Annu. Rev. Psychol. 2002. 53:187–213
Copyright c ? 2002 by Annual Reviews. All rights reserved
CAUSES OF EATING DISORDERS
Janet Polivy1and C. Peter Herman2
1Department of Psychology, University of Toronto, Erindale Campus, Mississauga,
Ontario, Canada L5L 1C6; e-mail: email@example.com
2Department of Psychology, University of Toronto, Toronto, Ontario, Canada M5S 1A1;
anorexia nervosa, bulimia nervosa, contributory factors, identity,
inant eating disorders. We review the recent research evidence pertaining to the de-
velopment of these disorders, including sociocultural factors (e.g., media and peer
influences), family factors (e.g., enmeshment and criticism), negative affect, low self-
eating disorders. Some contributory factors appear to be necessary for the appearance
of eating disorders, but none is sufficient. Eating disorders may represent a way of
coping with problems of identity and personal control.
Anorexia nervosa and bulimia nervosa have emerged as the predom-
INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187
DIAGNOSTIC CRITERIA AND CORE
PATHOLOGICAL FEATURES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188
Incidence and Prevalence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 189
Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190
CAUSES OF EATING DISORDERS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190
Sociocultural Contributors to Eating Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191
Familial Influences on Eating Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193
Individual Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
CONCLUSIONS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204
In the late 1960s, the previously obscure and extremely rare disorder anorexia ner-
middle- and upper-class families were starving themselves, sometimes to death.
The next decade saw the emergence of a new eating disorder, bulimia nervosa
(BN), wherein young women alternated self-starvation with bingeing, usually fol-
lowed by purging (i.e., active attempts to rid the body of calories). Clinicians and
the media focused intensively on these new disorders, which supplanted obesity
as the primary eating disorder; indeed, obesity was removed from the Diagnostic
esting historical research (Bemporad 1997) uncovered evidence of both AN and
BN having existed since ancient times, but certainly not to the same extent—and
possibly not in the same way—as at present. By the turn of the millennium, AN
and BN were well-established—as was the research enterprise—but a clear under-
standing of the source of the disorders or how to prevent or treat them remained
to a review of research (and speculation) on the causes of eating disorders, empha-
sizing the discriminant validity of causal factors (i.e., why one person develops an
eating disorder, whereas another seemingly similar person in a seemingly similar
situation does not). One major area we do not review is treatment research; this
decision is dictated mainly by space limitations, but also by the fact that studies
on treatment are only loosely related to research on eating disorder’s (ED) causes.
Another arguable decision is to ignore binge eating disorder and eating disorder
not otherwise specified, recently identified EDs; again, space limitations require
strict focus on the major EDs.
DIAGNOSTIC CRITERIA AND CORE
In this chapter we follow the convention of the research literature and consider
AN and BN as separate disorders. How—or even whether—to separate the eating
disorders, however, has been debated vigorously. The core symptoms (e.g., body
dissatisfaction; preoccupation with food, weight, and shape; certain ego deficits)
do not necessarily distinguish AN from BN patients, even if the diagnostic criteria
the EDs as one syndrome with different manifestations.
normal weight for age and height, an intense fear of fatness, disturbed experience
of one’s body weight or shape, and amenorrhea for at least three consecutive
menstrual cycles. Although many AN patients engage in compulsive exercising,
whereas bulimic-type AN patients regularly engage in binge eating and purging.
(Cachelin & Maher 1998, Garfinkel et al. 1996); we could extend the argument to
the 85% weight criterion.
The DSM-IV criteria for BN include recurrent episodes of both binge eating
(i.e., eating a larger amount of food than most people would eat in a similar time
CAUSES OF EATING DISORDERS
and circumstances, and a feeling of lack of control of one’s eating during the
episode) and compensatory behaviors (such as purging, exercising, or fasting) to
on body weight and shape. Note that bingeing and purging are characteristics of
one major type of AN, which leads to understandable confusion between AN and
BN1; BN may differ from bulimic-type AN only in that BN patients are unable to
suppress their weight below the 85% cut-off and thus fail to display amenorrhea.
AN is an exclusionary criterion for BN, which otherwise might be confused with
bulimic-type AN. A further subdivision of BN into purging-type (i.e., use of self-
induced vomiting or laxative, diuretic, or enema abuse) and nonpurging type
(i.e., fasting, exercising, or other nonpurging means of compensating for binge
eating) would seem to differ only in the preferred tactic for eliminating calories
and probably has little conceptual significance (APA 1994).
Although bingeing is a diagnostic feature of BN and bulimic-type AN, we have
little guidance as to how to identify a binge (Herman & Polivy 1996). Exactly how
much food is a larger-than-normal amount of food? How are we to assess the loss
of control that allegedly characterizes binges (Johnson et al. 2000)? If an eating
episode displayed only one aspect—a huge amount of food or loss of control but
not both—would it still be a binge?
One correlative feature that distinguishes BN from AN is impulsivity. Sexual
noted in BN patients (e.g., Matsunaga et al. 2000; Wiederman & Pryor 1996).
Indeed, impulsiveness may be what makes an aspiring anorexic into a bulimic;
if an individual intent on restricting her intake cannot resist food under certain
circumstances, she may capitulate to temptation, binge, and then feel obliged
to compensate afterward. This pattern would seem to characterize both BN and
Incidence and Prevalence
The incidence of AN and BN has increased markedly during the past 50 years,
although there is some reason to believe that at least some of the increase is due
to greater awareness and reporting of these disorders (Wakeling 1996). Precise
estimates of incidence and prevalence vary wildly, perhaps because those who
suffer from these disorders are often reluctant to reveal their condition. Prevalence
estimates tend to range from about 3% to 10% of at-risk females (those between
15 and 29 years of age), with BN patients outnumbering AN patients by at least
2 to 1. Those with AN frequently deny any illness and are often seen for treat-
ment only because of the concern of those close to them that their lives may be in
1Indeed, Gleaves et al. (2000) found that restrictor-type AN is more distinct from bulimic-
type AN than bulimic-type AN is from BN. It has been argued that bulimic-type AN should
simply be considered BN.
imminent danger. Those with BN, because their appearance is usually normal and
their bingeing and purging occur in private, are usually more difficult to detect,
although BN patients are more likely to present themselves for treatment, because
the binge-purge cycle is often profoundly disturbing to them. (AN patients fre-
quently appear to be indifferent to their disorder.) The prevalence of partial EDs
is at least twice that of full-syndrome EDs. Longitudinal studies suggest a pro-
gression from less to more severe disturbances, with normal dieters occasionally
becoming pathological dieters, who in turn occasionally progress to partial- or
full-syndrome EDs (Shisslak et al. 1995). It must be remembered, though, that
whereas normal dieting is a frequent precursor of EDs, most normal dieters do not
progress to the point of pathology. One of the most significant questions facing us
is why some dieters progress to EDs whereas most do not.
nostic criteria 5 years and longer after initial treatment (Fairburn et al. 2000, Keel
et al. 1999). Estimates of mortality (including suicide) rates range from just over
5% to just over 8% (Herzog et al. 2000, Steinhausen et al. 2000). Still, more than
50% of patients show significant improvement more than 5 years after beginning
2000). Some research (e.g., Keel et al. 1999) has explored predictors of success in
treatment, but there has been little investigation into natural recovery, self-cure, or
remission of EDs without treatment. Perhaps only the most intractable cases find
their way into treatment.
CAUSES OF EATING DISORDERS
The main purpose of this chapter is to survey the various attempts to explain why
some people develop eating disorders. The literature displays an uneasy balance
between studies exploring the role of particular putative causal factors and theo-
ries that attempt to combine such factors into a comprehensive whole. The main
obstacles facing these attempts are, first and foremost, the virtual impossibility of
conducting true experimental research in which a putative causal factor is manip-
ulated, and secondly, the difficulty of combining all such factors into a model that
is not unwieldy. A large proportion of studies examine AN and/or BN patients
(and sometimes a healthy or psychiatrically impaired control group) with an eye
to isolating correlates of the disorder, often in the vague hope that correlates can
be persuasively argued into causes. The difficulty of finding suitable samples of
ED patients to test has led to a proliferation of studies examining correlates of ED
symptomatology as it exists in more-or-less normal populations. Any sample of
reported symptoms (albeit far short of true pathology), which may be leveraged
CAUSES OF EATING DISORDERS
by extrapolation and the confusion of correlation and causation (especially in
cross-sectional data) into examinations of the causes of EDs. The difficulty of do-
ing proper research, along with the relative infancy of this field of research, should
are modest. Some theorists, such as Bruch (1973), have provided elegant theories;
however, empirical data to confirm this and other theories are incomplete and
inconclusive at this point.
Literally thousands of studies, plus numerous books and chapters, have at-
tempted to specify exactly what causes EDs. The consensual approach to inte-
grating the various factors that contribute to EDs is the “biopsychosocial” model.
This model has the advantage of taking into account all sorts of factors—ranging
from the broadly cultural to the narrowly biological, with stops along the way for
familial, social, cognitive, learning, personality, and other factors—that have been
ever; moreover, each version of the biopsychosocial model differs from the next.
Space limitations preclude an exhaustive review here, but we attempt to provide
an overview of the most salient findings and issues. We begin at the broadest level
with culture, proceed to familial and social factors, and then examine individual
factors such as personality, cognition, and physiology.
Sociocultural Contributors to Eating Disorders
Eating disorders do not occur uniformly in all cultures at all times. An obsession
with slimness—a core feature of EDs—is concentrated in cultures in which food
is abundant. In cultures of scarcity, the ideal body shape is much more likely to
be rotund, suggesting that ideals tend toward what is difficult to achieve. In this
sense, then, a culture of caloric abundance may be considered a cause of EDs.
It is important to note from the outset, however, that this cause is not specific;
growing up in a culture of abundance, while perhaps increasing the chances of
your developing an ED, does not make it likely that you will develop an ED; after
of abundance should be regarded as at most a background cause. Such a culture
may value slimness, but whether a particular individual takes this valuation to a
in the extent to which people internalize our culture’s valuation of slimness, and
the extent of such internalization predicts body dissatisfaction, drive for thinness,
We must refer to more individual factors (see below).
Initially, it was believed (see e.g., Garfinkel & Garner 1982) that the idealiza-
tion of slimness, and the consequent tendency toward EDs, was concentrated in
the upper-SES strata of the culture of abundance, where after all, abundance is
even greater. As our culture becomes increasingly homogenized, with media im-
ages of a thin ideal physique now permeating every corner of society, EDs have
A cross-cultural examination of weight-
related teasing, body image, and eating dis-
Int. J. Eat. Disord. 28:430–35
Matsunaga H, Kiriike N, Iwasaki Y, Miyata
bulimic patients in Japan. Int. J. Eat. Disord.
Milligan RJ, Waller G. 2000. Anger and bu-
limic psychopathology among nonclinical
women. Int. J. Eat. Disord. 28:446–50
Minuchin S, Rosman BL, Baker L. 1978. Psy-
chosomatic Families: Anorexia Nervosa in
Mogg K, Bradley BP, Hyare H, Lee S. 1998.
Selective attention to food-related stimuli in
hunger: Are attentional biases specific to
emotional and psychopathological states, or
are they also found in normal drives states?
Behav. Res. Ther. 36:227–37
Mumford DB, Choudry IY. 2000. Body dis-
satisfaction and eating attitudes in slimming
and fitness gyms in London and Lahore: a
cross-cultural study. Eur. Eat. Disord. Rev.
Mussell MP, Mitchell JE, Fenna CJ, Crosby
RD, MillerJP, HobermanHM.1997.Acom-
parison of onset of binge eating versus diet-
ing in the development of bulimia nervosa.
Int. J. Eat. Disord. 21:353–60
Neumark-Sztainer D, Story M, Hannan PJ,
Beuhring T, Resnick MD. 2000. Disor-
with sexual/physical abuse and other famil-
ial/psychosocial factors. Int. J. Eat. Disord.
O’Dea JA, Abraham S. 2000. Improving the
body image, eating attitudes, and behaviors
educational approach that focuses on self-
esteem. Int. J. Eat. Disord. 28:43–57
O’Dwyer AM, Lucey JV, Russell GF. 1996.
Serotonin activity in anorexia nervosa af-
ter long-term weight restoration: response
to D-fenfluramine challenge. Psychol. Med.
Ogden J, Steward J. 2000. The role of the
mother-daughter relationship in explaining
weight concern. Int. J. Eat. Disord. 28:78–
Paxton SJ, Schutz HK, Wertheim ES, Muir
SL. 1999. Friendship clique and peer influ-
ences on body image concerns, dietary re-
straint, extreme weight-loss behaviors, and
binge eating in adolescent girls. J. Abnorm.
Pike KM, Rodin J. 1991. Mothers, daughters,
and disordered eating. J. Abnorm. Psychol.
Pinel JPJ, Assanand S, Lehman DR. 2000.
Hunger, eating, and ill health. Am. Psychol.
PlominR, ChipuerHM, LoehlinJC.1990.Be-
havioral genetics and personality. In Hand-
book of Personality Theory and Research,
ed. LA Pervin, pp. 225–43. New York: Guil-
Polivy J, Herman CP. 1985. Dieting and bing-
ing: a causal analysis. Am. Psychol. 40:193–
Polivy J, Herman CP. 1987. The diagnosis and
treatment of normal eating. J. Consult. Clin.
Polivy J, Herman CP, Mills J, Wheeler HB.
Blackwell Handbook of Adolescence, ed. G
Pryor TL, Martin RL, Roach N. 1995. Obses-
sive-compulsive disorder, trichotollimania,
and anorexia nervosa: a case report. Int. J.
Eat. Disord. 18:375–79
Raffi AR, Rondini M, Grandi S, Fava GA.
2000. Life events and prodromal symptoms
in bulimia nervosa. Psychol. Med. 30:727–
Rieger E, Schotte DE, Touyz SW, Beumont
PJV, Griffiths R, Russell J. 1998. Attention-
al biases in eating disorders: a visual probe
detection procedure. Int. J. Eat. Disord. 23:
Rorty M, Yager J. 1996. Histories of
CAUSES OF EATING DISORDERS
sequelae in women with eating disorders.
Psychiatr. Clin. N. Am. 19:773–87
Rorty M, Yager J, Rossotto E, Buckwalter G.
2000. Parental intrusiveness in adolescence
recalled by women with a history of bulimia
nervosa and comparison women. Int. J. Eat.
Sanftner JL, Crowther JH. 1998. Variability
in self-esteem, moods, shame and guilt in
women who binge. Int. J. Eat. Disord. 23:
Schmidt U, Tiller J, Blanchard M, Andrews
B, Treasure J. 1997. Is there a specific
trauma precipitating anorexia nervosa? Psy-
chol. Med. 27:523–30
Sebastian SB, Williamson DA, Blouin DC.
1996. Memory bias for fatness stimuli in the
eating disorder. Cogn. Ther. Res. 20:275–86
Serpell L, Treasure J, Teasdale J, Sullivan V.
Eat. Disord. 25:177–86
Shisslak CM, Crago M, Estes LS. 1995. The
spectrum of eating disturbances. Int. J. Eat.
Shisslak CM, Crago M, McKnight KM, Estes
LS, Gray N, Parnaby OG. 1998. Potential
risk factors associated with weight control
behaviors in elementary and middle school
girls. J. Psychosom. Res. 44:301–13
Shoebridge P, Gowers SG. 2000. Parental
high concern and adolescent-onset anorexia
nervosa—a case-control study to investi-
gate direction of causality. Br. J. Psychiatry
Smolak L, Levine MP,
Parental input and weight concerns among
elementary school children. Int. J. Eat. Dis-
Spelt J, Meyer JM. 1995. Genetics and eating
disorders. In Behavior Genetic Approaches
in Behavioral Medicine, ed. JR Turner, LR
Cardon, JK Hewitt, pp. 167–85. New York:
Steiger H, Leung FYK, Puentes-Neuman G,
Gottheil N. 1992. Psychological profiles of
adolescent girls with varying degrees of eat-
ing and mood disturbances. Int. J. Eat. Dis-
Schermer F. 1999.
Steiger H, Stotland S, Trottier J, Ghadirian
transgenerational effects. Int. J. Eat. Disord.
Steinberg S,Tobin D,
The role of bulimic behaviors in affect reg-
ulation: different functions for different pa-
tient subgroups? Int. J. Eat. Disord. 9:51–
Steinhausen HC, Seidel R, Metzke CW. 2000.
long-term outcome of adolescent eating dis-
orders. Psychol. Med. 30:1089–98
Stice E. 1998. Modeling of eating pathology
and social reinforcement of the thin-ideal
predict onset of bulimic symptoms. Behav.
Res. Ther. 36:931–44
Stice E. 2001. A prospective test of the dual-
pathway model of bulimic pathology: medi-
ating effects of dieting and negative affect. J.
Abnorm. Psychol. 110:1–12
Stice E, Akutagawa D, Gaggar A, Agras WS.
between dieting and binge eating. Int. J. Eat.
Stice E, Hayward C, Cameron RP, Killen JD,
eating disturbances predict onset of depres-
sion among female adolescents: a longitu-
dinal study. J. Abnorm. Psychol. 109:438–
Stice E, Shaw H, Nemeroff C. 1998. Dual
pathway model of bulimia nervosa: longitu-
dinal support for dietary restraint and affect-
Stormer SM,Thompson JK. 1996. Expla-
nations of body image disturbance: a test
of maturational status, negative verbal com-
mentary, social comparison, and sociocul-
tural hypotheses.Int. J. Eat. Disord.19:193–
Striegel-Moore R. 1993. Etiology of binge eat-
ing: a developmental perspective. In Binge
Eating: Nature, Assessment and Treatment,
ed. CG Fairburn, GT Wilson, pp. 144–72.
New York: Guilford
Johnson C. 1989.
Striegel-Moore R. 1997. Risk factors for eat-
ing disorders. Ann. NY Acad. Sci. 817:98–
race in the development of eating disorders.
In The Developmental Psychopathology of
Prevention, and Treatment, ed. MP Levine,
LL Smolak, R Striegel-Moore, pp. 259–84.
Hillsdale, NJ: Erlbaum
Strober M. 1991. Disorders of the self in
anorexia nervosa: an organismic-develop-
mental paradigm. In Psychodynamic Treat-
ment of Anorexia Nervosa and Bulimia, ed.
CL Johnson, pp. 354–73. New York: Guil-
structural model for studies of the initiation
of dieting among adolescent girls. J. Psycho-
som. Res. 44:315–26
Study Group Anorexia Nervosa. 1995. Ano-
rexia nervosa: directions for future research.
Int. J. Eat. Disord. 17:235–41
Sunday SR, Halmi KA, Einhorn A. 1995. The
Yale-Brown-Cornell eating disorder scale: a
new scale to assess eating disorder symp-
tomatology. Int. J. Eat. Disord. 18:237–45
Thompson SH, Corwin SJ, Sargent RG. 1997.
Ideal body size beliefs and weight concerns
of fourth-grade children. Int. J. Eat. Disord.
Tiggemann M, Pickering AS. 1996. Role of
television in adolescent women’s body dis-
Troop NA. 1998. Eating disorders as coping
strategies: a critique. Eur. Eat. Disord. Rev.
Troop NA, Schmidt VA, Turnbull SJ, Trea-
Eur. Eat. Disord. Rev. 8:384–93
Valdiserri S, Kihlstrom J. 1995. Abnormal eat-
ing and dissociative experiences: a further
study of college women. Int. J. Eat. Disord.
VanderHam T, Meulman JJ, VanStrien DC,
vanEngeland H. 1997. Empirically based
subgrouping of eating disorders in adoles-
cents: a longitudinal perspective. Br. J. Psy-
VanderHam T, VanStrien DC, vanEngeland
H. 1998. Personality characteristics predict
Vanfurth EF, Vanstrien DC, Martina LML,
Vanson MJM, Hendrickx JJP, vanEngeland
H. 1996. Expressed emotion and the predic-
tion of outcome in adolescent eating disor-
ders. Int. J. Eat. Disord. 20:19–31
Vitousek KB, Hollon SD. 1990. The investiga-
tion of schematic content and processing in
eating disorders. Cogn. Ther. Res. 14:191–
VohsKD, BardoneAM, JoinerTE, Abramson
ceived weight status, and self-esteem inter-
act to predict bulimic symptoms: a model of
bulimic symptom development. J. Abnorm.
Wakeling A. 1996. Epidemiology of anorexia
nervosa. Psychiatry Res. 62:3–9
Waller G, Hodgson S. 1996. Body image dis-
tortion in anorexia and bulimia nervosa—the
role of perceived and actual control. J. Nerv.
Ment. Dis. 184:213–19
Ward A, Ramsay R, Treasure JL. 2000a. At-
tachment research in eating disorders. Br. J.
Med. Psychol. 73:35–51
Ward A, Ramsay R, Turnbull S, Benedettini
M, Treasure J. 2000b. Attachment patterns
in eating disorders: past in the present. Int. J.
Eat. Disord. 28:370–76
WardA, TillerJ, TreasureJ, RussellG.2000c.
Welch SL, Doll HA, Fairburn CG. 1997. Life
events and the onset of bulimia nervosa: a
controlled study. Psychol. Med. 27:515–22
Wertheim EH, Paxton SJ, Schutz HK, Muir
SL. 1997. Why do adolescent girls watch
their weight? An interview study examining
sociocultural pressures to be thin. J. Psycho-
som. Res. 42:345–55
Whelan E, Cooper PJ. 2000. The association
CAUSES OF EATING DISORDERS
between childhood feeding problems and
Psychol. Med. 30:69–77
Wichstrom L. 2000. Psychological and behav-
ioral factors unpredictive of disordered eat-
ing: a prospective study of the general ado-
lescent population in Norway. Int. J. Eat.
J. Eat. Disord. 20:359–65
Wilson GT. 1991. The addiction model of eat-
ing disorders: a critical analysis. Adv. Behav.
Res. Ther. 13:27–72
Woods SC, Brief DJ. 1988. Physiological fac-
tors. In Assessment of Addictive Behaviors,
ed. DM Donovan, GA Marlatt, pp. 296–322.
New York: Guilford