: effects of pharmacological challenge with
isoproterenol. Psychiatry Res 1990; 33:1–10.
45. Heufelder A, Warnhoff M, Pirke KM. Platelet alpha 2-adrenoceptor and adenylate
cyclase in patients with anorexia nervosa and bulimia. J Clin Endocrinol Metab
1985; 61:1053–1060.
46. Buckholtz NS, George DT, Davies AO, Jimerson DC, Potter WZ. Lymphocyte
beta-adrenergic receptor modification in bulimia. Arch Gen Psychiatry 1988; 45:
479–182.
47. Gill J, DeSouza V, Wakeling A, Dandona P, Jeremy JY. Differential changes in
alpha- and beta-adrenoceptor linked [45Ca2 +] uptake in platelets from patients
with anorexia nervosa. J Clin Endocrinol Metab 1992; 74:441–446.
48. Engstrom G, Alling C, Blennow K, Regnell G, Traskman-Bendz L.
Reduced cerebrospinal HVA concentrations and HVA/5-HIAA ratios in suicide
attempters: monoamine metabolites in 120 suicide attempters and 47 controls. Eur
Neuropsychopharmacol 1999; 9:399–405.
49. Hoebel BG. Brain neurotransmitters in food and drug reward. Am J Clin Nutr
1985; 42:1133–1150.
50. Jimerson DC, Lesem MD, Kaye WH, Brewerton TD. Low serotonin and
dopamine metabolite concentrations in CSF from bulimic patients with frequent
binge episodes. Arch Gen Psychiatry 1992; 49:132–138.
274 BREWERTON AND STEIGER
51. Kaye WH, Guido KWF, Frank GK, McConaha C. Altered dopamine activity after
recovery from restricting anorexia nervosa. Neuropsychopharmacology 1999; 21:
503–506.
52. Schultz W. Reward signaling by dopamine neurons. Neuroscientist 2001; 7:
293–302.
53. Hoebel BG, Hernandez L, Schwartz DH, Mark P, Hunter GA. Microdialysis
studies of brain norepinephrine, serotonin, and dopamine release during ingestive
behavior. The Psychobiology of Human Eating Disorders. Ann N Y Acad Sci 1989;
575:71–193.
54. Dayan P, Balleine BW. Reward, motivation, and reinforcement learning. Neuron
2002; 36:285–298.
55. Dally P, Sargant W. Treatment and outcome of anorexia nervosa. Br Med J 1966;
2:793–795.
56. Vandereycken W, Pierloot R. Pimozide combined with behavior therapy in the short-
term treatment of anorexia nervosa. A double-blind placebo-controlled cross-over
study. Acta Psychiatr Scand 1982; 66:445–450.
57. Vandereycken W. Neuroleptics in the short-term treatment of anorexia nervosa: a
double-blind placebo-controlled, cross-over trial with sulpride. Br J Psychiatry
1984; 144:288–292.
58. Hansen L. Olanzapine in the treatment of anorexia nervosa. Br J Psychiatry 1999;
175:592.
59. Jensen VS, Mejlhede A. Anorexia nervosa: treatment with olanzapine. Br J
Psychiatry 2000; 177:87.
60. LaVia M, Gray N, Kaye WH. Case reports of olanzapine treatment of anorexia
nervosa. Int J Eat Disord 2000; 27:363–366.
61. Bruins-Slot L, Gorwood P, Bouvard M, Blot P, Ades J, Feingold J, Schwartz JC,
Mouren-Simeoni MC. Lack of association between anorexia nervosa and D3
dopamine receptor gene. Biol Psychiatry 1998; 43:76–78.
62. Corcos M, Atger F, Levy-Soussan P, Avrameas S, Guilbert B, Cayol V, Jeammet P.
Bulimia nervosa and autoimmunity. Psychiatry Res 1999; 87:77–82.
63. Kaye WH, Weltzin TE. Serotonin activity in anorexia and bulimia nervosa:
relationship to the modulation of feeding and mood. J Clin Psychiatry 1991; 52
(suppl):41–48.
64. Dourish CT, Cooper SJ, Gilbert F, Coughlan J, Iversen SD. The 5-HT1A agonist
8-OH-DPAT increases consumption of palatable wet mash and liquid diets in the
rat. Psychopharmacology 1988; 94:58–63.
65. De Vry J, Schreiber R. Effects of selected serotonin 5-HT(l) and 5-HT(2) receptor
agonists on feeding behavior: possible mechanisms of action. Neurosci Biobehav
Rev 2000; 24:341–353.
66. Brewerton TD, Murphy DL, Jimerson DC. Testmeal responses following m-
chlorophenylpiperazine and L-tryptophan in bulimics and controls.
Neuropsychopharmacology 1994; 11:63–71.
67. Leibowitz SF, Alexander JT. Hypothalamic serotonin in control of eating behavior,
meal size, and body weight. Biol Psychiatry 1998; 44:851–864.
NEUROTRANSMITTER DYSREGULATION 275
68. Anderson IM, Mortimore C. 5-HT and human anxiety: evidence from studies using
acute tryptophan depletion. Adv Exp Med Biol 1999; 467:43–55.
69. Kaye WH, Gwirtsman HE, George DT, Ebert MH. Altered serotonin activity in
anorexia nervosa after long-term weight restoration. Arch Gen Psychiatry 1991a;
48:556–562.
70. Brewerton TD, Hand LD, Bishop ER. The Tridimensional Personality
Questionnaire in eating disorder patients. Int J Eat Disord 1993; 14:213–218.
71. Waller DA, Gullion CM, Petty F, Hardy BW, Murdock MV, Rush AJ.
Tridimensional Personality Questionnaire and serotonin in bulimia nervosa.
Psychiatry Res 1993; 48:9–15.
72. Linnoila M, Virkhunen M, Scheinin M, Nuutila A, Rimon R, Goodwin FK. Low
cerebrospinal fluid 5-hydroxyindoleacetic acid concentration differentiates
impulsive from nonimpulsive violent behavior. Life Sci 1983; 33:2609–2614.
73. Coccaro EF, Siever LJ, Klar H, Maurer G, Cochrane K, Cooper TB, Mohr RC,
Davis KL. Serotonergic studies in affective and personality disorder patients:
correlates with suicidal and impulsive aggressive behavior. Arch Gen Psychiatry
1989; 46:587–599.
74. Brewerton TD, Stellefson EJ, Hibbs N, Hodges EJ, Cochrane CE. A comparison of
eating disorder patients with and without compulsive exercising. Int J Eat Disord
1995; 17:413–416.
75. Epling F, Pierci D. Activity-based anorexia: a biological perspective. Int J Eat
Disord 1988; 7:475–485.
76. Carlsson M, Svensson K, Eriksson E, Carlsson A. Rat brain serotonin: biochemical
and functional evidence for a sex difference. J Neural Transm 1985; 63:297–313.
77. Goodwin GM, Fraser S, Stump K, Fairburn CG, Elliott JM, Cowen PJ. Dieting
and weight loss in volunteers increases the number of alpha2adrenoceptors and
5-HT receptors on blood platelets without effect on [3H]imipramine binding.
J Affect Disord 1987; 12:267–274.
78. Brewerton TD. Seasonal variation of serotonin function in humans: research and
clinical implications. Ann Clin Psychiatry 1989; 1:153–164.
79. Brewerton TD, Berrettini W, Nurnburger J, Linnoila M. An analysis of seasonal
fluctuations of CSF monoamines and neuropeptides in normal controls: findings
with 5-HIAA and HVA. Psychiatry Res 1988; 23:257–265.
80. Goldbloom DS, Olmsted MP. Pharmacotherapy of bulimia nervosa with fluoxetine:
assessment of clinically significant attitudinal change. Am J Psychiatry 1993; 50:
770–774.
81. Raleigh MJ, McGuire MT, Brammer GL, Yuwiler A. Social and
environmental influences on blood serotonin concentrations in monkeys. Arch Gen
Psychiatry 1984; 41:405–410.
82. Raleigh MJ, Brammer GL, McGuire MT, Yuwiler A. Dominant social status
facilitates the behavioral effects of serotonergic agonists. Brain Res 1985; 348:
274–282.
83. McQuire MT, Raleigh MJ. Serotonin-behavior interactions in vervet monkeys.
Psychopharmacol Bull 1985; 21:458–463.
276 BREWERTON AND STEIGER
84. Russell GF. The nutritional disorder in anorexia nervosa. J Psychosom Res 1967;
11:141–149.
85. Coppen AJ, Gupta RK, Eccleston EG, Wood KM, Wakeling A, de Sousa VF.
Plasma tryptophan in anorexia nervosa. Lancet 1976; 1:961.
86. Hassanyeh F, Marshall EF. Measures of serotonin metabolism in anorexia nervosa.
Acta Psychiatr Scand 1991; 84:561–563.
87. Askenazy F, Candito M, Caci H, Myquel M, Chambon P, Darcourt G, Puech AJ.
Whole blood serotonin content, tryptophan concentrations, and impulsivity in
anorexia nervosa. Biol Psychiatry 1998; 43:188–195.
88. Kaye WH, Ebert MH, Gwirtsman HE, Weiss SR. Differences in brain serotonergic
metabolism between nonbulimic and bulimic patients with anorexia nervosa. Am J
Psychiatry 1984; 141:1598–1601.
89. Gendall KA, Joyce PR. Meal-induced changes in tryptophan:LNAA ratio: effects on
craving and binge eating. Eat Behav 2000; 1:53–62.
90. Gerner RH, Cohen DJ, Fairbanks L, Anderson GM, Young JG, Scheinin M,
Linnoila M, Shaywitz BA, Hare TA. CSF neurochemistry of women with anorexia
nervosa and normal women. Am J Psychiatry 1984; 141:948–949.
91. Gillberg C. Low dopamine and serotonin levels in anorexia nervosa. Am J
Psychiatry 1983; 140:948–949.
92. Kaye WH. Persistent alterations in behavior and serotonin activity after recovery
from anorexia and bulimia nervosa. Ann N Y Acad Sci 1997; 817:162–178.
93. Kaye W, Frank G. Gene-environment interactions: Brain and behavior in anorexia
nervosa. Paper presented at the annual meeting of the Eating Disorder Research
Society, November 20–23, 2002, Charleston, South Carolina.
94. Brewerton TD, Zealberg JL, Lydiard RB, Glover V, Sandler M, Ballenger JC. CSF
isatin is elevated in bulimia nervosa. Biol Psychiatry 1995; 37:481–483.
95. Kaye WH, Greeno CG, Moss H, Fernstrom J, Fernstrom M, Lilenfeld LR,
Weltzin TE, Mann JJ. Alterations in serotonin activity and psychiatric symptoms
after recovery from bulimia nervosa. Arch Gen Psychiatry 1998; 55:927–935.
96. Brewerton TD, Brandt HA, Lesem DT, Murphy DL, Jimerson DC. Serotonin in
eating disorders. In: Coccaro E, Murphy D, eds. Serotonin in Major Psychiatric
Disorders. Washington, DC: American Psychiatric Press, 1990:153–184.
97. Brewerton TD, Jimerson DC. Studies of serotonin function in anorexia nervosa.
Psychiatry Res 1996; 62:31–42.
98. Hadigan CM, Walsh BT, Buttinger C, Hollander E. Behavioral and
neuro endocrine responses to metaCPP in anorexia nervosa. Biol Psychiatry 1995;
37:504–511.
99. Halmi KA, McBride PA, Sunday SR. Serotonin responsivity and hunger and satiety
in eating disorders. Primary and Secondary Eating Disorders: A
Psychoneuroendocrine and Metabolic Approach. Proceedings of the 2nd
International Symposium on Disorders of Eating Behaviour, Pavia, Italy, September
15–19, 1992:123–131.
NEUROTRANSMITTER DYSREGULATION 277
115. Wolfe BE, Metzger ED, Levine JM, Finkelstein DM, Cooper TB, Jimerson DC.
Serotonin function following remission from bulimia nervosa.
Neuropsychopharmacology 2000; 22:257–263.
116. Fernstrom JD. Dietary effects on brain serotonin synthesis: relationship to appetite
regulation. Am J Clin Nutr 1985; 42:1072–1082.
117. Kaye WH, Gwirtsman HE, Brewerton TD, George DT, Jimerson DC, Wurtman
RJ. Bingeing behavior and plasma amino acids: a possible involvement of brain
serotonin in bulimia. Psychiatry Res 1988; 23:31–43.
118. Kay WH, Frank GK, Meltzer CM, Price JC, McConaha CW, Crossan PJ, Klump
K, Rhodes L. Altered serotonin 2A receptor activity in women who have recovered
from bulimia nervosa. Am J Psychiatry 2001; 158:1152–1155.
119. Marazziti D, Macchi E, Rotondo A, Placidi GF, Cassano GB. Involvement of
serotonin system in bulimia. Life Sci 1988; 43:2123–2126.
120. Hallman J, Sakurai E, Oreland L. Blood platelet monoamine oxidase activity,
serotonin uptake and release rates in anorexia and bulimia patients and in healthy
controls. Acta Psychiatr Scand 1989; 81:73–77.
121. Goldbloom DS, Hicks LK, Garfinkel PE. Platelet serotonin uptake in bulimia
nervosa. Biol Psychiatry 1988; 28:644–647.
122. Steiger H, Leonard S, Kin NY, Ladouceur C, Ramdoyal D, Young SN. Childhood
abuse and platelet tritiated-paroxetine binding in bulimia nervosa:
implicationsofborderlinepersonalitydisorder.JClinPsychiatry2000;61:428–435.
123. Asberg M, Schalling D, Träskman-Bendz L, Wägner A. Psychobiology of
suicide, impulsivity and related phenomena. In: Meltzer HY, ed.
Psychopharmacology:Third Generation of Progress. NewYork: Raven Press, 1987:
655–688.
124. Coccaro EF, Siever LJ, Klar HM, Cochrane K, Cooper TB, Mohs RC, Davis KL.
Serotonergic studies in patients with affective and personality disorders: correlates
with suicidal and impulsive aggressive behaviour. Arch Gen Psychiatry 1989; 46:
587–599.
125. Swedo SE, Leonard HL, Krusei MJP, Rettew DC, Listwak SJ, Berrettini W,
Stipetic M, Hamburger S, Gold PW, Potter WZ, Rapoport JL. Cerebrospinal fluid
neurochemistry in children and adolescents with obsessive-compulsive disorder.
Arch Gen Psychiatry 1992; 49:29–36.
126. Fineberg NA, Roberts A, Montgomery SA, Cowen PJ. Brain 5-HT function in
obsessive-compulsive disorder. Prolactin responses to d-fenfluramine. Br J
Psychiatry 1998; 171:280–282.
127. Altemus M, Swedo SE, Leonard HL, Richter D, Rubinow DR, Potter WZ,
Rapaport JL. Changes in cerebrospinal fluid neurochemistry during treatment of
obsessive-compulsive disorder with clomipramine. Arch Gen Psychiatry 1994; 51:
846–849.
128. Germine RH, Goddard AW, Woods SW, Charnet DS, Henninger GR. Anger and
anxiety response to ra-chlorophenylpiperazine in generalized anxiety disorder. Biol
Psychiatry 1992; 32:457–461.
NEUROTRANSMITTER DYSREGULATION 279
145. Collier DA, Arranz MJ, Mupita D, Brown N, Treasure J. Association between the
5-HT2A receptor gene polymorphism and anorexia nervosa. Lancet 1997; 350:
412.
146. Nacmias B, Ricca V, Tedde A, Mezzani B, Rotella CM, Sorbi S. 5-HT2A receptor
gene polymorphisms in anorexia nervosa and bulimia nervosa. Neurosci Lett 1999;
277:134–136.
147. Enoch MA, Kaye WH, Rotondo A, Greenberg BD, Murphy DL, Goldman D.
5-HT2A promoter polymorphism—1438G/A, anorexia nervosa, and
obsessivecompulsive disorder. Lancet 1998; 351:1785.
148. Hinney A, Barth N, Ziegler A, vonPrittwitz S, Hamann A, Hennighausen K, Pirke
KM, Heils A, Rosenkranz K, Roth H, Coners H, Mayer H, Herzog W, Siegfried
A, Lehmkuhl G, Poustka F, Schmidt MH, Schafer H, Grzeschik KH, Lesch KP,
Lentes KU, Remschmidt H, Hebebrand J. Serotonin transporter gene-linked
polymorphic region, allele distributions in relationship to body weight and in
anorexia nervosa. Life Sci 1997; 61:295–303.
149. Sundaramurthy D, Pieri LF, Gape H, Markham AF, Campbell DA. Analysis of
serotonin transporter gene linked polymorphism (5-HTTLPR) in anorexia nervosa.
Am J Med Genet 2000; 96:53–55.
150. Han L, Nielsen DA, Rosenthal NE, Jefferson K, Kaye W, Murphy D, Altemus M,
Humphries J, Cassano G, Rotondo A, Virkkimen M, Linnoila M, Goldman D. No
coding variant of the tryptophan hydroxylase gene detected in seasonal affective
disorder, obsessive-compulsive disorder, anorexia nervosa, and alcoholism. Biol
Psychiatry 1999; 45:615–619.
151. Hinney A, Herrmann H, Lohr T, Rosenkranz K, Ziegler A, Lehmkuhl G, Poustka
F, Schmidt MH, Mayer H, Siegfried W, Remschmidt H, Hebebrand J. No evidence
for an involvement of alleles of polymorphisms in the serotonin1Dbeta and 7
receptor genes in obesity, underweight or anorexia nervosa. Int J Obes Relat
Metab Disord 1999; 23:760–763.
152. Ziegler A, Hebebrand J, Gorg R, Rosenkranz K, Fichter MM, HerpertzDahlmann
B, Remschimidt H, Hinney A. Further lack of association between the 5-HT2A
gene promoter polymorphism and susceptibility to eating disorders and a meta-
analysis pertaining to anorexia nervosa. Mol Psychiatry 1999; 4:410–412.
153. Nishiguchi N, Matsuchita S, Suzuki K, Murayama M, Shirakawa O, Higuchi S.
Association between 5HT2A receptor gene promoter region polymorphism and
eating disorders in Japanese patients. Biol Psychiatry 2001; 50:123–128.
154. Di Bella DD, Catalano M, Cavallini MC, Riboldi C, Bellodi I. Serotonin
transporter linked polymorphic region in anorexia nervosa and bulimia nervosa.
Mol Psychiatry 2000; 5:233–241.
155. Heils A, Teufel A, Petri S, Stober G, Riederer P, Bengel D. Lesch KP: Allelic
variations of human serotonin transporter gene expression. J Neurochem 1996; 66:
2621–2624.
156. Bondy B, Erfurth A, de Jonge S, Kriiger M, Meyer H. Possible association of the
short allele of the serotonin transporter promoter gene polymorphism (5HTTLPR)
with violent suicide. Mol Psychiatry 2000; 5:193–195.
NEUROTRANSMITTER DYSREGULATION 281
157. Lesch KP, Wolozin BL, Murphy DL, Reiderer P. Primary structure of the human
platelet serotonin uptake site: identity with the brain serotonin transporter. J
Neurochem 1993; 60:2319–2322.
158. Steiger H, Joober R, Israel M, Bruce K, NG Ying Kin NMK, Gauvin L, Young SN,
Joncas J, Torkaman-Xehi A. A polymorphism in the promoter region of the
serotonin transporter gene (5-HTTLPR) corresponds to impulsivity and reduced
paroxetine binding in eating-disordered and normal-eater woman. Presented at the
Annual Meeting of the Eating Disorders Research Society, Charleston, South
Carolina, November 23, 2002.
159. Fluoxetine Bulimia Nervosa Collaborative Group. Fluoxetine in the treatment of
bulimia nervosa: a multicenter, placebo-controlled, double-blind trial. Arch Gen
Psychiatry 1992; 49:139–147.
160. Attia E, Haiman C, Walsh BT, Flater SR. Does fluoxetine augment the inpatient
treatment of anorexia nervosa? Am J Psychiatry 1998; 155:548–551.
161. Strober M, Pataki C, Freeman R, DeAntonio M. No effect of adjunctive fluoxetine
on eating behavior or weight phobia during the inpatient treatment of anorexia
nervosa: an historical case-control study. J Child Adol Psychopharmacol 1999; 9:
195–201.
162. Faris PL, Kim SW, Meller WH, Goodale RL, Hofbauer RD, Oakman SA, Howard
LA, Stevens ER, Eckert ED, Hartman BK. Effect of ondansetron, a 5-HT3 receptor
antagonist, on the dynamic association between bulimic behaviors and pain
thresholds. Pain 1998; 77:297–303.
163. Faris PL, Kim SW, Meller WH, Goodale RL, Oakman SA, Hofbauer RD, Marshall
AM, Daughters RS, Banerjee-Stevens D, Eckert ED, Hartman BK. Effect of
decreasing afferent vagal activity with ondansetron on symptoms of bulimia
nervosa: a randomised, double-blind trial. Lancet 2000; 355:792–797.
164. Roychoudhury M, Kulkarni SK. Anti-anxiety profile of ondansetron, a selective 5-
HT3 antagonist, in a novel animal model. Methods Find Exp Clin Pharmacol 1997;
19:107–111.
165. Glover V, Halket JM, Watkins PJ, Clow A, Goodwin BL, Sandler M. Isatin:
identity with the purified endogenous monoamine oxidase inhibitor tribulin.
J Neurochem 1988; 51:656–659.
282 BREWERTON AND STEIGER
12
Neuroendocrine and Neuropeptide
Dysregulation in Anorexia Nervosa, Bulimia
Nervosa, and Binge Eating Disorder
Ursula F.Bailer and Walter H.Kaye
Western Psychiatric Institute and Clinic, University of Pittsburgh
School of Medicine
Pittsburgh, Pennsylvania, U.S.A.
NEUROENDOCRINOLOGY
Abnormal hormone profiles and responses to challenge are closely related to the
“starvation” status of anorexia nervosa (AN) and bulimia nervosa (BN) patients.
Hormone abnormalities may also be present, but to a lesser extent, in normal-
weight women with BN. The presence of starvation in AN is evident from the
weight loss, but it may not be recognized in normal-weight bulimics. Although
bulimic women often maintain a normal weight, they do so by restricting food
intake when not bingeing and purging, and they may have monotonous and
poorly balanced meals. Starvation-induced depletion of hepatic glycogen stores
results in free fatty acids and ketone bodies replacing glucose as the primary
energy source. This shift from glycogenolysis to lipolysis and ketogenesis is
associated with an increase in free fatty acids and their metabolites.
(β-Hydroxybutyric acid levels are elevated in both AN and BN (1), indicating
that bulimic patients are nutritionally depleted in spite of their normal body
weight.
The relationship of starvation and eating disorders to neuroendocrine
function is most clearly seen for the pituitary-gonadal axis.
Secondary amenorrhea is one of the criteria for AN in postmenarcheal women,
and oligomenorrhea occurs in about 50% of bulimics. The secondary
amenorrhea is a direct result of altered gonadotropin secretion. Serum sex
hormonebinding globulin may be increased, and both estrogen and testosterone
are decreased (2). The luteinizing hormone response to luteinizing
hormonereleasing hormone stimulation is blunted, but the follicle-stimulating
hormone response is usually normal.
With reference to the hypothalamic-pituitary-adreno-cortical (HPA) axis, it
is well known that plasma cortisol is increased at all times of the day and night,
but its circadian rhythm is preserved in terms of amplitude and timing.
284 BAILER AND KAYE
Stimulation and suppression tests of the HPA axis have been conducted mainly
in AN, and they are in accord with the baseline hormone findings.
Adrenocorticotropic hormone (ACTH) response to corticotropinreleasing
hormone (CRH) administration is reduced, undoubtedly secondary to enhanced
negative feedback on the pituitary corticotrophs exerted by elevated circulating
cortisol. The cortisol response to ACTH administration is increased, suggesting
increased secretory capacity of the adrenal cortex. The low-dose
dexamethasone suppression test is abnormal in 50–90% of anorexics and in 20%
to 60% of bulimics, depending on the weight loss. Because dexamethasone acts
primarily at the pituitary, ACTH and cortisol escape from dexamethasone
suppression, suggesting increased suprapituitary stimulation of corticotrophs by
CRH and vasopressin. Taken together, the pituitary-adrenocortical findings
indicate a mild to moderate activation of this hormone axis in AN and BN.
Interestingly, the abnormalities in AN and in reduced-weight BN (3,4) are
strikingly similar to those occurring in 30–50% of patients with major
depression, although malnutrition, and not mood disturbances, are likely to be
most contributory.
Obese women with binge eating disorder do not show abnormalities of
dexamethasone suppression, either before or after weight loss (5). Data are not
available on prolactin, growth hormone (GH) secretion, or 24-h cortisol
secretion in subjects with binge eating disorder (6). Among obese binge eaters
who do not purge, no abnormalities of glucose or insulin have been reported
relative to weight-matched controls (7). However, sophisticated methodologies
to evaluate cephalic-phase insulin release (CPIR) and glucose metabolism have
not been applied to this population.
With reference to the pituitary-thyroid axis, starvation leads to considerably
decreased plasma free triiodothyronine (T3) concentrations, along with
somewhat decreased plasma free thyroxine (T4) and increased plasma reverse
T3 concentrations. This represents the “euthyroid sick syndrome” hormone
profile (8,9). The decreased circulating T3 helps reduce energy expenditure and
minimizes muscle protein catabolism into amino acids for gluconeogenesis.
Cerebrospinal fluid (CSF) thyrotropin-releasing hormone also appears to be
reduced in AN (10). When bingeing, bulimic patients generally have normal
thyroid indices with perhaps reduced T3 and thyroidstimulating hormone
concentrations; however, when they become abstinent, their pituitary-thyroid
axis function resembles that of anorexic patients (11–13). Thyroid hormone
levels are similar in obese binge eaters and weightmatched controls (7,14).
Insulinlike growth factor, type I (IGF-1) concentrations are low in both AN
and BN, and circulating GH is increased, perhaps owing to diminished feedback
of IGF-1 on GH secretion. Circulating prolactin is usually unchanged in AN and
may be reduced in BN. Prolactin responses to serotonergic challenges such as
NEUROENDOCRINE AND NEUROPEPTIDE DYSREGULATION 285
NEUROPEPTIDES
The past decade has witnessed accelerating basic research on the role of
neuropeptides in the regulation of feeding behavior and obesity. The mechanisms
for controlling food intake involve a complicated interplay between peripheral
systems (including gustatory stimulation, gastrointestinal peptide secretion, and
vagal afferent nerve responses) and central nervous system (CNS)
neuropeptides and/or monoamines. Thus, studies in animals show that
neuropeptides, such as cholecystokinin, the endogenous opioids (such as
β-endorphin), and neuropeptide Y regulate the rate, duration, and size of meals,
as well as macronutrient selection (15,16). In addition to regulating eating
behavior, a number of CNS neuropeptides participate in the regulation of
neuroendocrine pathways. Thus, clinical studies have evaluated the possibility
that CNS neuropeptide alterations may contribute to dysregulated secretion of
the gonadal hormones, cortisol, thyroid hormones, and growth hormone in the
eating disorders (17,18).
While there are relatively few studies to date, most of the neuroendocrine
and neuropeptide alterations apparent during symptomatic episodes of AN and
BN tend to normalize after recovery. This observation suggests that most of the
disturbances are consequences rather than causes of malnutrition, weight loss,
and/or altered meal patterns. Still, an understanding of these neuropeptide
disturbances may shed light on why many people with AN or BN cannot easily
“reverse” their illness. In AN, malnutrition may contribute to a downward
spiral sustaining and perpetuating the desire for more weight loss and dieting.
Symptoms such as increased satiety, obsessions, and dysphoric mood may be
exaggerated by these neuropeptide alterations and thus contribute to the
downward spiral. In addition, mutual interactions between neuropeptide,
neuroendocrine, and neurotransmitter pathways may contribute to the
constellation of psychiatric comorbidity often observed in these disorders. Even
after weight gain and normalization of eating patterns, many individuals who
have recovered from AN or BN have physiological, behavioral, and
psychological symptoms that persist for extended periods. Menstrual cycle
dysregulation, for example, may persist for several months after weight
restoration. The following sections provide a brief overview of studies of
neuropeptides in AN and BN.
286 BAILER AND KAYE
Corticotropin-Releasing Hormone
When underweight, patients with AN have increased plasma cortisol secretion,
which is thought to be at least in part a consequence of hypersecretion of
endogenous CRH (3,19–21). In that the plasma and CSF measures return to
normal, it appears likely that activation of the HPA axis is precipitated by
weight loss. The observation of increased CRH activity is of great theoretical
interest in AN since intracerebroventricular CRH administration in
experimental animals produces many of the physiological and behavioral
changes associated with AN, including markedly decreased eating behavior (22),
hypothalamic hypogonadism (23), decreased sexual activity (24), and hyper
activity (25).
Opioid Peptides
Studies in laboratory animals raise the possibility that altered endogenous opioid
activity might contribute to pathological feeding behavior in eating disorders
since opioid agonists generally increase, and opioid antagonists decrease, food
intake (26). State-related reductions in concentrations of CSF (3-endorphin and
related opiate concentrations have been found in both underweight AN and ill
BN subjects (27–29). In contrast, using the T lymphocyte as a model system,
Brambilla et al. (30) found elevated β-endorphin levels in AN, although the
levels were normal in BN (31). If β-endorphin activity is a facilitator of feeding
behavior, then reduced CSF concentrations could reflect decreased central
activity of this system, which then maintains or facilitates inhibition of feeding
behavior in the eating disorders.
A disturbance in CNS opioid function may also contribute to the
neuroendocrine abnormalities in AN and BN (e.g., disturbances in HPA and
pituitary-gonadal axis function) (32,33). Brain opioid pathways inhibit ACTH
and cortisol release in humans, and they suppress pulsatile gonadotropin
secretion in rats and in sexually mature humans. Underweight anorexics
frequently have a blunted response of LH secretion to opiate antagonists (34),
and weight restoration tends to normalize this response. The failure of opioid
antagonists to increase luteinizing hormone secretion in underweight anorexics
suggests that another neurotransmitter system (or systems) may be responsible
for this neuroendocrine disturbance.
Cholecystokinin
Cholecystokinin (CCK) is a peptide secreted by the gastrointestinal system in
response to food intake. Release of CCK is thought to be one means of
transmitting satiety signals to the brain by way of vagal afferents (44). In parallel
to its role in satiety in rodents, exogenously administered CCK reduces food
intake in humans. The preponderance of data suggests that patients with BN, in
comparison to controls, have diminished release of CCK following ingestion of
a standardized test meal (45–48). Measurements of basal CCK values in blood
lymphocytes and in CSF also appear to be decreased in patients with
BN (31,49). It has been suggested that the diminished CCK response to a meal
may have a role in diminished postingestive satiety observed in BN. The
CCK response in BN patients was found to return to normal following
treatment (45).
Studies of CCK in AN have yielded less consistent findings. Some studies
have found elevations in basal levels of plasma CCK (46,50), as well as increased
peptide release following a test meal (46,51). One study found that blunting of
CCK response to an oral glucose load normalized in AN patients after
partial restoration of body weight (50). Other studies have found that
measures of CCK function in AN were similar to or lower than control
values (30,47,52,53). Further studies are needed to evaluate the relationship
between altered CCK regulation and other indices of abnormal gastric function
in symptomatic BN and AN patients (54).
Leptin
Leptin, the protein product of the ob gene, is secreted predominantly by adipose
tissue cells and acts in the CNS to decrease food intake, thus regulating body fat
stores. In rodent models, defects in the leptin coding sequence resulting in
leptin deficiency or defects in leptin receptor function are associated with
obesity. In humans, serum and CSF concentrations of leptin are positively
correlated with fat mass in individuals across a broad range of body weight,
including obesity (55,56). Thus, obesity in humans is not thought to be a result
of leptin deficiency per se, although rare genetic deficiencies in leptin
production have been associated with familial obesity (57).
Underweight patients with AN have consistently been found to have
significantly reduced serum leptin concentrations in comparison to normal
weight controls (53,58–61). Based on studies in laboratory animals, it has been
suggested that low leptin levels may contribute to amenorrhea and other
hormonal changes in the disorder (60). Although the reduction in fasting serum
leptin levels in AN is correlated with reduction in body mass index (BMI), there
NEUROENDOCRINE AND NEUROPEPTIDE DYSREGULATION 289
has been some discussion of the possibility that leptin levels in AN patients may
be higher than expected based on the extent of weight loss (62,63). Mantzoros
et al. (60) reported an elevated CSF to serum leptin ratio in AN compared to
controls, suggesting that the proportional decrease in leptin levels with weight
loss is greater in serum than in CSF. A longitudinal investigation during
refeeding in AN patients has shown that CSF leptin concentrations reach normal
values before full weight restoration, possibly as a consequence of the relatively
rapid and disproportionate accumulation of fat during refeeding (60). This
finding led the authors to suggest that premature normalization of leptin
concentration might contribute to difficulty in achieving and sustaining a normal
weight in AN. Plasma and CSF leptin levels appear to be similar to control
values in long-term recovered AN subjects (42).
Recent studies indicate that patients with BN, in comparison to carefully
matched controls, have significantly decreased leptin concentrations in serum
samples obtained after overnight fast (43,62,64–66). Initial findings in individuals
who have achieved sustained recovery from BN, when compared to controls
with closely matched percent body fat, suggest that serum leptin levels remain
decreased. This finding may be related to evidence for a persistent decrease in
activity in the hypothalamic-pituitary-thyroid axis in long-term recovered BN
individuals. These alterations could be associated with decreased metabolic rate
and a tendency to weight gain, contributing to the preoccupation with body
weight characteristic of BN.
Ghrelin
Ghrelin was originally discovered in the rat and the human stomach, and
stimulates GH secretion in rodents. This petide that antagonizes leptin action has
a role in the regulation of feeding behavior and energy metabolism in the
CNS (67). Ghrelin-producing neurons are located in the hypothalamus,
whrereas ghrelin receptors are expressed in various regions of the brain.
Intracerebroventricular injections of ghrelin strongly stimulated feeding
in rats and increased body weight gain. In addition, it has been reported
that fasting plasma ghrelin concentrations in humans are negatively correlated
with BMI (68,69), percentage body fat and fasting leptin and insulin
concentrations (70), which have an important role in the pathophysiology of
AN (71). In the latter study it could be shown that ghrelin was elevated in AN
patients and returned to normal levels after weight recovery. The possibility of
ghrelin resistance in cachectic states as caused by eating disorders could
be suggested. Fasting plasma ghrelin concentrations in patients with BN were
significantly higher than those in controls (69), although the BMIs between
bulimics and controls were not significantly different, suggesting that not only
290 BAILER AND KAYE
BMI, but also abnormal eating behavior with bingeing and purging, had an
influence on circulating ghrelin level in BN patients.
Gastrin-Releasing Peptide
Human gastrin-releasing peptide (GRP) is a 27-amino-acid peptide that shares
similar decapeptide with bombesin (BBS) (72). Peripheral and central
administration of GRP attenuates food intake in mammals and humans (73,74).
In the CNS, distinct BBS-like receptor subtypes have been identified in brain
tissue such as the bed nucleus of the stria terminalis, the olfactory tubercle, the
putamen, and the neocortex, with a neuromedin B- and a GRPpreferring
subtype (75,76). Both subtypes have been implicated in the modulation of BBS-
like peptide-induced food suppression (77). CSF GRP was significantly lower in
recovered bulimic patients (>1 year, normal weight, and regular menstrual
cycles, no bingeing or purging) compared to normal controls and recovered
anorectic patients (78). Lower CSF GRP in this group could be a trait-related
disturbance that might add to hyperphagic behavior, and thus to the
pathophysiology of this illness.
REFERENCES
1. Pirke KM, Pahl J, Schweiger U. Metabolic and endocrine indices of starvation in
bulimia: a comparison with anorexia nervosa. Psychiatry Res 1985; 15:33–39.
2. Tomova A, Kumanov P, Kirilov G. Factors related to sex hormone binding
globulin concentrations in women with anorexia nervosa. Psychosom Med 1995;
40:499–506.
3. Gold PW, Gwirtsman H, Avgerinos PC, Nieman LK, Gallucci WT, Kaye W,
Jimerson D, Ebert M, Rittmaster R, Loriaux DL. Abnormal hypothalamicpituitary-
adrenal function in anorexia nervosa. Pathophysiologic mechanisms in underweight
and weight-corrected patients. N Engl J Med 1986; 314:1335–1342.
4. Fichter MM, Pirke KM, Pollinger J, et al. Disturbances in the
hypothalamopituitary-adrenal and other neuroendocrine axes in bulimia. Biol
Psychiatry 1990; 27:1021–1037.
5. Yanovski SZ, Yanovski JA, Gwirtsman HE, Bernat A, Gold PG, Chrousos GP.
Normal dexamethasone suppression in obese binge and nonbinge eaters with rapid
weight loss. J Clin Endocrinol Metab 1993; 76:675–679.
6. Yanovski SZ. Biological correlates of binge eating. Addict Behav 1995; 20:
705–712.
7. Adami GF, Gandolfo P, Campostano A, Cocchi F, Bauer B, Scopinaro N. Obese
binge eaters: metabolic characteristics, energy expenditure, and dieting. Psychol
Med 1995; 25:195–198.
8. Wartofsky L, Burman KD. Alterations in throid function in patients with systemic
illness: the “euthyroid sick syndrome.” Endocr Rev 1982; 3:164–217.
9. Altemus M, Hetherington M, Kennedy B, et al. Thyroid function in bulimia
nervosa. Psychoneuroendocrinology 1996; 21:249–261.
10. Lesem MD, Kaye WH, Bissette G, et al. Cerebrospinal fluid TRH
immunoreactivity in anorexia nervosa. Biol Psychiatry 1994; 35:48–53.
11. Devlin MJ, Walsh BT, Kral JG, et al. Metabolic abnormalities in bulimia nervosa.
Arch Gen Psychiatry 1990; 47:144–148.
12. Altemus M, Hetherington M, Flood M. Decrease in resting metabolic rate during
abstinence from bulimic behavior. Am J Psychiatry 1991; 148:1071–1072.
13. Spalter AR, Gwirtsman HE, Demitrack MA, et al. Throid function in bulimia
nervosa. Biol Psychiatry 1993; 33:408–414.
292 BAILER AND KAYE
14. Wadden TA, Foster GD, Letizia KA, Wilk JE. Metabolic, anthropometric, and
psychological characteristics of obese binge eaters. Int J Eat Disord 1993; 14:
127–135.
15. Morley JE, Bhmdell JE. The neurobiological basis of eating disorders: some
formulations. Biol Psychiatry 1988; 23:53–78.
16. Schwartz MW, Woods SC, Porte D Jr, Seeley RJ, Baskin DG. Central nervous
system control of food intake. Nature 2000; 404:661–671.
17. Jimerson DC, Wolfe BE, Naab S. In: Anorexia nervosa and bulimia nervosa. CE,
Brumback RA, eds. Textbook of Pediatric Neuropsychiatry Coffee Washington,
DC: American Psychiatric Press, 1998:563–578.
18. Stoving RK, Hangaard J, Hansen-Nord M, Hagen C. A review of endocrine
changes in anorexia nervosa. J Psychiatr Res 1999; 33:139–152.
19. Kaye WH, Gwirtsman HE, George DT, Ebert MH, Jimerson DC, Tomai TP,
Chrousos GP, Gold PW. Elevated cerebrospinal fluid levels of immunoreactive
corticotropin-releasing hormone in anorexia nervosa: relation to state of nutrition,
adrenal function, and intensity of depression. J Clin Endocrinol Metab 1987; 64:
203–208.
20. Walsh BT, Roose SP, Katz JL, Dyrenfurth I, Wright L, Vande Wiele R, Glassman
AH. Hypothalamic-pituitary-adrenal-cortical activity in anorexia nervosa and
bulimia. Psychoneuroendocrinology 1987; 12:131–140.
21. Licinio J, Wong ML, Gold PW. The hypothalamic-pituitary-adrenal axis in
anorexia nervosa. Psychiatry Res 1996; 62:75–83.
22. Glowa JR, Gold PW. Corticotropin releasing hormone produces profound
anorexigenic effects in the rhesus monkey. Neuropeptides 1991; 18:55–61.
23. Rivier C, Vale W. Influence of corticotropin releasing factor on reproductive
functions in the rat. Endocrinology 1984; 114:914–921.
24. Sirinathsinghji DJ, Rees LH, Rivier J. Corticotropin-releasing factor is a potent
inhibitor of sexual receptivity in the female rat. Nature 1983; 305:232–235.
25. Sutton RE, Koob GF, LeMoal M. Corticotropin-releasing factor produces
behavioral activation in rats. Nature 1982; 297:331–333.
26. Morley JE, Levine AS, Gosnell BA, Mitchell JE, Krahn DD, Nizielski SE. Peptides
and feeding. Peptides 1985; 6:181–192.
27. Kaye WH, Berrettini WH, Gwirtsman HE, Chretien M, Gold PW, George DT,
Jimerson DC, Ebert MH. Reduced cerebrospinal fluid levels of immunoreactive
pro-opiomelanocortin related peptides (including beta-endorphin) in anorexia
nervosa. Biol Psychiatry 1987; 41:2147–2155.
28. Lesem MD, Berrettini W, Kaye WH, Jimerson DC. Measurement of CSF
dynorphin A 1–8 immunoreactivity in anorexia nervosa and normal-weight bulimia.
Biol Psychiatry 1991; 29:244–252.
29. Brewerton TD, Lydiard RB, Laraia MT, Shook JE, Ballenger JC. CSF
betaendorphin and dynorphin in bulimia nervosa. Am J Psychiatry 1992; 149:
1086–1090.
NEUROENDOCRINE AND NEUROPEPTIDE DYSREGULATION 293
46. Phillipp E, Pirke KM, Kellner MB, Krieg JC. Disturbed cholecystokinin secretion
in patients with eating disorders. Life Sci 1991; 48:2443–2450.
47. Pirke KM, Kellner MB, Friess E, Krieg JC, Fichter MM. Satiety and
cholecystokinin. Int J Eat Disord 1994; 15:63–69.
48. Devlin MJ, Walsh BT, Guss JL, Kissileff HR, Liddle RA, Petkova E. Post prandial
cholecystokinin release and gastric emptying in patients with bulimia nervosa. Am J
Clin Nutr 1997; 65:114–120.
49. Lydiard RB, Brewerton TD, Fossey MD, Laraia MT, Stuart G, Beinfeld MC,
Ballenger JC. CSF cholecystokinin octapeptide in patients with bulimia nervosa and
in normal comparison subjects. Am J Psychiatry 1993; 150:1099–1101.
50. Tamai H, Takemura J, Kobayashi N, Matsubayashi S, Matsukura S, Nakagawa T.
Changes in plasma cholecystokinin concentrations after oral glucose tolerance test
in anorexia nervosa before and after therapy. Metab Clin Exp 1993; 42:581–584.
51. Harty RF, Pearson PH, Solomon TE, McGuigan JE. Cholecystokinin, vasoactive
intestinal peptide and peptide histidine methionine responses to feeding in anorexia
nervosa. Regul Peptides 1991; 36:141–150.
52. Geracioti TD Jr, Liddle RA, Altemus M, Demitrack MA, Gold PW. Regulation of
appetite and cholecystokinin secretion in anorexia nervosa. Am J Psychiatry 1992;
149:958–961.
53. Baranowska B, Radzikowska M, Wasilewska-Dziubinska E, Roguski K, Borowiec
M. Disturbed release of gastrointestinal peptides in anorexia nervosa and in
obesity. Diabetes Obes Metab 2000; 2:99–103.
54. Geliebter A, Melton PM, McCray RS, Gallagher DR, Gage D, Hashim SA. Gastric
capacity, gastric emptying, and test-meal intake in normal and bulimic women. Am
J Clin Nutr 1992; 56:656–661.
55. Considine RV, Considine EL, Williams CJ, Hyde TM, Caro JF. The hypothalamic
leptin receptor in humans: identification of incidental sequence polymorphisms and
absence of the db/db mouse and fa/fa rat mutations. Diabetes 1996; 45:992–994.
56. Schwartz MW, Peskind E, Raskind M, Boyko EJ, Porte D Jr. Cerebrospinal fluid
leptin levels: relationship to plasma levels and to adiposity in humans. Nature Med
1996; 2:589–593.
57. Farooqi IS, Keogh JM, Kamath S, Jones S, Gibson WT, Trussell R, Jebb SA, Lip
GY, O’Rahilly S. Partial leptin deficiency and human adiposity. Nature 2001; 414:
34–35.
58. Hebebrand J, van der Heyden J, Devos R, Kopp W, Herpertz S, Remschmidt H,
Herzog W. Plasma concentrations of obese protein in anorexia nervosa. Lancet
1995; 346:1624–1625.
59. Grinspoon S, Gulick T, Askari H, Landt M, Lee K, Anderson E, Ma Z, Vignati L,
Bowsher R, Herzog D, Klibanski A. Serum leptin levels in women with anorexia
nervosa. J Clin Endocrinol Metab 1996; 81:3861–3863.
60. Mantzoros C, Flier JS, Lesem MD, Brewerton TD, Jimerson DC. Cerebrospinal
fluid leptin in anorexia nervosa: correlation with nutritional status and potential
role in resistance to weight gain. J Clin Endocrinol Metab 1997; 82: 1845–1851.
NEUROENDOCRINE AND NEUROPEPTIDE DYSREGULATION 295
61. Eckert ED, Pomeroy C, Raymond N, Kohler PF, Thuras P, Bowers CY. Leptin in
anorexia nervosa. J Clin Endocrinol Metab 1998; 83:791–795.
62. Frederich R, Hu S, Raymond N, Pomeroy C. Leptin in anorexia nervosa and bulimia
nervosa: importance of assay technique and method of interpretation. J Lab Clin
Med 2002; 139:72–79.
63. Jimerson DC. Leptin and the neurobiology of eating disorders. J Lab Clin Med
2002; 139:70–71.
64. Brewerton TD, Lesem MD, Kennedy A, Garvey WT. Reduced plasma leptin
concentration in bulimia nervosa. Psychoneuroendocrinology 2000; 25:649–658.
65. Jimerson DC, Mantzoros C, Wolfe BE, Metzger ED. Decreased serum leptin in
bulimia nervosa. J Clin Endocrinol Metab 2000; 85:4511–4514.
66. Monteleone P, Bortolotti F, Fabrazzo M, La Rocca A, Fuschino A, Maj M. Plasma
leptin response to acute fasting and refeeding in untreated women with bulimia
nervosa. J Clin Endocrinol Metab 2000; 85:2499–2503.
67. Nakazato M, Murakami N, Date Y, Kojima M, Matsuo H, Kangawa K, Matsukura
S. A role for ghrelin in the central regultion of feeding. Nature 2001; 409:
194–198.
68. Shiiya T, Nakazato M, Mizuta M, Date Y, Mondal MS, Tanaka M, Nozoe S,
Hosoda H, Kangawa K, Matsukura S. Plasma ghrelin levels in lean and obese
humans and the effect of glucose on ghrelin secretion. J Endocrinol Metab 2002;
87:240–244.
69. Tanaka M, Naruo T, Muranaga T, Yasuhara D, Shiiya T, Nakazato M, Matsukura S,
Nozoe S. Increased fasting plasma ghrelin levels in patients with bulimia nervosa.
Eur J Endocrinol 2002; 146:R1-R3.
70. Tschop M, Weyer C, Tataranni AP, Devanarayan V, Ravussin B, Heiman ML.
Circulating ghrelin levels are decreased in human obesity. Diabetes 2001; 50:
707–709.
71. Otto B, Cuntz U, Fruehauf E, Wawarta R, Folwaczny C, Riepl RL, Heiman ML,
Lehnert P, Fichter M, Tschöp M. Weight gain decrease elevated plasma ghrelin
concentrations of patients with anorexia nervosa. Eur J Endocrinol 2001; 145:
669–673.
72. Brown M, Marki W, Rivier J. Is gastrin releasing peptide mammalian bombesin?
LifeSci 1980; 27:125–128.
73. Bray GA. Nutrient intake is modulated by peripheral petide aministration. Obesity
Res 1995; 3(Suppl. 4):569S-572S.
74. Flynn FW. Bombesin-like peptides in the reglation of ingestive behavior. Ann NY
Acad Sci 1994; 739:120–134.
75. Ladenheim EE, Jensen RT, Mantey SA, Moran TH. Distinct distributions of two
bombesin receptor subtypes in the rat central nervous system. Brain Res 1992; 593:
168–178.
76. Wolf SS, Moody TW. Receptors for GRP/bombesin-like peptides in the rat
forebrain. Peptides 1985; 6(Suppl. 1):111–114.
296 BAILER AND KAYE
77. Ladenheim EE, Wirth KE, Moran TH. Receptor subtype mediation of feeding
suppression by bombesin-like peptides. Pharmacol Biochem Behav 1996; 54:
705–711.
78. Frank GK, Kaye WH, Ladenheim EE, McConaha C. Reduced gastrin releasing
peptide in cerebrospinal fluid after recovery from bulimia nervosa. Appetite 2001;
37:9–14.
13
Neuroimaging of the Eating Disorders
Janet Treasure
Thomas Guy House
London, England
Rudolf Uher
Institute of Psychiatry
London, England
It has been an unfortunate fact that eating disorders are all too often dismissed as
trivial complaints of spoilt princesses who are merely being stubborn and
willful. However, it will be difficult to continue to hold such a position in the
face of the evidence that is coming from research into brain imaging. Pictures
can be worth a thousand words, and the brain images, which show both
structural and functional brain changes, cannot be easily dismissed. Food
provokes a unique pattern of brain activation in people with eating disorders.
Moreover, food-induced activation of the orbitofrontal cortex continues after
recovery. Also structural abnormalities persist after recovery. Are these effects
scars from the illness or markers of a neurodevelopmental diathesis? The
answers may have implications for clinical evaluation, diagnostics, treatment,
and outcome. We therefore argue that brain imaging is not just an interesting
application of modern technology but an essential and exciting tool that can be
used to clarify the confusing tapestry of eating disorders.
Interest in imaging applied to eating disorders began with the increased
resolution offered by computed tomography (CT). This revealed that the brain,
in parallel with all other organs of the body, was shrunken especially in AN.
However, this was somewhat dismissed as a nonspecific side effect of starvation
and added to the list of numerous clinical consequences. However, the second
phase of this research, which relates to brain function, can be and has been
hypothesis driven. We predict that this may have a more profound effect on
thinking in the field.
For example, the level of resolution and the balance between cost, utility, and
acceptability varies among the different technologies. Functional magnetic
resonance scanning has the best resolution and does not involve injections of
radioactive substances; however, the design at the moment is limited to rapid
changes in blood flow. The other two technologies allow for investigation into
the chemistry of the brain but the time course and resolution are slower. Each of
the technologies is best suited to answering different questions, and there can be
useful synergy between the approaches.
Scanning experiments have to be carefully designed. They are expensive and
can be difficult to interpret. The experimental conditions (both internal and
external) need to be clearly defined. For example, if food is used as the
paradigm under investigation it is important to control for metabolic factors
such as time since the last meal. In earlier studies, all patients with an eating
disorder (anorexia nervosa or bulimia) were analyzed as a group with no attempt
to subcategorize according to eating behaviors. However, bingeing/disinhibited
eating appears to be associated with a distinct pattern of brain activation to food
whereas weight causes less of a differential response. Thus, the
subcategorization as defined in DSM-IV has some utility.
As in all aspects of science it helps to have a clear, specific hypothesis. Here
we have an advantage over those working in different fields of psychopathology
as the brain physiology and biochemistry of appetite control has been clearly
defined in animal models. Furthermore, it has been possible to develop this
research further in man. Thus, it is possible to develop testable hypotheses in
relationship to food, drawing from this body of research.
The statistical techniques used to analyze clusters of activation are complex,
but in the end all methods need to follow the basic principles of eliminating type
1 and 2 errors and adjusting for multiple testing. Unfortunately, in many
scanning studies, especially those in the first wave, these principles were
neglected. However, in later studies the statistical methods are more robust.
In this chapter we have focused on those studies that are of higher quality in
terms of all the features outlined above. However, as this is a new line of
investigation we have also included some studies, that would fail these quality
criteria but are important first steps into this area.
Anorexia Nervosa
Reduced total cerebral volume is a consistent finding in AN (5–9). The majority
of these studies were undertaken before AN was subdivided into the restricting
and the binge-purge subtypes, and often the generic term “eating disorders” was
used so it is not easy to relate anatomical changes to symptoms. The greater the
absolute weight loss and the faster the rate of weight loss, the smaller the brain
volume. Two small longitudinal studies examined the structural changes in the
brain of adolescents after full weight gain (10,11). Both found persistent deficits
in gray matter (cell bodies of neurons and glial cells), although there was
recovery of white matter (mainly myelinated axons). This supports the finding
of gray matter deficits in people who have made a full recovery from their
eating disorder (12). One postmortem study reported that there was a
reduction in basal dendritic fields and dendritic spine density (13). Similar
findings have been reported in schizophrenia and mood disorders where these
changes are most apparent in those with a positive family history (14).
300 TREASURE AND UHER
Bulimia Nervosa
The cerebral sulci are also widened in BN although the cerebral ventricles are
normal in size as are the thalamus and midbrain areas (17–19). One magnetic
resonance imaging (MRI) study found that the inferior frontal lobe cortex was
reduced in size (18). To our knowledge there are no data on brain structure in
binge eating disorder.
Brain Biochemistry
Brain biochemistry assessed using proton magnetic resonance spectroscopy is
perturbed in people with eating disorders. For example, lipid signals in the
frontal lobe were reduced to half of those seen in the normal population (20).
Lipid levels correlated with body mass index.
Animal Models
The control of food intake is of central importance to all living beings and
requires a complex integration between the individual and the environment.
The central information processing pathways for food stimuli in the visual,
olfactory, and gustatory modalities in the primate brain have been studied in
depth. Rolls (30,31) has summarized the findings from his meticulous series of
experiments involving electrophysiological recording from individual neu rons.
The initial processing of food stimuli occurs in the inferior temporal visual
cortex (visual), olfactory bulb and piriform cortex (smell), and nucleus of the
solitary tract, thalamus, and insula (taste). These areas project to the amygdala,
orbitofrontal cortex, lateral hypothalamus, and striatum where the reward value
of the stimuli is calibrated (Fig. 1).
302 TREASURE AND UHER
Food
Extrinsic food cues in a variety of sensory modalities lead to brain activation.
Visual images of food contrasted with nonfood produced changes in activation in
the left temperoinsular cortical region. The level of activation correlated with
the subjective rating of hunger (34,35). Taste and olfactory stimuli activated the
orbitofrontal cortex (36).
FIGURE 2 Areas of the brain activated in states of hunger (the orexogenic network).
The vertical lines are areas activated by hunger only and the crosshatched areas are those
activated by both hunger and satiety.
FIGURE 3 Areas of the brain activated by satiation (the anorexogenic network). The
horizontal lines are areas activated by hunger only and the cross-hatched areas are those
activated by both hunger and satiety.
306 TREASURE AND UHER
Brain regions: MO-PFC, medial and orbital prefrontal cortex; ACC, anterior cingulate
cortex; PCC, posterior cingulate cortex; L-PFC, lateral prefrontal cortex; IPL, inferior
parietal lobule; cerebell, cerebellum. ↑ significantly more active than in controls; ↓
significantly less active than in controls.
NEUROTRANSMISSION
Neuroimaging techniques have recently been used to examine the
neuropharmacology of eating disorders. The monoamines dopamine and
serotonin have an important role in feeding behavior in animals and humans.
Dopamine is linked to reward and it may modulate the hedonic response to
food. Serotonin inhibits feeding. The serotonin hypothesis of eating disorders
has as its essence the idea that abnormal 5-HT function may be a trait
vulnerability for eating disorders.
FIGURE 4 Areas of the brain activated by visual food stimuli in people with eating
disorders. It is based on functional fMRI studies (56, 57).
NEUROIMAGING OF THE EATING DISORDERS 309
310 TREASURE AND UHER
People with bulimia nervosa were found to have a 17% reduction in the
levels of serotonin transporter in the hypothalamus and thalamus and a 15%
reduction in levels of dopamine transporter in the striatum (60). A reduction in
serotonin transporter was also found in obese binge eaters (61).
In people with obesity an inverse relationship was found between BMI and
striatal dopamine receptor availability. Thus, this preliminary evidence suggests
that abnormal monamine systems may be associated with disinhibited eating.
The serotonin theory has also been tested by examining 5-HT receptor levels
in people who have recovered from an eating disorder. Reduced levels of
5-HT2A binding were found in the mesial temporal cortex (including the
amygdala and hippocampus) and to a lesser degree in the cingulate of women
with a history of restricting AN (62). The mechanism underlying this
phenomenon is unknown. The reduced receptor binding may be a process
compensating for increased extracellular 5-HT. (Earlier research had indeed
found increased 5-HT in the CSF of people who had recovered from AN; 63).
A similar study was undertaken with a smaller group of patients who had
recovered from BN. These people had reduced 5-HT2A in the lateral and
medial orbitofrontal cortex (64). Furthermore, this group of patients did not
have the expected age-related decline in 5-HT2A receptors. In conclusion,
abnormal levels of 5-HT2A receptor are found in various sites of the orexogenic
network after recovery from an eating disorder.
CONCLUSION
The information produced by brain scanning has implications for models used in
attempts to explain the etiology and maintenance of eating disorders. The
findings are consistent with a neurodevelopmental etiologic process. However,
there is also substantial evidence to suggest that many of the changes represent
acquired damage. Eating disorders occur at a critical time of brain development,
and toxic effects from malnutrition or stress may cause atrophic or dystrophic
changes. There is no doubt that these studies have generated many new ideas
about symptoms, causes, and consequences of eating disorders, and further
research linking genetics, precise definitions of the phenotypes of eating
314 TREASURE AND UHER
disorders, and scanning has great potential to increase our knowledge about
these confusing conditions.
SUMMARY
ACKNOWLEDGMENTS
This study was supported by grant QLKl-1999–916 from the
European Commission Framework V program http://www.cordis.lu/life/
home.html), the Nina Jackson Eating Disorders Research Charity, and a
Wellcome Trust Travelling Fellowship for Dr. R.Uher.
REFERENCES
1. Durston S, Hulshoff Pol HE, Casey BJ, Giedd JN, Buitelaar JK, van Engeland H.
Anatomical MRI of the developing human brain: what have we learned? J Am Acad
Child Adol Psychiatry 2001; 40(9): 1012–1020.
2. Huttenlocher PR. Synaptic density in human frontal cortex: developmental changes
and the effects of aging. Brain Res 1979; 163(2): 195–205.
3. McGivern R, Andersen J, Byrd D, Mutter K, Reilly J. Cognitive efficiency on a
match to sample task decreases at the onset of puberty in children. Brain Cogn
2002; 50(1):73.
4. Casey BJ, Trainor R, Giedd J, Vauss Y, Vaituzis CK, Hamburger S, et al. The role
of the anterior cingulate in automatic and controlled processes: a developmental
neuroanatomical study. Dev Psychobiol 1997; 30(l):61–69.
5. Dolan RJ, Mitchell J, Wakeling A. Structural brain changes in patients with
anorexia nervosa. Psychol Med 1988; 18(2):349–353.
6. Kohn MR, Ashtari M, Golden NH, Schebendach J, Patel M, Jacobson MS, et al.
Structural brain changes and malnutrition in anorexia nervosa. Ann N Y Acad Sci
1997; 817:398–399.
7. Kingston K, Szmukler G, Andrewes D, Tress B, Desmond P. Neuropsychological
and structural brain changes in anorexia nervosa before and after refeeding. Psychol
Med 1996; 26(l):15–28.
8. Krieg JC, Pirke KM, Lauer C, Backmund H. Endocrine, metabolic, and cranial
computed tomographic findings in anorexia nervosa. Biol Psychiatry 1988; 23(4):
377–387.
9. Swayze VW, Andersen A, Arndt S, Rajarethinam R, Fleming F, Sato Y, et al.
Reversibility of brain tissue loss in anorexia nervosa assessed with a computerized
Talairach 3-D proportional grid. Psychol Med 1996; 26(2):381–390.
10. Katzman DK, Lambe EK, Mikulis DJ, Ridgley JN, Goldbloom DS, Zipursky RB.
Cerebral gray matter and white matter volume deficits in adolescent girls with
anorexia nervosa. J Pediatr 1996; 129(6):794–803.
11. Golden NH, Ashtari M, Kohn MR, Patel M, Jacobson MS, Fletcher A, et al.
Reversibility of cerebral ventricular enlargement in anorexia nervosa,
316 TREASURE AND UHER
42. Del Parigi A, Chen K, Gautier JF, Salbe AD, Pratley RE, Ravussin E, et al. Sex
differences in the human brain’s response to hunger and satiation. Am J Clin Nutr
2002; 75(6):1017–1022.
43. Small DM, Zatorre RJ, Dagher A, Evans AC, Jones-Gotman M. Changes in brain
activity related to eating chocolate: from pleasure to aversion. Brain 2001; 124;
(Pt9):1720–1733.
44. Gautier JF, Chen K, Uecker A, Bandy D, Frost J, Salbe AD, et al. Regions of the
human brain affected during a liquid-meal taste perception in the fasting state: a
positron emission tomography study. Am J Clin Nutr 1999; 70(5):806–810.
45. Raynor HA, Epstein LH. Dietary variety, energy regulation, and obesity. Psychol
Bull 2001; 127(3):325–341.
46. O’Doherty J, Rolls ET, Francis S, Bowtell R, McGlone F, Kobal G, et al. Sensory-
specific satiety-related olfactory activation of the human orbitofrontal cortex.
Neuroreport 2000; ll(4):893–897.
47. Katzman DK, Lambe EK, Mikulis DJ, Ridgley JN, Goldbloom DS, Zipursky RB.
Cerebral gray matter and white matter volume deficits in adolescent girls with
anorexia nervosa [see comments]. J Pediatr 1996; 129(6):794–803.
48. Kingston K, Szmukler G, Andrewes D, Tress B, Desmond P. Neuropsychological
and structural brain changes in anorexia nervosa before and after refeeding. Psychol
Med 1996; 26(l):15–28.
49. Nozoe S, Naruo T, Nakabeppu Y, Soejima Y, Nakajo M, Tanaka H. Changes in
regional cerebral blood flow in patients with anorexia nervosa detected through
single photon emission tomography imaging. Biol Psychiatry 1993; 34(8):578–580.
50. Nozoe S, Naruo T, Yonekura R, Nakabeppu Y, Soejima Y, Nagai N, et al.
Comparison of regional cerebral blood flow in patients with eating disorders. Brain
Res Bull 1995; 36(3):251–255.
51. Naruo T, Nakabeppu Y, Sagiyama K, Munemoto T, Homan N, Deguchi D, et al.
Characteristic regional cerebral blood flow patterns in anorexia nervosa patients
with binge/purge behavior. Am J Psychiatry 2000; 157(9): 1520–1522.
52. Krieg JC, Lauer C, Leinsinger G, Pahl J, Schreiber W, Pirke KM, et al. Brain
morphology and regional cerebral blood flow in anorexia nervosa. Biol Psychiatry
1989; 25(8): 1041–1048.
53. Karhunen LJ, Vanninen EJ, Kuikka JT, Lappalainen RI, Tiihonen J, Uusitupa MI.
Regional cerebral blood flow during exposure to food in obese binge eating
women. Psychiatry Res 2000; 99(l):29–42.
54. Hirano H, Tomura N, Okane K, Watarai J, Tashiro T. Changes in cerebral blood
flow in bulimia nervosa. J Comput Assist Tomogr 1999; 23(2):280–282.
55. Ellison Z, Foong J, Howard R, Bullmore E, Williams S, Treasure J. Functional
anatomy of calorie fear in anorexia nervosa. Lancet 1998; 352(9135):! 192.
56. Uher R, Murphy T, Brammer M, Dalgleish T, Phillips M, Ng V, et al. Functional
neural correlates of eating disorders, personal communication, 2002
57. Uher R. Recovery and chronicity in anorexia nervosa: brain activity associated with
differential outcomes. Biol Psychiatry. (In press).
58. Damasio AR. How the brain creates the mind. Sci Am 1999; 281(6):112–117.
NEUROIMAGING OF THE EATING DISORDERS 319
59. Seeger G, Braus DF, Ruf M, Goldberger U, Schmidt MH. Body image distortion
reveals amygdala activation in patients with anorexia nervosa—a functional
magnetic resonance imaging study. Neurosci Lett 2002; 326(l):25–28.
60. Tauscher J, Pirker W, Willeit M, de Zwaan M, Bailer U, Neumeister A, et al.
[1231] Beta-CIT and single photon emission computed tomography reveal reduced
brain serotonin transporter availability in bulimia nervosa. Biol Psychiatry 2001; 49
(4):326–332.
61. Kuikka JT, Tammela L, Karhunen L, Rissanen A, Bergstrom KA, Naukkarinen H,
et al. Reduced serotonin transporter binding in binge eating women.
Psychopharmacology (Berl) 2001; 155(3):310–314.
62. Frank GK, Kaye WH, Meltzer CC, Price JC, Greer P, McConaha C, et al.
Reduced 5-HT2A receptor binding after recovery from anorexia nervosa. Biol
Psychiatry 2002; 52(9):896–906.
63. Kaye WH, Gwirtsman HE, George DT, Ebert MH. Altered serotonin activity in
anorexia nervosa after long-term weight restoration. Does elevated
cerebrospinal fluid 5-hydroxyindoleacetic acid level correlate with rigid and
obsessive behavior? Arch Gen Psychiatry 1991; 48(6):556–562.
64. Kaye WH, Frank GK, Meltzer CC, Price JC, McConaha CW, Crossan PJ, et al.
Altered serotonin 2A receptor activity in women who have recovered from bulimia
nervosa. Am J Psychiatry 2001; 158(7): 1152–1155.
65. Joseph R. Frontal lobe psychopathology: mania, depression, confabulation,
catatonia, perseveration, obsessive compulsions, and schizophrenia. Psychiatry
1999; 62(2): 138–172.
66. Cloninger RC. Functional neuroanatomy and brain imaging of personality and its
disorders. In: D’haenen H, den Boer JA, Willner P, eds. Biological Psychiatry.
Chichester: John Wiley & Sons Ltd, 2002:1377–1385.
67. Damasio AR. The somatic marker hypothesis and the possible functions of the
prefrontal cortex. Philos Trans R Soc Lond B Biol Sci 1996; 351(1346):
1413–1420.
68. Hornak J, Rolls ET, Wade D. Face and voice expression identification in patients with
emotional and behavioural changes following ventral frontal lobe damage.
Neuropsychologia 1996; 34(4):247–261.
70. Rolls ET. The orbitofrontal cortex and reward. Cereb Cortex 2000; 10(3):
284–294.
71. Kucharska-Pietura K, Nikolaou V, Masiak M, Treasure J. The recognition of
emotion in faces and voice in anorexia nervosa. Int J Eat Disord. In press.
72. Troop NA, Schmidt UH, Treasure JL. Feelings and fantasy in eating disorders: a
factor analysis of the Toronto Alexithymia Scale. Int J Eat Disord 1995; 18(2):
151–157.
73. Cochrane CE, Brewerton TD, Wilson DB, Hodges EL. Alexithymia in the eating
disorders. Int J Eat Disord 1993; 14(2):219–222.
74. Bruch H. Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within.
New York: Basic Books, 1973.
320 TREASURE AND UHER
* Current affiliation: University of Medicine and Dentistry of New Jersey, New Jersey
Medical School, Newark, New Jersey, U.S.A.
324 GRICE
GENETICS
Genetic study of disease yields evidence about the transmission and underlying
biology of the illness, two important factors related to treatment and
prevention. Psychiatric genetics is a very young field and thus far genes for
psychiatric disorders have been difficult to isolate. Eating disorders are complex
disorders, as are most psychiatric diagnoses. Genetic, biological,
developmental, and sociocultural forces contribute to vulnerabilities to and
etiologies of these disorders. These various influences are thought to have direct
and indirect effects, including synergistic influences, on the onset and
continuation of pathological eating disorders. Although clinical descriptions of
anorexic syndromes can be found in the literature dating back to the early
1870s (10,11), it is only in the past few decades that the genetic basis of eating
disorders has come to be appreciated and examined.
Understanding the genetic contributors to eating disorders presents
particular challenges. For example, there are strong social and cultural
presentations of ideal body weight and shape that influence an individual’s self-
perception of body size, in addition to any existing inherent genetic
vulnerabilities in this regard. Inheritance patterns of eating disorders in families,
useful in performing some genetic analyses, are often unclear and do not follow
traditional mendelian patterns. The often secretive and isolated nature of
pathological behaviors associated with eating disorders, particularly when
affected individuals display a normal or near-normal body mass index (BMI),
may compound the difficulty in identifying clinical cases and family patterns of
affectedness. These features, compounded by variability in clinical expression,
MOLECULAR BIOLOGY 325
can obscure phenotype classification. Lastly, from the clinical perspective there
is a spectrum of eating disorder diagnoses and pathology. AN and BN are
considered the most severe eating disorder diagnoses, each with diagnostic
subtypes; however, there is a residual category in DSM-IV that identifies eating
disorders not otherwise specified (ED-NOS), including subthreshold AN, BN,
and BED. Beyond DSM-IV diagnostic categories, many other pathological eating
behaviors and attitudes are associated with disruptions in psychological and/or
physical health, although the specific genetic factors that may contribute to these
states are largely unexamined (12).
GENETIC METHODS
Traditional methods of determining the role of genetic factors in the etiology of
a given disorder are twin, family, and adoption studies. Heritability (the
proportion of the population variance of a trait that can be explained by genetic
transmission) can be estimated from these types of studies. Once heritability is
established for a given disorder, genetic linkage analysis, association studies, and
candidate gene surveys are used to search for genes that underlie a particular
disorder. The bases for sound genetic studies include homogeneous phenotype
classification, unbiased ascertainment of index patients (probands), and accurate
clinical assessments. As discussed above, accurate assessment and definition of
AN and BN phenotypes requires particular attention. Study design should also
include appropriate ascertainment strategies to identify probands and families
and mimimize ascertainment bias (e.g., epidemiological studies or, lacking that,
multiple recruitment strategies to minimize ascertainment influence from a
single referral source) and to gather sufficient numbers of subjects for sound
statistical analysis. In addition to defined homogeneous phenotypes, it is also
important that the specific clinical assessment of study subjects be free from
inadvertent bias, such as can occur when subjects are assessed by multiple
researchers or phenotyped without structured criteria.
IDENTIFYING GENES
Several genetic analysis methods have been used to search for susceptibility
genes for eating disorders. Genetic association analyses, including casecontrol
studies, of candidate genes can identify gene variants that are statistically
associated with illness by comparing allele frequencies of presumably
biologically relevant genes in affected individuals (cases) and control individuals.
In a case-control study, when the allele frequencies of affected individuals are
compared to those of nonfamily controls, the control population should be
carefully selected since there are natural variations in gene frequencies that occur
326 GRICE
trait (14)], additional markers are used to narrow the region of interest and
positional cloning is used to identify genes for further study.
In each of these molecular genetic approaches, proband and family
assessments for phenotypical classification must be rigorous and controlled,
using instruments with good reliability and validity. Confidentiality must be
scrupulously guarded, both between family members and in general, with
adequate precautions taken to blind data and ensure protection of subjects’
privacy. The importance of control group selection is discussed above. Also
central to study integrity is sample size. Current hypotheses suggest that as
complex traits many psychiatric disorders are caused by several to many
susceptibility genes, each of small to modest effect, that likely interact to render
susceptibility to the disorder. Since this genetic susceptibility is parsed over
several to many genetic loci, large study populations are needed to generate
sufficient power to detect these genes (15,16). In uncommon disorders such as
eating disorders, large sample sizes are very difficult to achieve such that
multiple collaborative sites are necessary to generate a sufficient patient
population for genetic studies.
5-HT2A Subclass
The 5-HT2 receptor class is composed of the 5-HT2A, 5-HT2B, and 5-HT2C
receptors. These receptors demonstrate 46–50% sequence homology and have
been mapped to chromosome 13ql4-q21, 2q36.3–37.1, and Xq24,
respectively. The 5-HT2A receptor is expressed in many peripheral and central
tissues. In the central nervous system, the cortex, basal ganglia, and claustrum
are primary sights for 5-HT2A expression. In genetic studies of eating disorders,
the 5-HT2A receptor is the most extensively studied serotonin-related gene.
Several polymorphisms have been reported in the 5-HT2A receptor gene. The
variant that has received the most attention is a polymorphism in the promoter
(regulatory) region of the gene in which there is an A or G at nucleotide–1438.
A series of association studies (both population based using obese,
underweight, normal-weight, and non-psychiatrically ill controls, and family
based using the TDT) have examined the serotonin receptor 5-HT2A promoter
polymorphism—1438A/G. Five studies have found a positive association
between the 5-HT2A -1438A allele and eating disorders (18–22). The two
studies that focused solely on AN phenotypes found evidence for a positive
association between the—1438A allele and AN (all subtypes) (18,19) and/or
the AN restricting subtype (19). Three studies examined a broader range of
asdsadasd
TABLE 1 Association Studies (Population-Based and Family-Based) of Eating Disorders and the 5-HT2A Promoter Polymorphism -1438A/G
MOLECULAR BIOLOGY 329
330 GRICE
*,** Denotes comparison groups that yielded a p value ≤ 0.05. NS, Nonsignificant; p > 0.05.
TABLE 2 Association Studies of Eating Disorders and Serotonin-Related Genes3
aStudies of the 5-HT2A -1438 A/G promoter polymorphism are summarized in Table 1.
*,**,*#,## Denotes comparison group that yielded a p value ≤ 0.05 and associated authorship. NS, Nonsignificant; p > 0.05.
MOLECULAR BIOLOGY 331
332 GRICE
(n>300) but found neither an association between AN and 5HT2A -1438A allele
nor evidence of an interaction of this allele with age of onset of AN or minimum
lifetime BMI (27). Although the sample size in this study is the largest to date,
we still do not know for sure if it generates sufficient power when the odds ratio
associated with the A allele is small. Of note, however, is a follow-up study
based in part on this sample that used a quantitative TDT approach to suggest
that the A allele may act as a modifying factor, delaying age of AN onset (32).
Thus, the definitive role of the 5-HT2A polymorphisms in eating disorders
remains unclear but of great interest. There are some very interesting findings
and leads to follow, particularly related to the AN restricting subtype and the
5-HT2A -1438A allele. We must await verification of these results, likely
through large-scale controlled studies, before firm conclusions can be drawn
about the ultimate relevance of the -5-HT2A gene to the genetics of eating
disorders.
5-HT2C Subclass
Similar to the 5-HT2A receptor, the 5-HT2C receptor has been implicated
in the regulation of feeding-related behaviors such as satiety and eating
continuity (33). Supportive evidence also comes from mouse models in which
transgenic mice lacking the 5-HT2C receptor demonstrate abnormal feeding
behavior (34). A small number of studies have examined allele frequencies of
the 5-HT2C Cys23Ser polymorphism in subjects with a range of eating disorder
phenotypes. Although no association was found between Cys23Ser variants and
DSM-IV diagnoses of AN (neither restricting nor purging subtypes) (21),
BN (21,35), or BED (35), there was a significant association between the Ser23
allele and a clinically defined group of underweight teenage girls (some of whom
met criteria for AN) (36). If confirmed these data suggest that 5-HT2C may be
involved in the regulation of food intake or proneness to weight loss rather than
an eating disorder diagnosis per se.
5-HT, Subclass
The 5-HTi receptor class comprises five receptor subtypes (5-HT1A, 5-HT1B,
5-HT1D, 5-HT1E and 5-HT1F), which share 40–63% sequence homology in
humans (17). The 5-HT1Dβ, receptor, also known as 5-HT1B, has been mapped
to chromosome 6ql3. 5-HT1Dβ is expressed in the central nervous
system, particularly in the basal ganglia, striatum, and frontal cortex, and is
thought to function as an autoreceptor as well as a heteroreceptor that effects
release of acetylcholine, glutamate, dopamine, noradrenaline, and
γ–aminobutyric acid (for review, see 37). Population-based studies of the
334 GRICE
5-HT1Dβ receptor gene have examined its possible role in both AN and BN. In a
study of AN individuals, the Phel24Cys variant was studied using obese and
underweight individuals as comparison but found no significant association (38).
A study of the 5-HT1BG681C polymorphism examined the distribution of
genotypes in women with BN (39). When the minimum and maximum lifetime
BMIs were compared across the three genotypic groups (G/G, G/C, and CC)
both the G/C and C/C genotypes were associated with lower minimum
lifetime BMIs (and unrelated to lifetime AN rates), perhaps suggesting a role for
5-HT1B in a subphenotype not defined by DSM-IV schemas.
5-HT7 Subclass
The 5-HT7 receptor is located on chromosome 10q23.3–24.4 and shows less
than 50% homology to other receptors in the 5-HT family. 5-HT7 receptors are
found in the limbic and thalamocortical brain regions, regions implicated in
central regulation of feeding behavior (40). These localizations, together with
evidence that atypical antipsychotics have a high affinity for 5-HT7 (41), make it
an attractive candidate gene for psychiatric disorders. However, the sole study
of the 5-HT7 receptor in eating disorders examined the Pro279Leu
polymorphism in AN subjects and found no significant association between
allele frequencies in AN compared to obese and underweight controls (38).
Serotonin Transporter
The serotonin transporter is an integral component in regulating serotonin
function in the central nervous system and is the site of action for the
serotonin reuptake inhibitors. A 44-base-pair insertion/deletion (5-HTTLPR)
polymorphism in the promoter region of the 5-HT transporter gene (5-HTT)
confers differential transcription rates on gene expression. The so-called short
variant of 5-HTTLPR (the deletion variant) is associated with significant
decreases in 5-HTT expression and 5-HT uptake (42), making 5-HTT a
candidate gene of great interest for many psychiatric disorders, including eating
disorders. Several groups have examined this variant, using populationbased
methods and a variety of control groups, and found conflicting results regarding
the role of 5-HTT in a range of eating disorders phenotypes. One positive
association was found between the 5-HTTLPR deletion (short) variant in AN
compared to obese and normal-weight controls (43). Three studies did not
support this finding (44–46), although one group found a positive association
MOLECULAR BIOLOGY 335
between this same variant and BN (46). Also of note is a positive association
between the 5-HTTLPR insertion (long) variant and abnormal eating
behaviors (defined by high scores on the Eating Attitudes Test) in nonclinical
subjects (47). Since these studies have not been replicated, as with other
candidate genes, we will have to await further research on 5HTTLPR to show
us how, if at all, this gene influences susceptibility to abnormal eating behaviors
or clinically defined eating disorder diagnoses.
Tryptophan Hydroxylase
Since tryptophan hydroxylase (TPH) is the rate-limiting enzyme in the serotonin
synthesis pathway it has been seen as a potential candidate gene in eating
disorders. TPH is mapped to chromosome 11p15.3-p14. In the one published
study on TPH and AN, there was no evidence for association (48).
Estrogen Receptors
There are two types of estrogen receptors: ER-α and ER-β mapped to
chromosomes 6q25.1 and 14q23.2, respectively. ERs belong to the nuclear
hormone receptor family and are found in brain areas involved in regulation of
sdgfsdfsdf
TABLE 3 Association Studies of Eating Disorders and Candidate Genes Displayed in Chronological Order3
336 GRICE
a Studies of the 5-HT A-1438 A/G promoter polymorphism and other serotonin-related genes are summarized in Table 1 and Table 2,
2
respectively.
b RFLP, restriction fragment length polymorphism.
c LEGLUR, leptin gene-linked upstream region.
d VNTR, variable number of tandem repeats.
e Microsatellite markers that flank the gene.
f hSKCa3, small-conductance calcium-activated potassium channel 3.
food intake (for review, see 64). Since high estrogen levels are known to inhibit
food intake (65) and in the brain, ERs colocalize with corticotropinreleasing
factor (CRF), it is theorized that interactions between estrogen and CRF may
modulate the hypothalamic-pituitary-adrenal axis and be involved in the
molecular basis of feeding, satiety, and, perhaps, eating disorders, especially
AN (66). Two studies have looked specifically at the association between ERs
and eating disorders (52,61). ER-(3 was screened for variations in subjects
with a range of weight extremes (extremely obese, AN, BN, healthy
underweight) (52). Although five different sequence variants were identified,
the association results were negative except for a suggestive association between
a G/A polymorphism at nucleotide 1082 and the AN phenotype. A second
study examined ER-α and ER-β in AN subjects (61). There were no significant
findings related to ER-α, but in ER-β the heterozygous genotype GA at
nucleotide 1082 was associated with AN.
Catechol-O-Methyltransferase
Catechol-O-methyltransferase (COMT) catalyzes the transfer of a methyl group
to catecholamines (dopamine, epinephrine, and norepinephrine) and is the major
degradative pathway of these neurotransmitters. COMT has been mapped to
chromosome 22q 11.21. In humans there is a functional polymorphism
(Val/Met 158) that determines high and low enzymatic activity. COMT has
been considered a candidate gene for several psychiatric disorders and associated
with positive findings in a subset of these studies (e.g., substance use disorders,
schizophrenia, attention deficit disorder). Relevant to this summary, the Val/
Met polymorphism was studied in a family-based association study and the high-
activity allele was significantly associated with AN, indicating a possible role in
eating disorders (58).
MOLECULAR BIOLOGY 339
hSKCa3
hSKCa3 is a small-conductance calcium-activated potassium channel involved in
regulating neural excitability. hSKCa3 has been mapped to chromosome 1q21.
In one model, small-conductance calcium-activated potassium channels
may contribute to the genetic susceptibility to bipolar disorder and
schizophrenia (71,72). To date, one study has examined hSKCa3 polymorphisms
in AN (60). Using a family-based association method, a positive association was
found, with longer alleles from the hSKCa3 gene found at higher rates in the AN
sample compared to controls.
340 GRICE
Norepinephrine Transporter
Norepinephrine transporter (NET) expression is regulated by norepinephrine;
thus, it has an important role in noradrenergic transmission. This system
regulates many neuroendocrine systems implicated in the pathophysiology of
eating disorders as well as anxiety disorders. In clinical research, reduced
noradrenergic activity is found in AN patients following normal-weight
restoration (73,74) although the mechanism underlying these findings are
unknown. Using a family-based association method, a polymorphic region in the
promoter of the NET gene was studied in the restricting subtype of AN (62). A
significant association was found between an insertion in this region and the
restricting AN subtype, suggesting that this NET gene variant, or a variant in
linkage disequilibrium with it, increases risk for restricting AN.
signal of 2.92 was found on chromosome 10p. A second peak in this same
region of 10p approached significance and a smaller suggestive linkage signal
was found on chromosome 14. The sample was then narrowed by selecting only
those families in which at last one other affected relative had regular vomiting
behavior (by design, the proband had already met this criteria). When this subset
of 133 families was studied, the initial linkage signal at chromosome 10p
increased to 3.39. This chromosomal region has been implicated in other
disorders, such as obesity, alcoholism, schizophrenia, and bipolar disorder,
perhaps reflecting that this region harbors a gene(s) that generically increases
susceptibility to a range of psychiatric and related disorders (as summarized
in (76)). It is also possible that a gene(s) in this region may specifically alter
susceptibility to BN and obesity, two disorders that may have overlapping
vulnerabilities and/or manifestations.
OBESITY
Compared to the genetic studies of DSM-IV-defined eating disorders, there are
a plethora of studies of human obesity. This intensity of research has identified
putative regions affecting obesity phenotypes on all chromosomes except
chromosome Y and with over 250 significant regions of interest in the genome
under study, a summary of which is beyond the scope of this chapter (for review,
see 77). Well over 150 studies covering approximately 60 candidate genes have
reported significant associations with obesity. Genome-wide linkage analyses of
obesity-related phenotypes have uncovered similar numbers of loci linked to
obesity indicators. As in eating disorders, a variety of phenotypes related to
obesity have been defined, including BMI, body fat mass, percentage of body
fat, fat-free mass, skinfolds, resting metabolic rates, and plasma leptin levels—
again indicating the importance of phenotypical definition beyond absolute
clinical categories. Relevant to this review of the genetics of eating disorders,
many of the genes discussed in this chapter also have been examined in obesity.
Significant findings in obesity genetics have been associated with serotonergic
genes (5-HTlB, 5-HT2C, 5HT2A), melanocortinergic genes (MC4-r, POMC,
NPY, AGRP), ER-α, UCP-2/UCP-3, and tumor necrosis factor-α. As research
continues to delve into the genetic basis of eating disorders we should expect to
see greater understanding of which pathways (e.g., those related to feeding
behavior, satiety, and/or energy metabolism) are affected in both obesity
disorders and eating disorders. Delineation of the specific genetic variations
associated with relevant phenotypes will allow us to discover if abnormal eating
behaviors can be seen as a spectrum of disorders ranging from obesity to
anorexia or if the genetic bases for these disorders are in fact distinct.
342 GRICE
SUMMARY
Although research in the genetics of obesity syndromes far outdistances research
in the genetics of eating disorders at this time, our knowledge and research in
AN and BN far exceeds that for other eating disorder syndromes or diagnoses.
It is apparent that AN and BN are heritable eating disorders that result from
complex interactions of genetic liabilities and environmental factors. The
positive case-control studies associated with several genes of interest (e.g., the
5-HT2A receptor, melanocortinergic system genes) have piqued interest in the
molecular genetic basis of eating disorders. Recent findings of significant linkage
peaks on chromosome 1p and 1q (related to an AN subtype) and on chromosome
10p (related to a BN subtype) have spurred the field forward with new
enthusiasm. Thus, many promising leads are emerging from genetic linkage
studies and candidate gene analyses; however, we must await further molecular
studies to confirm the specific genes that confer heritability to eating disorders.
Impediments to progress are due in part to the low population prevalence of eating
disorders and perhaps also the low rates of clinical identification of eating
disorder phenotypes, both of which make it very difficult to ascertain samples
sufficiently powerful to detect genes of less than major effect. In addition, it is
only in the past few years that molecular geneticists have had the means to examine
the human genome with the level of specificity and detail required for human
genetic studies. As a result of these technological and methodological advances,
the field of molecular genetics in eating disorders is growing rapidly. The large-
scale linkage studies of AN and BN and the larger TDT and association studies
are evidence of the more methodologically robust and controlled analyses that
have recently been undertaken. Collaborations such as these, combined with
ongoing developments in molecular genetic and genomic analytical tools, will
further strengthen genetically based studies and bring us closer still to the
identification of specific genes that confer susceptibility to eating disorders.
REFERENCES
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC, 1994:544–545.
2. Walters EE, Kendler KS. Anorexia nervosa and anorexic-like syndromes in a
population-based female twin sample. Am J Psychiatry 1995; 152:64–71.
3. Hoek HW, van Harten PN, van Hoeken D, Susser E. Lack of relation between
culture and anorexia nervosa-results of an incidence study on Curacao. N Engl J
Med 1998;338(17):1231–1232.
4. Timmerman MG, Wells LA, Chen SP. Bulimia nervosa and associated alcohol
abuse among secondary school students. J Am Acad Child Adol Psychiatry 1990; 29
(1):118–122.
MOLECULAR BIOLOGY 343
repeat: a candidate for schizophrenia and bipolar disorder? Mol Psychiatry 1998; 3:
32–37.
72. Dror V, Shamir E, Ghanshani S, Kimhi R, Swartz M, Barak Y, et al. hSKca3/
KCNN3 potassium channel gene: association of longer CAG repeats with
schizophrenia in Israeli Ashkenazai Jews, expression in human tissues and
localization to chromosome Iq21. Mol Psychiatry 1999; 4:254–260.
73. Kaye WH, Jimeson DC, Lake CR, Ebert MH. Altered norepinephrine metabolism
following long-term weight recovery in patients with anorexia nervosa. Psychiatry
Res 1985; 14:333–342.
74. Pirke KM, Kellner M, Phillip E, Laessle R, Krieg JC, Fichter MM. Plasma
norepinephrine after a standardized test meal in acute and remitted patients with
anorexia nervosa and healthy controls. Biol Psychiatry 1992; 31:1074–1077.
75. Devlin B, Bacanu SA, Klump KL, Bulik CM, Fichter MM, Halmi KA, Kaplan AS,
Strober M, Treasure J, Woodside DB, Berrettini WH, Kaye WH. Linkage analysis
of anorexia nervosa incorporating behavioral covariates. Hum Mol Genet 2002; 11
(6):689–696.
76. Bulik CM, Devlin B, Bacanu SA, Thornton L, Klump KL, Fichter MM, Halmi KA,
Kaplan AS, Strober M, Woodside DB, Bergen AW, Ganjei JK, Crow S, Mitchell J,
Rotondo A, Mauri M, Cassano G, Kellp P, Berrettini WH, Kaye WH. Significant
linkage on chromosome 10p in families with bulimia nervosa. Am J Hum Genet
2003; 72:200–207.
77. Rankinen T, Perusse L, Weisnagel SJ, Snyder EE, Chagnon YC, Bouchard C. The
human obesity gene map: the 2001 update. Obesity Res 2002; 10 (3): 196–243.
15
Management of Eating Disorders: Inpatient
and Partial Hospital Programs
Wayne A.Bowers, Arnold E.Andersen, and Kay Evans
University of Iowa Hospital & Clinics
Iowa City, Iowa, U.S.A.
It was the best of times; it was the worst of times. One might use that phrase
when examining the current state in the management of eating disorders,
especially when management occurs in an inpatient or partial hospitalization
setting. Inpatient treatments for eating disorders have evolved considerably,
with increasing acceptance of a multidisciplinary approach, but still remain
overly variable even with the current amount of evidence-based information.
Earlier hospital-based treatments included one or several of the following: high
doses of antipsychotic medications, tube feeding, nursing management, bed rest
with a high-calorie diet, strict behavioral contingency management,
hyperalimentation, and a variety of medical regimes (1–5). The literature also
describes a variety of variably successful psychological interventions to restore
weight among persons with an eating disorder. Several controlled trials of
behavior therapy have been reported (6–8). Strict behavioral interventions have
recently been criticized as being narrow minded, leading to short-term
compliance but frequent relapse. Long-term outcome studies suggested that
weight restoration alone by strictly medical or behavioral methods was a
temporary phenomenon, which at times produced negative effects (9).
A multidimensional perspective to the management of eating disorders was
developed (10–13) that advocated that weight gain achieved by compre hensive
management of eating disorders in the context of identifying, challenging, and
changing distorted cognitions was more enduring. Behavior therapy was best
seen as one aspect of a total treatment program that included additionally
required cognitive, family, and medical interventions (14,15). The complex
nature of eating disorders suggested the need for a coordinated,
multidisciplinary approach to treatment, focusing on the combined biological,
social, behavioral, and psychological needs of the patient. Successful treatment
was described as a skillful blend of weight restoration, psychotherapy
(individual, group, family), psychoeducational interventions, medical
management, and, at times, pharmacotherapy (10,14). Pharmacotherapy was
seen as an adjunct to the other therapies. Low-dose antipsychotics and
350 BOWERS ET AL.
antianxiety agents are at times useful to reduce anxiety associated with fear
of loss of control surrounding meals and weight gain, but are not used to
increase hunger. While antidepressant medication was suggested to treat
concomitant depressive symptoms or to reduce obsessive-compulsive symptoms
sometimes seen in these patients, such agents are relatively ineffective in starved
patients (16,17). Some classes of antidepressants have been found to be useful in
maintenance of weight after restoration (18).
Over the past 15 years the most progress has been made in creating effective
outpatient treatments for bulimia nervosa (19,20). The use of cognitive-
behavioral therapy and interpersonal therapy has been shown to be effective in
both short- and long-term treatment (21,22) and have reduced the need for
hospitalization for many individuals with bulimia nervosa. In a similar manner,
the use of psychopharmacological agents, often layered on top of manual-based
proven psychotherapies, have been shown to be effective in the management of
bulimia nervosa (18,23,24). With a greater understanding of treatment options
for bulimia nervosa the need for hospital-based intervention has decreased
except where outpatient treatments have failed or patients have severe
comorbidity.
In the same time period, less progress has been made in the effective
management of anorexia nervosa. Although the use of family therapy has been
shown to work effectively with adolescents and this approach has been
manualized (25), it is still not widely used in practice. However, it may be very
effective in a limited number of younger patients. Although many patients are
successfully treated in an outpatient setting, hospital-based care by a skilled team
remains the intervention of choice for those individuals who fail outpatient
treatment settings or are too ill. The literature has shown that inpatient care is
an effective method to manage both the physical and psychological aspects of
anorexia nervosa (14). However, the change in health care influenced by health
maintenance organizations (HMOs) has altered the face of inpatient treatment.
The pressure to reduce length of stay (LOS) for hospitalized patients and
reduced insurance coverage for the management of eating disorders has limited
treatment. Bezold et al. (26) reported that the average length of stay in a
psychiatric hospital decreased 25% between 1988 and 1992. The pressure to
reduce cost is translated into reductions in LOS for individuals with an eating
disorder. The same type of decrease in LOS has been reported regarding
hospitalization for eating disorders. Over a 15-year period from 1984 to 1998,
the length of stay for a hospitalized eating disorder patient went from 149.5
days in 1984 to 22.7 days in 1998 (27). The reduction in LOS affects the health
of the patient, adversely influencing long-term care, and contributing to high
readmission rates (28).
INPATIENT AND PARTIAL HOSPITAL PROGRAMS 351
One positive result of managed care creating pressure to reduce LOS has
been the development of day treatment or partial hospitalization programs
(PHPs) (29). Although these programs are influenced by their own health care
climates, there are similarities among PHPs (30). Among the common elements
are use of a multidisciplinary staff, group treatment as a primary method of
treatment, and the use of the PHP as part of a continuum of care for some
programs. The design of the program often reflects the area in which the
program works, such as a freestanding program or as part of a hospitalbased
treatment model. Most programs run from 3 to 5 days a week and integrate
some form of cognitive-behavioral therapy, readiness, or motivational therapy
into the treatment (31). Empirical data about the effectiveness of PHPs is
sparse. However, there is an indication that these programs can be effective in
continuing gains from an inpatient treatment program as well as assist reduction
in symptoms when patients “step up” from outpatient status (28,32). One
study (28) documented empirical decision rules for optimizing successful
transition from inpatient to PHP.
The American Psychiatric Association guidelines for the management of eating
disorders (33) give both specific and broad recommendations for evidence-
based, current best-practice treatment of eating disorders resulting from
research studies and clinical consensus (34). The revised guidelines have detailed
the necessity of integrating nutritional rehabilitation, psychosocial treatments,
medical procedures, and psychopharmacological interventions, and summarize
levels of care for a treatment continuum. This continuum includes outpatient,
intensive outpatient, partial hospitalization and full-day programming, and
residential and inpatient care. The remainder of the chapter presents a
prototype for inpatient and partial hospitalization based on APA guidelines in
the management of eating disorders.
INPATIENT TREATMENT
The comprehensive treatment of anorexia nervosa often requires inpatient care
as part of a continuum of care to restore healthy mental, physical, and social
functioning. This type of program must achieve safe, prompt, and effective
short-term hospital-based improvement. It must also prepare patients for
transition to a less intense, step-down, partial hospitalization treatment,
followed by long-term continued outpatient care emphasizing relapse
prevention and health promotion. The conceptual model most appropriate for
guiding the management of anorexia nervosa is that of a multifactorial etiologic
process. Eating disorders have never been adequately explained by single
etiologic factors but require a more complex, multifactorial understanding of
both origin and treatment. Since treatments logically grow out of assumptions of
352 BOWERS ET AL.
The broad goals of inpatient care are weight restoration and beginning
treatment for the psychological and environmental factors that contribute to
maintenance of the disorder, especially overvalued beliefs and cognitive
distortions, and dysfunctional family systems. Table 2 summarizes significant
but achievable goals for the inpatient care of persons with anorexia nervosa.
Weight restoration (a vital but not exclusive goal) means restoration of a fully
healthy body weight, with rebuilding of body and organ tissue as well as organ
functioning, not excessive fluid weight, as may occur with hyperalimentation.
Restoration to a healthy body weight is a means, not an end, to comprehensive
treatment. The conclusive work of treatment involves a fundamental and
enduring change in distorted thinking concerning weight, shape, size, and
appearance. Treatment is focused on decreasing the overinvestment in thinness
as a means of dealing with crucial central issues in life, such as mood regulation,
personal identity, or family stability.
The initial goal of inpatient care is medical stabilization. Medical stabilization
is intended to differentiate between slowly produced symptoms of starvation
that are part of the body’s adaptive response to decreased energy intake and
which will generally respond to simple nutritional rehabilitation versus those
medical signs and symptoms that are life threatening or atypical. This distinction
requires the clinician to thoroughly understand the adaptive responses of the
body to starvation. Many of the social behaviors and psychological symptoms
attributed to anorexia nervosa are, in fact, due to starvation and will normalize
by restoration to a healthy body weight. The rapidity of weight loss, methods of
weight loss, physical examination results, and laboratory tests are some of the
factors that need to be understood in the acute medical stabilization of the
patient. Some medical symptoms will improve with weight restoration alone
(stable bradycardia in most cases) whereas others require acute intervention
(prolonged QT interval). The key is to distinguish between adaptive responses
INPATIENT AND PARTIAL HOSPITAL PROGRAMS 353
population ideal weight at the onset of dieting. There is a rationale for setting the
goal weight of these patients at 5–15% above the “ideal” weight. Since many of
these patients may be biologically normal only when above the ideal in weight.
However, few patients accept this reasoning and few clinicians practice
individualization of weight goals within the normal range.
Where practical considerations dictate a short inpatient treatment period,
moderate weight gain to 85–90% of normal may have to be accepted. In this
case, close follow-up is required in a partial hospitalization program or an
outpatient clinic. A goal weight range, rather than a single point, should be set
so that patients can fluctuate comfortably within a 4- to 5-pound (1.4 kg) range.
The weight goal is not firmly set when the patient comes to the hospital but
only after treatment has been underway for several weeks. The weight range is
made as a decision among the team members if variation from protocol is
needed. Not telling patients their goal weight range until they are in the middle
of it allows changes to be made by staff without incurring the wrath or fear of
patients perceiving that a promise is being broken about a given weight range.
The initial food prescribed begins with 1200–1500 calories per day,
according to the patient’s admission weight, low in fat, salt, and lactose. No
diet foods of any kind are allowed. The dietitian has an essential role in relating
to patients, families, and staff. They take a complete nutritional history from the
patient upon admission. However, they do not discuss treatment directly with
the patient until weight is in the maintenance range. Every day the dietitian is
present at staff rounds to help make decisions about changes in dietary
programs. If the dietitian and the patients interact directly during nutritional
rehabilitation, patients may demand endless changes in menu. Patients name
three specific foods to delete from their menu, but other than these three
specific choices (e.g., artichoke, pork chops, scrambled eggs), they do not
determine the foods prescribed. Vegetarianism is permitted only if part of an
established religious or philosophical practice (for example, Seventh-Day
Adventist) preceding the eating disorder. Most adolescent vegetarianism in
eating-disordered patients represents an early phase of their eating disorder.
Calories are increased by 500 every 4–5 days until a maximum of 3500–4500
calories per day is achieved. The exact number will depend on the individual
rate of weight gain, the height of the patient, and the presence of gastrointestinal
discomfort. Once nutritional rehabilitation has been underway for several
weeks, most calories can be prescribed in fairly dense form, including a
moderate amount of fats and sweets. A safe continuing weight restoration
averaging 3 pounds a week in females and 4 pounds a week in males can be
achieved without significant medical symptoms, except for occasional pedal
edema (easily managed without diuretics by feet elevation, limitation of salt,
and psychoeducation).
356 BOWERS ET AL.
distress and dysphoria (40,44). Dieting, weight loss, and attaining thinness
become factors these individuals manipulate in an attempt to exercise control
over their internal and external environments (44,45). Continued weight loss,
which has become a sign of control, leads to social praise at first; then, shortly
after, social criticism that may be threatening to these patients’ sense of internal
and external control. This perceived criticism leads to increased social isolation
that reinforces distorted cognitions and maladaptive behaviors of an eating
disorder.
We use a design called the comprehensive model of cognitive therapy (46) to
organize an inpatient unit. Unit leaders, primary therapists, and adjunctive
therapists are all trained in cognitive therapy when using a comprehensive model.
Each intervention is designed to blend with the other psychotherapies. The
milieu (a) fully accommodates cognitive therapy; (b) supports individual,
family, and group therapies with cognitive therapy interventions; and
(c) integrates psychoeducational programs to complement and reinforce the
learning of cognitive therapy principles. Beck’s (47) original model,
modifications of this model for inpatient settings (39,48), and adaptations by
Garner et al. (44) for outpatient management of anorexia nervosa along with
Fairburn’s (49) approach to managing bulimia nervosa are the foundation of unit
structure.
The cognitive therapy milieu operates on the premise that patients are
affected by their environment and in turn influence that environment. The
milieu is a microcosm of the patient’s world providing the treatment staff and
patient with an opportunity to understand their problems. Recreation of the
patient’s world assists the treatment team in identifying cognitive distortions,
basic assumptions, schemas, and core beliefs as they occur, with recognition of
transference relationships as conveying vital information about family and peer
relationships. Through recognition, acknowledgment, and acceptance of their
problems, patients can gain new insight that allows them to address and modify
their distorted thinking patterns and beliefs.
PROGRAM SCHEDULING
Patients are involved in some form of treatment much of the day. A detailed
weekly schedule is displayed in Table 3, which includes several types of group
treatments. Typically they begin with a psychoeducational group, in which they
learn about basic cognitive therapy principles, the effects of starvation, and
principles of healthy social and psychological functioning. Patients participate in
an activities therapy group three times per week with content focusing on
building leisure time skills. An occupational therapy group meets twice a week.
The first session focuses on meal planning and purchasing. The second session
358 BOWERS ET AL.
Group Therapy
Psychoeducational Group
All groups are ongoing and a patient will enter group immediately after
admission to the unit. The psychoeducational group explores various aspects of
cognitive therapy (i.e., cognitive distortions, automatic thoughts) in a didactic
fashion and its relationship to an eating disorder. The purpose of this group is to
teach patients the basic concepts of cognitive therapy and information about the
effects of the disorder. After each group, assignments using these concepts are
given to the patients to complete before the next group. Some of the objectives
of this group are that the patient will:
The instructional methods used by the group leaders are didactic, role plays,
discussions, practice sessions, homework, peer feedback, and creative
expression exercises (artwork, etc.). The psychoeducational groups run daily
for 1 hour. Outcomes of the group are measured by satisfactory completion of
homework assignments, active participation in the group discussions, and
activities that reflect an understanding of the content being taught.
The materials and information given to each patient have been adapted from
various authors in the area of cognitive therapy. Ancillary areas covered in this
group include exploring self-identity and self-esteem, values clarification,
feelings identification, and problem solving. Other psychoeducational material
has been integrated directly relating to eating disorders. Included is information
on the effects of starvation, how the disorder functions psychologically, and the
social and media views of an individual’s appearance (54).
situations that arose during the day or between groups. In addition, material
that comes from the group itself is available to show how the ideas of cognitive
therapy are ever present with patients. It is also an opportunity for more skilled
members of the group to assist newer group members in first identifying
automatic thoughts, schemas, and core beliefs.
A cognitive therapy group challenges the weight- and shape-centered view of
the world that patients have established through their distorted cognitions. In
our experience, much of the group work lends itself toward helping the patients
understand how their cognitions affect their mood and consequent behaviors.
Another healing factor is the ability of group members to easily identify in
others the ramifications of their own eating disorder. As patients help others
identify and change negative cognitions, they also improve their own, often
coming to resolution of their issues as reflected in others.
Family Therapy
Family therapy maintains a cognitive framework designed to work with family
communications and schemas (57). Family therapy is important to treatment
outcome with this patient population and is an ongoing process in our program
of care. Parents and siblings frequently exhibit a sense of hopelessness regarding
the recovery of their family member, often intermixed with anger and anxiety,
with fathers more often showing the former and mothers the latter. Many of the
families we have worked with have been told that their family member will
probably not survive. Family therapy sessions are held on a regular basis with
the patient, family members, and/or a significant other. The content is
determined by the patient’s issues that have been pinpointed in the day-to-day
treatment process. These families often have difficulty identifying feelings and
expressing emotions, and not infrequently there are underlying family secrets
and unspoken issues that impair open communication. The hopelessness and
anger these individuals are feeling must also be addressed and assisted to
resolution. The focus of the sessions is on the interactions between the patient
and the family and resolution of the eating disorder. Our premise is that the
eating disorder maybe a symptom of other unresolved underlying problems.
However, families are assumed to be blameworthy for any aspect of the illness,
and often need to be relieved of the belief that they could have prevented the
illness, and that in fact this is an illness rather than a personal or family failing.
This work is always done within the CBT framework. The families are taught
through the therapy sessions to identify feelings and automatic thoughts, to
challenge automatic thoughts, and to reframe and examine the changes in their
feelings before and after the challenge. Some of the parents have marital issues
that need to be resolved, and such couples are referred to a therapist in their
locale or within the facility of treatment where they can pursue these issues
more intensely. Such issues may include triangulating, untreated mood
disorders, waning marital bonding, and so forth.
Another form of family therapy is increasingly important while working with
inpatients and partial hospitalization programs. A manual for psychotherapeutic
interventions with families for adolescent AN has recently been developed (25)
incorporating elements of the Maudsley treatment program that have been
found effective for adolescent AN patients (58). This protocol underscores the
central role of parents as a resource in the treatment of adolescent patients with
AN. Unlike more traditional family therapy models in which the patient is seen
INPATIENT AND PARTIAL HOSPITAL PROGRAMS 367
weight restoration and should be reevaluated after weight restoration before anti-
OCD medications are used. Exceptions may of course occur. Occasionally
patients benefit from prokinetic agents (Reglan) to decrease bloating, or H2
blockers or proton pump inhibitors (Zantac or Prilosec) where reflux
esophagitis is present.
constant observation during meals or just after meals, as these are gradually
diminished.
Decision to admit a patient to a partial program is usually based on failure to
make progress during outpatient treatment or as a step-down from inpatient
care. Often progress is measured by weight restoration or weight stabilization,
as well as by ability to challenge cognitive distortions, and improvement in
comorbid symptoms, such as depression, obsessive-compulsive disorder, etc.
Third-party payers when working with inpatients with anorexia often request
movement to partial hospitalization. A partial program as part of a continuum
of treatment allows patients to move to less restrictive care. It would be prudent
to move from inpatient to partial hospitalization when a patient is at least
80–85% of target weight range, but individuals may need more time in
inpatient treatment based on empirical studies. Weight is not the only criteria
for movement to a less restrictive level of treatment. The ability to engage in
psychotherapy must also be taken into consideration. Also, there needs to be
criteria for when to bring a patient back onto an inpatient treatment program if
partial hospitalization is ineffective.
Treatment in a partial/day hospitalization program is primary handled in a
group format, both for cost and effectiveness reasons. Group treatment can be
varied for those patients who are more or less advanced in the use of cognitive
therapy. Group approaches also offer more socialization in the context of the
cognitive model, as well as more chances to practice the concepts during the
day. A psychoeducation group functions much as in inpatient treatment, but it
can be split into more or less advanced tracks. If a patient has begun the partial/
day program after failure in outpatient treatment the psychoeducational group
would focus on more basic principles of cognitive therapy. Groups would build
on the principles of cognitive therapy with an emphasis on the use of mood
ratings, mastery and pleasure, graded task assignments, identification of
automatic thoughts, cognitive distortions, and use of thought records. In
addition, information regarding the effects of starvation on the body and
psychological processing would be introduced with an emphasis on how these
affect the interaction of thoughts, feelings, and behavior.
Patients who are more advanced in the principles of cognitive therapy would
have a different track for the psychoeducational group with a greater focus on
the ideas of schemas and core beliefs. This group would also focus on the
societal aspects of eating disorders and discuss how these unrealistic standards
influence and perhaps contribute to their own cognitive distortions about
weight, shape, and appearance. The main influence of this group would be on
the identification of their own schemas in order to understand the
developmental aspects of their disorder. Patients would be shown methods to
spot their core distorted beliefs by monitoring their emotional shifts and
INPATIENT AND PARTIAL HOSPITAL PROGRAMS 371
situations in which they find themselves using their disorder as a method for coping
with intense emotions. This group would also use other existing material to
assist in changing schemas and core beliefs.
Cognitive group therapy is the main psychotherapeutic vehicle in the partial/
day hospitalization program. This type of group (depending on availability of
therapists) can be run daily but must occur at least twice a week. The length of
the session also is dependent on the frequency of the meetings, ranging from
four to five times each week to longer sessions twice a week. This group can
have two possible formats. One format is based on the individual cognitive
therapy session, with definite structure. At the beginning of the group an agenda
is developed from topics presented by the group members. All members are
encouraged to be a part of the group, but more often time is spent with an
individual topic on an individual member. Other members of the group and the
group leaders give feedback to the member(s) involved. In this format group
leaders are more interactive and lead the discussion among the group members.
The alternative format is to develop a more process-oriented group in the partial/
day hospitalization program. This cognitive group therapy is similar to that
discussed in the chapter on inpatient treatment, blending of process
orientation (56), and cognitive-behavioral principles (15,55). These two models
allows more group latitude to deal with various personal and interpersonal issues.
The curative factors of group (56) and cognitive therapy principles create a
focus on cognitive and developmental factors involved with eating disorders. This
group format influences the perceptions of the patients and assists patients in
recovering from their disorder through self-disclosure and confrontation of
symptomatic behavior, distorted ideas, and schematic material. It also provides
an environment that validates emotions and assists patients in tolerating
uncomfortable feelings while facilitating self-understanding.
The body image group also parallels the group run in an inpatient setting with
a focus on helping patients understand their body distortions and how these
distortions affect their lives and sustain the eating disorder. Patients are
supportive yet confrontive with one another, helping each other face their
distortions and bring their cognitions into basis in fact.
Unlike inpatients, the patients in partial hospitalization spend part of the day
outside of a formal treatment setting. This time may be very anxiety producing
but represents an essential practical format for gaining mastery in an everyday
unstructured setting. Urges to restrict, exercise, or purge can be strong. In
order to prepare patients for these urges and for efficient use of free time, each
day is ended with a planning group emphasizing a plan for healthy thinking and
behavior when not in treatment. Format is structured around alternative healthy
plans that each member needs to practice as an alternative to not engaging in the
disorder. This may include alternatives to the urge to restrict, exercise/purge,
372 BOWERS ET AL.
Involuntary Patients
One subject that has important bearing on inpatient treatment and, to a lesser
degree, on partial hospitalization is the use of involuntary treatment. Although a
controversial subject, involuntary commitment to treatment, through a
judiciously applied legal process, is at times a life-saving way to assist individuals
who have a life-threatening disorder but refuse hospitalization. There is a very
modest literature that looks at the usefulness of legal commitment, and
suggestions have been made that in some cases eating disorder patients who
desire not to be treated should be respected even if it may mean their
death (60). We strongly disagree. The literature that exists is generally positive
INPATIENT AND PARTIAL HOSPITAL PROGRAMS 373
REFERENCES
1. Dally P, Sargent W. Treatment and outcome of anorexia nervosa. Br Med J 1960;
1:1770–1773.
2. Silverman J. Anorexia nervosa: clinical observations in a successful treatment
program. J Pediatrics 1974; 84:68–73.
3. Russell GFM. The present status of anorexia nervosa. Psychol Med 1977; 7:
353–367.
4. Maloney MJ, Farrell MK. Treatment of severe weight loss in anorexia nervosa with
hyperalimentation and psychotherapy. Am J Psychiatry 1980; 137:310–314.
5. Vandereycken W. The use of neuroleptics in the treatment of anorexia nervosa
patients. In: Garfinkel PE, Garner DM, eds. The Role of Drug Treatment in Eating
Disorders. New York: Brunner/Mazel, 1987.
6. Agras WS, Schneider JA, Arnow B, Rathburn SD, Telch CF. Cognitivebehavioral
treatment with and without exposure plus response prevention in the treatment of
bulimia nervosa: a reply to Leitenberg and Rosen. J Consult Clin Psychol 1989; 57:
778–779.
7. Eckert ED, Goldberg SC, Halmi KA, Casper RC, Davis JM. Behavior therapy and
anorexia nervosa. Br J Psychiatry 1979; 134:55–59.
8. Touyz SW, Beumont PJV, Glaun D, Philips T, Cowie I. A comparison of lenient
and strict operant conditioning programs in refeeding patients with anorexia
nervosa. Br J Psychiatry 1984; 144:517–520.
9. Vandereycken W. The place of behavior therapy in the inpatient treatment of
anorexia nervosa. Br Rev Bulimia Anorexia Nervosa 1989; 3:55–60.
374 BOWERS ET AL.
10. Andersen AE, Morse C, Santmyer K. Inpatient treatment of anorexia Nervosa. In:
Garner DM, Garfinkel PE, eds. Handbook of Psychotherapy for Anorexia Nervosa
and Bulimia. Guilford Press, 1985:311–343.
11. Andersen, A.E. New York:Inpatient and outpatient treatment of anorexia nervosa.
In: Brownell KD, Foreyt J.P, eds., Handbook of Eating Disorders: Physiology,
Psychology, and Treatment of Obesity, Anorexia and Bulimia. New York:Basic
Books, 1986.
12. Garner DM, Garfinkel PE, Irvine MJ. Integration and sequencing of treatment
approaches for eating disorders. Psychother Psychosom 1986; 67–75.
13. Vandereycken W. Inpatient treatment of anorexia nervosa: some researchguided
changes. J Psychiatr Res 1985; 19:413–422.
14. Andersen AE, Bowers WA, Evans KK. Inpatient treatment of anorexia nervosa. In:
Garner DM, Garfinkel PE, eds. Handbook of Treatment for Eating Disorders.
2d ed. New York: Guilford Press, 1997:327–353.
15. Bowers WA, Andersen AE. Inpatient treatment of anorexia nervosa: review and
recommendations. Harvard Rev Psychiatry, 1994.
16. Strober M, Pataki C, Freeman R, DeAntonio M. No effect of adjunctive fluoxetine
on eating behavior or weight phobia during the inpatient treatment of anorexia
nervosa: an historical case-control study. J Child Adolesc Psychopharmacol 1999;
9:195–201.
17. Mitchell JE, Peterson CB, Myers T, Wonderlich S. Combining pharmacotherapy
and psychotherapy in the treatment of patients with eating disorders. Psychiatr Clin
North Am 24:315–324.
18. Kaye WH, Weltzin TE, Bulik CM. An open trial of fluoxetine in patients with
anorexia nervosa. J Clin Psychiatry 1991; 52:464–471.
19. Keel PK, Mitchell JE, Davis TL, Crow SJ. Long-term impact of treatment in
women diagnosed with bulimia nervosa. Int J Eating Disord 2002; 31:151–158.
20. Rosenblum J, Forman S. Evidenced-based treatment of eating disorders. Curr Opin
Pediatrics 2002; 14:379–383.
21. Bowers WA, Ansher LS. Cognitions in anorexia nervosa: changes at discharge from
a cognitive therapy milieu inpatient program. J Cognitive Psychother 2000; 14:
393–401.
22. Wilson GT, Fairburn CC, Agras WS, Walsh BT, Kraemer H. Cognitivebehavioral
therapy for bulimia nervosa: time course and mechanisms of change. J Consult Clin
Psychol 2002; 70:267–274.
23. Nakash-Eisikovits O, Dierberger A, Westen D. A multidimensional metaanalysis of
pharmacotherapy for bulimia nervosa: summarizing the range of outcome in
controlled clinical trials. Harvard Rev Psychiatry 2002; 10:193–211.
24. Zhu AJ, Walsh BT. Pharmacologic treatment of eating disorders. Can J Psychiatry
2002; 47:227–234.
25. Lock J, Le Grange D, Agras WS, Dare C. Treatment Manual for Anorexia Nervosa:
A Family-Based Approach. New York: Guilford Press, 2001.
26. Bezold H, MacDowell M, Kunkel R. Predicting psychiatric length of stay. Admin
Policy Men Health 1996; 23:407–423.
INPATIENT AND PARTIAL HOSPITAL PROGRAMS 375
27. Wiseman CV, Sunday SR, Klapper F, Harris WA, Halmi KA. Changing patterns of
hospitalization in eating disorder patients. Int J Eating Disord 2001; 30:69–74.
28. Howard WT, Evan KK, Quintero-Howard CV, Bowers WA, Andersen AE.
Predictors of success or failure of transition to day hospital treatment for inpatients
with anorexia nervosa. Am J Psychiatry 1999; 156:1697–1702.
29. Anzai N, Lindsey-Dudley K, Bidwell RJ. Inpatient and partial hospital treatment
for adolescent eating disorders. Child Adol Psychiatr Clin North Am 2002; 11:
279–309.
30. Zipfel S, Reas DL, Thorton C, Olmsted MP, Williamson DA, Gerlinghoff M,
Herzog W, Beumont PJ. Day hospitalization programs for eating disorders: a
systematic review of the literature. Int J Eating Disord 2002; 31:105–107.
31. Thorton C, Beumont P, Touyz S. The Australian experience of day programs for
patients with eating disorders. Int J Eating Disord 2002; 1–10.
32. Kaplan AS, Omlsted MP. Partial Hospitalization. In: Garner DM, Garfinkel PE,
eds. Handbook of Treatment for Eating Disorders. 2nd ed. New York: Guilford
Press, 1997:354–360.
33. American Psychiatric Association. Practice guideline for eating disorders (revised).
Am J Psychiatry 157(suppl):l-39.
34. Yager J. Implementing the Revised American Psychiatric Association Practice
Guidelines for the treatment of patients with eating disorders. Psychiatr Clin North
Am 2001; 24:185–199.
35. Metropolitan Life Insurance Company. Metropolitan height and weight tables.
NewYork, 1983.
36. Frisch RE, McArthur JW. Menstrual cycles: fatness as a determinant of minimum
weight for height necessary for their maintenance or onset. Science 1974; 185:
949–951.
37. Fairburn CG. Eating disorders. In: Clark DM, Fairburn CG, eds. Science and
Practice of Cognitive Behavior Therapy. New York: Oxford University Press,
1997:209–242.
38. Eckert ED, Mitchell JE. An overview of the treatment of anorexia nervosa.
Psychiatr Med 1989; 7:293–315.
39. Bowers WA. Cognitive therapy for eating disorders. In: Wright JH, Thase ME,
Beck AT, Ludgate JW, eds. Cognitive Therapy with Inpatients: Developing a
Cognitive Therapy Milieu. New York: Guilford Press, 1993.
40. Garfinkel PE, Garner DM. Anorexia Nervosa: A Multidimensional Perspective.
New York: Brunner/Mazel, 1982.
41. Garner DM. Individual psychotherapy for anorexia nervosa. J Psychiatr Res 1985;
19:423–433.
42. Beck JS. Cognitive Therapy: Basics and Beyond. New York: Guilford Press, 1995.
43. Freeman A. A psychosocial approach to conceptualizing schematic development for
cognitive therapy. In: Kuehlwein KT, Rosen H, eds. Cognitive Therapies in
Action. New York: Jossey-Bass, 1993:54–87.
376 BOWERS ET AL.
44. Garner DM, Vitousek KM, Pike KM. Cognitive-behavioral therapy for Anorexia
Nervosa. In: Garner DM, Garfinkel PE, eds. Handbook of Psychotherapy for
Anorexia Nervosa and Bulimia. New York: Guilford Press, 1997:94–144.
45. Bowers WA. Cognitive model of eating disorders. J Cognitive Psychother An Int
Quart2001; 15:331–340.
46. Wright JH, Thase ME, Beck AT, Ludgate JW. Cognitive Therapy with Inpatients:
Developing a Cognitive Therapy Milieu. New York: Guilford Press, 1993.
47. Beck AT, Rush J, Shaw BF, Emery G. Cognitive Therapy of Depression. New
York: Guilford Press, 1979.
48. Bowers WA. Basic principles for applying cognitive-behavioral therapy to anorexia
nervosa. Psychiatr Clin North Am 2001; 24:293–304.
49. Wilson GT, Fairburn CC, Agras WS. Cognitive-behavioral therapy for
bulimia nervosa. In: Garner DM, Garfinkel PE, eds. Handbook of Treatment for
Eating Disorders. 2d ed. New York: Guilford Press, 1997:67–93.
50. Fairburn CG, Cooper PJ. The Eating Disorders Examination. 12th ed. In: Fairburn
CG, Wilson GT, eds. Binge Eating: Nature, Assessment and Treatment. New
York: Guilford Press, 1993:317–360.
51. Garner DM, Olmsted MP. Manual for the Eating Attitudes Test (EDI). Odessa,
FL: Psychological Assessment Resources, Inc., 1993.
52. Garner DM, Garfinkel PE. The eating attitudes test. An index of the symptoms of
anorexia nervosa. Psychol Med 1979; 9:273–279.
53. Garner DM, Garfinkel PE. Handbook of Treatment for Eating Disorders. 2d ed.
New York: Guilford Press, 1997:145–177.
54. Garner DM. Psychoeducational principles in treatment. In: Garner DM, Garfinkel
PE, eds. Handbook of Treatment for Eating Disorders. 2d ed. New York: Guilford
Press, 1997:145–177.
55. Bowers WA. Eating disorders. In: White JR, Freeman AS, eds.
CognitiveBehavioral group therapy for specific problems and populations.
Washington, DC: American Psychological Association, 2000:127–148.
56. Yalom I. The Theory and Practice of Group Psychotherapy. 4th ed. New York: Basic
Books, 1995.
57. Dattilio FM. Families in crisis. In: Dattilio FM, Freeman A, eds.
CognitiveBehavioral Strategies in Crisis Intervention. New York: Guilford Press,
1994: 2789–3010.
58. Dare C, Eisler I. Family therapy for anorexia nervosa. In: Garner DM, Garfinkel
PE, eds. Handbook of Treatment for Eating Disorders. 2d ed. New York: Guilford
Press, 1997:307–326.
59. Strober M, Freeman R, Morrell W. The long-term course of severe anorexia
nervosa in adolescents: survival analysis of recovery, relapse, and outcome
predictors over 10–15 years in a prospective study. Int J Eating Disord 1997; 22:
339–360.
60. Draper H. Anorexia nervosa and respecting a refusal of life-prolonging therapy:
limited justification. Bioethics 2000; 14:120–133.
INPATIENT AND PARTIAL HOSPITAL PROGRAMS 377
Anorexia Nervosa
Nutritional Assessment
The initial nutritional assessment of a person suffering from anorexia nervosa
should include a detailed history of the onset of the eating disorder, a thorough
recall of typical eating patterns and eating disorder symptom use, and questions
regarding potential precipitating events (e.g., weight-related teasing, bodily
changes associated with puberty, comments by family or friends, etc.). A
detailed description of a typical day should include times of eating occasions,
type and amount of food eaten, beverages consumed, and if and when bingeing
and purging occurs. Research comparing reported intake to observed intake has
NUTRITION COUNSELING 381
shown that diet history given by patients with anorexia nervosa provides a quite
reliable picture of nutritional intake (4). It is also important to assess the food
rules dictated by anorexia. Typical food-related rules commonly seen with
anorexia nervosa include the following: no eating after a certain time in the
evening, no eating of specific foods (such as meat, sweets, fats, snacks), eating
foods in a specific order, following certain caloric or fat gram daily limits, trying
to go all day without eating, and isolating self from others while eating. Foods
are often categorized as “good” or “bad” or “safe” or “scary,” and these
categorizations often determine eating behaviors (5). While these behaviors and
rules are largely the result of semistarvation, they can perpetuate the eating
disorder. Most tend to significantly decrease or abate with nutritional
rehabilitation (6–8). A detailed exercise history, including type of exercise,
duration, intensity, and compulsivity, is a necessary part of the evaluation to
determine energy expended on physical activity. As with eating patterns,
particular attention should be given to assessing exercise patterns in all settings:
at home, at school, at health clubs, as part of clubs or teams, or in other
settings. The physical activity level is often high in patients with anorexia
nervosa and contributes significantly to energy balance (9,10). Thorough
assessment is necessary, as anorexia imposes many rules and regulations.
Clinicians may need to ask many questions, as patients may not readily
volunteer information regarding eating disorder-related eating and exercise
patterns and may have altered perceptions of these behaviors. Family members
or friends, if present at the assessment, can often provide additional valuable
historical data regarding the patient’s eating habits and change in eating (e.g.,
onset of dieting; whether certain eating behaviors, like vegetarianism, predated
the eating disorder or co-occurred with the eating disorder; etc.).
Nutritional Rehabilitation
In addition to weight restoration, nutritional interventions seek to correct any
nutritional deficiencies resulting from the illness. Research has shown that
patients with anorexia nervosa may have abnormal vitamin status, specifically
indicators of low riboflavin and vitamin B6, deficiencies in essential fatty acids,
low serum albumin and other nutrients (11,12). Osteopenia is common among
patients with anorexia nervosa (13–15), making dietary calcium intake a critical
part of nutritional rehabilitation. Research suggests that weight restoration in
conjunction with adequate dietary calcium and vitamin D is associated with
improvement in bone mineralization (16,17).
Adequate nutrition rehabilitation can be a significant challenge. Many
patients experience and are frustrated by delayed gastric emptying resulting
from ongoing food restriction and complain of feeling excessively full in the
382 CROLL AND NEUMARK-SZTAINER
FIGURE 2 Calculation of energy requirements. (From Harris JA, Benedict FG. (1919)
Biometric studies of basal metabolism in man. Carnegie Institute of Washington:
Publication No. 279.)
activity, and kilocalories needed for weight restoration (see Fig. 2 for details
regarding these calculations). It is important to note that this provides only an
estimate, and patients will respond differently at different times in the process,
as resting energy expenditure has been shown to increase and peak during
refeeding (23–26). Kilocalorie levels may need frequent adjustment until the
desired rate of weight restoration is achieved and weight restoration is
adequate (1–3).
At high caloric levels, consuming adequate food may present a challenge to
patients. Calorically dense foods, more frequent meals and snacks, or oral
liquid supplements can be utilized to meet the high-energy needs of these patients.
Some inpatient, partial, and residential programs use nasogastric tube feedings
or total parenteral nutrition (TPN) to increase caloric consumption, but both
require close medical monitoring, may increase the risk of refeeding syndrome,
and may be unnecessarily overwhelming for some patients (1–3). Use of food
384 CROLL AND NEUMARK-SZTAINER
Meal Plans
The individualized meal plan serves many purposes. On a broad level, it can
serve as the client’s personalized road map to successful, normal eating. On a
more detailed level, it provides the patient with a concrete presentation of what
she or he needs to eat on a daily basis to progress in treatment. The meal plan is
typically created with the client, taking into account true food likes and dislikes
and the current prescribed caloric level. The meal plan encourages patients to
challenge the eating disorder and themselves to reintroduce foods forbidden by
the eating disorder. Meal plans, while calculated based on caloric needs, are
usually presented in terms of servings from each food group, similar to the food
guide pyramid recommendations (27), rather than calories. See Table 1 for
examples of typical meal plans at different caloric levels and Table 2 for
recommended portion sizes of foods in each food group.
NUTRITION COUNSELING 385
a Number of servings per groups varies; based on individualized meal plan created for
patient.
b Liquid supplements may be used at higher calorie levels, if desired, to meet caloric
needs. If liquid supplements are used, the number of grain and dessert servings may be
reduced accordingly to meet required caloric level.
sugar, and other foods, patients face a difficult task in overcoming those
messages and incorporating challenging foods in their meal plan. Education
regarding the concepts of normal eating is critical, including learning to eat
when hungry, eating until full, including a wide variety of foods, not avoiding
or fearing specific foods, eating with others, eating in a variety of settings,
eating from all the food groups, not being obsessed with thoughts of food, not
purging or exercising to counteract food eaten, etc. Normal eating includes
NUTRITION COUNSELING 387
having all kinds of foods, not categorizing foods as positive or negative, and
incorporating variety and moderation as mainstays (28).
Ongoing Treatment
While many patients with anorexia nervosa experience inpatient or partial
hospitalization treatment, most of the time spent in treatment is in an
outpatient setting with a multidisciplinary team. Regular follow-up with the
dietitian is necessary and generally occurs on a weekly basis, typically until
weight restoration is complete and has been maintained for at least 2 weeks.
Once the patient is within their goal weight range, visits with the dietitian may
decrease in frequency to bimonthly or monthly. Visits often include taking the
patient’s weight. Weights should be taken with the patient wearing only a gown
and undergarments, preferably with them facing away from the numbers on the
scale. Weight changes are used as a guideline for meal plan changes and
strategies and are an integral piece of medical monitoring. Because of the
intense focus on weight associated with anorexia nervosa, discussions with the
patient regarding current weight, weight change, and goal weights should focus
on progress and strategies for change rather than be overly focused on numbers.
As adequate weight restoration is achieved, energy needs decrease and the meal
plan can be changed accordingly. Weight maintenance energy levels vary by
individual based on age, gender, physical activity, and weight, but are typically
in the range of 2000–2800 kcal/day. Figure 2 provides an equation for
calculating weight restoration and weight maintenance needs.
Nutritional care in an outpatient setting incorporates a number of techniques
to aid patients in the process of incorporating variety into their meal plan and
regaining foods lost to the eating disorder. Usually clients will be asked to eat at
structured, regular intervals and participate in selfmonitoring, cognitive-
behavioral therapy techniques (29,30) involving planning meals and snacks
ahead of time, eating at set times, and keeping daily food records. Eating
specific amounts and types of foods at appropriate set times throughout the day,
even if not hungry, allows for relearning of hunger and satiety cues and normal
eating patterns.
Food records include information about food and beverage intake, including
time of meal or snack, location, whether alone or with others, what and how
much was eaten, rating of hunger and satiety levels, as well as any thoughts or
feelings associated with eating. If patients also struggle with bingeing and/or
purging, urges or occurrences of the behaviors can be tracked on these forms as
well. Review of the patient’s food records provides an opportunity to discuss
progress made with the meal plan and challenges faced with specific foods or
situations. Self-monitoring can be challenging for some patients for a variety of
388 CROLL AND NEUMARK-SZTAINER
reasons. It may be difficult for patients to write down what they are eating. It may
seem overwhelming and anxiety provoking to see it all down on paper, or it
may be difficult to record symptoms. For others, it may be another avenue for
the perfectionism of anorexia to take hold, driving them to have perfectly
written and detailed food records each week. Initially, patients often struggle
with rating hunger and satiety levels because the eating disorder has resulted in
loss of connection between hunger signals and eating behaviors. Reconnection
to innate hunger and satiety signs may take considerable time. Clinicians should
encourage patients to consider food records as another tool in the fight against
anorexia and a way for them to remind themselves of their meal plan and their
goals, rather than something to obsess about or feel like they have to do
perfectly (see Fig. 3 for an example of a comprehensive food record form).
Family Involvement
With adolescent patients, parents need to be included in initial education
sessions regarding the meal plan, portion sizes, expectations for the patient
while in treatment, and ways family members can support the patient. While
parents are often not present during ongoing follow-up sessions, they generally
need to be regularly apprised of weight changes, progress with the meal plan,
and strategies or goals for the week, as well as given the opportunity to ask
questions regarding the meal plan. Parents also can provide insight regarding the
patient’s eating behaviors, successes, and difficulties at home that patients may
not fully reveal to the clinician. For younger patients, there is evidence to
suggest that the patient’s family can be integrally involved in the
reestablishment of normal eating patterns (31). This approach aids parents in
supporting the recovery of their child by giving them primary jurisdiction over
implementation of the meal plan and the patient’s eating. Such approaches must
be carefully implemented so as not to set up a power struggle between the
patient and the parents, but rather should help parents to support their child in a
constructive and productive manner. In this type of approach, parents would be
more involved in ongoing nutrition sessions.
Regardless of their level of involvement in the meal plan, families often need
assistance in knowing what to say to help patients have success with their meal
plan. No one approach works well with all families, and families should be
encouraged to ask the patient what they should and should not do or say to be
supportive when it seems like the patient is struggling with the eating disorder
during a meal or snack. To be most effective and productive, these conversations
should take place outside of meal and snack times.
FIGURE 3 Example of a Food Record Form.
NUTRITION COUNSELING 389
390 CROLL AND NEUMARK-SZTAINER
Bulimia Nervosa
Nutritional Assessment
The initial nutritional assessment of a person suffering from bulimia nervosa is
similar to that of anorexia nervosa (see Fig. 1 for typical assessment questions).
A detailed description of a typical day should include all eating occasions,
including binge and purge occurrences as well as nonbinge meals and snacks. A
careful exploration of type and amount of food eaten and beverages consumed
through the day can reveal an accurate picture of foods commonly eaten during
a binge, triggers for binge and purge episodes, and those foods the patient is
comfortable eating without feeling the need to purge. Typically, foods that are
high in fat or sugar, such as fast food, bakery items, salty snack foods, candy,
and ice cream, are foods considered “bad foods” or binge foods and are avoided
unless purging is possible or planned (32). When purging is not planned or
possible, patients with bulimia nervosa will usually restrict food intake or limit
intake to foods considered to be healthy, such as fruit, vegetables, and other low-
fat foods. Research has shown that when not engaging in binge eating, persons
with bulimia nervosa exhibit significant dietary restraint, eat fewer meals and
snacks, and take in significantly less energy and fat than controls (33,34). These
findings, along with studies examining energy retained from binge eating after
purging [approximately 1200 kcal/binge (35,36)], explain why many patients
with bulimia nervosa have a relatively normal body weight despite characteristic
restrictive eating alternating with binge eating and purging.
Nutritional Rehabilitation
Nutritional rehabilitation focuses on helping patients set goals around reducing
binge-purge and restricting behaviors, increasing variety in food choices,
practicing eating foods that are considered binge foods without purging,
planning approaches for eating in challenging situations (e.g., restaurants,
special occasions), and encouraging healthy, moderate exercise (1–3). Because
individuals with bulimia nervosa typically maintain a normal or near-normal
NUTRITION COUNSELING 391
a variety of restaurants and social situations with the patient and supporting the
patient’s efforts to follow the meal plan in these challenging situations.
Nutritional intervention often focuses on helping patients to manage
overwhelming situations that involve food by focusing on the component parts
of the situation and making a plan for success using the meal plan as a guide. For
example, if a patient has a great deal of difficulty going grocery shopping without
it resulting in a binge-purge episode, the clinician can help the patient break
down the task into manageable parts. First, together they can make a grocery
list and determine what area of the store each food is in. Next they can
determine what type and quantity of each food the patient needs to buy to meet
his or her meal plan. At this point, it is important to explore what challenges
may exist for particular foods and how those challenges can be overcome. For
example, the meal plan discourages use of fat-free food items, but the patient
feels compelled by the eating disorder to buy only fat-free cream cheese. So the
patient takes a friend shopping and asks the friend to put regular cream cheese in
the cart. Patients may need education regarding the nutritional benefits of
challenging foods to understand that such foods generally provide more
nutrients and satiety than fat-free or lowfat versions. After making the list and
determining what needs to be purchased and where it is located, the dietitian
may have the patient practice by going to the grocery store with the list, confirm
the location of all the items, but not buy anything on this occasion. It is probably
a good idea for the patient to take no money alone so as to help prevent a binge-
purge episode. After this practice run, the patient may feel more assured of
success because he or she is familiar with the location of items in the store. Then
the patient would be asked to go to the grocery store, with a support person if
necessary, to actually purchase the foods on the list in the specified quantities
and report back to the clinician regarding success and challenges.
In addition to these techniques used in an outpatient setting, experiential
nutritional activities are often part of partial day treatment or intensive
outpatient treatment. Such activities typically include supported exposure to
difficult foods or situations, such as meals out at restaurants, grocery shopping,
or meal preparation for guests as a group. These experiential activities are
commonly supervised by a dietitian and a psychologist or other clinician, and
include a process group cofacilitated by both clinicians for the most effective
utilization of the experience. Patients are often able to overcome challenging
foods or situations in these types of experiential activities and recognize that
they can complete food-related tasks that they thought were overwhelming.
Overall, as with anorexia nervosa, nutritional intervention and education is a
critical part of a multifaceted approach to management of bulimia nervosa and
seems most effective for patients when paired with cognitivebehavioral work
with a psychologist or other clinician. Ongoing nutrition counseling helps
NUTRITION COUNSELING 395
patients with bulimia nervosa establish regular eating patterns and decrease
symptom use, develop skills for use when reintroducing challenging foods, and
have better understanding of nutritional needs and physiological effects of
symptom use.
Nutritional Assessment
Given that patients with binge eating disorder often seek treatment for obesity
and that nutritional counseling is generally a service incorporated into obesity
treatment, a nutrition professional may be the primary clinician discussing binge
eating with the patient. Binge eating disorder research is in the relatively early
stages and as such numerous assessment and treatment recommendations and
protocols are under evaluation, many of which have nutritional therapy or
nutrition education components. The initial nutritional assessment for binge
eating disorder should include a detailed account of the onset of binge eating, a
weight and dieting history, and any historical events the patient believes may be
related to the binge eating (e.g., weight-related teasing; comments by parents,
friends, significant other; etc.). In general, people experiencing binge eating are
more likely to have had a history of being overweight since childhood, have a
significant history of large weight fluctuations (20 pounds or more), and
experience an increase in binge eating as weight increases (48–51). Because
binge eating may develop during periods of dietary restriction, such as a very-
low-calorie diet (52), a careful history of diet attempts and outcomes should be
taken. Assessment should include a thorough recall of typical eating patterns and
binge eating occurrence and duration, along with an assessment of the out-of-
control nature of the reported binge eating episodes.
A detailed description of a typical day, including all eating occasions, can help
identify patterns in eating and triggers for binge eating. As with bulimia
nervosa, a careful exploration of type and amount of food eaten and beverages
consumed through the day can reveal an accurate picture of foods commonly
eaten during a binge, as well as those foods the patient eats outside of binge
episodes. Typically, foods that are high in fat or carbohydrates and lower in
protein, such as candy, baked goods, and ice cream, are foods included in binge
episodes (49,52). Caloric contribution from binge eating to total daily intake
varies greatly depending on the episode, ranging from a minor contribution of
fewer than 100 kilocalories to a large contribution of several thousand
kilocalories (49,53). Studies have shown an average caloric intake difference of
396 CROLL AND NEUMARK-SZTAINER
for binge eating disorder. If necessary, focus on healthy, moderate weight loss
or lifelong weight control can be incorporated as patients are able to reduce or
cease binge eating behaviors.
Adequate weight restoration through increased energy intake via food rather than
enteral or parenteral nutrition products
Meal plan education and guidance focused on food groups, portion sizes, and
variety to promote normalization of eating patterns
Supported reintroduction of foods eliminated from the diet to dispel fears related
to these foods
Adequate nutrient intake to support nutritional recovery, possibly including a
low-dose multivitamin and multimineral supplement
Nutrition education regarding normal, healthy eating; and normalization of
dieting, restrictive eating, and excessive energy expenditure behaviors.
Binge eating disorder nutritional treatment goals and components include the
following, with particular attention to strategies for managing eating in high-risk
or triggering situations and establishment of regular meals and snacks.
REFERENCES
1. American Psychiatric Association. Practice guideline for the treatment of patients
with eating disorders. Am J Psychiatry 2000; 157(1): 1–39.
2. American Dietetic Association. Nutrition intervention in the treatment of anorexia
nervosa, bulimia nervosa, and eating disorder not otherwise specified (EDNOS).
J Am Diet Assoc 2001; 101(7):810–819.
3. Rock CL, Curran-Celentano J. Nutritional management of eating disorders.
Psychiat Clin North Am 1996; 19(4):701–713.
4. Hadigan CM, Anderson EJ, Miller KK, Hubbard JL, Herzog DB, Klibanski A,
Grinspoon SK. Assessment of macronutrient and micronutrient intake in women
with anorexia nervosa. Int J Eating Disord 2000; 28(3):284–292.
5. Sunday SR, Einhorn A, Halmi KA. Relationship of perceived macronutrient and
caloric content to affective cognitions about food in eating-disordered, restrained,
and unrestrained subjects. Am J Clin Nutr 1992; 55(2):362–371.
6. Garner DM. Pathogenesis of anorexia nervosa. Lancet 1993; 341:1631–1635.
7. Keys A, Brozek J, Henschel A, Mickelsen O, Taylor HL. The Biology of Human
Starvation. Minneapolis: University of Minnesota Press, 1950.
8. Rock CL, Curran-Celentano J. Nutritional disorder of anorexia nervosa: a review.
Int J Eating Disord 1994; 15(2): 187–203.
9. Casper RC, Schoeller DA, Kushner R, Hnilicka J, Gold ST. Total daily
energy expenditure and activity level in anorexia nervosa. Am J Clin Nutr 1991;
53(5): 1143–1150.
400 CROLL AND NEUMARK-SZTAINER
10. Pirke KM, Trimborn P, Platte P, Fichter M. Average total energy expenditure in
anorexia nervosa, bulimia nervosa, and healthy young women. Biol Psychiatry
1991; 30(7):711–718.
11. Rock CL, Vasantharajan S. Vitamin status of eating disorder patients: relationship
to clinical indices and effect of treatment. Int J Eating Disord 1995; 18(3):257–262.
12. Holman RT, Adams CE, Nelson RA, Grater SJ, Jaskiewicz JA, Johnson SB,
Erdman JW Jr. Patients with anorexia nervosa demonstrate deficiencies of selected
essential fatty acids, compensatory changes in nonessential fatty acids and decreased
fluidity of plasma lipids. J Nutr 1995; 125(4):901–907.
13. Bachrach LK, Katzman DK, Litt IF, Guido D, Marcus R. Recovery from
osteopenia in adolescent girls with anorexia nervosa. J Clin Endocrinol Metab 1991;
72(3):602–606.
14. Rigotti NA, Neer RM, Skates SJ, Herzog DB, Nussbaum SR. The clinical course of
osteoporosis in anorexia nervosa. A longitudinal study of cortical bone mass. JAMA
1991; 265(9): 1133–1138.
15. Rigotti NA, Nussbaum SR, Herzog DB, Neer RM. Osteoporosis in women with
anorexia nervosa. N Engl J Med 1984; 311(25):1601–1606.
16. Abrams SA, Silber TJ, Esteban NV, Vieira NE, Stuff JE, Meyers R, Majd M,
Yergey AL. Mineral balance and bone turnover in adolescents with anorexia
nervosa. J Pediatrics 1993; 123(2):326–331.
17. Hay PJ, Delahunt JW, Hall A, Mitchell AW, Harper G, Salmond C. Predictors of
osteopenia in premenopausal women with anorexia nervosa. Calc Tissue Int 1992;
50(6):498–501.
18. Waldholtz BD, Andersen AE. Gastrointestinal symptoms in anorexia nervosa. A
prospective study. Gastroenterology 1990; 98(6):1415–1419.
19. Vaisman N, Corey M, Rossi MF, Goldberg E, Pencharz P. Changes in body
composition during refeeding of patients with anorexia nervosa. J Pediatrics 1988;
113(5):925–929.
20. Solomon SM, Kirby DF. The refeeding syndrome: a review. J Parent Ent Nutr
1990; 14:90–97.
21. Rock CL. Nutritional and medical assessment and management of eating disorders.
Nutr Clin Care 1999; 2:332–343.
22. Fisher M, Simpser E, Schneider M. Hypophosphatemia secondary to oral refeeding
in anorexia nervosa. Int J Eating Disord 2000; 28(2): 181–187.
23. Obarzanek E, Lesem MD, Jimerson DC. Resting metabolic rate of anorexia
nervosa patients during weight gain. Am J Clin Nutr 1994; 60(5):666- 675.
24. Krahn DD, Rock C, Dechert RE, Nairn KK, Hasse SA. Changes in resting energy
expenditure and body composition in anorexia nervosa patients during refeeding.
J Am Diet Assoc 1993; 93(4):434–438.
25. Salisbury JJ, Levine AS, Crow SJ, Mitchell JE. Refeeding, metabolic rate, and
weight gain in anorexia nervosa: a review. Int J Eating Disord 1995; 17(4):
337–345.
26. Platte P, Pirke KM, Trimborn P, Pietsch K, Krieg JC, Fichter MM. Resting
metabolic rate and total energy expenditure in acute and weight recovered patients
NUTRITION COUNSELING 401
with anorexia nervosa and in healthy young women. Int J Eating Disord 1994; 16
(l):45–52.
27. Department of Health and Human Services and the United States Department of
Agriculture. The food guide pyramid. 1996. http://www.nal.usda.gov/fnic/Fpyr/
pyramid.html.
28. Satter E. How to Get Your Kid to Eat…But Not Too Much. Palo Alto, CA: Bull
Publishing, 1987.
29. Wilson GT. Cognitive behavior therapy for eating disorders: progress and
problems. Behav Res Ther 1991; 37(suppl 1):S79-S95.
30. Garner DM, Vitousek KM, Pike KM. Cognitive-behavioral therapy for anorexia
nervosa. In: Garner DMG ed. Handbook of Treatment of Eating Disorders. New
York: Guilford Press, 1997:94–144.
31. Lock J, LeGrange D, Agras WS, Dare C. Treatment Manual for Anorexia Nervosa:
A Family-Based Approach. New York: Guilford Press, 2001.
32. Hetherington MM, Altemus M, Nelson ML, Bernat AS, Gold PW. Eating behavior
in bulimia nervosa: multiple meal analyses. Am J Clin Nutr 1994; 60(6):864–873.
33. Hadigan CM, Kissileff HR, Walsh BT. Patterns of food selection during meals in
women with bulimia. Am J Clin Nutr 1989; 50(4):566–759.
34. Weltzin TE, Hsu LK, Pollice C, Kaye WH. Feeding patterns in bulimia nervosa.
Biol Psychiatry 1991; 30(11):1093–1110.
35. Kaye WH, Weltzin TE, Hsu LK, McConaha CW, Bolton B. Amount of calories
retained after binge eating and vomiting. Am J Psychiatry 1993; 150(6):969–971.
36. Goldfein JA, Devlin MJ, Spitzer RL. Cognitive behavioral therapy for the
treatment of binge eating disorder: what constitutes success? Am J Psychiatry
2000; 157(7): 1051–1056.
37. Miller WR, Rollnick S. Motivational Interviewing: Preparing People to Change
Addictive Behavior. New York: Guilford Press, 1991.
38. Sundgot-Borgen J, Rosenvinge JH, Bahr R, Schneider LS. The effect of exercise,
cognitive therapy, and nutritional counseling in treating bulimia nervosa. Med Sci
Sports Exercise 2002; 34(2): 190–195.
39. Hsu LK, Rand W, Sullivan S, Liu DW, Mulliken B, McDonagh B, Kaye WH.
Cognitive therapy, nutritional therapy and their combination in the treatment of
bulimia nervosa. Psychol Med 2001; 31(5):871–879.
40. Hsu LK, Holben B, West S. Nutritional counseling in bulimia nervosa. Int J Eating
Disord 1992; 11:55–62.
41. Fairburn CG, Agras WS, Wilson GT. The research on the treatment of bulimia
nervosa: Practical and theoretical implications. In: Anderson GH, Kennedy SH,
eds. The Biology of Feast and Famine: Relevance to Eating Disorders. San Diego:
Academic Press, 1992:318–340.
42. Hsu LK, Santhouse R, Chesler BE. Individual cognitive behavioral therapy for
bulimia nervosa: the description of a program. Int J Eating Disord 1991; 10:
273–283.
43. Story M. Nutrition management and dietary treatment of bulimia. J Am Diet Assoc
1986; 86:517.
402 CROLL AND NEUMARK-SZTAINER
44. Cowen PJ, Smith KA. Serotonin, dieting, and bulimia nervosa. Adv Exp Med Biol
1999; 467:101–104.
45. Kaye WH, Gendall KA, Fernstrom MH, Fernstrom JD, McConaha CW, Weltzin
TE. Effects of acute tryptophan depletion on mood in bulimia nervosa. Biol Psychiatry
2000; 47(2):151–157.
46. Smith KA, Fairburn CG, Cowen PJ. Symptomatic relapse in bulimia nervosa
following acute tryptophan depletion. Arch Gen Psychiatry 1999; 56:171–176.
47. Mitchell JE, Specker SM, DeZwann M. Comorbidity and medical complications of
bulimia nervosa. J Clin Psychiatry 1991; 52:13.
48. Telch CF, Agras WS, Rossiter EM. Binge eating increases with increasing
adiposity. Int J Eating Disord 1992; 7:115–119.
49. Marcus MD. Binge eating in obesity. In: Fairburn CG, Wilson GT, eds. Binge
Eating: Nature, Assessment, and Treatment. New York: Guilford Press, 1993:
77–96.
50. Wilfley DE, Grillo GM. Eating disorders: a women’s health problem in primary
care. Nurs Prac Forum 1993; 5:34–45.
51. Telch CF, Agras WS. The effects of a very low calorie diet on binge eating. Behav
Ther 1993; 24:177–193.
52. Yanovski SZ, Leet M, Yanovski JA, Flood M, Gold PW, Kissileff HR, Walsh BT.
Food selection and intake of obese women with binge-eating disorder. Am J Clin
Nutr 1992; 56(6):975–980.
53. Rossiter EM, Agras WS, Telch CF, Bmce B. The eating patterns of non-purging
bulimic subjects. Int J Eating Disord 1992; 11:111–120.
54. Timmerman GM. Caloric intake patterns of nonpurge binge-eating women. West J
Nurs Res 1000; 20:103–118.
55. Yanovski SZ, Sebring NG. Recorded food intake of obese women with binge eating
disorder before and after weight loss. Int J Eating Disord 1994; 15:135–150.
56. Wilson GT. Assessment of binge eating. In: Fairburn CG, Wilson GT, eds. Binge
Eating: Nature, Assessment, and Treatment. New York: Guilford Press, 1999:
3227–3249.
57. Grillo GM. The assessment and treatment of binge eating disorder. J Pract
Psychiatry Behav Health 1998; 4:191–200.
58. Williamson DA, Martin CK. Binge eating disorder: a review of the literature after
publication of the DSM-IV. Eating Weight Disord: Stud Anorexia. Bulimia, and
Obesity 1999; 4(3):103–114.
59. National Heart, Lung, and Blood Institute. Clinical guidelines on the identification,
evaluation, and treatment of overweight and obesity in adults—The evidence
report. Obesity Res 1998; 6(suppl 2):51S-209S.
60. Fairburn CG, Cooper Z, Doll HA, Norman P, O’Connor M. The natural course of
bulimia nervosa and binge eating disorder in young women. Arch Gen Psychiatry
2000; 57(7):659–665.
61. Pendleton VR, Goodrick GK, Poston WS, Reeves RS, Foreyt JP.
Exercise augments the effects of cognitive-behavioral therapy in the treatment of
binge eating. Int J Eating Disord 2002; 31(2): 172–184.
NUTRITION COUNSELING 403
62. Goodrick GK, Poston WS II, Kimball KT, Reeves RS, Foreyt JP. Nondieting
versus dieting treatment for overweight binge-eating women. J Consult Clin
Psychol 1998;66(2):363–368.
63. Fariburn CG, Marcus MD, Wilson GT. Cognitive-behavioral treatment of binge
eating and bulimia nervosa. In: Fairburn CG, Wilson GT, eds. Binge Eating:
Nature, Assessment, and Treatment. New York: Guilford Press, 1993:361–404.
64. Tanco S, Linden W, Earle T. Well-being and morbid obesity in women: a
controlled therapy evaluation. Int J Eating Disord 1998; 23(3):325–339.
65. Devlin MJ. Binge-eating disorder and obesity. A combined treatment approach.
Psychiatr Clin North Am 2001; 24(2):325–335.
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17
An Overview of Cognitive-Behavioral
Approaches to Eating Disorders
Stephen A.Wonderlich, James E.Mitchell, and Lorraine
Swan-Kremier
University of North Dakota School of Medicine and Health
Sciences and the Neuropsychiatric Research Institute
Fargo, North Dakota, U.S.A.
Carol B.Peterson and Scott J.Crow
University of Minnesota
Minneapolis, Minneapolis, U.S.A.
CBT, cognitive behavioral therapy; BT, behavioral therapy; ERP, exposure and response preventions; ss, single site; ms, multiple sites; IPT,
interpersonal psychotherapy; SPT, supportive therapy; Imip, imipramine; Desip, desipramine; NT, nutritional counseling.
COGNITIVE-BEHAVIORAL APPROACHES 411
Initiating CBT
The initial sessions of CBT must take into account the patient’s likely
ambivalence about making a change and emphasize the development of
therapeutic rapport. In particular, eating-disordered individuals with highly
obsessional, paranoid, or avoidant cognitive styles may enter treatment with
considerable hesitation. Several authors (37,40) have discussed approaches to
managing such ambivalence that are consistent with CBT. These interventions
typically include recognizing the adaptive functions of the disorder for the
patient, accepting the patient’s thought processes as genuine, and a
demonstration by the clinician of a clear knowledge of both general
psychopathology and also eating disorders.
COGNITIVE-BEHAVIORAL APPROACHES 413
Self-Monitoring
Early in CBT, the patient is provided with some type of self-monitoring form,
which may include information about time of day, environmental situations,
food and liquid consumed, presence of eating disorder symptoms, and
asso ciated maladaptive thoughts and feelings. Such a self-monitoring approach
is a clinically useful way to gather a considerable amount of information about
the patient’s day-to-day “ecological niche” surrounding their eating disorder
symptoms. Patients should be instructed about the importance of
selfmonitoring, which is designed to provide them with a greater sense of
control over and knowledge about their eating disorder symptoms.
Early in treatment, patients may be encouraged to record the consumption of
meals, snacks, and bulimic symptoms (binges) in their selfmonitoring records.
This allows the clinician to see the presence or absence of well-structured
schedules of eating that are reasonably dispersed throughout the day.
Obviously, anorexic individuals’ food records will reveal the absence of healthy
and diversified eating, while the record of a bulimic individual may reveal a
more chaotic and unpredictable pattern of eating. Self-monitoring may
ultimately include an identification of environmental cues for particular types of
eating behaviors, including binge eating, skipping meals, and purging.
Eventually, the patient may also include data on particular thoughts and feelings
in the face of specific environmental events or cues. Thus, the selfmonitoring
may help the clinician and patient to identify a pattern of particular
environmental stimuli, associated intrapsychic activity in the form of cognitions
and feelings, and overt behavioral activity such exercising, binge eating, or
purging.
Cognitive Restructuring
Figure 1 depicts a basic cognitive model underlying CBT. This model
emphasizes the close relationship between thoughts, feelings, and behaviors. In
CBT, cognitions or thoughts are a central operational construct. It is not
stressful environmental stimuli that are ultimately thought to result in eating
disorder symptoms but the cognitive appraisal of those stimuli. For example, an
eating-disordered individual may see her body in the mirror (stimulus) and have
the thought “Oh no, I can’t believe how fat I’ve become.” Such a thought is
associated with a negative emotional response, and in combination this thought
and feeling may increase the likelihood of some selfdestructive behavior
COGNITIVE-BEHAVIORAL APPROACHES 415
employed in CBT for the eating disorders: (a) behavioral experimentation and
(b) testing the validity of the thought-through questions.
Behavioral experimentation refers to identifying a negative thought and the
logical or predicted consequence or outcome associated with that thought.
Then, the individual intentionally creates a behavioral situation, that should result
in the predicted outcome if the thought is accurate. Typically, because of the
high degree of distortion in the maladaptive thought, the behavioral prediction
is not confirmed through the experiment. For example, if an individual has the
thought “eating three meals a day will make me fat,” the patient and clinician can
devise an experiment to test this thought. For example, the patient may agree
that if she was able to eat three meals a day for at least 5 days, this would
provide a good test of whether or not she would gain weight, as oppose to
staying the same or perhaps even losing weight. If the patient were willing to try
this on a trial basis for 5 days, she could actually weigh herself before starting
and again 5 days later. Of course, the patient would have to agree to engage in
the experiment and be willing to report on the outcome. Most likely, at least in
BN, there would be little change in weight because calories may be ingested
through meals rather than traditional binge eating patterns. The patient should
be encouraged to identify the inference that can be drawn from the experiment
and whether or not it conflicts with the prediction associated with the eating
disorder.
The second means of restructuring thought patterns is to assist the patient in
questioning the actual thought. For example, if a patient had the thought “I will
be happy when I am below 100 pounds,” the therapist may ask a series of
questions to test the validity of this idea. For example, the patient may be asked
if she had ever been below 100 pounds previously and whether or not she was
happy then. If not, the therapist may ask what it means that she weighed less
than 100 pounds and was not happy. If she states that she was happy, the
therapist may ask if she was happy all the time. It would be expected that she
was not happy all the time, and that could lead to a discussion of what other
factors must have influenced her mood besides weight, given that she was under
a 100 pounds but still had periods of unhappiness. Also, the patient may be
asked if she knew any other people who weighed less than a 100 pounds and
whether or not they were happy. In general, the therapist should take the
approach of asking the patient what evidence there is to support the thought
that weighing less than 100 pounds will make her happy and, alternatively, what
evidence there is that fails to support the thought. Ideally, the therapist and
patient collaboratively examine the evidence for the thought, examine its
validity, and begin to develop more adaptive and accurate alternative thought
patterns.
COGNITIVE-BEHAVIORAL APPROACHES 417
with practice help the individual to identify solutions to problems that are
outside the realm of eating disorder symptoms.
One specific type of problem solving lies in the area of interpersonal
relationships. Many problems in living involve relationships to other people.
When this is the situation, patients should be encouraged to carefully identify
the nature of the problem they are having with the other person. Assertiveness
training is a helpful approach to several types of interpersonal problems,
including difficulty in expressing negative emotions, problems setting limits,
and problems expressing positive feelings. In therapy, role playing may
greatly facilitate the patient’s ability to effectively deal with problematic
interpersonal situations. Seeing the clinician model appropriate social responses
in a role play with the patient may facilitate imitation. The old teaching axiom
of “see one, do one, teach one,” is an appropriate way to think about improving
social skills.
Case Study
Cindy was a 28-year-old, married mother of a 6-year-old son and 3-year-old
daughter at the time of presentation to the outpatient eating disorders clinic.
She had recently relocated to the area after her husband took a managerial
position with a local manufacturing company. The impetus to her seeking
treatment was the distress and shame she’d been experiencing since her daughter
walked into the bathroom and observed her mother vomiting.
Cindy was seen for an initial evaluation, which included a detailed review of
the onset of eating disorder symptoms, current eating patterns and
compensatory behaviors, thoughts and feelings associated with weight and shape,
weight and menstrual history, as well as assessment of comorbid
psychopathology, chemical use, medical status, and psychosocial history.
Cindy reported the onset of eating disordered behavior at the age of 15 when
she entered a new high school following her family’s relocated. She recalls her
volleyball teammates ridiculing others’ appearance and feared that she would
also be the subject of ridicule. Cindy began skipping breakfast and lunch (a
practice common to her peer group) and consuming only low-calorie and low-
fat foods at the evening meal with her family. She was motivated to continue
dieting by the attention she received from peers. Cindy recalled first self-
inducing vomiting after she ate pizza and sweets at a postgame celebration.
Vomiting behavior quickly escalated, and Cindy also began to binge-eat. She
indicated that because she could vomit she would “make it worth my while” and
consume “forbidden foods” she enjoyed. Binge eating and vomiting continued at
a rate of two or three times a week throughout high school and her early college
years. Although she continued to be extremely concerned about her weight and
COGNITIVE-BEHAVIORAL APPROACHES 419
shape, Cindy maintained a 6-year abstinence from binge eating and vomiting
after she left college, married, had a child, and breast-fed.
Cindy described a gradual relapse in eating disorder symptoms in the year
before her relocation. Anticipating loneliness in a new town, frustrated that she
had not met her goal of completing her degree, and increasingly disparaging of
her body and abilities, Cindy attempted to lose weight through dietary
restriction believing she would feel more confident and better about herself in
general. Binge eating and vomiting quickly returned and escalated. At the time
of presentation to the outpatient eating disorder clinic, Cindy weighed
145 pounds at a height of 5 foot 4 inches (body mass index = 24.9). She
reported extreme dissatisfaction with her shape, feeling extremely fat and
unworthy as a result of her weight. Cindy reported her ideal weight as
110 pounds, believing she would be more confident, a better mother, and more
acceptable to others.
In attempts to achieve her ideal weight, Cindy had a daily plan to avoid
dietary fat, restrict calories to 1000 kcal/day, and exercise for 60 min. Cindy
described “losing the battle” to follow her strict plan and admitted to binge
eating and purging daily. Each day began with attempting to avoid eating, only
to be preoccupied with food, often distracting her from tasks at hand and time
with her children. She typically nibbled on food she prepared for her daughter’s
snack and midday meal. Chastising herself, concluding she had already “blown
it” for the day, and vowing to begin anew the next day, Cindy reported binge
eating on her children’s uneaten meals, 12 ounces of chips, and 6 cups of ice
cream in the early afternoon during the children’s nap time.
Cindy denied use of laxatives, enemas, diuretics, syrup of ipecac, chewing
and spitting, or rumination of food. She denied exercising in an excessive
manner, in fact berated herself for not achieving her plan of daily exercise.
Cindy had been on an antidepressant for 15 months; however, she continued to
struggle with dysphoric mood, amotivation, low energy, poor concentration,
and low self-esteem. Based on evaluation results, it was recommended that
Cindy participate in individual CBT for bulimia. She was referred to her
primary physician for review of medications and serum electrolytes.
Cindy’s treatment began with a detailed description of the cognitive model
of the maintenance of bulimia with particular emphasis on the cyclic relationship
between strict dieting (avoidance of eating, restriction of intake, and food
avoidance), binge eating, and purging. Cindy agreed that insecurity and low self-
esteem precipitated and exacerbated concerns about her weight and shape, and
she believed that her eating disorder had become a way to cope with these
negative mood states. Self-monitoring was presented as the initial treatment
assignment. Cindy was instructed to record the time and place of eating
episodes; type and amount of food eaten; whether the episode was considered a
420 WONDERLICH ET AL.
meal, snack, or binge; whether vomiting occurred; and thoughts, feelings, and
circumstances surrounding the episode of eating (Fig. 2). She was informed of
the importance of accurate self-monitoring and its part in providing vital
information on triggers for eating disorder behaviors as well as guiding
treatment sessions. Despite anticipating embarrassment about the therapist
being aware of the intimate details of her eating disorder, Cindy left the session
stating an understanding of and commitment to the CBT plan.
Despite her stated commitment, Cindy arrived at her second scheduled
appointment having not self-monitored. Time was taken to explore with Cindy
what had interfered with her completing this crucial first assignment, and the
discussion gave way to identifying the advantages and disadvantages of
addressing her eating disorder. Cindy expressed significant ambivalence
regarding treatment, embarrassment and shame about her symptoms, and fear of
becoming fat were she to change her behavior. Cindy was provided with
reassurance that most normal-weight patients do not gain weight as a result of
CBT.
Cindy presented to her third session having completed self-monitoring,
which was reviewed in great detail with particular emphasis on potential cues of
binge eating and vomiting. A pattern of dietary restriction, avoiding foods
thought to be “fattening,” and avoiding eating in general were highlighted as
examples of strict dieting which left Cindy vulnerable to binge eating. The
importance of eating consistently throughout the day was stressed, and Cindy
collaborated on developing a plan for having regular meals and snacks consisting
of food and portion sizes that she was prepared to consume without vomiting.
Cindy was easily able to adapt her eating to the scheduled eating pattern she
provided for her young children and found that three meals and three snacks
could be consumed in the presence of others, which would further decrease the
risk of binge eating and vomiting.
The next several sessions focused on implementing Cindy’s plan for
consistent eating while continuing to monitor her weight through weekly
weighing. Cindy was surprised by an improvement in energy and mood as well
as renewed interest in spending time with her children. Given her significant
fear of weight gain and subsequent food avoidance, Cindy was instructed to
develop a hierarchy of feared foods. Each day, Cindy developed a plan for
introducing a food from the bottom of the hierarchy that may trigger binge
eating and engaging in an alternative behavior immediately following the
consumption until the urge to vomit subsided. Weekly weighing provided
Cindy with valuable evidence that these foods could be consumed without
weight gain, which in turn provided motivation for continuing to add previously
avoided foods.
As episodes of binge eating and vomiting decreased and became intermittent,
Cindy’s treatment began to focus on those factors that had been maintaining her
eating disorder, in particular distorted thoughts and beliefs about food, eating,
weight and shape, and the use of dietary restricting, binge eating, and vomiting
as a means of managing life stress and negative mood. The presence of
maladaptive thoughts as cues for eating disorder behaviors was identified using
self-monitoring forms where Cindy had also been monitoring her thoughts
associated with eating episodes. These thoughts were then challenged using
cognitive restructuring. For example, Cindy identified her belief that “eating fat
will make me fat” and more specifically indicated a belief that she would gain
422 WONDERLICH ET AL.
5 pounds if she consumed a food containing more than 5 grams of dietary fat per
serving. Cindy was challenged to test this belief by setting up an experiment in
which she consumed ice cream without vomiting and later in the week
monitored her weight. She was instructed to consume the ice cream in the
presence of her husband, utilize alternative behaviors for a specified period of
time and/or spend time out of the house should the urge to vomit occur. This
process of challenging maladaptive thoughts through empirical testing and
evidence gathering was repeated as Cindy worked through her list of feared
foods, exposed herself to high-risk situations, and confronted negative thoughts
about her weight and shape.
Cindy’s participation in CBT also revealed a longstanding pattern of engaging
in binge eating and vomiting in response to a variety of negative mood states,
including loneliness, frustration, interpersonal conflict, and selfdisparagement.
Cindy was increasingly able to implement cognitive restructuring and
alternative behaviors at such times, but struggled with extreme negative self-
appraisal, which continued to place her at risk for binge eating and vomiting.
Not completing her educational degree and the lack of social contacts since
relocating were identified as cues for self-disparagement and subsequent eating
disorder behavior. Problem solving was applied wherein Cindy clearly identified
why social isolation was problematic, generated options for solving the problem,
including joining a parents-of-preschoolers group, taking courses to finish her
degree, attending community functions, and joining a church. A similar process
of problem solving was applied to Cindy’s struggle with not completing her
degree, as well as a variety of problems of daily life.
After 4 months of treatment, Cindy achieved abstinence from binge eating
and purging, was consistently eating a variety of foods, and reported increasing
confidence as she tackled what had previously been viewed as insurmountable
environmental stressors. The final stage of treatment focused on maintaining the
changes that Cindy had made in treatment and developing a relapse prevention
plan. Cindy considered what situations may place her at risk for relapse (e.g.,
another relocation, her daughter’s transition into school) and developed a plan
for managing eating disorder symptoms should they arise. She was informed of
the possibility of a reemergence of symptoms in times of stress or transition and
was reassured that utilizing the skills she developed in treatment would likely
curtail a relapse. Cindy reviewed the techniques she had learned and devised a
plan for returning to self-monitoring, making sure she was utilizing alternative
behaviors and remaining connected with her social supports. Cindy agreed that
three consecutive weeks of binge eating and vomiting should signal the need to
return to treatment; however, she felt confident that she would be able to
interrupt the cycle of binge eating and vomiting.
COGNITIVE-BEHAVIORAL APPROACHES 423
CONCLUSION
CBT is a treatment for a wide variety of eating disorder symptoms that has
received considerable empirical support and continues to be the modality of
choice for a variety of eating disorder clinical presentations. CBT may evolve
and be modified in future studies; already applications in telemedicine,
CDROM, and Palm Pilot applications have emerged. Furthermore, variations
of CBT have been developed with a greater emphasis on interpersonal
functioning, emotional responding, and alternative cognitive structures. There
continues to be a need for enhanced approaches to educating mental health
professionals about the applications of CBT to eating-disordered patients, and a
lack of dissemination of these treatments remains a limiting factor for eating-
disordered individuals.
ACKNOWLEDGMENTS
Supported by research grants from the McKnight Foundation and the National
Institute of Mental Health (ROl-MH59234) and the National Institute of
Diabetes, Digestive and Kidney Diseases (R01-DK61912; R01-DK60432;
P30-DK50456), and the Neuropsychiatric Research Institute.
REFERENCES
1. Beck AT, Emery G. Anxiety Disorders and Phobias. New York: Basic Books,
1985.
2. Beck AT, Rush AJ, Shaw BF, Emery G. Cognitive Therapy of Depression. New
York: Guilford Press, 1979.
3. Peterson CP, Mitchell JE. Cognitive behavior therapy. In: Gabbard GO, ed.
Treatment of Psychiatric Disorders. 2d ed. Washington, DC: APA Press, 1995.
4. Fairburn CG, Marcus MD, Wilson GT. Cognitive behavioral therapy for binge
eating and bulimia nervosa: a comprehensive treatment manual. In: Fairburn CG,
Wilson GT, eds. Binge Eating: Nature Assessment and Treatment. New York:
Guilford Press, 1993:361–404.
5. Mitchell JE, Peterson CB. Cognitive-behavioral treatment of eating disorders.
Dickstein LD, Riba MB, Oldham JM, eds. Review of Psychiatry. Vol. 16:.
Washington, DC: APA Press, 1995:1–107–1-134.
6. Crow S, Mitchell JE. Bulimia nervosa. In: Mitchell JE, ed. The Outpatient
Treatment of Eating Disorders: A Guide for Therapists Dietitians and Physicians.
Minneapolis: University of Minnesota Press, 2001:26–59.
7. Lacey JH. An outpatient treatment program for bulimia nervosa. Int J Eat Disord
1983; 286:1609–1613.
8. Connors ME, Johnson CL, Stuckey MK. Treatment of bulimia with brief
psychoeducational group therapy. Am J Psychiatry 1984; 141:1512–1516.
424 WONDERLICH ET AL.
9. Yates AJ, Sambrailo F. Bulimia nervosa: a descriptive and therapeutic study. Behav
Res Ther 1984; 5:505–517.
10. Kirkley BG, Schneider JA, Agras WS, Bachman JA. Comparison of two group
treatments for bulimia. J Consult Clin Psychol 1985; 53:43–48.
11. Ordman AM, Kirschenbaum DS. Cognitive behavioral therapy for bulimia: an
initial outcome study. J Consult Clin Psychol 1985; 53:305–313.
12. Lee NF, Rush AJ. Cognitive-behavioral group therapy for bulimia. Int J Eat Disord
1986; 5:599–615.
13. Wolchik SA, Weiss L, Katzman MA. An empirically validated short-term
psychoeducational group treatment program for bulimia. Int J Eat Disord 1986; 5:
21–34.
14. Wilson GT, Rossiter E, Kleifeld EI, Lindholm L. Cognitive behavioral treatment of
bulimia nervosa: a controlled evaluation. Behav Res Ther 1986; 24:227–238.
15. Fairburn CG, Kirk J, O’Connor M, Cooper PJ. A comparison of two psychological
treatments for bulimia nervosa. Behav Res Ther 1986; 24:629–643.
16. Laessle RG, Waadt S, Pirke KM. A structured behaviorally oriented group
treatment for bulimia nervosa. Psychother Psychosom 1987; 48:141–145.
17. Leitenberg H, Rosen JC, Gross J, Nudelman S, Vara LS. Exposure plus response
prevention treatment of bulimia nervosa. J Consult Clin Psychol 1988; 56:
535–541.
18. Freeman CPL, Barry F, Dunkeld-Turnbull J, Henderson A. Controlled trial of
psychotherapy for bulimia nervosa. Br Med J; 296:521–525.
19. Agras WS, Schneider JA, Arnow B, Raeburn SD, Telch CF. Cognitive behavioral
and response prevention treatments for bulimia nervosa. J Consult Clin Psychol
1989; 57:215–221.
20. Mitchell JE, Pyle RL, Eckert ED, Hatsukami D, Pomeroy C, Zimmerman R. A
comparison study of antidepressants and structured intensive group psychotherapy
in the treatment of bulimia nervosa. Arch Gen Psychiatry 1990; 47:149–157.
21. Fairburn CG, Jones RT, Peveler RC, Carr SJ, Solomon RA, O’Connor ME,
Burran J, Hope RA. Three psychological treatments for bulimia nervosa. Arch Gen
Psychiatry 1991; 48:463–469.
22. Fichter MM, Leibl K, Rief W, Brunner E, Schmidt-Auberger S, Engel RR.
Fluoxetine versus placebo: a double-blind study with bulimic inpatients undergoing
intensive psychotherapy. Pharmacopsychiatry 1991; 24:1–7.
23. Wilson GT, Eldredge KL, Smith D, Niles B. Cognitive behavioral treatment with
and without response prevention for bulimia. Behav Res Ther 1991; 29:575–583.
24. Laessle RG, Beumont PJV, Butow P, Lennerts W, O’Connor M, Pirke KM, Touyz
SW, Waadt S. A comparison of nutritional management with stress management in
the treatment of bulimia nervosa. Br J Psychiatry 1991; 159:250–261.
25. Garner DM, Rockert W, Davis R, Garner MV, Olmsted MP, Engle M.
Comparison of cognitive behavioral and supportive expressive therapy for bulimia
nervosa. Am J Psychiatry 1993; 150:37–46.
COGNITIVE-BEHAVIORAL APPROACHES 425
26. Agras WS, Rossiter EM, Arnow B, Schneider JA, Telch CG, Raeburn SD, Bruce B,
Perl M, Koran LM. Pharmacologic and cognitive behavioral treatment for bulimia
nervosa: a controlled clinical comparison. Am J Psychiatry 1992; 149: 82–87.
27. Mitchell JE, Pyle RL, Pomeroy C, Zollman M, Crosby R, Seim H, Eckert ED,
Zimmerman R. Cognitive behavioral group psychotherapy for bulimia nervosa: the
importance of logistical variables. Int J Eat Disord 1993; 14:277–288.
28. Thackwray DE, Smith MC, Bodfish JW, Meyers AW. A comparison of behavioral
and cognitive behavioral interventions for bulimia nervosa. J Consult Clin Psychol
1993; 61:639–645.
29. Goldbloom DS, Olmsted M, Davis R, Clews J, Heinmaa M, Rockert W, Shaw B.
A randomized controlled trial of fluoxetine and cognitive behavioral therapy for
bulimia nervosa. Behav Res Ther 1997; 35:803–811.
30. Walsh BT, Wilson GT, Loeb KL, Devlin MJ, Pike KM, Roose SP, Fleiss J,
Waternaux C. Medication and psychotherapy in the treatment of bulimia nervosa.
Am J Psychiatry 1997; 154:523–531.
31. Agras WS, Walsh BT, Fairburn CG, Wilson GT, Kraemer HC. Multicenter
comparison of cognitive behavioral therapy and interpersonal therapy for bulimia
nervosa. Arch Gen Psychiatry 2000; 57:459–468.
32. Hsu LK, Rand W, Sullivan S, Liu DW, Milliken B, McDonagh B, Kaye WH.
Cognitive therapy, nutritional therapy and their combination in the treatment of
bulimia nervosa. Psychol Med 2001; 32:871–879.
33. Bulik CM, Sullivan PF, Carter FA, McIntosh VV, Joyce PR. The role of exposure
with response prevention in the cognitive-behavioural therapy for bulimia nervosa.
Psychol Med 1998; 28:611–623.
34. Agras WS, Crow SJ, Halmi KA, Mitchell JE, Wilson CT, Kraemer HC. Outcome
predictors for the cognitive behavior treatment of bulimia nervosa: data from a
multisite study. Am J Psychiatry 2000; 157:1302–1308.
35. Jacobi C, Dahme B, Dittmann R. Cognitive-behavioural, fluoxetine and combined
treatment for bulimia nervosa: short-and long-term results. Eur Eat Disord
Rev2002; 10:179–198.
36. Agras WS, Rossiter EM, Arnow B, Telch CF, Raeburn SD, Bruce B, Koran L. One
year follow up of psychosocial and pharmacologic treatments for bulimia nervosa.
J Clin Psychiatry 1991; 52:29–33.
37. Peterson CB, Mitchell JE. Cognitive behavioral therapy for eating disorders. In:
Mitchell JE, ed. The Outpatient Treatment of Eating Disorders: A Guide for
Therapists, Dietitians, and Physicians. Minneapolis: University of Minnesota Press,
2001:145–167.
38. Smith DE, Marcus MD, Kaye W. Cognitive behavioral treatment of obese binge
eaters. Int J Eat Disord 1992; 12:257–262.
39. Wilfley DE, Agras WS, Telch CF, Rossiter EM, Schneider JA, Cole AG, Sifford L,
Raeburn SD. Group cognitive behavioral therapy and group interpersonal therapy
for the nonpurging bulimic: a controlled comparison. J Consult Clin Psychol 1993;
61:296–305.
426 WONDERLICH ET AL.
40. Wilfley DE, Welch RR, Stein RI, Spurrell EB, Cohen LR, Saelens BE, Dounchis JZ,
Frank MA, Wiseman CV, Matt GE. A randomized comparison of group cognitive
behavioral therapy and group interpersonal psychotherapy for the treatment of
overweight individuals with binge eating disorder. Arch Gen Psychiatry 2002; 59:
713–721.
41. Garner DM, Vitousek KM, Pike KM. Cognitive behavioral therapy for anorexia
nervosa. In: Garner DM, Garfinkel PE, eds. Handbook of Treatment for Eating
Disorders. 2nd ed. New York: Guilford Press, 1997:94–144.
42. Serpell L, Treasure J. Bulimia nervosa: Friend or foe? The pros and cons of bulimia
nervosa. Int J Eat Disord 2002; 32:164–170.
43. Channon S, De Silva P, Hemsley D, Perkins R. A controlled trial of
cognitivebehavioural and behavioural treatment of anorexia nervosa. Behav Res
Ther 1989; 27:529–535.
44. Pike KM. Relapse prevention for anorexia nervosa. Paper presented at the Seventh
New York International Conference on Eating Disorders, New York, 1996.
45. American Psychiatric Association. Practice guideline for the treatment of patients
with eating disorders (revision). Am J Psychiatry 2000; 157(Suppl):l-39.
46. D’zurilla TJ, Goldfried MR. Problem solving and behavior modification. J Abnorm
Psychol 1971; 78:197–226.
18
An Overview of Family Evaluation and
Therapy for Anorexia Nervosa, Bulimia
Nervosa, and Binge Eating Disorder
Deborah Marcontell Michel and Susan G.Willard
Tulane University School of Medicine
New Orleans, Louisiana, U.S.A.
Foley (2) described the family unit as an open system. A system comprises sets of
different parts that are interconnected with all parts affecting the other parts.
Furthermore, each part has a relationship to the other parts in a stable manner.
The family system is considered open because it has a continuous flow of
elements entering and leaving the system. Open systems are further
characterized by wholeness, relationship, and equifinality. Wholeness is the
interdependence between the parts of the system. This principle emphasizes not
only the individuals in the family but also the relationships among them.
Relationship, then, examines the interactions between the parts of the family and
focuses on what is happening, not why it is happening. The family therapist
therefore carefully analyzes interactions among all family members. Finally,
equifinality refers to the tenet that open systems are not dictated by their initial
conditions; thus, difficulties can be eliminated if changes are made at any point
in time within the system. Consequently, a family therapist focuses on the
present, not the past, with the idea that an intervention can be made at any time
to change the system.
According to Foley (2), family relationships are made up of interlocking
triangles that lend stability to the system and function to reduce or increase its
emotional intensity. Thus, whenever the emotional balance between two family
members becomes too distant or too close, a third family member can restore
equilibrium and stability. One of the tasks of the family therapist is to analyze
the existing triangles in the family system and intervene to change the system. The
process by which the system adjusts itself is termed feedback. When negative
feedback is given in response to deviation from the existing system, the deviation
is corrected and balance is restored. By contrast, positive feedback prevents the
system from returning to its original state, forces it to change, and thereby
destroys the former system. Instead of attempting to directly correct a
problematic behavior, the family therapist may use this principle to exaggerate a
symptom to the point at which it causes the original dysfunctional system to
collapse.
appreciated through the observations and writings of Hilde Bruch (6). She noted
the association between eating disorders and difficulty with individuation and
emotional separation from the family of origin. In the mid to late 1970s, Mara
Selvini-Palazzoli (7) and Salvador Minuchin and colleagues (8,9) pioneered the
systematic application of family therapy to the treatment of AN with their schools
of systems therapy and structural therapy, respectively. More recently, a group
of clinicians at the Maudsley Hospital in London have developed the Maudsley
model of family therapy for AN (10).
Obviously, the history of family therapy in the treatment of eating disorders
has focused on the development of methods to treat individuals with AN. These
approaches have also been applied to the family treatment of bulimia nervosa
(BN) and will be discussed later. For a more detailed account of the history and
development of family therapies in the treatment of eating disorders, see Dare
and Eisler (10).
then, is to maintain the child role and to not grow up. Family loyalty to retain
homeostasis is often chosen over normal development, which would lead to
separation and independence. Other characteristics that may be observed
include a highly critical parent, parental depression, or marital problems. In the
latter case, the child may receive the spoken or unspoken message that
independence, autonomy, and leaving home will cause the family system to fall
apart.
We are aware of only one study describing the family characteristics of
individuals with binge eating disorder (BED). Hodges et al. (14) compared the
families of those with BED, AN-restricting type (AN-R), AN-binge/eating
purging type (AN—B+P), BN, and normal controls. The investigators found
that those with BED endorsed less family cohesion and less encouragement to
express honest feelings than the other eating disorder groups. They also
described their families as more isolated, more sedentary, and limited in terms
of emphasis on independence. Furthermore, the BED group rated their families
lower on achievement orientation, intellectual-cultural orientation, and moral-
religious emphasis. Finally, they described their families as having less structure,
fewer rules, and less predictability than the other eating disorder groups. When
compared to individuals with AN-R and AN-B+P, the BED group reported
more conflict that was similar to the group with BN.
Compared to subjects without an eating disorder, individuals with BED in
the Hodges et al. (14) study reported more familial conflict and described their
families as more rigid in terms of rules and procedures used to regulate family
life. The BED group also endorsed less independence, cohesiveness, and
expressiveness in addition to less focus on pursuit of political, social, cultural,
and intellectual endeavors or participation in social or recreational activities.
The authors caution that data were gathered via self-report and no other means
of corroboration obtained, yet the patients’ accounts may provide useful
information for treatment.
FAMILY EVALUATION
In order to determine the needs of the family and to decide what therapeutic
interventions are appropriate, an evaluation of the family is in order. This is in
accordance with the APA Practice Guidelines for the Treatment of Eating
Disorders (15). The evaluation should include all members living within the
home and, at times, the clinician may bring in other family members who do
not live in the home but have been identified as family members having
significant relationships with the identified patient. The purpose of the
assessment is to ascertain what role, if any, the family environment played in the
432 MICHEL AND WILLARD
development and maintenance of the eating disorder and to what degree those
issues, if present, remain (16).
Evaluation of the family includes basic psychosocial information about
members such as demographic data, present and past living arrangements,
psychiatric history, medical history, educational and occupational history, and
social history. Inquiry into significant family events is also important as is the
assessment of family traditions. Gathering background information on each
parent’s family of origin is helpful so that multigenerational patterns of relating
and behaving can be identified. Regarding the evaluation of physical or sexual
abuse, our family and individual assessments are conducted separately by
different therapists. Although we acknowledge that not all clinicians are in a
position to practice in this manner, it is our opinion that this arrangement
makes it comparatively easier for the identified patient to disclose such sensitive
information. Our experience in most cases of ongoing abuse, however, is that it
will not be disclosed until a stronger therapeutic relationship has been
established with the individual psychotherapist. Though we are unaware of any
published data to directly support this clinical observation in a psychotherapy
setting, it is consistent with research demonstrating significant delay in child and
adolescent disclosure of sexual abuse, if the abuse is disclosedatall(17).
In addition to conducting a standard psychosocial interview of the family,
Andersen (18) compiled a list of areas which should be investigated including
(a) interactional patterns, (b) flexibility, (c) sensitivity, (d) family supports and
stresses, (e) performance of stage-appropriate tasks, and (f) family knowledge
of the illness. Examination of interactional patterns includes such topics as
quality of the marital relationship, spousal agreement on parenting behavior,
family satisfaction and companionship, communication patterns, and the general
affective atmosphere of the family. Flexibility refers to how easily the family
system allows members to change in terms of communication and roles they
play in response to situations and stressors. In evaluating the sensitivity
component, the practitioner assesses whether family members demonstrate
emotional hypersensitivity and overreactivity, or un involvement and
insensitivity, to one another. Evaluation of family supports and stresses includes
the degree of support, or lack thereof, that family members provide to one
another as well as any sources of significant strength and stress within the
family. In addition, evaluation of outside supports and stressors is important.
Regarding the performance of stage-appropriate tasks, the clinician assesses the
age appropriateness of rules and responsibilities that are assigned to family
members, particularly children. Finally, the clinician needs to know family
members’ understanding of the illness in terms of etiology, treatment, and
recovery as well as their thoughts, feelings, and behaviors associated with it. In
particular, knowledge of family attitudes and behaviors that may hinder the
FAMILY EVALUATION AND THERAPY 433
patient’s ability to recover is critical so that they may be quickly examined and
resolved (16). Similarly, family members’ preoccupation with weight and
appearance, which may sabotage the identified patient’s efforts at recovery,
must be addressed early on (19).
Vanderlinden and Vandereycken (20) stress that family assessment is a
continuous process throughout family treatment. They recommend performing
a functional analysis of the eating disorder within the family system. The goal is
to formulate hypotheses about how the eating disorder functions within the
family. The following questions, then, are important to remember throughout
the process: (a) How does the symptom serve to stabilize the family? (b) What
role does the family play in stabilizing the symptom? (c) Around what central
theme is the problem organized? (d) What consequences will follow change in
the family? (e) What is the therapeutic dilemma?
Standardized, self-report instruments that the practitioner may find helpful in
assessing quality of familial relationships and interactions from an individual
family member’s point of view are available. A selection of these include the
Leuven Family Questionnaire (21), the Family Evaluation Scale (FES; 22), the
Family Adaptation and Cohesion Evaluation Scale (FACES; 23), and the Family
Assessment Measure (FAM; 24). Of course, it is incumbent on the linician to be
familiar with the purposes, strengths, and limitations of any questionnaire
chosen for use as explained by the test developer.
Minuchin’s group also advocated that the parents take charge of their anorexic
child’s eating by instituting “family meal sessions.” During these sessions, it was
the job of the parents to unite in taking control over their child’s eating
behavior while the therapist monitored family interactions, intervening when
necessary.
Evidence in support of the structural approach, as reported by Minuchin
et al. (9), consists of a detailed study spanning 7 years. During that time,
assessment, treatment, and follow-up data were collected on 50 families having
a child with AN. Six of the identified patients were males. The median age was
14.5 years with a range from 9 to 21 years. All patients received treatment less
than 3 years after the onset of illness. The average length of treatment was
6 months with a range of 2–16 months. Family therapy was typically conducted
on a weekly basis.
Therapists in the study (9) described three trends in treatment that emerged
based on the identified patient’s age. Preadolescents were not seen individually.
Instead, conjoint therapy (identified patient seen with family) was conducted
initially with a shift to marital therapy later. Familial issues centered on
increasing parental control and effectiveness as well as improving the parental
coalition. For the adolescent group, conjoint family therapy and marital therapy
were conducted along with individual sessions. Siblings were seen alone with
the identified patient when judged appropriate. Issues centered on increasing
autonomy and independence in the adolescent. In the young adult sample, the
primary therapeutic issue was separation from the family of origin. Conjoint
family sessions alone were therefore done in the beginning, with a quick shift to
separate individual plus nonconjoint family sessions.
Of the original sample, 80% were followed for 2 years or more. The total
follow-up time ranged from 1.5 to 7 years. Results of the investigation showed
that 86% of the patients achieved full recovery from anorexic symptoms and
correlated psychosocial deficits. Four percent improved somewhat in both
areas, 6% did not improve, and 4% relapsed (9). Martin (as cited in Dare and
Eisler, 10) demonstrated similar findings with a related model of therapy.
Though considered a landmark in family treatment of anorexia nervosa,
Minuchin’s study has been criticized for various methodological weaknesses,
including inadequate sample sizes, overlapping meanings of constructs, a focus
on pathological polarities regarding familial interactions, and a lack of empirical
measures to assess outcome (25,26).
To address some of the criticisms of Minuchin’s psychosomatic model,
authors of a Flemish study operationally defined and measured the concepts by
behavioral methods and self-report (26). The concepts were behaviorally
redefined as follows: “intensity of intrafamilial boundaries” for enmeshment,
“degree of family adaptability” for rigidity, “the family’s way of handling
FAMILY EVALUATION AND THERAPY 435
that these practitioners do not assume that the family is dysfunctional (10).
Instead, this London-based group posited that a significant amount of the
“dysfunction” reported in families with a child with AN may be the result of the
development of a life-threatening illness, changes in the child’s mood and
behavior, potential blaming by professionals, and failure of initial therapeutic
efforts (10). Nevertheless, the Maudsley clinicians observed many of
the same family characteristics as described by Minuchin and Palazzoli (29).
Le Grange (30) explains that therapy is time limited and typically proceeds
through three clearly defined phases: (a) refeeding the person with anorexia
nervosa, (b) negotiating new patterns of relationships, and (c) termination.
During the refeeding phase, the focus is on eating disorder symptoms. Like the
structural family therapists, the Maudsley group advocates that the parents take
charge of the child’s eating and a family meal session may be included in this
phase. Once the child begins to cooperate with increased food intake and there
is a discernible change of mood within the family, patterns of relationships and
other family issues can be discussed. Such discussion takes place around how these
problems affect the parents in their efforts to ensure that the child’s weight
increases steadily. Following weight restoration, the termination phase begins
with an emphasis on the child establishing a healthy adolescent or young adult
relationship with the parents that does not include the eating disorder. Some
clinicians also see the patient individually (10).
In adult patients with AN, the approach is modified so that attempts are made
to remove the eating disorder from its central and controlling role in the
relationships between the identified patient and other family members.
Furthermore, there is not typically a push for the parents to take charge of the
adultchild’seating(31).
Recently, the Maudsley approach was used to develop a professional, family-
based treatment manual targeting adolescents with AN (32,33). Favorable
results were reported for weight restoration and associated psychological
features at 6-month follow-up. The authors caution, however, that the results
are preliminary, short term, and include only 19 cases. A larger, longer term
treatment trial is underway at this writing.
The Maudsley group has conducted a number of controlled trials comparing
different forms of therapy for adolescents with AN in an effort to shape their
own approach (10). In addition, they have shown that adolescents under age 19
with anorexia nervosa for less than 3 years respond very well to the Maudsley
model of family therapy in the short term (34,35) and at 5year follow-up (36).
In adults with AN, an early study tentatively demonstrated that adult patients
derive greater benefit from individual supportive therapy than from the
Maudsley model of family therapy for adults (34). A more recent study (31)
found that adult patients benefited from 1 year of family therapy, but not
FAMILY EVALUATION AND THERAPY 437
issues. The boundary problems encompassed physical space and privacy, rules
about respect for boundaries, and tolerance of emotional distance. Boundaries
were sometimes lacking or impermeable. Regarding organization, systems need
rules or organization to regulate actions or expressions. Thus, a system can be
too rigidly organized or it can be disorganized. In the experience of Root and her
coworkers, all the families they treated had difficulty expressing and resolving
feelings, particularly anger, resentment, jealousy, grief, depression, anxiety,
and insecurity. The clinicians argued that difficulties in this arena resulted in the
actual bulimic symptoms; they postulated that a system that disallows certain
feelings and cannot adapt encourages either an explosive discharge of feelings or
development of psychosomatic illnesses. Thus, a child in this type of system
subsequently learns that directly expressing certain emotions causes a parent to
become explosive or ill.
Another purely theoretical approach to family treatment for BN has been
described by Jack Brandes (43) of the University of Toronto. He asserted that
families having a child with BN have difficulties with attachment and loss. In his
practice, many families related accounts of actual loss and abandonment through
illness, death, change in socioeconomic status, and immigration followed by
social isolation. He hypothesized that the concerns these families have with
appearance, demeanor, and performance may represent worries about being
unacceptable and unappealing to society. Symptomatic behavior, i.e., bulimic
behavior, may therefore be a means of coping with social isolation, separation,
and loss. The treatment model Brandes (43) proposed to treat families having a
child with BN consisted of four phases that embraced structural, cognitive, and
psychoeducational components. He noted that the family may be seen
exclusively, or individual and/or marital sessions may be added as clinically
appropriate. The first phase of treatment is assessment in which the therapist
“joins” with the family (establishes a therapeutic alliance), performs a family
history, works to reduce shame and blame, and educates the family about BN.
The second phase, early treatment, focuses on dietary reeducation and
encouraging the identified patient to own the bulimic symptoms. There is also
an emphasis on loss and abandonment themes, self-sacrifice of the identified
patient, and individual identity in the family. The third stage of treatment
addresses individual concerns, marital issues, separation, and integration into
the community. Termination, the final phase of treatment, focuses on feelings
of loss and abandonment regarding treatment. To ease the difficulty of
termination, the therapist contracts for future contacts with the family.
An investigation by Schwartz et al. (11) involved 30 families having an
adolescent or adult child with BN treated from a structural-systemic approach.
The treatment model focused on patient differentiation from the family of
origin, with work in this area initiated prior to directly targeting bulimic
440 MICHEL AND WILLARD
subject had a good outcome, five had an intermediate outcome, and one had a
poor outcome. Overall, average outcome scores significantly improved
following treatment, although the study was limited by a small sample and lack
of a control group.
Despite the relative dearth of empirical information on the effectiveness of
family treatment in BN, family therapy is clinically accepted as an important
component in the comprehensive treatment of BN, particularly in younger
patients. Our experience has shown family therapy to be quite helpful in
resolving issues that may contribute to the development and maintenance of the
eating disorder. It is particularly useful when used in conjunction with
individual psychotherapy focused on individuation and identity formation
combined with the use of cognitive-behavioral techniques to address symptom
reduction.
SUMMARY
The family therapy movement began in the 1950s and represented a change in
the way in which behavior was viewed, emphasizing present interactions and
relationships between family members. The majority of family treatment
models and studies on the efficacy of family therapy in treating eating disorders
have focused on AN. Nevertheless, it is widely accepted in clinical practice that
family therapy is required in comprehensive treatment for both AN and BN,
particularly in younger patients still living at home. Empirical support for family
treatment of AN and BN exists, but well-controlled outcome investigations are
somewhat limited (3). In the case of BED, a recently defined problem, family
treatment has not been studied. However, there may be a role for family
therapy in treatment if the clinician determines that family members have a role
in the origin or maintenance of the illness.
Dysfunctional family characteristics of those with eating disorders have been
identified and, for those with AN or BN, clinicians have described family
typologies. Whether or not these attributes are part of a dysfunctional system
that produces an individual with an eating disorder is debatable, as some experts
446 MICHEL AND WILLARD
believe that it may be the result of the stress associated with having a child with
AN or BN. In addition, the importance of biological factors in the development
of AN and BN is becoming more evident, along with environmental influences.
Regarding the environmental factors, we have previously noted (12) that the
family may contribute to the development of, or exacerbate, an eating disorder
by providing an environment that can hinder an adolescent in establishing an
identity, practicing effective communication skills, and/or learning adaptive
coping skills. Within the context of the family, his or her eating disorder may
function to establish an identity separate from the family, to cope with
stressors, to distract from negative feelings, and to provide what the patient
considers to be a means of “safe” self-expression of feelings.
With regard to clinical practice, it is usually essential for patients living with
their families of origin to participate in family therapy, as everyone in the family
is affected by these disorders. For those no longer living at home, family therapy
may be limited to couples therapy, marital therapy, or the current family system.
If, however, members of the family of origin are found to still stimulate the
eating disorder, it will be necessary to include them in family treatment. In very
critical or abusive families, family therapy may need to take the form of parent
counseling or nonconjoint family therapy. A thorough evaluation of the family
and family dynamics at the outset will assist the clinician in sorting out these
issues and in conducting effective family therapy. In addition, the combination of
family therapy and individual therapy appears to be quite prevalent as each form
of treatment can provide a useful and complementary function, which facilitates
recovery. Finally, some families present obstacles to assessment and treatment,
including denial of the eating disorder, minimization of the problem, and/or
denial of the psychological underpinnings. These issues must be resolved and the
family engaged in a therapeutic alliance in order to increase the likelihood of
achieving a successful outcome.
REFERENCES
1. Hoffman L. Foundation of Family Therapy: A Conceptual Framework for Systems
Change. New York: Basic Books, 1981:16–19.
2. Foley VD. Family therapy. In: Corsini RJ, ed. Current Psychotherapies. 3rd ed.
Itasca, IL: F.E. Peacock, 1984:447–490.
3. Lemmon CR, Josephson AM. Family therapy for eating disorders. Child Adol
Psychiatry Clin of North Am 2001; 10:519–542.
4. Gull WW. Anorexia nervosa (apepsia hysterica, anorexia hysterica). Trans Clin Soc
London 1874; 7:22–28.
5. Lasegue C. De 1’anorexie hysterique. Arch Gen Med 1873; 1:384–403.
FAMILY EVALUATION AND THERAPY 447
6. Bruch H. Eating Disorders: Obesity, Anorexia Nervosa, and the Person Within.
New York: Basic Books, 1973.
7. Selvini-Palazzoli M. Self-Starvation. New York: Jason Aronson, 1974.
8. Minuchin S, Baker L, Rosman BL, Liebman R, Milman L, Todd TC. A conceptual
model of psychosomatic illness in children. Arch Gen Psychiatry 1975; 32:
1031–1038.
9. Minuchin S, Rosman BL, Baker L. Psychosomatic Families: Anorexia Nervosa in
Context. Cambridge, MA: Harvard University Press, 1978.
10. Dare C, Eisler I. In: Garner DM, Garfinkel PE, eds. Handbook of Treatment for
Eating Disorders. New York: Guilford Press, 1997:307–324.
11. Schwartz RC, Barrett MJ, Saba G. Family therapy for bulimia. In: Garner DM,
Garfinkel PE, eds. Handbook of Psychotherapy for Anorexia Nervosa and Bulimia.
New York: Guilford Press, 1985:280–307.
12. Michel DM, Willard SG. When Dieting Becomes Dangerous: Understanding and
Treating Anorexia and Bulimia. New Haven, CT: Yale University Press, 2003.
13. Root MPP, Fallon P, Friedrich WN. Bulimia: A Systems Approach to Treatment.
New York: W.W. Norton and Co., 1986.
14. Hodges EL, Cochrane CE, Brewerton TD. Family characteristics of binge-eating
disorder patients. Int J of Eat Disord 1998; 23:145–151.
15. American Psychiatric Association Work Group on Eating Disorders. Practice
guideline for the treatment of patients with eating disorders. Rev Am J Psychiatry
2000; 57(suppl l):l-39.
16. Woodside DB, Shekter-Wolfson LF, Garfinkel PE, Olmsted MP. Family
interactions in bulimia nervosa II: complex intrafamily comparisons and clinical
significance. Int J Eat Disord 1999; 17:117–126.
17. Paine ML, Hansen DJ. Factors influencing children to self-disclose sexual abuse.
Clin Psychol Rev 2002; 22:271–295.
18. Andersen AE. Practical Comprehensive Treatment of Anorexia Nervosa and
Bulimia. Baltimore, MD: The Johns Hopkins University Press, 1985:135–148.
19. Pelch BL. Eating disordered families: Issues between the generations. In: Lemberg
R, Cohn L, eds. Eating Disorders: A Reference Sourcebook. Phoenix: OryxPress,
1999:121–123.
20. Vanderlinden J, Vandereycken W. Family therapy within the psychiatric hos pital:
Indications, pitfalls, and specific interventions. In: Vandereycken W, Kog E,
Vanderlinden J, eds. The Family Approach to Eating Disorders: Assessment and
Treatment of Anorexia Nervosa and Bulimia. New York: PMA Publishing, 1989:
263–310.
21. Kog E, Vertommen H, DeGroote T. Family interaction research in anorexia
nervosa: the use and misuse of a self-report questionnaire. International Journal of
Family Psychiatry 1985; 6:227–243.
22. Moos RH, Moos BS. Family Environment Scale Manual. 2d ed. Palo Alto, CA:
Consulting Psychologists Press, 1986.
23. Waller G, Slade P, Calam R. Family adaptability and cohesion: relation to eating
attitudes and disorders. Int J Eat Disord 1990; 9:225–228.
448 MICHEL AND WILLARD
41. Robin AL, Siegal PT, Koepke T, Moye AW, Tice S. Family therapy versus
individual therapy for adolescent females with anorexia nervosa. J Dev Behavi
Pediat 1994; 15:111–116.
42. Robin AL, Gilroy M, Dennis AB. Treatment of eating disorders in children and
adolescents. Clin Psychol Rev 1998; 18:421–446.
43. Brandes J. Outpatient family therapy for bulimia nervosa. In: Woodside DB,
Shekter-Wolfson L, eds. Family Approaches in Treatment of Eating Disorders.
Washington, DC: American Psychiatric Press, 49–66.
44. Jager B, Liedtke R, Kunsebeck HW, Lempa W, Kersting A, Seide L.
Psychotherapy and bulimia nervosa: evaluation and long-term follow-up of two
conflict-orientated treatment conditions. Acta Psychiatr Scand 1996; 93:268–278.
45. Dodge E, Hodes M, Eisler I, Dare C. Family therapy for bulimia nervosa in
adolescents: an exploratory study. J Fam Ther 1995; 17:59–77.
46. American Psychiatric Association. Diagnostic and Statistical Manual of Mental
Disorders. 4th ed. Washington, DC, 1994.
47. Gorin AA, Le Grange D, Stone AA. Effectiveness of spouse involvement in
cognitive behavioral therapy for binge eating disorder. Int J Eat Disord 2003: 421–
433.
48. Perednia C, Van Vreckem E, Vandereycken W. Parent counseling: From guidance
to treatment. In: Vandereycken W, Kog E, Vanderlinden J, eds. The Family
Approach to Eating Disorders: Assessment and Treament of Anorexia Nervosa and
Bulimia. New York: PMA Publishing, 1989:249–261.
49. Klump K. A genetic link to anorexia. In: DeAngelis T, ed. Monitor on Psychology.
March 2002; 33(3):34–36.
50. Goldner EM, Birminghan CL. Anorexia nervosa: methods of treatment. In:
Alexander-Mott L, Lumsden DB, eds. Understanding Eating Disorders: Anorexia
Nervosa, Bulimia Nervosa, and Obesity. Washington, DC: Taylor & Francis, 1994:
135–157.
51. Gowers S, Norton K, Halek C, Crisp AH. Outcome of outpatient psychotherapy in
a random allocation treatment study of anorexia nervosa. Int J Eat Disord 1994; 15:
165–177.
52. Michel DM. Psychological assessment as a therapeutic intervention in hospitalized
patients with eating disorders. Prof Psychol Res Pract. In press.
53. Casper RC, Troiani M. Family functioning in anorexia nervosa differs by subtype.
Int J Eat Disord 2001; 30:338–342.
54. Powers P. Management of patients with comorbid medical conditions. In: Garner
DM, Garfinkel PE, eds. Handbook of Treatment for Eating Disorders. 2d ed. New
York: Guilford Press, 1997:424–436.
55. Willard SG. Anorexia and Bulimia: The Potential Devastation of Dieting. Plainfield,
NJ: Patient Education Press, 1990.
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19
Interpersonal Psychotherapy for Anorexia
Nervosa, Bulimia Nervosa, and Binge Eating
Disorder
M.Joy Jacobs
San Diego State University/University of California San Diego
Joint Doctoral Program in Clinical Psychology
San Diego, California, U.S.A.
R.Robinson Welch and Denise E.Wilfley
Washington University School of Medicine
St. Louis, Missouri, U.S.A.
INTRODUCTION
Originally developed by Gerald Klerman and colleagues (1) for the
management of unipolar depression, interpersonal psychotherapy (IPT) is a
brief, time-limited therapy that has been successfully adapted for the
management of eating disorders. First successfully adapted for the management
of bulimia nervosa (BN) (2,3), IPT has since proven effective, via an innovative
group format, for binge eating disorder (BED). Currently, the role of IPT in the
management of anorexia nervosa remains unclear.
THEORETICAL FOUNDATIONS OF
INTERPERSONAL PSYCHOTHERAPY
IPT was initially developed not as a novel therapy, but as an attempt to reflect
interpersonally focused treatment for depression already in practice in the
1970s and 1980s (4,5). IPT is theoretically rooted in theories developed by
Adolf Meyer, Henry Stack Sullivan, and John Bowlby. In the 1950s, Meyer
postulated that psychopathology was rooted in maladjustment to one’s social
environment (6). During the same time period, Henry Stack Sullivan (who was
responsible for popularizing the term “interpersonal”) theorized that a patient’s
interpersonal relationships, rather than intrapsychic processes alone, constituted
the relevant focus of therapeutic attention. Sullivan believed that individuals could
not be understood in isolation from their interpersonal relationships and posited
452 JACOBS ET AL.
Treatment Structure
IPT for eating disorders typically lasts 15–20 sessions over a 4- to 5-month
period (33,34). The treatment is demarcated by three phases. The initial phase is
dedicated to identifying the problem area that will be the target for treatment.
The intermediate phase is devoted to working on the target problem area(s). The
termination phase is devoted to consolidating gains made during treatment and
preparing patients for future work on their own. Each phase of treatment for
eating disorder patients, along with clinical vignettes illustrating implementation
of the treatment, will be described in detail below.
Therapeutic Stance
Similar to other therapies, IPT places importance on establishing a positive
therapeutic alliance between therapist and patient. Specifically, the IPT
therapeutic stance is one of warmth, support, and empathy. The therapist is
active and advocates for the patient rather than remaining neutral. By phrasing
things positively, the therapist helps the patient feel comfortable and aims to
foster a safe and supportive working environment. Confrontations and
clarifications are offered in a gentle and timely manner, and the therapist is
careful to encourage the patient’s positive expectations of the therapeutic
relationship. In addition, the therapist conveys a hopeful stance and optimistic
attitude about the patient’s ability to recover.
Source: Adapted from Wilfley DE, Stein Rl, Welch RR. Interpersonal psychotherapy for
the treatment of eating disorders. In: Treasure, J, Schmidt U, Dare C, Van Furth E, eds.
Handbook of Eating Disorders, 2nd ed. Sussex: John Wiley & Sons, 2003; 253–270.
formulation, the therapist links the patient’s eating disorder to one of the four
interpersonal problem areas. The patient’s concurrence with the therapist’s
identification of the problem area and agreement to work on this area are essential
before beginning the intermediate treatment phase.
DIAGNOSIS AND ASSIGNING THE SICK ROLE. After a thorough
psychiatric review has been conducted, the patient is formally diagnosed with an
eating disorder and assigned the “sick role.” The purposes of assigning the sick
role are both theoretical and practical. Consistent with the medical model,
receiving a formal diagnosis reinforces the idea that the patient has a known
condition that can be managed. Accurate diagnosis is essential to effective
treatment. The giving of a diagnosis also explicitly identifies the patient as in
need of help. The sick role is assigned not to condescend to the patient but
rather to temporarily exempt the individual from other responsibilities in order
to devote full attention to recovery. This is particularly important for eating-
disordered patients, many of whom tend to set aside their own needs and
desires in order to care for and please others. If this applies in a particular case,
the therapist may explicitly highlight the patient’s excessive caretaking
458 JACOBS ET AL.
tendencies and encourage the patient to redirect this energy from others to her
own recovery. In doing so, the therapist clarifies the rationale behind IPT—that
by improving the patient’s patterns of interpersonal functioning, the patient’s
eating disorder symptoms are expected to improve as well.
THE INTERPERSONAL INVENTORY. At the beginning of IPT, an
interpersonal inventory examining the patient’s interpersonal history is
conducted. The interpersonal inventory may take 1–3 sessions to complete. A
thorough interpersonal inventory is essential for adequate case formulation and
development of an optimal treatment plan. The clinical importance of investing
the time involved in conducting a comprehensive interpersonal inventory
cannot be overemphasized; accurate identification of the patient’s primary
problem area can be difficult and is key to success in therapy.
Included in the interpersonal inventory is a review of the patient’s current
close relationships, current social functioning, relationship patterns, and
expectations. Changes in interpersonal relationships are explored and discussed
with reference to the onset and maintenance of eating disorder symptoms. For
each person who is important in the patient’s life, the following information is
assessed: frequency of contact, activities shared, satisfactory and unsatisfactory
aspects of the relationship, and ways that the patient would like to change the
relationship. The therapist obtains a chronological history of significant life
events, fluctuations in mood and self-esteem, interpersonal relationships, and
eating disorder symptoms. From this review, the therapist can work with the
patient to make connections between certain life experiences and eating disorder
symptoms. Thorough exploration of this interrelationship typically helps
patients to more clearly understand the rationale behind IPT. Upon completion
of the interpersonal inventory, the therapist should have helped the patient
identify a primary interpersonal problem area(s).
THE INTERPERSONAL FORMULATION. Upon completion of the
interpersonal inventory, the therapist should have developed an individualized
interpersonal formulation, including identification of the patient’s primary
problem area. Although some patients may present for treatment with
difficulties in several problem areas, the time-limited nature of the treatment
necessitates a focused approach. The therapist, with the agreement of the
patient, should assign one, or at most two, problem area(s) upon which to
develop a treatment plan. The goals developed at this stage will be referenced at
each future session and will guide the day-to-day work of the treatment. For
examples of individual case formulations, the reader is referred to (35). If more
than one problem area is identified, the patient may choose to work
simultaneously on both or may decide to first address the problem area
that seems most likely to be responsive to treatment. For example, when a
patient has role disputes and interpersonal deficits, clinical attention might first
INTERPERSONAL PSYCHOTHERAPY 459
Therapeutic Techniques.
FOCUSING ON GOALS. IPT is a directed, goal-oriented therapy. Thus, it
is important that the therapist maintain a focus each week on how the patient is
working on his or her goals between sessions. Phrases such as “moving forward
on your goals” and “making important changes” are used to encourage patients
INTERPERSONAL PSYCHOTHERAPY 461
* Please note that in order to most clearly illustrate the therapeutic principles discussed
in the text, this and the other clinical vignettes included below appear to offer more
rapid results than may typically be expected clinically.
462 JACOBS ET AL.
you can more clearly see that connection, how would you like to
start working on your relationship with your father?
REDIRECTING ISSUES RELATED TO EATING, SHAPE, AND/OR
WEIGHT. Eating disorder patients may frequently bring up issues in session
relating to distressing eating behavior (e.g., binge episodes) or may want to
engage in extended discussion relating to eating, shape, and weight. Although
these issues are relevant insofar as they reflect the clinical status of the patient’s
eating disorder, the therapist must be attentive to keep the session “on track,”
i.e, focused on the patient’s treatment goals. In such situations, the therapist
should gently but firmly redirect the patient back to work on the treatment
goals. As discussed above, dialogue related to eating disorder symptomatology
must be repeatedly linked to its functional role in the interpersonal domain. The
following example illustrates how a therapist can redirect discussion and help
the patient focus on the treatment goals:
Therapist: What did you want to work on today, Jim?
Jim: I’ve been really stressed out lately. I have two exams this week and
a research paper due. I didn’t have much time to eat, which was
good, but I had a huge binge on Saturday night. I found myself in
the kitchen gorging on chips, cookies, pizza, basically anything that
didn’t move. I was so embarrassed when my roommate walked in
and saw what I was doing. I probably would still be eating if he
hadn’t walked in.
Therapist: One of the things you shared with me last week was that eating is a
way for you to relieve stress, to unwind. Instead of allowing
yourself a break or sharing your feelings with friends, you’ll turn to
food.
Jim: I definitely did that. You wouldn’t believe how I was shoving food
in by the mouthful, I couldn’t eat fast enough, I wanted…
Therapist: Jim, let me refocus you for a moment, back to your goals. How
have your efforts to reach out to other students been coming?
Jim: Pretty good. I’ve started studying in the library, so that I can hang
out in the student lounge when I need a break. I’ve met a few
people that way. It’s hard for me though because I always feel
insecure in social situations. I feel like other people may be judging
me or don’t like me.
Therapist: As we discussed last week, for a long time you’ve been sheltering
yourself from that insecurity by avoiding others and using food to
cope with stress. I wonder if as you practice being more social and
build up your support system, you’ll start to feel more comfortable
socially. You’ll have more friends to turn to when you’re stressed
464 JACOBS ET AL.
and be less likely to turn to food. In the short time we’ve been
working together, you’ve already met several new people. Not
surprisingly, you only had one overeating episode this past week.
You said earlier that you were bingeing nightly during similarly
stressful times in the past.
The above discussed therapeutic techniques (i.e., focusing on goals;
connecting eating symptoms and interpersonal problems; redirecting eating,
weight, or shape issues) are utilized with patients in all four problem areas.
By the end of the intermediate phase, patients are often acutely aware that
treatment will soon be ending. The therapist should begin to discuss termination
explicitly and address any anxiety the patient may be experiencing regarding it.
The therapist should begin to prepare the patient for emotions that may arise
with termination, including grief related to the ending of treatment.
The Termination Phase. The termination phase typically lasts four to five
sessions. During this phase, the therapist should encourage the patient to reflect
on progress made during therapy and to outline goals for remaining work.
Patients are encouraged to identify early warning signs of relapse (e.g.,
overeating, restricting, negative mood) and to identify potential plans of action.
Patients are reminded that eating disorder symptoms tend to arise in times of
difficulty and are encouraged to view such symptoms as important early
warning signals. Identifying potential plans of action in such situations will serve
to increase the patient’s sense of competence and security. Nevertheless, it is
also essential to assist patients in identifying warning signs and symptoms that
may indicate a need for professional intervention in the future.
with your husband.” Once this has generated discussion, progressively more
specific questioning would ensue.
Encouraging Affect. IPT’s focus on affect evocation and exploration is especially
relevant for eating disorder patients, given that problematic eating often
functions as a way to regulate negative affect. Specifically, the IPT therapist
helps patients: (a) acknowledge and accept painful affects, (b) use affective
experiences to bring about desired interpersonal changes, and (c) experience
suppressed affects.
Frequently, eating-disordered patients are emotionally constricted in
situations when others would typically experience strong emotions. For
example, sometimes patients will deny feeling upset when it is clear that an
upsetting interaction has just occurred. In this situation, the therapist might say,
“Although you said you were not upset, it appears to me that you have shut down
since mentioning the situation with your husband.” By explicitly noting the
discrepancy, the therapist will attempt to draw out affect that has been
suppressed.
Clarification. This technique is useful in calling attention to contradictions that
may have occurred in the patient’s presentation of material and increases the
patient’s awareness about what she or he has actually communicated. For
example, contradictions between the patient’s affect and speech may be
noteworthy (i.e., “While you were telling me how upset you are about your
father, you had a smile on your face. What do you think that’s about?”).
Communication Analysis. This technique is used to identify any communication
difficulties that the patient may be experiencing and to help the patient alter
ineffective communication patterns. Typically, the therapist will ask the patient
to recall in great detail a recent interaction or argument with a significant other.
Together, patient and therapist work to identify any communication difficulties
and to find more effective communication strategies.
Use of the Therapeutic Relationship. The premise behind this technique is that
people have characteristic patterns of interacting with others. The technique is
utilized by exploring the patient’s thoughts, feelings, expectations, and behavior
in the therapeutic relationship and relating these to the patient’s characteristic way
of behaving and/or feeling in other relationships. This technique is particularly
relevant and useful for patients with interpersonal deficits and interpersonal role
disputes. Use of this technique offers the patient the opportunity to understand
the nature of his or her difficulties in interacting with others and provides the
patient with helpful feedback on his or her interaction style.
466 JACOBS ET AL.
and goals are incorporated into the treatment plan. The primary problem area is
determined by conducting a thorough interpersonal inventory and devising an
individualized interpersonal formulation for each patient. IPT has resulted in
significant and well-maintained improvements for the management of BN and
BED; its role in the management of AN has yet to be determined.
The interpersonal focus of IPT has traditionally been more readily embraced
by clinicians than CBT; IPT may also be an easier therapy in which to become
proficient. In the future, the efficacy of IPT in eating-disordered populations
may be further enhanced by including a specific focus on eating disorder
symptomatology in the treatment. In addition, further adaptations of the group
format, which has demonstrated promise with BED patients, may be usefully
extended to other patient subpopulations who would likely benefit from the
support of a group modality (i.e., adolescents). Additional research is needed
regarding the mechanisms by which IPT achieves its effects, predictors of
treatment outcome, and the effectiveness of IPT for eating disorders in clinical
settings. Finally, advances in neuroscience, specifically increased sophistication
in neuroimaging techniques, offer the potential to investigate the impact of IPT
on brain function in eating disorder patients. Such studies have revealed changes
in brain function in depressed patients treated with IPT (53,54); similar studies
of IPT for eating disorders may provide useful information regarding
physiological mechanisms influencing treatment response. Such empirically
based refinements of the content and delivery of IPT may thus further enhance
its clinical utility in the management of eating disorders.
REFERENCES
1. Klerman GL, Weissman MM, Rounsaville BJ, Chevron ES. Interpersonal
Psychotherapy of Depression. New York: Basic Books, 1984.
2. Fairburn CG, Jones R, Peveler RC, Carr SJ, Solomon RA, O’Connor ME, Burton
J, Hope A. Three psychological treatments for bulimia nervosa: a comparative
trial. Arch Gen Psychiatry 1991; 48:463–469.
3. Fairburn CG, Peveler RC, Jones R, Hope RA, O’Connor ME. Predictors of
12-month outcome in bulimia nervosa and the influence of attitudes to shape and
weight. J Consult Clinical Psychol 1993; 61:696–698.
4. Klerman GL, Weissman MM. Interpersonal psychotherapy for depression:
background and concepts. In: Klerman GL, Weissman MM, eds. New Applications
of Interpersonal Psychotherapy. Washington, DC: American Psychiatric
Association, 1993:3–26.
5. Frank E, Spanier C. Interpersonal psychotherapy for depression: overview, clinical
efficacy, and future directions. Clin Psychol Sci Pract 1995; 2:349–369.
6. Meyer A. Psychobiology: A Science of Man. Springfield, IL: Charles C Thomas,
1957.
470 JACOBS ET AL.
25. Stice E, Akutagawa D, Gaggar A, Agras WS. Negative affect moderates the relation
between dieting and binge eating. Int J Eating Disord 2000; 27:218–229.
26. Telch CF, Agras WS. Do emotional states influence binge eating in the obese? Int J
Eat Disord 1996; 20:271–279.
27. Powell AL, Thelen MH. Emotions and cognitions associated with bingeing and
weight control behavior in bulimia. J Psychosom Res 1996; 40:317–328.
28. Schupak-Neuberg E, Nemeroff CJ. Disturbances in identity and self-regulation in
bulimia nervosa: implications for a metaphorical perspective of “body as self.” Int J
Eat Disord 1993; 13:335–347.
29. Steiger H, Gauvin L, Jabalpurwala S, Seguin JR, Stotland S. Hypersensitivity to
social interactions in bulimic syndromes: relationship to binge eating. J Consult
Clin Psychol 1999; 67:765–775.
30. Fairburn CG, Peveler RC, Jones R, Hope RA, O’Connor ME. Predictors of
12-month outcome in bulimia nervosa and the influence of attitudes to shape and
weight. J Consult Clinical Psychol 1993; 61:696–698.
31. Wilfley DE, Welch RR, Stein RI, Spurrell EB, Cohen LR, Saelens BE, Dounchis JZ,
Frank MA, Wiseman CV, Matt GE. The psychological treatment of binge eating
disorder (BED): a comparison group of cognitive behavioral therapy and
interpersonal psychotherapy. Arch Gen Psychiatry 2002; 59:713–721.
32. McIntosh VV, Bulik CM, McKenzie JM, Luty SE, Jordan J. Interpersonal
psychotherapy for anorexia nervosa. Int J Eat Disord 2000; 27:125–139.
33. Wilfley DE, Frank MA, Welch R, Spurrell EB, Rounseville BJ. Adapting
interpersonal psychotherapy to a group format (IPT-G) for binge eating disorder:
toward a model for adapting empirically supported treatments. Psychother Res
1998; 8:379–391.
34. Fairburn CG, Doll HA, Welch SL, Hay PJ, Davies BA, O’Connor ME. Risk factors
for binge eating disorder: a community-based, case-control study. Arch Gen
Psychiatry 1998; 55:425–432.
35. Wilfley DE, Stein RI, Welch RR. Interpersonal psychotherapy for the treatment of
eating disorders. In: Treasure J, Schmidt U, Dare C, Van Furth E, eds. Handbook
of Eating Disorders. 2d ed. Sussex: John Wiley & Sons, 2003; 253–270.
36. Frank E, Kupfer DJ, Wagner EF, McEachran AB, Cornes C. Efficacy of
interpersonal psychotherapy as a maintenance treatment of recurrent depression:
contributing factors. Arch Gen Psychiatry 1991; 48:1053–1059.
37. Wilson GT, Fairburn CG Eating disorders. In: Nathan PE, Gorman JM, eds.
Treatments That Work. 2d ed. New York: Oxford University Press, 2002.
38. Fairburn CG, Norman PA, Welch SL, O’Connor ME, Doll HA, Peveler RC. A
prospective study of outcome in bulimia nervosa and the long-term effects of three
psychological treatments. Arch Gen Psychiatry 1995; 52:304–312.
39. Agras WS, Walsh BT, Fairburn CG, Wilson GT, Kraemer HC. A multicenter
comparison of cognitive-behavioral therapy and interpersonal psychotherapy for
bulimia nervosa. Arch Gen Psychiatry 2000; 57:459–466.
472 JACOBS ET AL.
40. Fairburn CG, Jones R, Peveler RC, Carr SJ, Solomon RA, O’Connor ME, Burton
J, Hope A. Three psychological treatments for bulimia nervosa: a comparative
trial. Arch Gen Psychiatry 1991; 48:463–469.
41. Wilfley DE, MacKenzie KR, Welch RR, Ayres VE, Weissman MM. Interpersonal
Psychotherapy for Group. New York: Basic Books, 2000.
42. Wilfley DE, Agras WS, Telch CF, Rossiter EM, Schneider JA, Cole AG, Sifford L,
Raeburn SD. Group cognitive-behavioral therapy and group interpersonal
psychotherapy for the nonpurging bulimic individual: a controlled comparison.
J Consult Clin Psychol 1993; 61:296–305.
43. Grilo CM, Masheb RM, Heninger G, Wilson GT. Controlled comparison of
cognitive behavior therapy and fluoxetine for binge eating disorder. Paper
presented at the Academy for Eating Disorders International Conference on Eating
Disorders, Boston, MA, April 2002.
44. Devlin MJ. Psychotherapy and medication for binge eating disorder. Paper
presented at the Academy for Eating Disorders International Conference on Eating
Disorders, Boston, MA, April 2002.
45. Ricca V, Mannucci E, Mezzani B, et al. Fluoxetine and fluvoxamine combined with
individual cognitive-behavior therapy in binge eating disorder: a one-year follow-up
study. Psychother Psychosom 2001; 70:298–306.
46. Nauta H, Hospers H, Kok G, Jansen A. A comparison between a cognitive and a
behavioral treatment for obese binge eaters and obese non-binge eaters. Behavior
Therapy 2000; 21:441–461.
47. Kenardy J, Mensch M, Bowen K, Green B, Walton J. Group therapy for binge
eating in type 2 diabetes: A randomized trial. Diabet Med March 2002; 19(3):
234–239.
48. Marcus MD, Wing RR, Fairburn CG. Cognitive behavioral treatment of binge
eating vs. behavioral weigh control on the treatment of binge eating disorder. Ann
Behav Med 1995; 17:SO90.
49. Telch CF, Agras WS, Rossiter EM, Wilfley DE, Kenardy J. Group
cognitivebehavioral treatment for the non-purging bulimic: an initial evaluation.
J Consult Clin Psychol 1990; 58:629–635.
50. Eisler I, Dare C, Russell GF, Szmukler GI, Le Grange D, Dodge E. Family and
individual therapy in anorexia nervosa: a 5-year follow-up. Arch Gen Psychiatry
1997; 54:1025–1030.
51. Eisler I, Dare C, Hodes M, Dodge E, Russell G, Le Grange D. Family therapy for
adolescent anorexia nervosa: the results of a controlled comparison of two family
interventions. J Child Psychol Psychiatry 2000; 41:727–736.
52. McIntosh VV, Jordan J, Carter FA, Luty SE, McKenzie JM, Bulik CM, Joyce PR.
Three psychotherapies for anorexia nervosa: a randomized controlled trial. Paper
presented at the Academy for Eating Disorders International Conference on Eating
Disorders, Boston, MA, April 2002.
INTERPERSONAL PSYCHOTHERAPY 473
53. Brody AL, Saxena S, Stoessel P, et al. Regional brain metabolic changes in patients
with major depression treated with either paroxetine or interpersonal therapy.
Arch Gen Psychiatry 2001; 58:631–640.
54. Martin SD, Martin E, Rai SR, et al. Brain blood flow changes in depressed patients
treated with interpersonal psychotherapy or venlafaxine hydrochloride. Arch Gen
Psychiatry 2001; 58:641–648.
474 JACOBS ET AL.
20
Use of Dialectical Behavior Therapy in the
Eating Disorders
Marsha D.Marcus and Michele D.Levine
Western Psychiatric Institute and Clinic, University of Pittsburgh
School of Medicine
Pittsburgh, Pennsylvania, U.S.A.
who work with these individuals to understand the validity of eating disorder
symptoms as efforts to cope with aversive circumstances is a critical tool in the
establishment and maintenance of an effective working relationship. Similarly, a
dialectical world view recognizes and accepts the difficulty of change and the
ambivalence that eating disorder patients have about modifying or relinquishing
their symptoms. The deliberate balance between acceptance and pulling for
change also serves to reduce ambivalence about the therapist, who may be
perceived as intrusive or controlling.
regulation, and (d) distress tolerance. The practice and application of the skills
is reinforced continually during individual therapy and are a specific focus of
telephone consultations with a patient. An overview of the content in each of
these skill areas follows.
Mindfulness practice is rooted in the Zen tradition of acceptance and
nonjudgmental attitude. The skills taught in this module involve learning to
observe, identify, and participate in a range of experiences with awareness. The
module begins by describing the idea of “wise mind,” a term used to refer to the
synthesis, of “emotion mind,” which includes feelings, wishes, and impressions,
and “rational mind,” which consists of thoughts, logic, and facts. Patients
cultivate the ability to focus attention on one thing at a time, and the concept of
focusing on what is effective or doing what works in a given situation is
reinforced.
Distress tolerance skills focus on coping with unpleasant and painful
emotions and situations. DBT provides concrete crisis survival strategies to
increase the ability to tolerate distress and accept life as it is in the moment.
There are several classes of distress tolerance strategies, including distraction
strategies, self-soothing strategies (we utilize all of the self-soothing strategies
with eating disorder patients except for self-soothing with food), strategies to
improve the moment, and thinking of pros and cons. Acceptance skills include
cultivation of radical acceptance and willingness. Radical acceptance involves
acknowledging and accepting current emotions, thoughts, and environmental
situations and developing a capacity to accept painful emotions as a part of life.
Willingness describes the development of a capacity to be fully alive at every
moment.
Emotion regulation skills involve identifying and labeling emotions, and
effectively managing extreme emotional states. The module includes lessons on
the function of emotions, as well as skills to decrease emotional vulnerability
and increase positive emotional experiences. With eating disorder patients, the
emphasis on identifying and labeling emotions is particularly important because
severe calorie restriction and other eating disorders symptoms may serve to
numb feelings, with the result that patients have a significantly narrowed
affective range. Thus, it is often necessary to help the eating disorder patient to
recognize feelings so as to learn how to regulate them.
Interpersonal effectiveness skills include assertiveness and interpersonal
problem solving. Effective strategies for identifying a goal and developing a plan
to obtain the changes an individual wants without sabotaging important
relationships or losing self-respect in an interpersonal situation are taught.
Within the group setting, ways of asking for what one needs, saying no, and coping
with interpersonal conflict also are modeled and practiced.
486 MARCUS AND LEVINE
consultation team meets weekly to discuss cases with the goal of encouraging
therapists’ motivation, enhancing their skills, and promoting a dialectical view of
the patient and her problems.
In summary, DBT requires a considerable commitment of time and energy
on the part of the patient and the treatment team, as individual therapy, skills
training, telephone use, and a therapist consultation team are standard. However,
in the context of the considerable morbidity of BPD and other difficult-to-treat
psychiatric disorders, such as chronic eating disorders, the investment required
for DBT is regarded as cost effective.
dinner, and two shorter days (9 a.m. to 1 p.m.) with breakfast and lunch. The
average length of stay in Partial Hospital is 3 weeks. The Intensive Outpatient
Program provides 9 hours of program over three evenings from 5 p.m. to 8 p.m.,
and includes dinner. This provides a step-down level of care for patients who
have been in Partial Hospital, or a step up for patients who are not benefiting
from regular outpatient treatment. Standard DBT, as described above, is offered
to appropriate patients as part of our outpatient clinic that provides
psychotherapy, family therapy, nutrition counseling, and medical monitoring
for patients with the full spectrum of eating disorders.
We have incorporated DBT principles in each level of care in our program.
Some of the strengths of DBT are that it provides an overall philosophy for
understanding refractory symptoms, encourages a compassionate and
nonjudgmental stance for all treaters, and offers nonpejorative, easily
understood language to describe patient behaviors and staff responses to
patients. Although it is not feasible or appropriate to provide formal DBT
training to all of the professional and paraprofessional staff that work with
patients, we have disseminated the assumptions of DBT and provided training
on the use of consultation to help staffdeal with feelings they have about
working with patients. We also have provided training to ensure that staff
members temper cognitive-behavioral strategies for change with balancing doses
of validation and acceptance. DBT language is used across the program, and
patients as well as staff members understand the meaning of terms used in DBT
skills training. The use of common terminology promotes the development of
cohension and sense of purpose in the therapeutic milieu.
In the inpatient unit, patients are exposed to the DBT skills modules,
particularly mindfulness and distress tolerance as well as to the use of behavior
chain analyses. Exposure to DBT skills is intensified in the Partial Hospital
Program, and patients are encouraged to make use of DBT skills throughout acute
treatment. Patients in the partial program also must commit to working on
recovery and not to engage in symptom behavior on the premises. Thus, eating-
disordered behaviors that occur on the premises, such as food restriction or
purging, are considered therapy interfering regardless of the patient’s degree of
medical risk. If patients engage in problem behaviors they are asked to do
behavior chain analyses, which are then reviewed with the therapist. The
therapist and patient then agree on a plan to repair any negative consequences of
the problem behavior.
SUMMARY
We have successfully utilized DBT in the management of chronic eating
disorders as it provides a treatment context in which change not only is possible
490 MARCUS AND LEVINE
but also is explicitly nurtured and reinforced in the context of respect for and
acceptance of patients’ struggles and ambivalence. DBT principles can be
disseminated to ancillary staff who work with patients and to families to
promote positive and constructive means for understanding difficult
behavior. Although research is needed to determine if DBT confers benefits for
chronic eating disorder patients over and above care as usual, our clinical
experience suggests that DBT benefits patients and the staff who work with
them.
REFERENCES
1. Paul T, Schroeter K, Dahme B, Nutzinger DO. Self-injurious behavior in women
with eating disorders. Am J Psychiatry 2002; 159:408–411.
2. McCabe EB, Marcus MD. Is dialectical behavior therapy useful in the management
of anorexia nervosa? Eat Disorders J Treat Prevent 2002; 10:335–337.
3. Linehan MM. Cognitive Behavioral Treatment of Borderline Personality Disorder.
New York: Guilford Press, 1993.
4. Linehan MM. Skills Training Manual for Treating Borderline Personality Disorder.
New York: Guilford Press, 1993.
5. Linehan MM, Armstrong HE, Suarez A, Allmon D, Heard HL.
Cognitivebehavioral treatment of chronically parasuicidal borderline patients. Arch
Gen Psychiatry 1991; 48:1060–1064.
6. Linehan MM, Heard HL, Armstrong HE. Naturalistic follow-up of a behavioral
treatment for chronically parasuicidal borderline patients. Arch Gen Psychiatry
1993; 50:971–974.
7. Dimeff L, Rizvi SL, Brown M, Linehan MM. Dialectical behavior therapy for
substance abuse: a pilot application to methamphetamine-dependent women with
borderline personality disorder. Cogn Behav Prac 2000; 7:457–468.
8. Linehan MM, Schmidt H, Dimeff LA, Craft JC, Kanter J, Comtois KA. Dialectical
behavior therapy for patients with borderline personality disorder and drug-
dependence. Am J Addict 1999; 8:279–292.
9. Linehan MM, Dimeff LA, Reynolds SK, Comtois KA, Welch SS, Heagerty P,
Kivlahan DR. Dialectical behavior therapy versus comprehensive validation therapy
plus 12-step for the treatment of opioid dependent women meeting criteria for
borderline personality disorder. Drug Alcohol Depend 2002; 67:13–26.
10. Telch CF, Agras WS, Linehan MM. Group dialectical behavior therapy for binge-
eating disorder: a preliminary, uncontrolled trial. Behav Ther 2000; 31: 569–582.
11. Telch CF, Agras WS, Linehan MM. Dialectical behavior therapy for binge eating
disorder. J Consult Clin Psychol 2001; 69:1061–1065.
12. Wiser S, Telch CF. Dialectical behavior therapy for binge-eating disorder. J Clin
Psychol 1999; 55:755–768.
13. Safer DL, Telch CF, Agras WS. Dialectical behavior therapy for bulimia nervosa.
Am J Psychiatry 2001; 158:632–634.
21
Psychopharmacology of Anorexia Nervosa,
Bulimia Nervosa, and Binge Eating Disorder
Joanna E.Steinglass and B.Timothy Walsh
New York State Psychiatric Institute, Columbia University
New York, New York, U.S.A.
ANOREXIA NERVOSA
Anorexia nervosa is characterized by a relentless pursuit of thinness and fear of
becoming fat: patients starve themselves to extremes of low weight, resulting in
amenorrhea and risk of death. Treatment must target multiple aspects of the
disorder as patients need to gain weight, extinguish eating-disordered
behaviors, and alter cognitions that foster these behaviors. Current
recommendations focus on a multidisciplinary approach to treatment, including
psychotherapies with cognitive-behavioral components. Inpatient treatment for
patients at very low weight focuses on behavioral interventions and nutritional
counseling to encourage eating and weight gain in conjunction with beginning to
challenge cognitive disturbances. Nonetheless, AN has been difficult to treat and
has a high relapse rate. Thus medications are under investigation both to
facilitate initial treatment and to prevent relapse.
Study of the management of AN lends itself to multiple possible outcome
measures. The major initial concern is weight restoration, which can be readily
assessed by the amount and the rate of weight gain. In the long term, rate of
relapse is an important outcome, defined as significant weight loss or
reemergence of restrictive or binge-purge behaviors. Interwoven through both
phases of treatment (weight gain and relapse prevention) is the complex
problem of body image dissatisfaction.
Many psychopharmacological interventions have been tried, beginning with
the work of Dally and Sargant on antipsychotics in the 1960s. Due to the limited
understanding of the biological basis of AN, medication trials have been driven
by unproven theoretical models and/or by an interest in taking advantage of
medication side effects. While anecdotal reports of successful treatments have
been published, only a small number of randomized controlled trials have been
conducted, and definitive psychopharmacological treatment has not been
identified.
Antidepressants
Antidepressant treatment for AN is a reasonable notion given the common
concomitant symptoms of anxiety and depression. Many patients with AN
describe low mood, low energy, poor concentration, loss of interest, and social
isolation. The ritualized behaviors around eating and the obsessive
preoccupation with shape and weight can be conceptualized as on the spectrum
of obsessive-compulsive disorder (OCD), a syndrome that is also responsive to
antidepressant medication.
Controlled trials of several different medications to promote weight gain
have been generally discouraging. Initial studies involved tricyclic
PSYCHOPHARMACOLOGY 493
antidepressants (TCAs), with the hope that the side effect of weight gain would
add to the benefits of treating mood disturbance. There have been three
randomized controlled trials of TCAs. In one, clomipramine was associated
with a slower rate of weight gain than placebo despite increased appetite, and
there were no long-term effects at 1 and 4 years (2). In a study of amitriptyline
versus placebo, there was no significant difference in weight gain (3). A second
study of amitriptyline, which also had a third arm in which subjects received the
serotonin (5-HT) antagonist cyproheptadine, showed no major benefit of
amitriptyline (4). TCAs are known to prolong the QTc interval, which is also
affected by AN. These observations, coupled with concerns that TCAs in
children and adolescents may be linked to sudden death (5), suggest that TCAs
should be rarely used for patients with AN at low weight.
In light of their benign side effect profile and efficacy in many other disorders,
selective serotonin reuptake inhibitors (SSRIs) would appear promising in the
management of in AN. Initial anecdotal evidence that fluoxetine might be
beneficial for weight gain and mood symptoms (6) was supported in an open
trial (7). However, the single randomized placebocontrolled trial of fluoxetine
did not support these results. Attia et al. (8) conducted this trial of 33 patients
with AN at low weight. All patients received inpatient care in addition to either
fluoxetime (60 mg/day) or placebo for 7 weeks or until they reached 90% of
ideal body weight and maintained it for a week. Fluoxetine conferred no benefit
on weight gain, irrespective of subtype (restricting versus binge-purge). This
finding is consistent with an open trial of Strober et al. (9) who administered
fluoxetine to 33 inpatients.
While the studies of medication treatment in the acute phase focused on
weight gain, some studies also included measures of other dimensions of AN.
Mood symptoms have been found to improve with weight gain, with no
added benefit from medication (8,34). The open trial of Strober et al. described
above (9) examined severity of weight phobia and abnormal eating behaviors
and found no evidence that fluoxetine treatment was of benefit. Attia and
colleagues (8) assessed the effect of medication on body image dissatisfaction, a
core component of AN, and noted significant improvement with weight gain in
scores on Body Satisfaction Questionnaire (BSQ) in both placebo and fluoxetine
groups, although not to within the normal range in either group.
Somewhat more promising results have been found in the relapse prevention
phase, but there is just one randomized controlled trial. Thirtyfive women with
AN, restricting subtype, entered a double-blind, randomized, controlled trial
after inpatient weight restoration and received either fluoxetine (10–60 mg/
day) or placebo for 11 months (10). Subjects receiving medication were
significantly more likely than those who received placebo to maintain near-
normal weight for one year. Interpretation of data from the randomized trial is
494 STEINGLASS AND WALSH
limited in that dosage of fluoxetine was not controlled for, nor was
additional treatment (i.e., psychotherapy) restricted. Subjects were limited to
those with restricting subtype, and there is no information on the effect of
medication on parameters other than weight. In addition, a naturalistic study of
Strober et al. (11) comparing relapse among patients receiving open fluoxetine
treatment to relapse among a group of matched, historical controls failed to
detect evidence of a benefit from fluoxetine. Nonetheless, the study of
Kaye et al. (10) is virtually the only placebo-controlled examination of
medication in AN that found a statistically and clinically significant impact
of medication compared to placebo. Further study is needed to determine
replicate and extend this finding.
In summary, there is little reason to think that antidepressants add
substantially to the standard inpatient management of AN. Given the
widespread benefits of antidepressant medication in other, seemingly related
psychiatric disorders, the lack of impact of antidepressants is surprising.
Kaye et al. (12) have shown that patients at low weight have low levels of
5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of serotonin, which
improve with weight gain. Low levels of 5-HIAA suggest that patients have low
levels of brain serotonin, which is consistent with the finding that dieting in non-
eatingdisordered women reduces tryptophan levels (the amino acid that is the
substrate for serotonin) and reduces serotonin production (13). Thus, it may be
that antidepressants are ineffective at low weight because they have insufficient
substrate (14). This is supported by the finding that tryptophan depletion has
been shown to reverse the effects of SSRIs in depressed patients (13).
Notably, virtually all studies of patients at low weight have been conducted in
an inpatient setting, where nonpharmacological interventions are effective in
producing weight gain. At least theoretically, there is potential for benefit from
medication in an outpatient setting, where weight gain tends to be slower.
Antipsychotics
Pharmacological treatment in AN began with antipsychotics. The theoretical
rationale for the use of this class of medication derives from the neardelusional
quality of beliefs about shape and weight held by some patients with AN. Dally
and Sargant (15) studied chlorpromazine (1600 mg/day) and found that while
the rate of weight gain was enhanced compared to historical controls, there
were significant negative effects including seizures and the emergence of binge-
purge behavior. Furthermore, benefits were not sustained over long-term
follow-up. Pimozide was studied subsequently in a randomized, controlled trial
of hospitalized patients (16). The authors found a trend toward slightly higher
daily weights while on pimozide, but effects on psychological symptoms were
PSYCHOPHARMACOLOGY 495
Other Agents
A number of other medication classes have been tried, targeting primarily the
weight gain phase of AN. Cyproheptadine, an antihistaminic agent that acts
centrally to decrease serotonin activity, has been studied in several controlled
trials after it was noted to cause weight gain in other conditions. Results have
been mixed. In the first placebo-controlled trial (21), cyproheptadine did not
improve weight gain. A second study found that cyproheptadine was associated
with improved weight gain in a subgroup of severely ill patients (22). In a trial
comparing amitriptyline, cyproheptadine, and placebo (mentioned above) (4),
the authors noted no significant weight gain in the cyproheptadine group.
However, they did note a difference between subtypes such that individuals
with the restricting subtype showed an increased rate of weight gain with
cyproheptadine whereas individuals with the binge-purge subtype showed an
increased rate of weight gain with amitriptyline.
496 STEINGLASS AND WALSH
Other novel approaches to improving weight gain have included lithium, for
its weight gain and mood stabilizing properties, and tetrahydrocannabinol (THC)
for its appetite-enhancing effect. Lithium was associated with a small weight
increase in one small, short-duration placebo-controlled trial (34). THC was
compared to diazepam in a small randomized, doubleblind trial using a
crossover design (35). There was no benefit from THC with respect to food
intake or weight gain, and THC was associated with significant side effects,
including paranoia, sleep disturbance, and interpersonal sensitivity.
A major medical complication of AN is osteoporosis/osteopenia. Estrogen
replacement therapy has been used to treat osteoporosis in postmenopausal
women and therefore has been explored as an adjunctive treatment in AN.
However, a randomized controlled trial assessing the bone densities of subjects
receiving estrogen and progestin versus no medication found no significant
changes in the hormone-treated group (36). Those patients who resumed
menses showed improvement in bone density. These data suggest that, at
present, the best documented intervention to arrest bone loss in AN is weight
gain sufficient to restore regular menstruation.
BULIMIA NERVOSA
Bulimia nervosa is characterized by recurrent binge eating followed by
inappropriate compensatory behaviors, such as vomiting. Because in DSMIV,
AN has diagnostic precedence over BN, patients with AN who meet criteria for
BN are considered as having the binge-purge subtype of AN. Thus, most
patients with BN are of normal weight. Like patients with AN, those with BN
have a disturbance of body image and unduly value their shape and weight when
evaluating their self-esteem. Bulimia nervosa is more common than AN, with a
prevalence of 1–5% in adolescent and young adult women (37). BN tends to be
managed in the outpatient setting, making clinical trials less complicated and
costly than with AN and, presumably for these reasons, more numerous. In
addition, studies of medications in the management of BN have yielded more
promising results, most notably with antidepressants.
Antidepressants
The study of antidepressant medications resulted from the observation that
patients with BN, like those with AN, often describe depressive symptoms.
Over the past 20 years, many antidepressants have been found to be more
effective than placebo in reducing binge-purge episodes in normal-weight
women with BN (38,39). While TCAs (40–45), monoamine oxidase
inhibitors (46–48) and SSRIs (49–51) have all been shown to be effective, there
498 STEINGLASS AND WALSH
Areas for further study include the optimal duration of treatment and the long-
term efficacy of antidepressants.
Anticonvulsants
An early clinical model conceptualized BN as a seizure disorder, with
bingepurge episodes thought to represent paroxysmal events. Small trials with
the anticonvulsants phenytoin (63) and carbamazepine (64) did not suggest a
robust response to medication. A recent case report (65) of a woman with
epilepsy and BN who was treated with topiramate and showed improvement in
binge-purge behaviors and in attitude about shape and weight raised the
possibility that topiramate may have benefit in the management of BN. Results
from a randomized, double-blind, placebocontrolled trial of topiramate
(25–400 mg/day) have been presented, showing reduction in binge and purge
duration and frequency (66). Although preliminary, these results are
encouraging.
Other Agents
Some agents have been studied based on biological models, as opposed to
clinical models, of BN. These models have focused mainly on the potential role
of serotonin, which has been shown to impact various aspects of feeding. As
increased serotonergic function tends to decrease food intake, it was
hypothesized that medications that increase serotonin would decrease binge
eating behavior (67). L-Tryptophan, the amino acid precursor of serotonin, was
examined in a randomized, placebo-controlled trial (N = 13), but no drug-
placebo difference was detected (68). Fenfluramine, a serotonergic agent that
both blocks reuptake and increases release, was studied with mixed results. In a
randomized, placebo-controlled trial using a crossover design, fenfluramine was
shown to decrease binge-purge frequency (69). However, in two subsequent
placebo-controlled trials, the medication showed no benefit (70,71).
Fenfluramine was withdrawn from the market in 1997 due to an association
with cardiac valve abnormalities.
Another model for treatment of BN focuses on the feeding behaviors of
patients, specifically their difficulty in identifying satiety. This model postulates
that binge eating and purging might lead to desensitization of the vagal nerve
afferents, which have a key role in signaling satiety. Subjects with BN were
found to have an increased somatosensory pain threshold, which may indirectly
reflect altered vagal nerve activity (72). Based on these observations, Faris and
colleagues (73) conducted a 4-week randomized, placebocontrolled trial in BN
and found that ondansetron (24 mg/day), a medication that blocks 5-HT3
500 STEINGLASS AND WALSH
receptors involved in visceral stimulation of the vagal nerve, was associated with
a significant decrease in binge-purge behaviors.
One clinical model of BN focused on the similarities between bingepurge
behaviors and addictive behaviors, drawing on the evidence that endogenous
opiates may be involved in appetite changes. In a small, open trial of
naltrexone, an opiate antagonist, 7 of 10 patients with BN improved with
complete or partial remission (74). One randomized, controlled trial including
AN and BN patients found a decrease in binge-purge behaviors with naltrexone
(100–200 mg/day) (29), whereas a randomized, controlled trial using a lower
dose (50 mg/day) showed no benefit (75).
Lithium has also been studied. Hsu et al. (60) conducted a randomized,
placebo-controlled, 8-week trial of lithium (mean lithium level = 0.62) in
patients with BN. Both placebo and medication groups improved, and there was
no significant difference between the groups.
Combination Treatment
While the above data clearly support the efficacy of antidepressants in BN,
controlled trials have also shown the efficacy of psychotherapy alone (see
Chapters 17,19, and 20). Seven randomized controlled trials have, in different
ways, compared treatments in an attempt to assess the benefits of psychotherapy
versus pharmacotherapy versus a combination of the two. Overall, the studies
suggest that cognitive-behavioral therapy (CBT) alone is probably more
effective in reducing binge eating and purging behaviors, but that the addition of
medication provides some additional benefit.
The first study, conducted by Mitchell and colleagues (62), randomized
subjects to one of four treatment arms for 10 weeks: imipramine alone, placebo
alone, intensive group therapy alone, or imipramine with intensive group
therapy. The psychotherapy intervention provided was an unusually intensive
group therapy, which included joint meals with the therapist on five occasions
during the first week of treatment. Outcome measures assessed eating
behaviors, affective symptoms, and attitudinal measures. The reduction in
eating-disordered behaviors in response to intensive group therapy was
impressive, and no added benefit from imipramine could be detected. On the
other hand, combination treatment significantly improved affective symptoms
more than either treatment alone. In a follow-up study, Keel et al. (76) found
that 10 years posttreatment, all three active treatment groups showed
significant improvement in social functioning as compared with placebo. There
were no significant differences on measures of depression, body image, or
eating disorder behavior.
PSYCHOPHARMACOLOGY 501
Conclusions drawn from the above studies must be considered with caution.
One major problem is that the largest studies were conducted before the
widespread use of SSRIs, making it difficult to extrapolate from these data to
current clinical practice. The limited information available suggests that CBT is
likely to be more effective and more acceptable to patients than is a course of
antidepressant medication. However, the data are reasonably consistent in
indicating that the addition of an antidepressant to psychotherapy modestly
augments improvement in psychological symptoms and, perhaps, in disturbance
of eating behavior. The effectiveness of medication in reducing relapse is
uncertain.
Antidepressants
Based on the efficacy of antidepressants in the management of BN and the
similarities between these two disorders, most research has focused on
antidepressants. An early placebo-controlled trial of “nonpurging BN”
found that desipramine was effective in the short-term reduction of binge
eating (82). However, symptoms reemerged 4 weeks after medication
discontinuation. A randomized, controlled trial has also shown imipramine to
be effective (83). More recently, two studies have found benefits from SSRIs. In
one randomized controlled trial of fluvoxamine (50–300 mg/day) (84) and one
randomized controlled trial of sertraline (50–200 mg/day) (85), the authors
reported a significant reduction in binge eating behavior as well as a decrease in
BMI in the medication groups as compared with placebo. As with most of the
medication trials in eating disorders, these short-term results do not provide
information as to sustained benefit of medications.
PSYCHOPHARMACOLOGY 503
Other Agents
As with AN and BN, a number of other classes of medication have received
some attention as being of possible use in the management of BED. Topiramate
is the latest to show promise. In one open label-study of 13 patients with BED,
topiramate was associated with weight loss (86). Appolinario et al. (87)
reported a case study of a patient who responded to topiramate after other
treatments had been unsuccessful. McElroy et al. (88) conducted a placebo-
controlled, double-blind trial of topiramate in 61 patients with BED.
Topiramate-treated subjects showed significantly greater reductions in binge
frequency, binge day frequency, and other measures of symptom severity, as
well as significant reduction in BMI.
Trials of dexfenfluramine yielded some promising results. Dexfenfluramine
was associated with a decrease in binge eating, and when used in combination
with phentermine, with weight loss, as well (89,90). However,
dexfenfluramine has since been withdrawn from the market due to its
association with cardiac valve abnormalities. An open trial of sibutramine, an
appetite suppressant approved for the management of obesity, suggested that
use of this agent was associated with improvement in both binge eating and
weight loss (91). A controlled trial has been conducted, but results are not yet
available. The opiate antagonist naltrexone was studied in a randomized placebo-
controlled trial which also included an imipramine arm (89). While both
medication groups showed improvement, there was no difference from
placebo.
Combination Treatment
Antidepressant medications appear to provide short-term benefit in the
management of BED, but the benefits do not appear to be sustained beyond the
discontinuation of the medication. Several studies have examined the benefits of
combined treatment, but, at present, the data are insufficient to support clear
conclusions (83,92–95).
Anorexia Nervosa
Psychopharmacological interventions have not been shown to provide
significant benefit to underweight patients with AN. The mainstays of treatment
are nonpharmacological, and focus on nutritional rehabilitation and relapse
504 STEINGLASS AND WALSH
Bulimia Nervosa
The data on the use of antidepressants in the treatment of BN are convincing in
indicating that that fluoxetine is safe and beneficial. While it is likely that other
SSRIs would be effective, only fluoxetine has been examined in
placebocontrolled trials, and should be used in a dose of 60 mg/day. Most
patients can be rapidly titrated to this dose over the course of a week. There are
no available data to guide treatment for relapse prevention or to suggest
recommended length of treatment. Bupropion is not recommended in the
management of BN because of the risk of seizure. There are consistent
indications that medications modestly enhance the benefits of psychological
treatment.
REFERENCES
1. American Psychiatric Association. Practice guidelines for the treatment of patients
with eating disorders (Revision). Am J Psychiatry (Supplement) 2000; 157(l):l-39.
2. Lacey J, Crisp AH. Hunger, food intake and weight: the impact of clomipramine
on a refeeding anorexia nervosa population. Postgrad J Med 1980; 56(suppl 1):
79–95.
3. Biederman J, Herzog D, Rivinus T, et al. Amitriptyline in the treatment of
anorexia nervosa: a double-blind, placebo-controlled study. J Clin
Psychopharmacol 1985; 5, 10–16.
4. Halmi K, Eckert E, LaDu T, Cohen J. Anorexia nervosa: treatment efficacy of
cyproheptadine and amitriptyline. Arch Gen Psychiatry 1986; 43:177–181.
5. Wilens T, Biederman J, Baldessarini R, et al. Cardiovascular effects of therapeutic
doses of tricyclic antidepressants in children and adolescents. J Am Acad Child
Adolesc Psychiatry 1996; 35:1491–1501.
6. Ferguson J. Treatment of an anorexia nervosa patient with flouxetine. Am J
Psychiatry 1987; 144:1239.
7. Gwirtsman H, Guze B, Yager J, Gainsley B. Fluoxetine treatment of anorexia
nervosa: an open clinical trial. J Clin Psychiatry 1990; 51:1378–1382.
PSYCHOPHARMACOLOGY 505
treatment of obese binge eaters and non-binge eaters. Am J Psychiatry 1990; 147:
876–881.
95. Grilo C, Masheb R, Heninger G, Wilson G. Controlled comparison of cognitive
behavorial therapy and fluoxetine for binge eating disorder. In: Mitchell J, ed.
Scientific II Session. International Conference on Eating Disorders. BED and
Obesity. Boston: Academy for Eating Disorders, April 28, 2002.
22
Eating Disorders, Victimization, and
Comorbidity: Principles of Treatment
Timothy D.Brewerton
Medical University of South Carolina
Charleston, South Carolina, U.S.A.
Comorbidity is the rule rather than the exception when it comes to eating
disorders (EDs), particularly bulimia nervosa (BN). The common types of
comorbid psychiatric disorders (on axes I and II) and comorbid medical
disorders (on axis III) are reviewed in Chapters 8, 9, and 10, respectively.
Comorbidity is simply the coexistence of one disorder with another disorder in
the same person. When one disorder, e.g., major depressive disorder (MDD),
occurs with another in the present time this constitutes current prevalence or
history, whereas when another disorder occurs at any point during the lifetime
of the individual it constitutes lifetime prevalence or previous history of that
comorbid disorder. While current comorbidity is more strongly the purview of
clinicians managing acute EDs, particularly in an inpatient setting, obtaining the
lifetime history of all forms of comorbidity is extremely important in order for
the clinician to see the “big picture,” the “forest” and the “trees,” and the
wholistic, developmental, and biopsychosocial perspective.
The themes of this chapter are that (a) a cluster of comorbid disorders and
their symptoms co-occur together more often than chance would dictate, and
that this link is highly associated with a history of victimization and subsequent
PTSD; and (b) the victimization and PTSD must be specifically and adequately
addressed in order to optimize full recovery from not only the ED but all
associated comorbid disorders. Victimization usually refers specifically to major
physical boundary violations, such as rape, molestation, and aggravated assault.
All of these common events are crimes in all developed countries, and there
may be important legal ramifications for these patients to process in therapy. Of
course, victimization may also involve other traumatic experiences, such as
witnessing a homicide, severe emotional abuse, and neglect (physical and
emotional).
Just as there is a spectrum of trauma and victimization, there is also a
spectrum of trauma-related disorders (1–4). The disorders that group together
within this trauma-related spectrum include eating (especially BN), affective
(especially MDD), anxiety (especially post-traumatic stress disorder, PTSD),
512 BREWERTON
especially genital rape, predicted an odds ratio of 5.62 for the development of
BN and 5.05 for the development of two or more psychiatric disorders (12). This
was an especially important and powerful study given that it controlled for
genetic influences.
1. Childhood sexual abuse (CSA) is associated with BN, which was supported
by 8 of 12 studies.
2. CSA is more common in BN than AN, which was supported by 4 of 6
studies.
3. CSA is a specific risk factor for EDs, which was not at all supported.
4. CSA is associated with greater severity, which was not supported by the
data (but only three studies were included).
5. Particular features of CSA are associated with ED symptoms, which was
supported by 4 of 5 studies; these included decreased social competence;
poor maternal relationship; unreliable parenting; severity of CSA, and
presence of lifetime PTSD, which was a finding from the NWS (14).
6. CSA is associated with comorbidity in ED subjects, which was supported
by 5 of 6 studies.
One of the studies included in this review was the NWS (14), which remains
the most comprehensive study of the relationship of trauma history and PTSD to
EDs and comorbidity in a large national sample. Structured telephone interviews
of a representative sample of over 4000 U.S. women from four stratified
geographical areas assessed detailed histories of crime victimization experiences
(rape, molestation, attempted sexual assault, and aggravated assault), PTSD,
MDD, EDs and substance abuse/dependence using DSM-IIIR and DSM-IV
(binge eating disorder, BED) criteria. The lifetime prevalence rates for the EDs
were as follows: BN = 2.4%, BED = 1.0%; AN = 0.23%. In comparing BN
and non-BN/BED subjects who completed the survey, the following lifetime
prevalence rates were obtained: completed rape: 26.6% v. 3.3% (p < 0.01);
contact sexual molestation: 22.0% v. 12.0% (p < 0.05); attempted assault:
514 BREWERTON
26.8% v. 8.4%, p < 0.001; any direct crime victimization (one or more of the
above): 54.4% v. 31.0% (p < 0.001); lifetime PTSD: 37% v. 12% (p < 0.001);
current PTSD: 21% v. 4% (p < 0.001). In comparing BED versus non-BN/BED
subjects, there were no significant differences except for lifetime PTSD:
22% v. 12% (p < 0.01). In the AN group there were no reports of rape,
molestation, aggravated assault, or PTSD at all. The age of first rape occurred
before the age of first binge in 84% of all BN cases. The corresponding numbers
for only adolescent rapes (12–17 years) and only child rapes (≤11 years) were
96% and 100%, respectively. These data provide substantial validity to the
notion that victimization is a causative risk factor for BN, albeit a nonspecific
one. In addition, the age of first binge for BN subjects was significantly earlier in
cases of rape resulting in PTSD compared to those with rape without PTSD or
no rape. Interestingly, the prevalence rates for BN were significantly higher in
those subjects with histories of rape with PTSD (10.4%) compared to those
with rape without PTSD (2.0%) or those with no rape (2.0%), which strongly
suggests that PTSD rather than prior abuse per se best predicts the development
of BN. In the NWS links between trauma, dissociative symptoms, and BN were
also found (15). BN subjects had significantly more “forgetting” or psychogenic
amnesia of traumatic events (27%) than BED subjects (12%) or non-ED
subjects. This was defined as an endorsement by subjects that they forgot all or
part of traumatic events. Multiple linear regression using psychogenic amnesia
as the dependent variable identified the following significant variables (in
decreasing order of significance): lifetime PTSD, childhood rape, lifetime major
depression, molestation, emotional problems in the family, laxative abuse, total
number of victimization experiences, age, and vomiting (15). Based on these
and other data, it was hypothesized that purging behaviors, such as vomiting and
laxative abuse, rather than binge eating per se, are maladaptive behaviors linked
to PTSD and MDD that facilitate avoiding, numbing, and forgetting traumatic
memories.
Since the publication of the review by Wonderlich and colleagues, there have
been two large reviews on sexual abuse and EDs, both of which support the
importance of this link in at least a subgroup of ED patients (16,17).
Of course, not all patients with EDs have been victimized. However, the
index of suspicion rises substantially as the number of comorbid psychiatric
disorders rises. In the NWS there were clear links between trauma, PTSD, and
comorbidity with affective, anxiety, and substance use disorders (SUDs). A very
robust linear relationship exists between the number of comorbid axis I
diagnoses and the percentage of subjects with histories of child rape, rape at any
age, and any direct victimization experience (unpublished data). 100% of the
subjects with all four diagnoses (BN, MDD, PTSD, SUD) had experienced at
least one major direct victimization experience in their life (rape, molestation,
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 515
aggravated assault). Fifty percent of these same subjects with all four diagnoses
reported a childhood rape (≤ 17 years old).
There have been a number of more recent studies on EDs, victimization, and
comorbidity, all of which lend further support to this relationship. Some of
these studies will be reviewed below.
Kenardy showed links between past sexual and/or physical abuse and weight
dissatisfaction and/or disordered eating in young and middle-aged women (18),
while Romans reported higher rates of EDs in women who have experienced
CSA (19). In this study, the factors that increased the risk of developing an ED
in women who had experienced CSA were belonging to a younger age cohort,
experiencing menarche at an early age, and experiencing high paternal
overcontrol. Low maternal care was specifically associated with the
development of AN, whereas early age of menarche differentiated women with
BN. Younger age and early age of menarche also differentiated the CSA + ED
women from the psychiatric comparison group.
In a clinical study that supports the link between PTSD and EDs, Gleaves and
colleagues stated that 74% of 293 women admitted to a residential treatment
center who completed a PTSD symptom scale reported a traumatic experience
and 52% reported symptoms consistent with a diagnosis of PTSD (20). Of
112 AN patients, 47% met PTSD criteria, and of 103 BN patients 62% met
PTSD criteria. In a clinical sample of recovered BN patients, abused subjects
showed a trend toward more frequent lifetime diagnoses of PTSD and substance
dependence compared with nonabused subjects (21). These results suggest that
abusive experiences may be associated with some of the psychopathology of BN,
particularly that which is related to anxiety, substance abuse, and more severe
core ED pathology. In another study, women comorbid for BN and substance
dependence were found to have the highest frequency and the most severe
histories of sexual abuse compared to bulimic women without substance
dependence (22).
In an Australian sample of hospitalized patients, nearly one-half of ED
patients reported a history of child sexual abuse and one-quarter reported child
physical abuse, and these rates were significantly higher than those for the
control group (23). In addition, dissociative experiences were found to be
common and strongly associated with history of abuse and self-mutilation (24).
In a Japanese study of ED patients and controls, physical punishment histories
tended to be more prevalent among patients with AN-BP or BN than among
AN-R or controls. AN-BP and BN patients with physical punishment histories
had twofold higher scores on the Dissociative Experiences Scale (DES) and
significantly more frequent histories of self-mutilation (67% v. 33%) compared
with patients without such histories (25). Multi-impulsivity in Japanese ED
patients was associated with suicide attempts, self-mutilation, BPD, and parental
516 BREWERTON
United States (33) and Sweden (34). These links have also been shown to
persist in sexually abused children long past the time of abuse (35).
Data supporting a role for various forms of abuse as a risk factor for BED
have also emerged in the literature over the last several years. Grilo and
colleagues showed higher rates of childhood psychological, physical, and sexual
maltreatment in outpatients with BED (36). A total of 83% of BED patients
reported some form of childhood maltreatment, including 59% reporting
emotional abuse, 36% physical abuse, 30% sexual abuse, 69% emotional
neglect, and 49% physical neglect. There were no differences in the distribution
of any form of childhood maltreatment by gender, obesity status, body mass
index, binge eating, or attitudinal features. Only physical neglect was associated
with dietary restraint in women, whereas emotional abuse was associated with
greater body dissatisfaction, higher depression, and lower self-esteem in men
and women, and sexual abuse was associated with greater body dissatisfaction in
men. Another study also identified other forms of victimization besides abuse,
like bullying and discrimination, as risk factors for BED (37). Unfortunately,
these studies did not report on rates of PTSD in these patients.
Other investigators have also expanded the spectrum of abuse that may
contribute to the development of EDs, including neglect (38), childhood
emotional abuse (39,40), adverse family background (41), and extreme food
deprivation (42).
In terms of studies of mediating variables between prior child abuse and BN,
research have shown that impulsivity and core beliefs involving shame, self-
esteem, and perceived control are significant mediating variables to consider in
terms not only of etiology but of treatment planning as well (43–48).
Affective Disorders
A lifetime prevalence of major depressive disorder (MDD) has been found in
association with AN and BN in 24–88% of reported cases, depending on the
study (see Chapter 8). To a much lesser extent, this pattern of higher affective
disorders in ED patients runs true for dysthymia (19–20%) and bipolar disorder
(4–13%) as well, particularly BPD type II with a seasonal pattern. Depressive
symptoms that do not meet full criteria for an affective disorder are also
common in ED patients (depression NOS).
Each of these affective disorders has been reported to have higher than
expected rates of a history of trauma or victimization, and more often than not
the trauma occurred during childhood or adolescence. It is important for the
clinician to realize that fully two-thirds of all rapes of women in the United
States occur before the age of 18 (NWS). The frequency of rape in decreasing
order is in girls aged 12–17 years, then in girls at or below 11 years old, then in
women ages 18–24 years. After this age period, the frequency of rape decreases
with age precipitously. Childhood sexual and physical abuse has been found to
be highly associated with MDD and affective disturbances in general (7,49–55),
and Gladstone reported that depressed patients with childhood abuse histories
were more likely associated with BPD (see “Axis II Comorbidity” below) (54).
In addition, a history of physical or sexual abuse in childhood has been
found to be particularly associated with MDD with reversed neurovegetative
features, e.g., hyperphagia and hypersomnia, whether or not manic subjects are
included (55). A significant relationship between mania and childhood physical
abuse was also found. Across analyses there was a significant main effect of
female gender on risk of early sexual abuse, which has been a consistent finding
in the literature. These results suggest an association between early traumatic
experiences and particular symptom clusters of depression, mania, or both in
adults.
Anxiety Disorders
Just about all of the anxiety disorders, with the possible exception of panic
disorder, also occur in ED patients (23–75%) at higher than expected rates
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 519
when compared to rates in the general population. These data have been much
more extensively reviewed in Chapter 8 and will not be discussed at length.
However, the general ranges reported are as follows: PTSD (37–62%),
obsessive-compulsive disorder (OCD) (3–66%), social phobia (16–55%), panic
disorder (5–10%), generalized anxiety disorder (GND) (12%), simple phobia
(13%). Taken together, it is evident from this research that one of the most
common anxiety disorders presenting in the ED population is PTSD, a finding
from the NWS (14). Although there are many studies of the rates of child abuse
and other victimization experiences in ED samples (13,14,16,17,56), a paucity
of reliable data exists on the prevalence of PTSD in subjects with EDs.
An important and consistent finding is that anxiety disorders are usually
primary and the ED is usually secondary. Much has been published on this
particular comorbid dyad in the last few years, as noted in Chapters 6 and 8. It
appears that anxiety symptoms, particularly those involving behavioral
inhibition and obsessionality, are important risk factors for the development of
EDs. Anxiety typically persists and often worsens following the onset of an ED.
In the NWS, sexual assault and PTSD symptoms began before the first binge
ever occurred in 84% of all rapes and nearly 100% of rapes occurring during
childhood (≤17 years old) (in subjects with BN only).
A diagnostic sine qua non for PTSD is of course the occurrence of a traumatic
event. However, all of the other anxiety disorders have been reported to have
high rates of victimization, including OCD, panic disorder, GAD, social phobia,
simple phobia, as well as separation anxiety disorder and overanxious disorder
in kids (29,51–53,57–62).
colleagues demonstrated in the NWS that the major reason alcohol abuse so
commonly coexists with BN is because they share comorbid PTSD (66).
Dissociative Disorders
Next to PTSD, which requires an identified traumatic event, the DDs as a group
are most closely linked to trauma. This link between trauma and dissociative
phenomena has been well described in the literature (4,67,68). DDs and their
symptoms have been described all over the world and are commonly related to
severely overwhelming traumatic experiences, particularly when occurring
during childhood, and include derealization, depersonalization, time
distortions, cognitive and memory alterations (including amnesia), identity
alterations, and somatic sensations. Dissociative disorders (particularly
dissociative identity disorder, DID) are very real disorders of memory,
consciousness, and identity that represent the devastating effects of unusually
severe and often chronic violent abuse during childhood. Axis I comorbidity is
quite common, and several investigators have reported high frequencies of EDs
and behaviors in DID patients (69–71). Conversely, high frequencies of
dissociative symptoms have been reported in ED patients, particularly BN
(72–85), and in nonclinical samples with ED pathology (86,87). Previously,
there were no detailed studies of both dissociative symptoms, such as psychogenic
amnesia (PA), and victimization experiences, such as rape, in a representative
group of women with and without EDs. Data generated as part of the NWS
provided an opportunity for a more controlled examination of these
relationships.
As part of the PTSD screening, respondents were designated as having PA if
they endorsed ever “forgetting” all or part of a significant traumatic event, a
question that was part of the PTSD module. Respondents with BN endorsed PA
2.5 times more often than non-BN/non-BED respondents (27% v. 11%,
p < 0.000033, χ2square), and there was a trend for a similar difference between
BN and BED (11%, p < 0.09). These results imply that purging, rather than
bingeing per se, is more closely associated with an endorsement of PA. It is
likely that bulimic behaviors are maladaptive mechanisms with psychobiological
underpinnings linked to PTSD and depression that facilitate avoiding, numbing
and forgetting traumatic memories (15).
Somatoform Disorders
Disturbances in body perception and overt body distortion are somatoform
symptoms inherent to the EDs, especially AN. Links between somatoform
disorders (SDs) and EDs have also been reported in the literature (88–91). A
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 521
recent family study showed clustering of OCD with EDs and SDs (89),
particularly body dysmorphic disorder (BDD). BDD and EDs are similarly
characterized by obsessive and compulsive phenomenology targeted on the body
despicable. Other investigators have noted the connection between EDs and
BDD (90,91).
Links between SDs and prior victimization, especially CSA, are well
known (92–97). Among adult females, child abuse contributes not only to
general somatic preoccupation but to specific somatic symptoms in the chest and
throat areas as well (97). Interestingly, these body areas are those that are
involved in vomiting behavior. SDs are intimately linked to DDs as well as to
other axis I comorbidity. Somatoform dissociation is a unique construct that is
highly characteristic of DD patients, a core feature in many patients with SDs,
and an important symptom cluster in a subgroup of patients with EDs (88). Other
studies report that measures of somatization are significantly positively
correlated with measures of dissociation.
Axis II Comorbidity
The most common personality disorders (PDs) associated with the EDs have
been extensively reviewed in Chapter 9. In short, cluster C disorders [obsessive-
compulsive personality disorder (OCPD), avoidant personality disorder (APD),
and dependent personality disorder (DPD)] are common to both AN and BN. In
particular, OCPD and its traits are the best studied of this cluster and have been
shown to be important risk factors in the development of EDs (125).
Although there are no clear links between cluster C disorders and
victimization or PTSD, childhood emotional neglect has been associated with an
increased risk for APD during adolescence and early adulthood (126). It is
important to note that the presence of APD may contribute more avoidance to
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 523
that already inherent to PTSD and therefore make it even harder for the
traumatized ED patient to disclose abuse and face the exposure work required.
Childhood emotional neglect has also been associated with increased risk for
paranoid and cluster A PD symptom levels during adolescence and early
adulthood, and childhood physical neglect has been associated with an increased
risk for schizotypal PD and with cluster A PD symptom levels (126).
It is also noted in Chapter 9 that cluster B disorders, and their associated trait
of impulsivity, decidedly occur more frequently in the BN and AN bingepurge
type than in the AN restricting type of ED. Data show strong links not only
between BPD and patients with binge-purge symptomatology, but also between
BPD and histories of victimization, PTSD, affective disorders, other anxiety
disorders, SUDs, DDs, SDs, ICDs, DBDs, and ADHD (127–130). BPD is also
highly associated with multiple comorbid axis I disorders (131–133) as well as
with prior abuse and neglect. Other cluster B personality disorders, such as
narcissistic personality disorder (NPD) and antisocial personality disorder
(APD), have also been associated with child abuse and neglect(134).
first in relation to the other identified comorbid disorders? What disorders are
concurrent? What are the traumas and when did they happen in relation to the
disorders identified? It is useful over time to work with the patient to construct
a phenomenological, cause-and-effect-based time line and schema in which the
development and evolution of their problems makes overall sense to them. It is
likely that this information will evolve gradually and be referred to in therapy
again and again. Identifying the functional links of meaning between comorbid
disorders and life events can be very informative and instructive for patient,
family, and therapist in terms of identifying and challenging cognitive
distortions. One very common theme underlying the link between EDs and
trauma-related comorbidity is that maladaptive coping mechanisms, such as
bingeing, purging, dieting, substance abuse, dissociation, self-mutilation,
compulsive behavior, etc., are ways to avoid trauma-related states, i.e.,
memories, affects, behaviors, and thoughts, which are often triggered by any
number of cues. This phenomenon is another type of “compensatory behavior”
and is essentially another variation of the selfmedication hypothesis (141). Self-
punishment also has a lot of cognitive explanatory power for many traumatized
ED patients.
What disorder is primary and what disorder is secondary, tertiary, etc.? If the
onset of the ED came before the onset of the MDD, then the ED is the primary
disorder and MDD is the secondary disorder, which may in part be due to the
ED. If the ED came after the MDD, then the ED is secondary and may in part
be due to the MDD. In other words, as discussed in Chapter 6, primary
disorders may be risk factors for the development of secondary disorders. There
has been a long tradition in medicine to ascertain this type of information, to
develop a chronology of events and their subsequent sequelae, as a way to guide
treatment and “go to the source” of a patient’s problems. A secondary
depression may be more likely to respond to weight restoration and successful
management of the ED, whereas a primary depression may more likely linger
on or be an impediment to the ED recovery process unless it is managed more
aggressively. Interestingly, research shows that most episodes of MDD are
secondary, and they tend to be more persistent and severe than primary MDD
episodes (142). Similar to the above example, to the extent that an ED is
secondary to victimization and the posttraumatic stress process, it is important
to eventually and adequately address this primary problem.
Whenever possible, comorbid disorders should be managed concurrently, but
again, it is a matter of emphasis and prioritization. Which disorder or problem
should the clinician focus on first? A useful guideline that should determine the
clinician’s initial emphasis, for both ethical and medicolegal reasons, is the
current level of danger, risk, and/or brain/body impairment. It is necessary to
normalize or stabilize brain function in order for the psychotherapeutic
528 BREWERTON
enterprise to “take hold” and succeed. The idea that the nutritional instability
common to all ED patients must be addressed before more intensive
psychotherapy can be effectively utilized is common knowledge among experts
in the field. Garner and Garfinkel noted that the typical stages or phases of
treatment start with refeeding, nutritional stabilization, and rehabilitation,
which sometimes require a structured setting and program (143). Walter
Vandereycken put it succinctly when he said, “First we eat, then we talk” (144).
In short, all patients should receive nutritional education and counseling as
reviewed in Chapter 16, and these messages must be in sync with the primary
psychotherapeutic process.
The body of knowledge that must be conveyed includes several key points,
including (a) the powerful semistarvation effects in conscientious objectors
reported by Keys (8) and discussed in Chapter 8, and which lead to the
conclusion that dieting induces mental and physical symptoms de novo, and
(b) the implications of the tryptophan depletion studies to EDs as noted
in Chapters 11 and 16, which basically indicate that dieting depletes
neurotransmitters and this in turn has significant and rapid clinical effects (145).
It is also important to explain to patients and families that refeeding alone may
alleviate mood and anxiety dysregulation to some degree, but that it is also not
going to “fix everything.” In some ways certain symptoms of the traumatized ED
comorbid patient may get worse before they get better, and this is useful to
predict. Refeeding may allow patients to start “feeling their feelings” again and
to therefore begin to process them, usually with increasing intensity. Their
eating-disordered brains slowly but surely start to function better and better as
neurotransmitter and neurohormone levels move toward normalization (see
Chapters 11, 12, and 13). For this reason, nutritional rehabilitation, especially
weight gain in AN, not only allows antidepressants to work but also allows
psychotherapy to work. In effect, once patients begin to think and feel more clearly
as a result of refeeding, the real psychological issues can “rise” to awareness and
become clarified, processed, and “digested.” Nevertheless, the alexithymia that
is characteristic of ED patients and other psychosomatic conditions may be an
important clinical issue to address (146).
When substance abuse complicates the picture, one should always manage
withdrawal and dependence aggressively and as much as possible achieve
abstinence (“Say no, then go”). Just as starved brains can’t learn very well,
intoxicated brains can’t either. Basic requirements for effective psychotherapy
include grossly intact brain function, including the ability to attend and the
ability to learn-unlearn. In addition, sufficient motivation, the willingness to
change, and the presence of supportive relationship(s) are important ingredients
for progress. If necessary, motivational enhancement therapy (MET) may be
beneficial in highly resistant patients (147).
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 529
Once brain function has been stabilized and the process of normalization is
well on its way, more intensive psychotherapy can begin or intensify. The
phases of nutritional rehabilitation and intensive psychotherapy are not
absolutely distinct, but instead tend to overlap and merge into one another. The
major forms of psychotherapy that have been shown to have empirical evidence
for their effectiveness in the EDs are cognitive-behavioral therapy (CBT),
interpersonal therapy (IPT), family therapy (FT), and dialectical behavior
therapy (DBT), all of which are reviewed in Chapters 17, 18, 19, and 20,
respectively. Experiential psychotherapies have not been rigorously studied, but
may have important roles in the recovery of comorbid ED patients, particularly
in dealing with body image concerns, accessing emotional states, and
being exposed to one’s own self, so to speak. Likewise, elements of
psychodynamically oriented psychotherapy may be useful adjuncts in treatment,
but this should never be the only or primary modality used.
It is imperative that the clinician who wants to effectively manage EDs and
their comorbid psychiatric disorders familiarize themselves not only with the
American Psychiatric Association’s Practice Guidelines for the Treatment of
Eating Disorders (www.psych.org/clin_res/guide.bk.cfm), but with other
practice guidelines and treatment manuals as well on an as-needed
basis (www.psychguides.com; www.issd.org; www.psych.org) (148,149).
Therapeutic techniques adequate for the non-comorbid ED are not likely to
address other problems and disorders, so the clinician must rely on his or her
own resources, creativity, and ability to integrate a multitude of approaches in
order to tailor the best treatment to match the uniqueness of each patient.
Specific aspects and approaches regarding specific comorbid combinations are
outlined in Table 2.
Lest it seem too overwhelming or daunting, it is important to realize that
there are a number of commonalities inherent to the treatment of ED patients with
comorbid trauma-related disorders, including psychoeducation, CBT, and
pharmacotherapy. When using general relaxation techniques it is, in my
opinion, better to avoid progressive muscle relaxation in ED patients. This
inadvertently focuses attention on specific body parts that are “emotionally
loaded” for ED patients, which often serves to heighten anxiety rather than
lower it. Techniques that focus on the breath with or without the use of
visualization appear to work best in my view. When anxiety disorders
enter the clinical picture, the addition of prolonged exposure to CBT is clearly
indicated (149–154). Adequate time needs to be spent educating the patient
about the rationale for in vivo exposure using lay explanations for extinction,
conditioned cues, experiential learning, and why anxiety is a necessary
component for exposure to work. Hence, medicating away anxiety with
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530 BREWERTON
REFERENCES
1. Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress
disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995; 52:
1048–1060.
2. Kessler RC, Davis CG, Kendler KS. Childhood adversity and adult psychiatric
disorder in the US National Comorbidity Survey. Psychol Med 1997; 27:
1101–1119.
3. Kessler RC. Posttraumatic stress disorder: the burden to the individual and to
society. J Clin Psychiatry 2000; 61(Suppl 5):4–12; discussion 13–14.
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 537
19. Romans SE, Gendall KA, Martin JL, Mullen PE. Child sexual abuse and later
disordered eating: a New Zealand epidemiological study. Int J Eat Disord 2001; 29:
380–392.
20. Gleaves DH, Eberenz KP, May MC. Scope and significance of posttraumatic
symptomatology among women hospitalized for an eating disorder. Int J Eat Disord
1998; 24:147–156.
21. Matsunaga H, Kaye WH, McConaha C, Plotnicov K, Pollice C, Rao R, Stein D.
Psychopathological characteristics of recovered bulimics who have a history of
physical or sexual abuse. J Nerv Ment Dis 1999; 187:472–477.
22. Deep AL, Lilenfeld LR, Plotnicov KH, Pollice C, Kaye WH. Sexual abuse in eating
disorder subtypes and control women: the role of comorbid substance dependence
in bulimia nervosa. Int J Eat Disord 1999; 25:1–10.
23. Brown L, Russell J, Thornton C, Dunn S. Experiences of physical and sexual abuse
in Australian general practice attenders and an eating disordered population. Aust N
Z J Psychiatry 1997; 31:398–404.
24. Brown L, Russell J, Thornton C, Dunn S. Dissociation, abuse and the eating
disorders: evidence from an Australian population. Aust N Z J Psychiatry 1999; 33:
521–528.
25. Nagata T, Kiriike N, Iketani T, Kawarada Y, Tanaka H. History of childhood
sexual or physical abuse in Japanese patients with eating disorders: relationship with
dissociation and impulsive behaviours. Psychol Med 1999; 29: 935–942.
26. Nagata T, Kawarada Y, Kiriike N, Iketani T. Multi-impulsivity of Japanese patients
with eating disorders: primary and secondary impulsivity. Psychiatry Res 2000; 94:
239–250.
27. Favaro A, Dalle Grave R, Santonastaso P. Impact of a history of physical and sexual
abuse in eating disordered and asymptomatic subjects. Acta Psychiat Scand 1998;
97:358–363.
28. Striegel-Moore RH, Garvin V, Dohm FA, Rosenheck RA. Eating disorders in a
national sample of hospitalized female and male veterans: detection rates and
psychiatric comorbidity. Int J Eat Disord 1999; 25:405–414.
29. Lipschitz DS, Winegar RK, Hartnick E, Foote B, Southwick SM. Posttraumatic
stress disorder in hospitalized adolescents: psychiatric comorbidity and clinical
correlates. J Am Acad Child Adol Psychiatry 1999; 38:385–392.
30. Neumark-Sztainer D, Story M, Hannan PJ, Beuhring T, Resnick MD. Disordered
eating among adolescents: associations with sexual/physical abuse and other familial/
psychosocial factors. Int J Eat Disord 2000; 28:249–258.
31. Wonderlich SA, Crosby RD, Mitchell JE, Roberts JA, Haseltine B, DeMuth G,
Thompson KM. Relationship of childhood sexual abuse and eating disturbance in
children. J Am Acad Child Adol Psychiatry 2000; 39:1277–1283.
32. Thompson KM, Wonderlich SA, Crosby RD, Mitchell JE. Sexual victimization and
adolescent weight regulation practices: a test across three community based
samples. Child Abuse Neglect 2001; 25:291–305.
33. Ackard DM, Neumark-Sztainer D, Hannan PJ, French S, Story M. Binge and purge
behavior among adolescents: associations with sexual and physical abuse in a
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 539
63. Cochrane CE, Malcolm R, Brewerton TD. Eating disorders in cocaine abusers.
AddictiveDisl998;23:l-7.
64. Gross H, Ebert MH, Faden VB, Goldberg SC, Kaye WH, Caine ED, Hawks R,
Zinberg N. A double-blind trial of delta 9-tetrahydrocannabinol in primary
anorexia nervosa. J Clin Psychopharmacol 1983; 3:165–171.
65. Kessler RC, Crum RM, Warner LA, Nelson CB, Schulenberg J, Anthony JC.
Lifetime co-occurrence of DSM-III-R alcohol abuse and dependence with other
psychiatric disorders in the National Comorbidity Survey. Arch Gen Psychiatry
1997; 54:313–321.
66. Dansky BS, Brewerton TD, Kilpatrick DG. Comorbidity of bulimia nervosa and
alcohol use disorders: results from the National Women’s Study. Int J Eat Disord
2000; 27:180–190.
67. Putnam F, Guroff JJ, Silberman EK, Barban L, Post RM. The clinical
phenomenology of multiple personality disorder: a review of 100 cases. J Clin
Psychiatry 1986; 47:285–293.
68. Putnam F. Dissociation in Children and Adolescents: A Developmental Perspective.
New York: Guilford Press, 1997.
69. Torem MS. Dissociative states presenting as an eating disorder. Am J Clin
Hypnosis 1986; 29:137–142.
70. Torem MS. Covert multiple personality underlying eating disorders. Am J
Psychotherapy 1990; 44:357–368.
71. Torem MS. Eating disorders in patients with multiple personality disorder. In:
Kluft RP, Fine CG, eds. Clinical Perspectives on Multiple Personality Disorder.
Washington, DC: American Psychiatric Press, 1993:343–353.
72. Demitrack MA, Putnam FW, Brewerton TD, Brandt HA, Gold PW. Dis sociative
phenomena in eating disorders: relationship to clinical variables. J Psychaitry 1990;
147:1184–1188.
73. Goodwin JM, Attias R. Eating disorders in survivors of multimodal childhood
abuse. In: Kluft RP, Fine CG, eds. Clinical Perspectives on Multiple Personality
Disorder. Washington, D.C.: American Psychiatric Press, 1993:327–341.
74. Abraham SF, Beaumont PJV. How patients describe bulimia or binge eating.
Psychol Med 1984; 12:625–635.
75. Everill J, Waller G, Macdonald W. Dissociation in bulimic and non-
eatingdisordered women. Int J Eat Disord 1995; 17:127–134.
76. Tobin DL, Molteni AL, Elin MR. Early trauma, dissociation, and late onset in the
eating disorders. Int J Eat Disord 1995; 17:305–308.
77. Valdiserri S, Kihlstrom JF. Abnormal eating and dissociative experiences. Int J Eat
Disord 1995; 17:373–380.
78. Gleaves DH, Eberenz KP. Correlates of dissociative symptoms among women with
eating disorders. J Psychiatr Res 1995; 29:417–4426.
79. Vanderlinden J, Spinhoven P, Vandereycken W, van Dyck R. Dissociative and
hypnotic experiences in eating disorder patients: an exploratory study. Am J Clin
Hypnosis 1995; 38:97–108.
542 BREWERTON
96. Farley M, Patsalides BM. Physical symptoms, posttraumatic stress disorder, and
healthcare utilization of women with and without childhood physical and sexual
abuse. Psychol Rep 2001; 89:595–606.
97. Sansone RA, Gaither GA, Sansone LA. Childhood trauma and adult somatic
preoccupation by body area among women in an internal medicine setting: a pilot
study. Int J Psychol Med 2001; 31:147–154.
98. George MS, Brewerton TD, Cochrane CE. Trichotillomania, trichophagy and
bulimia nervosa. N Engl J Med 1990; 322:470–471.
99. Goldman MJ. Kleptomania: making sense of the nonsensical. Am J Psychiatry 1991;
148:986–996.
100. Baum A, Goldner EM. The relationship between stealing and eating disorders: a
review. Harvard Review of Psychiatry 1995; 3:210–221.
101. McElroy SL, Hudson JI, Pope HG, Keck PE. Kleptomania: clinical characteristics
and associated psychopathology. Psychol Med 1991; 21:93–108.
102. Favaro A, Santonastaso P. Self-injurious behavior in anorexia nervosa. J Nerv Ment
Dis 2000; 188:537–542.
103. Paul T, Schroeter K, Dahme B, Nutzinger DO. Self-injurious behavior in women
with eating disorders. Am J Psychiatry 2002; 159:408–411.
104. McElroy SL, Keck PE Jr, Phillips KA. Kleptomania, compulsive buying, and binge-
eating disorder. J Clin Psychiatry 1995; 56(suppl 4): 14–26; discussion 27.
105. Zlotnick C, Mattia JI, Zimmerman M. Clinical correlates of self-mutilation in a
sample of general psychiatric patients. J Nerv Ment Dis 1999; 187:296–301.
106. Lowenstein LF. The etiology, diagnosis and treatment of the fire-setting behaviour
of children. Child Psychiatry Hum Dev 1999–1999; 19:186–194.
107. McElroy SL, Phillips KA, Keck PE Jr. Obsessive compulsive spectrum disorder. J
Clin Psychiatry 1994; 55(suppl):33–51; discussion 52–53.
108. Stein DJ. Neurobiology of the obsessive-compulsive spectrum disorders. Biol
Psychiatry 2000; 47:296–304.
109. Hollander E, Rosen J. Impulsivity. J Psychopharmacol 2000; 14(suppl 1, 2):
S39-S44.
110. Messman-Moore TL, Long PJ, Siegfried NJ. The revictimization of child sexual
abuse survivors: an examination of the adjustment of college women with child
sexual abuse, adult sexual assault, and adult physical abuse. Child Maltreatment
2000; 5:18–27.
111. Humphrey JA, White JW. Women’s vulnerability to sexual assault from
adolescence to young adulthood. J Adol Health 2000; 27:419–424.
112. Field NP, Classen C, Butler LD, Koopman C, Zarcone J, Spiegel D.
Revictimization and information processing in women survivors of childhood
sexual abuse. J Anxiety Disord 2001; 15:459–469.
113. Kellogg ND, Hoffman TJ. Child sexual revictimization by multiple perpetrators.
Child Abuse Neglect 1997; 21:953–964.
114. Drimmer EJ. Stimulant treatment of bulimia nervosa with and without attention-
deficit disorder: three case reports. Nutrition 2003; 19:76–77.
544 BREWERTON
115. Sokol MS, Gray NS, Goldstein A, Kaye WH. Methylphenidate treatment for bulimia
nervosa associated with a cluster B personality disorder. Int J Eat Disord 1999; 25:
233–237.
116. Schweickert LA, Strober M, Moskowitz A. Efficacy of methylphenidate in bulimia
nervosa comorbid with attention-deficit hyperactivity disorder: a case report. Int J
Eat Disord 1997; 21:299–301.
117. Glod CA, Teicher MH. Relationship between early abuse, posttraumatic stress
disorder, and activity levels in prepubertal children. J Am Acad Child Adol
Psychiatry 1996; 35:1384–1393.
118. Hinshaw SP. Preadolescent girls with attention-deficit/hyperactivity disorder: I.
Background characteristics, comorbidity, cognitive and social functioning, and
parenting practices. J Consult Clin Psychol 2002; 70:1086–1098.
119. Heffron WM, Martin CA, Welsh RJ, Perry P, Moore CK. Hyperactivity and child
abuse. Can J Psychiatry 1987; 32:384–386.
120. Cohen AJ, Adler N, Kaplan SJ, Pelcovitz D, Mandel FS. Interactional effects of
marital status and physical abuse on adolescent psychopathology. Child Abuse
Neglect. 2002; 26:277–288.
121. Thompson KM, Wonderlich SA, Crosby RD, Mitchell JE. The neglected link
between eating disturbances and aggressive behavior in girls. J Am Acad Child
Adol Psychiatry 1999; 38:1277–1284.
122. Geist R, Davis R, Heinmaa M. Binge/purge symptoms and comorbidity in
adolescents with eating disorders. Can J Psychiatry 1998; 43:507–512.
123. Ford JD, Racusin R, Ellis CG, Daviss WB, Reiser J, Fleischer A, Thomas J. Child
maltreatment, other trauma exposure, and posttraumatic symptomatology among
children with oppositional defiant and attention deficit hyperactivity disorders.
Child Maltreatment 2000; 5:205–217.
124. Ford JD, Racusin R, Daviss WB, Ellis CG, Thomas J, Rogers K, Reiser J,
Schiffman J, Sengupta A. Trauma exposure among children with
oppositional defiant disorder and attention deficit-hyperactivity disorder. J Consult
Clin Psychol 1999; 67:786–789.
125. Zaider TI, Johnson JG, Cockell SJ. Psychiatric comorbidity associated with eating
disorder symptomatology among adolescents in the community. Intl J Eat Disord
2000; 28:58–67.
126. Johnson JG, Cohen P, Kotler L, Kasen S, Brook JS. Psychiatric disorders associated
with risk for the development of eating disorders during adolescence and early
adulthood. J Consult Clin Psychol 2002; 70:1119–1128.
127. Zanarini MC, Frankenburg FR, Dubo ED, Sickel AE, Trikha A, Levin A, Reynolds
V. Axis I comorbidity of borderline personality disorder. Am J Psychiatry 1998;
155:1733–1739.
128. Yen S, Shea MT, Battle CL, Johnson DM, Zlotnick C, Dolan-Sewell R, Skodol AE,
Grilo CM, Gunderson JG, Sanislow CA, Zanarini MC, Bender DS, Rettew JB,
McGlashan TH. Traumatic exposure and posttraumatic stress disorder in
borderline, schizotypal, avoidant, and obsessive-compulsive personality disorders:
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 545
145. Smith KA, Fairburn CG, Cowen PJ. Symptomatic relapse in bulimia nervosa
following acute tryptophan depletion. Arch Gen Psychiatry 1999; 56:171–176.
146. Cochrane CE, Brewerton TD, Hodges EL, Wilson D. Alexithymia in the eating
disorders. Int J Eat Disord 1993; 14:219–222.
147. Feld R, Woodside DB, Kaplan AS, Olmsted MP, Carter JC. Pretreatment
motivational enhancement therapy for eating disorders: a pilot study. Int J Eat Disord
2001; 29:393–400.
148. American Psychiatric Association. Practice guideline for the treatment of patients
with borderline personality disorder. Am J Psychiatry 2001; 158(suppl 10): 1–52.
149. Expert consensus guidelines for the treatment of posttraumatic stress disorder.
J Clin Psych 1999; 60(suppl 16):6–76.
150. Ballenger JC, Davidson JR, Lecmbier Y, Nutt DJ, Foa EB, Kessler RC, McFarlane
AC, Shalev AY. Consensus statement on posttraumatic stress disorder from the
International Consensus Group on Depression and Anxiety. J Clin Psychiatry 2000;
61(Suppl 5):60–66.
151. Schnicke M, Resick PA. Cognitive Processing Therapy for Rape Victims: A
Treatment Manual. London: Sage Publications, 1993.
152. Foa E, Rothbaum B. Treating the Trauma of Rape: Cognitive-Behavioral Therapy
for PTSD. New York: Guilford Press, 2001.
153. Keane T, Foa E, Friedman M. Effective Treatments for PTSD: Practice Guidelines
from the International Society for Traumatic Stress Studies. New York: Guilford
Press, 2000.
154. Heflin AH, Deblinger E. Treating Sexually Abused Children and Their
Nonoffending Parents: A Cognitive Behavioral Approach. London: Sage
Publications, 1996.
155. Shapiro F. Eye Movement Desensitization and Reprocessing (EMDR). 2d ed. Basic
Principles, Protocols, and Procedures. New York: Guilford Press, 2001.
156. Brewerton TD, Shannon M. Possible clozapine exacerbation of bulimia nervosa.
Am J Psychiatry 1992; 149:1408–1409.
157. McElroy SL, Casuto LS, Nelson EB, Lake KA, Soutullo CA, Keck PE Jr, Hudson
JI. Placebo-controlled trial of sertraline in the treatment of binge eating disorder.
Am J Psychiatry 2000; 157:1004–1006.
158. Ricca V, Mannucci E, Mezzani B, Moretti S, Di Bernardo M, Bertelli M, Rotella
CM, Faravelli C. Fluoxetine and fluvoxamine combined with individual cognitive-
behaviour therapy in binge eating disorder: a one-year follow-up study. Psychother
Psychosom 2001; 70:298–306.
159. Albert U, Aguglia E, Maina G, Bogetto F. Venlafaxine versus clomipramine in the
treatment of obsessive-compulsive disorder: a preliminary single-blind, 12week,
controlled study. J Clin Psychiatry 2002; 63:1004–1009.
160. Anderson JW, Greenway FL, Fujioka K, Gadde KM, McKenney J, O’Neil PM.
Bupropion SR enhances weight loss: a 48-week double-blind, placebocontrolled
trial. Obesity Res 2002; 10:633–641.
EATING DISORDERS, VICTIMIZATION, COMORBIDITY 547
Making predictions about the future is fraught with uncertainty, and humility is
always in order for those foolish enough to offer more than the most general of
prognostications. Professional futurologists employ a variety of specific
technical methods, including trend extrapolation, genius forecasting, consensus
methods, simulations, cross-impact matrix methods, scenario building, decision
trees, and creative disorder (a method that relies on innovations coming from
grass-roots levels). None of these methods may be capable of capturing
unanticipated events, known as “wild cards,” or successfully anticipating their
impacts. Lacking genius, a group capable of achieving consensus, and suitable
simulations, the safest statements one can offer are based on trend analyses, and
some imaginative scenario building and cross-matrix thinking(1,2).
A few lessons learned from futurist studies can guide our thinking about
eating disorders treatment from the start: First, technical changes always occur
more rapidly than social changes. Second, futurists usually tend to be more
optimistic about the occurrence and rates of change, particularly social change,
than is usually born out by history. Third, futurists tend to underestimate the
expenses involved in producing the changes they envision. Fourth, to help put
things into perspective, Arthur Clarke’s three laws of the future should always
be born in mind, to wit: (a) when a distinguished but elderly scientist says that
something is possible, he is almost certainly right. When he states that
something is impossible, he is very probably wrong. (b) The only way to
discover the limits of the possible is to go beyond them to the impossible.
(c) Any sufficiently advanced technology is indistinguishable from magic (3).
With respect to medicine and psychiatry, the rapid advances in neuroimaging
and genomics of the past few decades might seen like magic to those working in
this field a few decades ago. Where “magical” technological advances will appear
and how they will manifest in the next few decades can only be imagined.
Where the funds and necessary public will come from to pay for the services
that are likely to be possible, even demanded, is anyone’s guess.
550 YAGER
field will have to wait for such a system to be achieved. However, we might
anticipate that advances in functional as well as structural neuroimaging, genetic
analyses, complex systems, information processing, and related cognitive
sciences may lead to more discriminating diagnostic groupings based on
meaning biological differences within similar phenotypes. For the foreseeable
future, however, we will still rely on diagnostic systems based on clinical and
laboratory observations—phenomenology.
Already, the process of reviewing current diagnostic thinking for DSMV has
begun. Particular attention will be paid to what has been called “bioecological”
perspective, focusing on the first two decades of life, when rapid changes occur
in behavior, emotion, and cognition. Considerable attention will be paid to
developmental neuroscience, genetics, brain imaging, postmortem studies, and
animal models (4).
Well-recognized gaps exist in current categorical methods for diagnosing
personality disorders and their relationship with axis I disorders, and in the
limited provisions for the diagnosis of relational disorders in the current
nomenclature. These gaps have led to suggestions for dimensional
classifications, at least for personality disorders. Relationships between mental
disorders and measures of disability and impairment are likely to be revisited.
Particularly salient for eating disorders, the relationships of cultural factors to
psychopathology and the main cultural variables that operate in diagnostic
processes will be carefully reconsidered.
Crossing this DSM-V matrix with emerging discussions in the literature,
simple trend analysis suggests how several themes of the last several years may
color future discussions about eating disorders diagnoses. First, with regard to
nosological criteria, controversial questions have been raised regarding whether
amenorrhea, included as a diagnostic criterion for anorexia nervosa from DSM-
III on, should continue to be required as a criterion for anorexia nervosa (5).
Since experienced clinicians have seen many cases of otherwise frank anorexia
nervosa in which some degree of menstrual bleeding manages to persist, and
since this finding appears to have little if any significance regarding course or
outcome, amenorrhea may not be categorically required for distinctions
between “caseness” and “noncaseness” of anorexia nervosa. In addition,
controversies regarding whether the syndrome of binge eating disorder merits
elevation from its current lowly position, lumped in the EDNOS category, to
official diagnostic status as a distinct entity will be better informed by studies in
the next decade (6).
Regarding the relationship between axis II personality disorders and axis I
disorders, the recent research of Westen and Harnden-Fischer is informative.
Their studies support previous work suggesting that the course of anorexia
nervosa is strongly related to comorbid personality configuration. To
552 YAGER
been increasing substantially in spite of huge outcries from public health officials
about the importance of proper diet and exercise. To the extent that eating
disorders partly result from reactions against obesity-oriented tendencies,
pressures to develop eating disorders will remain strong in the community at
large and continue to affect those who are most vulnerable. Second, we can
think about how shifting social pressures may affect vulnerability factors such as
perfectionism, anxiety disorders, and depressive disorders. Might there be
relationships between the extent to which Western society continues to provide
increasing opportunities for self-fulfillment and individuation for women and
the extent to which perfectionistic tendencies are unleashed in those who
believe that excelling is of paramount importance? To what extent does today’s
society select for perfectionistic traits? Among the hypotheses recently advanced
to account for a seemingly significant increase in the numbers of children with
Asperger’s disorder in California’s Silicon Valley area is one based on the
observation that many of these children emerge from families in which both
parents were “computer nerds” (10). The question raised is whether the
selective breeding of “nerds” is more likely to breed Asperger’s children. In
parallel fashion, to what extent do contemporary societal pressures increase the
selective and assortive mating of perfectionistic men with perfectionistic
women, thereby producing higher likelihoods of perfectionistic offspring
vulnerable to anorexia nervosa? Are children with anorexia nervosa more likely
to emerge from homes parented by hard-driving, status-seeking couples than
from others?
In another vein, Sapolsky points to factors he believes are likely to contribute
to his prediction of increased rates of major depression in society. He posits that
ongoing rapid rates of social change and reductions in those social structures
that probably counter depressogenic tendencies, signaling breakdown of
community, add considerably to the stresses likely to produce depression (and,
from our perspective, potentially eating disorders as well) (11). Factors include
the increasing fragmentation of families into nuclear and one-parent families
that lack easily accessible grandparents, aunts, uncles, and cousins as
overstressed youth raised by overtaxed parents grow up. Absent the immediate
availability of extended families, youth may miss the benefits afforded by the
mediating, moderating, and supportive influences these other relatives may
provide regarding how to live. Studies concerning the relative risk for eating
disorders among adolescents raised in proximity to large extended families
versus those reared in more isolated environments may illuminate this intriguing
possibility.
Finally, it seems reasonable to predict that as globalization extends the ready
availability of fat-rich foods, opportunities for individuation and personal
choice, and the trend-setting influences of MTV and the Style Channel, the
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mood and anxiety disorders in particular are likely to be used for patients with
eating disorders, initially “off label,” and then, where interesting findings are
obtained, in systematic clinical trials. The pipeline for new medications is large.
Emerging new medications for mood disorders that may merit investigation for
eating disorders include selective noradrenergic uptake inhibitors such as
reboxetine; antiglucocorticoids such as mifepristone (RU486); corticotropin-
releasing factor (CRF) antagonists and other neurosteroid-modulating agents;
5-adenosylmethionine; the serotonin enhancer tianeptine; substance P
antagonists and other agents affecting neurokinins; and reversible monoamine
oxidase inhibitors such as moclobemide. Also of interest are new anxiolytics
such as pregabalin, and talipexole, a dopamine D2 and α2-adrenergic agonist
currently used for Parkinson’s disease, now being studied for managing
symptoms of dissociation and hyperarousal (29).
In addition to pharmacological treatments, other biological treatments using
light therapy, vagus nerve stimulation and transcranial magnetic stimulation for
associated depression, and other physiologically active procedures remain to be
explored for specific types of complex eating disorders (30).
Psychotherapies
Several trends can be identified. It is likely that research will continue on
delineating evidence-based effective individual, family, and group
psychotherapies for eating disorders, and on deconstructing and reassembling the
underlying effective elements to give better guidance to practitioners facing
complex clinical situations. Although these studies are expensive and difficult to
carry out, a number of developments may facilitate such studies in the future.
These include the development of multisite and, indeed, multinational clinical
trials, permitting larger studies. In addition, one can envision the organization
of intraprofession or multiprofession “practice research net works,” essentially
aggregations of up to several thousand practitioners organized to answer specific
clinical questions in their practices. Such networks have already proven effective
for answering clinical and health services research questions in pediatrics, family
medicine, and psychiatry (31). While psychotherapies based on cognitive-
behavioral and interpersonal psychotherapy models have been dominant, fusions
of these approaches as in cognitive-analytical therapies are exciting.
Motivational enhancement techniques, dialectic behavior therapy for complex,
multi-impulsive patients, and experimental manual-based psychotherapies based
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75% have used the Internet at least once to find health information and about
one in four has looked up information on weight issues, mental health, drugs
and alcohol, and violence (34).
A huge amount of information is currently available for the “on-line seeker,”
and information will predictably increase. In November 2002, one of the most
popular search engines, Google, listed about 1,040,000 sites pertinent to eating
disorders. Numerous organizations devoted to eating disorders are on-line. The
Center for Counseling and Health Resources, an on-line clearinghouse, posted
about 330 links related to eating disorders. Fortunately, the “top hits” on search
engines include a large number of wellregarded sites. Easily accessed, too, are
many commercial sites and personal web pages, some of which are very helpful,
but among which are many of uncertain quality. In mid-2002 the top eating
disorder sites listed on Google included Eating Disorders Awareness and
Prevention (EDAP; now becoming National Eating Disorders Association),
Something Fishy, Eating Disorders Mirror Mirror (Canada), ANRED,
EDReferral.com, the Eating Disorders Association (England), the Harvard
Eating Disorders Center, and the Academy for Eating Disorders. Although data
to estimate the extent to which these sites are accessed are hard to obtain, one
site, Something Fishy, indicated more than 2.9 million hits since 1995.
How good are these sites? Many questions remain concerning what criteria
should be used to evaluate them. In the future, well-respected eating disorders
organizations, such as the Academy for Eating Disorders, may take on the task
of defining criteria by which to judge eating disorders sites using parameters
such as their use of standard diagnostic criteria, the quality of information they
provide about these conditions, the range of reputable treatment options they
present, and the links they offer to reputable sources and facilities.
What do these sites provide? First, they provide considerable information
about diagnostic criteria, permitting individuals to do reasonably good
screenings for the existence of active or subclinical disorders in themselves or
others. Second, they provide considerable information about the causes
and courses of eating disorders, treatment, treatment resources, research, and
clinical trials. Of importance, on-line sites offer considerable social and
emotional support, personal narratives, chats, stories, poems, and memorials.
One year long qualitative study of an on-line support group assessed the
emotional and social support provided (alt.support.eating-disord, [ASED]). The
group developed its own rules, etiquette, and norms to create safe
communications and support and to explicitly reduce competitiveness. The
group provided a mix of problem solving and emotional support. In contrast to
face-to-face support groups, the lack of physical cues and presence seemed to
reduce competition regarding who is thinnest (35). Many other general and
specific eating disorders groups appear on-line. For example, the site
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http://www.healthy-place.com/Communities/Eating_Disorders/Site/comm_
calender.htm offers 12 different types of eating disorder on-line support groups
with different themes, including groups for eating disorder sufferers who also self-
injure and groups for parents of children with eating disorders. Clearly such
groups are not always available locally.
But some sites provide misinformation and misguidance. Of note, thanks to a
vigorous campaign initiated by ANAD, many former “proanorexia” sites that
appeared in abundance have been eliminated. However, some pro-anorexia
messages may still be encountered, and may deleteriously influence and
encourage young browsers who are intrigued and enchanted by the idea of
becoming anorexic.
Given the extent to which patients, families, and friends are likely to be using
the internet to acquire information about eating disorders, guidelines have been
developed to assist clinicians in dealing with their “wired” patients. Clinicians
are advised to be open minded and diplomatic about information patients bring
in from their net searches, understanding that the patient wants more
knowledge. Take the information seriously, discuss accurate and questionable
issues, suggest other web sites that might help, and suggest that patients not act
on information without consulting the provider (36).
the complex clinical safety, legal, and ethical issues emerging in the context of
computer-based treatments and distant medicine. These derive in part from the
fact that clinicians do not have access to patients’ nonverbal/behavioral cues,
lack control over the participant’s environment, and cannot assure the validity or
accuracy of information, among other factors. These issues resemble problems
of telephone encounters. Of particular concern, the potential for
miscommunication and delayed response to clinical emergencies, such as
postings of suicidal ideation, requires attention (41). In part, these concerns
have been addressed by reminding and reiterating that on-line communications
are not effective for crises, and by assuring that clinicians have accurate home
and work phone numbers for patients.
Emerging Technologies
Wireless two-way appliances increasingly used for chronic disease management,
the so-called “personal health buddy,” may be employed for eating disorders,
facilitating reporting of eating, exercise, mood and associated features, and
responses from clinicians (http://www.healthhero.com). Research conducted
by Wonderlich et al. using personal digital assistants exemplifies these
developments (48). Other emerging clinical applications include computer-
based body image assessments (49,50) and virtual reality-based body image
assessment and treatment (51).
Computer technology may provide better ways to train larger numbers of
health professionals, families, and patients about eating disorders using well-
established distance education models that integrate the Internet, audio tapes
and videotapes, telephone supervision, etc. Such methods are already being used
internationally (A.Parker, personal communication; A.Barriguete, personal
communications).
564 YAGER
Futuristic Applications
Further into the future, a number of additional applications may be developed,
limited only by imagination, funding, and zeal. Of potential value for the
management of eating disorders are the following possibilities: PDAbased
intelligent agents linked to patient’s cognitive style; voice, face, and emotion
recognition artificial intelligence systems for computer-assisted selfguided
therapy; outsourcing distance psychotherapy internationally in a global market;
video-telemedicine for family therapy with disconnected families. Finally,
research and treatment may be aided by sophisticated simulations capable of
portraying increasingly complex models of individual and family dynamics.
Envision future versions of “Sim Family,” including the emergence of the Sims
On-Line, permitting patients and families to demonstrate and work out
important issues in family relationships (www.the sims.ea.com). This is not
science fiction.
A cautionary note: Use of electronic communications and information
technology in applications such as those described above introduces a huge set
of confidentiality, patient safety, professional boundary, liability, and related
ethical and legal concerns that must be carefully addressed through informed
consents and practice protocols. All those writing in these fields emphasize
these issues, and several offer important ethical and legal guidelines (52).
judicial decisions that support insurance coverage based on medical rather than
psychiatric benefits for treatment of malnutrition associated with severe eating
disorders may be precedent setting and help patients, families, and clinicians
obtain needed services (53).
Even if decent funding were to be made available, many communities lack
appropriate facilities and health providers properly trained to assess and treat
patients with severe eating disorders. Responsibility for increasing the
availability of training opportunities will fall to academic centers and
organizations with strong eating disorders capacities, and, as alluded to above,
should be enhanced by the increasing availability of distance learning. However,
distance learning will never substitute for live supervised clinical experience.
Funding and incentives for training providers will determine the extent to which
these needs are met in the future.
Regardless of the extent to which funding may improve, it should be clear
that the costs of medical care will always increase so as to consume more than
the available resources. No doubt, as technologically sophisticated methods for
assessing genes, brains, and fluids become increasingly available, costs of care
are likely to continue to increase substantially just to pay for these tests and
procedures. However, the fact that new tests and treatments become available
does not assure that they will necessarily contribute materially to better
outcomes. Therefore, excellent judgment will always be required to ascertain
the actual value of performing new procedures and treatments.
As the various health professionals involved in assessing and treating eating
disorder patients continue to carefully observe and evaluate their experiences,
ongoing attention will be required for continually revising, updating, and
optimizing not only the evidence-based treatments and practices that command
respect but also the judgment-infused future editions of practice guidelines.
One hopes that tomorrow’s practice guidelines will better delineate how
collaborating health providers can best employ potential tests and treatments to
assure that outcomes become progressively better for patients and their
families. One also hopes that tomorrow’s research, on which such
recommendations will be based, will be guided by an unending supply of
curiosity and increasingly sophisticated questions.
REFERENCES
1. Yager J. A futuristic view of psychiatry. In: Yager J, ed. The Future of Psychiatry as
a Medical Specialty. Washington, DC: American Psychiatric Press, 1989:135–159.
2. Brockman J, ed., The Next Fifty Years: Science in the First Half of the TwentyFirst
Century. New York: Vintage, 2002.
566 YAGER
3. Clarke AC. Technology and the future. In: Clarke AC, ed. Report on Planet
Three. New York: Signet, 1972:129–141.
4. Kupfer DJ, First MB, Regier DA, eds. A Research Agenda for DSM-V.
Washington, DC: American Psychiatric Association, 2002.
5. Garfinkel PE, Lin E, Goering P, Spegg C, Goldbloom D, Kennedy S, Kaplan AS,
Woodside DB. Should amenorrhoea be necessary for the diagnosis of anorexia
nervosa? Evidence from a Canadian community sample. Br J Psychiatry 1996; 168:
500–506.
6. Pincus HA, First M. Critical differences between binge eating and overeating. Arch
Gen Psychiatry 1999; 56:951.
7. Westen D, Harnden-Fischer J. Personality profiles in eating disorders: rethinking
the distinction between axis I and axis II. Am J Psychiatry 2001; 158:547–562.
8. Strober M, Freeman R, Morrell W. Atypical anorexia nervosa: separation from
typical cases in course and outcome in a long-term prospective study. Int J Eat
Disord 1999; 25:135–142.
9. Rieger E, Touyz SW, Beumont PJ. The Anorexia Nervosa Stages of Change
Questionnaire (ANSOCQ): information regarding its psychometric properties. Int
J Eat Disord 2002; 32:24–38.
10. Silberman S. The Geek Syndrome: Autism—and its milder cousin Asperger’s
syndrome—is surging among the children of Silicon Valley. Are math-and-tech
genes to blame? Wired Dec 2001; 9(12). http://www.wired.com/wired/archive/
9.12/aspergers.html.
11. Sapolsky RM. Will we still be sad fifty years from now? In: Brockman J, ed. The
Next Fifty Years: Science in the First Half of the Twenty-First Century. New York:
Vintage Press, 2002:105–113.
12. Becker AE, Burwell RA, Gilman SE, Herzog DB, Hamburg P. Eating behaviours
and attitudes following prolonged exposure to television among ethnic Fijian
adolescent girls. Br J Psychiatry 2002; 180, 509–514.
13. Gorwood P, Bouvard M, Mouren-Simeoni MC, Kipman A, Ades J. Genetics and
anorexia nervosa: a review of candidate genes. Psychiatr Genet 1998; 8(1): 1–12.
14. Treasure JL, Owen JB. Intriguing links between animal behavior and anorexia
nervosa. Int J Eat Disord 1997; 21:307–311.
15. Levitan RD, Kaplan AS, Masellis M, Basile VS, Walker ML, Lipson N, Siegel GI,
Woodside DB, Macciardi FM, Kennedy SH, Kennedy JL. Polymorphism of the
serotonin 5-HT1B receptor gene (HTRIB) associated with minimum lifetime body
mass index in women with bulimia nervosa. Biol Psychiatry 2001; 50:640–643.
16. Westberg L, Bah J, Rastam M, Gillberg C, Wentz E, Melke J, Hellstrand M,
Eriksson E. Association between a polymorphism of the 5-HT2c receptor and
weight loss in teenage girls. Neuropsychopharmacology 2002; 26:789–793.
17. Klump KL, Kaye WH, Strober M. The evolving genetic foundations of eating
disorders. Psychiatr Clin North Am 2001; 24:215–225.
18. Hu X, Murphy F, Karwautz A, Li T, Freeman B, Franklin D, Giotakis O, Treasure
J, Collier DA. Analysis of microsatellite markers at the UCP2/UCP3 locus on
chromosome 1 Iql3 in anorexia nervosa. Mol Psychiatry 2002; 7:276–277.
FUTURE DIRECTIONS 567
19. Eastwood H, Brown KM, Markovic D, Pieri LF. Variation in the ESR 1 and ESR2
genes and genetic susceptibility to anorexia nervosa. Mol Psychiatry 2002; 7:
86–89.
20. Vink T, Hinney A, van Elburg AA, van Goozen SH, Sandkuijl LA, Sinke RJ,
Herpertz-Dahlmann BM, Hebebrand J, Remschmidt H, van Engeland H, Adan RA.
Association between an agouti-related protein gene polymorphism and anorexia
nervosa. Mol Psychiatry 2001; 6:325–328.
21. Klump KL, Wonderlich S, Lehoux P, Lilenfeld LR, Bulik CM. Does environment
matter? A review of nonshared environment and eating disorders. Int J Eat Disord
2002; 31:118–135.
22. Schork NJ, Fallin D, Lanchbury JS. Single nucleotide polymorphisms and the future
of genetic epidemiology. Clin Genet 2000; 58:250–264.
23. Katzman DK, Zipursky RB, Lambe EK, Mikulis DJ. A longitudinal magnetic
resonance imaging study of brain changes in adolescents with anorexia nervosa.
Arch Pediatr Adol Med 1997; 151:793–797.
24. Gordon I, Lask B, Bryant-Waugh R, Christie D, Timimi S. Childhood-onset
anorexia nervosa: towards identifying a biological substrate. Int J Eat Disord 1997;
22:159–165.
25. Robb AS, Silber TJ, Orrell-Valente JK, Valadez-Meltzer A, Ellis N, Dadson MJ,
Chatoor I. Supplemental nocturnal nasogastric refeeding for better short-term
outcome in hospitalized adolescent girls with anorexia nervosa. Am J Psychiatry
2002; 159:1347–1353.
26. Bodkin JA, Amsterdam JD. Transdermal selegiline in major depression: a double-
blind, placebo-controlled, parallel-group study in outpatients. Am J Psychiatry
2002; 159(11):1869–1875.
27. Levine J. Controlled trials of inositol in psychiatry. Eur Neuropsychopharmacol
1997; 7:147–155.
28. Mendelson SD. Treatment of anorexia nervosa with tramadol. Am J Psychiatry
2001; 158:963–964.
29. Boschert S. Novel antidepressant therapies near approval. Clin Psychiatry News
2002; 30(10): 1–20.
30. Rush AJ, George MS, Sackeim HA, Marangell LB, Husain M, Giller C, Nahas Z,
Haines S, Simpson RK Jr, Goodman R. Vagus nerve stimulation (VNS) for
treatment-resistant depressions: a multicenter study. Biol Psychiatry 2000; 47:
276–286.
31. Pincus HA, Zarin DA, Tanielian TL, Johnson JL, West JC, Pettit AR, Marcus SC,
Kessler RC, McIntyre JS. Psychiatric patients and treatments in 1997: findings from
the American Psychiatric Practice Research Network. Arch Gen Psychiatry 1999;
56:441–449.
32. Lock J, Le Grange D, Agras S, Dare C. Treatment Manual for Anorexia Nervosa: A
Family-Based Approach. New York: Guilford Press, 2001.
33. Ferguson T. Health Online: How to Find Health Information, Support Groups, and
Self-Help Communities in Cyberspace. Boston: Addison-Wesley, 1996.
568 YAGER
34. Kaiser Family Foundation. How young people use the internet for health
information. GenerationX.Com.,http://www.kff.org/content/2001/2001121
la/GenerationRx.pdf.
35. Walstrom MK. “You know, who’s the thinnest?”: Combating surveillance and
creating safety in coping with eating disorders online. Cyber Psychol Behav 2000;
3:761–783.
36. Chin T. Site reading: physicians grapple with recommending websites. Am Med
News, Oct 23–30, 2000, 24 (http://www.ama-assn.org/sci-pubs/amnews/
pick_00/tesa 102 3. htm).
37. Balas EA, Jaffrey F, Kuperman GJ, Boren SA, Brown GD, Pinciroli F, Mitchell JA.
Electronic communication with patients. Evaluation of distance medicine
technology. JAMA 1997; 278:152–159.
38. Winzelberg AJ, Eppstein D, Eldredge KL, Wilfley D, Dasmahapatra R, Dev P,
Taylor CB. Effectiveness of an internet-based program for reducing risk factors for
eating disorders. J Consult Clin Psychol 2000; 68:346–350.
39. Celio AA, Winzelberg AJ, Wilfley DE, Eppstein-Herald D, Springer EA, Dev P,
Taylor CB. Reducing risk factors for eating disorders: comparison of an internetand
a classroom-delivered psychoeducational program. J Consult Clin Psychol 2000;
68:650–657.
40. Zabinski MF, Wilfley DE, Pung MA, Winzelberg AJ, Eldredge K, Taylor CB. An
interactive internet-based intervention for women at risk of eating disorders: a
pilot study. Int J Eat Disord 2001; 30:129–137.
41. Humphreys K, Winzelberg A, Klaw E. Psychologists’ ethical responsibilities in the
Internet-based groups: issues, strategies, and a call for dialogue. Prof Psychol Res
Pract 2000; 31:493–496.
42. Yager J. E-mail as a therapeutic adjunct in the outpatient treatment of anorexia
nervosa: illustrative case material and discussion of the issues. Int J Eat Disord
2001; 29:125–138.
43. Robinson PH, Sefaty MA. The use of e-mail in the identification of bulimia nervosa
and its treatment. Eur. Eat Disord Rev 2001; 9:182–193.
44. Bakke B, Mitchell J, Wonderlich S, Erickson R. Administering cognitivebehavioral
therapy for bulimia nervosa via telemedicine in rural settings. Int J Eat Disord 2001;
30:454–457.
45. Sansone R. Patient to patient e-mail support for clinical practices. Eat Disord Treat
Prev 2001; 9:373–375.
46. Kenwright M, Liness S, Marks I. Reducing demands on clinicians by offering
computer-aided self-help for phobia/panic. Feasibility study. Br J Psychiatry 2001;
179:456–459.
47. Thiels C, Schmidt U, Treasure J, Garthe R, Troop N. Guided self-change for bulimia
nervosa incorporating use of a self-care manual. Am J Psychiatry 1998; 155:
947–953.
48. Smyth J, Wonderlich S, Crosby R, Miltenberger R, Mitchell J, Rorty M. The use of
ecological momentary assessment approaches in eating disorder research. Int J Eat
Disord 2001; 30:83–95.
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