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
Not surprisingly, the media are often blamed for the (increasing) incidence of
EDs, on the grounds that media images of idealized (slim) physiques motivate or
of distorting reality, in that the models and celebrities portrayed in the media are
either naturally thin (i.e., at the tail of the normal distribution of body weight)
and thus unrepresentative of normality, or unnaturally thin (i.e., the products of
of abundance, idealized media images are at best a background cause of EDs.
Exposure to the media is so widespread that if such exposure were the cause
of EDs, then it would be difficult to explain why anyone would not be eating-
disordered. Furthermore, as Tiggemann & Pickering (1996, p. 202) noted upon
discovering that among girls, body dissatisfaction and drive for thinness were
associated with increased exposure to certain types of TV shows, “although it
is tempting to conclude that watching a large dose of thin idealized images on
television leads to dissatisfaction with one’s body, a correlation cannot determine
with their bodies or wishing to be thinner, seek out or are more interested in
particular types of television.”
The idealization of slimness and derogation of fatness in cultures of abundance
is more intense for females than for males (Striegel-Moore 1993, 1997). This sex-
linked valuation of thinness is usually invoked to account for the fact that EDs
are more than 10 times more prevalent in females than in males (Striegel-Moore
1997). As a result of the societal disparagement of overweight and glorification of
underweight, many—perhaps most—young women express dissatisfaction with
their weight and shape. This dissatisfaction often has emotional overtones of self-
disgust. Body dissatisfaction, in fact, may be regarded as an essential precursor
(and continuing accompaniment) of EDs. The more intense this dissatisfaction,
the more likely that one will undertake attempts to lose weight. When combined
with other pathogens (see below), these attempts may well eventuate in AN (if the
individual has particularly strong restraints on eating) or BN (if she does not).
and by way of teasing for failure to adhere to peer norms. Adolescent female
friendship cliques tend to be homogenous with respect to body-image concerns
(Paxton et al. 1999), suggesting direct peer influence; however, the possibility
remains that cliques do not influence their members so much as “recruit” them on
the basis of shared concerns (Ennett & Bauman 1994). It is difficult to weigh the
or the family, which teach the same lessons; some evidence suggests that peers
and family are more potent influences than the media (Stice 1998), whereas other
CAUSES OF EATING DISORDERS
other influences, is so broad and pervasive that it ought to cause more pathology
than actually occurs. Paxton et al.’s (1999) analysis reminds us that not all peers
are equally concerned about attaining a slim physique, so blanket condemnation
of peer influence or pressure is unwarranted.
Media and peer pressure no doubt impinge more powerfully on females than
on males, but we should not be too complacent about explaining the huge dis-
proportion of females among ED patients solely in terms of these influences. At
the very least, we must consider the possibility that it is not simply that our cul-
ture exhorts females (more than males) to be thin; it may be the case that females
are more attentive than are males to such exhortations, for various reasons that are
Among American women, blacks were thought to be “protected” from EDs
than do white men (see e.g., Greenberg & Laporte 1996), and black women (e.g.,
Powell & Kahn 1995) and children (Thompson et al. 1997) have larger ideal
physiques. Thus, when black women develop an ED, it is more likely to be binge
eating disorder, an ED that does not prominently feature a drive toward thinness
(Striegel-Moore & Smolak 1996). Still, recent case reports (Striegel-Moore 1997;
Striegel-Moore & Smolak 1996) suggest that the diffusion of the thin ideal has
reached the black subculture as well. The widespread adoption of the dominant
American cultural ideals (in American ethnic subcultures and indeed around the
world) has meant that “ethnicity” no longer protects individuals from AN and BN
(e.g., Chamorro & Flores-Ortiz 2000, Mumford & Choudry 2000, Polivy et al.
income white women suggests that whatever black-white differences may exist in
population samples may be more a function of SES than of race (Caldwell et al.
The influence of sociocultural factors in the context of EDs can be summa-
rized succinctly as the idealization of thinness, which is sometimes regarded as a
isfactions and distress toward a focus on body shape and size, providing an outlet
for individual pathology; thinness is thus relentlessly pursued by those who see
no better way to solve their problems. As we narrow our focus toward individual
pathology, we now move to family influences.
Familial Influences on Eating Disorders
In what ways might families contribute to EDs? The most obvious way is by
encouraging EDs. Families (and friends) often praise AN patients’ slenderness,
and envy the self-control and discipline required to achieve it (Branch & Eurman
1980); this reinforcement frequently persists even when the anorexic becomes
severely emaciated. Of course, this reinforcement does not cause the disorder so
much as help to perpetuate it. Certainly, people with AN do not require family
approval in order to starve themselves. In fact, those with AN as often as not use
their families’ increasing concerns about their inordinate slimness as a manipula-
tive tool (Branch & Eurman 1980, Minuchin et al. 1978).
Family dynamics have been implicated not only in the perpetuation of EDs but
also in their development (e.g., Minuchin et al. 1978). Case reports and studies of
family interaction show eating-disordered families to be enmeshed, intrusive, hos-
tile, and negating of the patient’s emotional needs (Minuchin et al. 1978) or overly
concerned with parenting (Shoebridge & Gowers 2000); some, such as Minuchin,
have argued that the entire family unit must be treated if therapy is to be effective.
Within the past few years, several studies have found that attachment processes
are abnormal in eating-disordered populations; insecure attachment is common
in this group (Ward et al. 2000a,b). Ward and colleagues (Ward et al. 2000b,
p. 279), however, conclude that “many of these (family dysfunction) characteris-
tics are regarded as secondary to the presence of an ill family member, rather than
ED patients generally describe a critical family environment, featuring coer-
communication, parental caring, and parental expectations as low and those who
report sexual or physical abuse are at increased risk for developing EDs (Haudek
intrusiveness, specifically maternal invasion of privacy, jealousy, and competition,
encouragement of autonomy is associated with less dieting behavior (Strong &
Huon 1998), possibly serving a protective function against EDs.
Mothers of girls with EDs may well have an influence on their daughters’
pathology. They think that their daughters should lose more weight and describe
them as less attractive than do comparison mothers or the girls themselves (Hill &
Franklin 1998, Pike & Rodin 1991). Mothers of ED patients are more dissatisfied
with the general functioning of the family system and are themselves more eating-
disordered than are mothers of girls who do not have EDs (Hill & Franklin 1998,
Pike & Rodin 1991). Direct maternal comments appear to be more powerful influ-
ences than is simple modeling of weight and shape concerns (Ogden & Steward
2000, Smolak et al. 1999), although even modeling does appear to affect elemen-
tary schoolchildren’s weight and shape-related attitudes and behaviors (Smolak
et al. 1999). Mothers’ critical comments prospectively predicted ED outcome for
their daughters (Vanfurth et al. 1996).
Mothers who themselves have an ED tend to have a negative influence on
their children’s attitudes and behaviors, feeding them irregularly, using food for
nonnutritive purposes, and expressing concern about their daughters’ weight as
early as the age of 2. By 5 years of age, these children exhibit greater negative
affect than do the offspring of mothers without EDs and are at serious risk for the
later development of an ED (Agras et al. 1999). In fact, maternal EDs produce
childhood feeding problems in offspring (Whelan & Cooper 2000), and 50% of
children of mothers with EDs have psychiatric disorders (Hodes et al. 1997).
CAUSES OF EATING DISORDERS
ficult to determine whether family dysfunction contributes to EDs, EDs contribute
to family dysfunction, or some common factor contributes to both. Moreover, the
role of the family is often ascertained by retrospective questioning, further under-
eating-disordered families, in the absence of control families, preclude any cer-
tainty about whether these family problems are unique to families with a member
who suffers from an ED.2
If we were to conclude that negative family influences were in fact responsible
family induces EDs. Below, we consider the possibility that problems of identity
and/or control are central to EDs, with the individual attempting to resolve these
problems by investing emotionally and behaviorally in the pursuit of slimness.
The family, of course, may contribute directly to problems of identity or control
and may also suggest the solution, by emphasizing slimness as a panacea. Steiger
et al. (1996) conclude that families (including so-called normal families as well)
may transmit eating concerns, but such transmission may not be sufficient for
the emergence of an ED, which requires “some additional vulnerability factor”
(p. 156), either biological or experiential. This brings us to the consideration of
individual factors that conduce to the development of EDs.
Individual Risk Factors
There are many factors specific to the individual that have been proposed as con-
tributors to the development of EDs. Some of these factors (e.g., personality traits,
self-esteem deficits) are seen as resident in the individual, whereas others involve
personal experiences and seem to fall somewhere between the environment and
the individual. The latter accordingly is examined first.
EXPERIENCES CONTRIBUTING TO EATING DISORDER DEVELOPMENT
experiences that have been most frequently linked to the development of EDs in-
clude abuse, trauma, and teasing. Self-reports of having been teased about one’s
appearance or body shape are associated with increased ED symptomatology
2A dramatically different approach to assessing familial influences on EDs is behavior
genetic analysis, which includes common (familial) environment as a potential explanation
of twin concordance. The Virginia group found a substantial familial influence on BN
(Kendler et al. 1995) but later reversed itself, deciding that “the tendency to focus on
common or familial environment as playing a primary causal role in the development of
disordered eating is overemphasized” (Bulik et al. 1998, p. 1216). The often implausibly
draw conclusions about family influence on the basis of genetics-vs.-environment models.
Moreover, as Spelt & Meyer (1995) point out, the absence of common family environment
influences, not that such influences do not exist.
(Lunner et al. 2000). Similarly, ED patients report more premorbid life stresses
and difficulties than do controls (e.g., Raffi et al. 2000, Schmidt et al. 1997, Welch
et al. 1997). The joint occurrence (and possible mutual influence) of stressful life
events and affective deficiencies such as low self-esteem, depressed mood, anhe-
donia, generalized anxiety, and irritability may be particularly pathogenic for BN
(Raffi et al. 2000).
tology (Everill & Waller 1995), although CSA is also associated with depression
and other psychological disturbances. Not surprisingly, all of these problems are
more likely to be associated with CSA in conjunction with other physical and
emotional abuse and when the family does not provide support (deGroot & Rodin
1999). Some, however, maintain that BN patients do not have an elevated inci-
dence of CSA, although the severity of the abuse may be greater (Groth-Marnat
& Michel 2000). Casper & Lyubomirsky (1997) argue that sexual abuse causes
BN only indirectly, by conducing to individual psychopathology. Kent & Waller
found influence on self-esteem and anxiety—is the only type of childhood trauma
that predicts eating pathology in adults.
How might abuse lead to EDs? It has been argued abuse induces intolerable
emotions and undermines identity. EDs serve as desperate attempts to regulate
overwhelming negative affect and to construct a coherent sense of self when inter-
nal structures are lacking (Rorty & Yager 1996). Similarly, EDs have been seen as
coping mechanisms favored by women who do not have more constructive ways
of dealing with personal crises (Troop 1998).
How do EDs serve to deal with continuing emotional or identity problems? By
refocusing one’s attention onto weight, shape, and eating, one enters a domain
in which one can gain some emotional control. The AN patient achieves at least
partial emotional gratification by avoiding food and achieving slimness (albeit
never enough). The BN patient gains emotional relief by bingeing (and then by
a narrow, apparently viable way to channel identity concerns (and to avoid dealing
with broader issues). More recent theorists concur that an extreme need to control
both eating and other aspects of behavior is a central feature of EDs (Fairburn
et al. 1999). Gaining a sense of control and pride in one’s ability to control one’s
eating combats the feeling of being taken over by thoughts of food or of lacking
induction of loss of perceived control led ED patients to report feeling fatter and
more pessimistic (Waller & Hodgson 1996).
ative emotionality is unlikely to lead to EDs in and of itself, stress and nega-
tive mood are commonly reported antecedents for EDs (e.g., Ball & Lee 2000,
Leon et al. 1997). For example, BN patients have elevated self-directed hostility
scores, even controlling for other factors such as mood and family hostility level
Although a temperamental characteristic such as neg-
CAUSES OF EATING DISORDERS
(Friedman et al. 1997), and women with EDs score higher than controls in guilt,
covert hostility (BN) (Allen et al. 1998), and suppressed anger (AN) (Geller et al.
dieting and binge eating, although dieting and negative affect remain independent
risk factors for binge eating (Stice et al. 2000a). It may be, though, that negative
mood and self-perceptions predict later ED symptomatology, none of these pre-
dictors remain significant if initial disordered eating is ruled out. Thus, affective
factors may not be etiologically important for EDs, although they may be asso-
ciated with subclinical eating problems (Wichstrom 2000).
A functional relation between negative affect and ED symptoms has been pro-
posed (e.g., Steinberg et al. 1989). According to Johnson & Larson (1982), people
with BN attempt to elevate their mood by eating; purging allows them to avoid
gaining weight. Unfortunately, the bulimic eventually realizes that the binges are
the guilt, as well as discharging anger. It is thus possible that purging eventually
replaces bingeing as a means of tension reduction (Johnson & Larson 1982). In
fact, BN patients report reduced anxiety and depression following a binge/purge
episode (Sanftner & Crowther 1998, Steinberg et al. 1989). After bingeing in the
laboratory, bulimics reported reduced anxiety, tension, and guilt, although depres-
sion was unchanged (Kaye et al. 1986). Bulimic behaviors also reduce anger,
particularly when the individual has a strong tendency to avoid expressing that
emotion (Milligan & Waller 2000).
secondary to EDs, or common third variables (biological or psychosocial) leading
to both, such as genetic or familial transmission. The lack of a well-organized
body- and self-image is unique to EDs, however (Steiger et al. 1992). Some evi-
subsequent depression in initially nondepressed individuals (Stice et al. 2000b).
Some studies find that ED onset follows that of mood disorder (Godart et al.
2000, Gruber & Dilsaver 1996), whereas still others suggest that depression and
anxiety are more state-dependent features that resolve when ED symptoms remit
(Lehoux et al. 2000). Actually inducing negative affect increases body dissatisfac-
tion and body-size perception in BN patients (Carter et al. 1996; Kulbartz-Klatt
et al. 1999), suggesting that whichever is primary, negative affect can contribute
to ED symptoms.
ing EDs (e.g., Fairburn et al. 1997, Leary et al. 1995, Striegel-Moore 1997).
Self-esteem reflects how others react to the individual; thus, (perceived) rejection
may cause lower self-esteem and maladaptive behaviors, including EDs. Further-
more, dieting, which is highly prone to disruptions that result in overeating, often
Low self-esteem may conduce to a variety of disorders, includ-
produces a downward spiraling of self-esteem that contributes more specifically
to EDs (as opposed to, say, depression) (Heatherton & Polivy 1992). Shape-
and weight-based self-esteem is reduced in ED patients (Geller et al. 1998), and
prospective research confirms that girls with low self-esteem are more likely to
develop disordered eating in the next few years (Button et al. 1996).
Empirically, self-esteem has been found to moderate perfectionism and feel-
ing overweight in predicting bulimic symptoms (Bardone et al. 2000, Vohs et al.
1999). Women high in perfectionism, who consider themselves overweight ex-
hibit bulimic symptoms only if they have low self-esteem (i.e., if they doubt they
can attain their high body standards); women with high self-esteem and the same
diathesis-stress conditions are less likely to exhibit bulimic symptoms. Similarly,
low self-esteem and negative affect predicted ED symptomatology 4 years later
(Leon et al. 1997). Moreover, a program aimed at improving self-esteem in 11- to
14-year-olds resulted in lowered incidence of weight loss and ED symptomatol-
ogy 1 year later in participants considered at risk when the program began (O’Dea
& Abraham 2000). Finally, lower self-esteem in ED patients predicts worse out-
come (Hesse-Biber et al. 1999, VanderHam et al. 1998). Alternatively, women
who recover from BN report an increase in their self-esteem (Troop et al. 2000).
channeled in ED more specifically into negative feelings about the body or body
dissatisfaction (BD).3BD is sometimes operationalized as the gap between one’s
assessment of BD involves asking people specifically how (dis)satisfied they are
with their bodies or parts thereof.
Virtually all conceptualizations of EDs—including the DSM criteria—make
reference to BD. Most models of EDs involving multiple factors (e.g., Stice 2001)
assign BD a prominent causal role. BD (sometimes referred to as weight concern)
is often associated with dieting behavior; indeed, BN and AN are sometimes
referred to as the dieting disorders. Dieting has been posited to precipitate, if not
cause, bingeing (Polivy & Herman 1985) and EDs in general (Polivy & Herman
1987; Stice 2000a, 2001), and it is BD that presumably causes dieting. Weight
concern and dieting help to predict the emergence of an ED (e.g., Joiner et al.
1997, Steiger et al. 1996, Stice et al. 1998), and bulimic women seek out the
Negative affect and negative feelings about the self are
3The broader construct of “negative body image” comprises both body dissatisfaction and
body misperception—typically, overestimation of one’s actual body size. Although both
types of body image problems can in principle drive weight loss attempts, and although
& Thompson 1996). For a time, misperception was considered a critical aspect of EDs and
in misperception are much weaker than are comparable differences in dissatisfaction (Cash
& Deagle 1997).
CAUSES OF EATING DISORDERS
very appearance feedback that is likely to aggravate these concerns (Joiner 1999).
of later symptoms, via the mediating effects of increased body dissatisfaction.
girls who are otherwise at high risk for developing EDs (Chandy et al. 1995).
Most of the alleged causes of EDs that we have reviewed operate through
BD. Thus, media influence is thought to precipitate EDs by making women feel
dissatisfied with their appearance. Family and peer pressure, teasing, and more
individual psychological influences such as general anxiety converge on the “final
common pathway” of BD (Paxton et al. 1999).
do anything about it. Why is it that of two dissatisfied people, one throws herself
into (usually futile) attempts to achieve a satisfactory body, whereas the other
remains dissatisfied but does not diet/starve, binge, or purge? The determining
factor, we suggest, is whether or not the individual seizes upon weight and shape
invested in achieving a “perfect” body as an existential project (i.e., as a way of
lacking). Some become invested in achieving complete control over their eating,
weight, and shape, believing that control in these domains is possible even though
such control is not possible elsewhere in their lives. For many with EDs, these
two goals overlap. In the final analysis, BD may contribute to EDs primarily by
conferring purpose: The narrow ambitions of the ED patient—in particular, the
exclusive focus on weight—may make her life simpler, more certain, and more
of inadequacy by identifying herself with her weight” (Vitousek & Hollon 1990,
sive thoughts, inaccurate judgments, and rigid thinking patterns. The prominence
ity for weight, and using one’s weight as a basis for self-evaluation, are central
features of both AN and BN and contribute to the persistence of EDs (Vitousek &
Hollon 1990). An obsession with becoming thin may be seen as driving AN (and
is present in BN as well). Judging one’s own body to be larger than it really is
may justify a relentless pursuit of thinness. Examination of cognitions in EDs has
been stimulated by two developments: (a) the ascendancy of cognitive-behavior
therapy for EDs, which is premised on the notion that normalizing cognitions may
paradigms for studying cognition.
EDs feature several cognitive aberrations, including obses-
of time obsessing about food/eating, weight/shape, and related matters (Gleaves
Individuals with EDs tend to spend an inordinate amount
et al. 2000). One survey (Sunday et al. 1995) found that 74% of ED patients
spent more than 3 hours/day on obsessional thoughts; 42% spent more than
8 hours/day! Sixty-two percent had fewer than 3 hours/day entirely free of such
obsessive thoughts, and 37% had no free hours at all. Most (72%) patients tried
to suppress these obsessive thoughts, but “50% were not successful and felt that
they had little or no control over the preoccupations” (Sunday et al. 1995, p. 241).
About 20% of the patients—especially restricting anorexics—found the obsessive
thoughts comforting and did not wish to be rid of them; more than half the patients
considered the obsessions to be ego-syntonic.
(strive to) be perfect. Perfectionism can easily be applied to eating, weight, and
shape. Perfectionism is not a defining characteristic of eating disorders but it has
long been thought to be involved in AN and, to a lesser extent, BN (Garner et al.
1983, 1984). Hewitt et al. (1995) argue that perfectionism can contribute to eating
disorders by making normal shortcomings more traumatic or by making a normal
body a sign of imperfection. The eating disorder inventory (EDI) (Garner et al.
1983) includes a perfectionism subscale.
AN patients display elevated scores on paper-and-pencil measures of perfec-
tionism (Bastiani et al. 1995). The fact that some indices of perfectionism remain
high even after weight restoration suggests that perfectionism may be a precur-
sor of AN; this view accords with Strober’s (1991) theory in which self-doubting
perfectionism is one of a small number of characteristics that predispose one to
AN. Bruch (1973) and Casper (1983) also accord perfectionism a causal role in
AN. Recent debates contrasting self-imposed perfectionism and other-imposed
perfectionism add further complexities to the analysis of EDs (Hewitt et al. 1995);
whom are ANs trying to please, themselves or others?
Related to obsession is perfectionism, the belief that one must
unpleasant realities is to adopt the dynamic defense of dissociation, in which trau-
thing more tractable. In BN “immersion” in the binge may protect the individual
from emotional distress (Heatherton & Baumeister 1991, Lacey 1986). Evidence
for dissociative tendencies in EDs—as measured using the self-report Dissocia-
tive Experiences Scale (Bernstein & Putnam 1986)—is not very impressive, how-
ever. In their review Everill & Waller (1995) claim that “high levels of dissocia-
tive tendencies have been reported in eating-disordered women” (p. 4), but these
that “within the population of normal college-age women ... there appears to be
no particular relationship between abnormal eating and dissociative experiences”
(1995, p. 149).
One of the more profound psychological tactics used to escape
the Matching Familiar Figures Test, reflecting their greater impulsiveness (Kaye
CAUSES OF EATING DISORDERS
et al. 1995). Such aberrations might contribute to their disorder; Bruch (1973)
argued that ANs engaged in unwarranted all-or-none thinking, which might lead
them to regard themselves as failures after even minor infractions.
are many controversies pertaining to technical issues, the consensus from studies
assessing cognitive bias such as those using the modified Stroop (color-naming)
(e.g., Green et al. 1999) and dot/visual probe (e.g., Rieger et al. 1998) paradigms
is clear: BNs tend to show bias for weight/shape words (compared with control
is the value of this discovery. We already knew that ED patients have an emotional
concern with weight and shape; this is a defining feature of the disorders. That
attentional bias to shape and food stimuli renders the findings in ED patients even
Studies of memory bias make the same point, with ED patients showing differ-
ential memory for disorder-related material (e.g., Hermans et al. 1998, Sebastian
for weight, shape, and food information, “it is, however, still unclear what role (if
any) these schemata play in the etiology of anorexia nervosa” (Hermans et al.
1998, p. 199) or in BN. It seems just as likely that a preoccupation with food is a
result as it is a cause of weight loss (see Herman & Polivy 1993).
ED patients display aberrations in information processing and
apparent lack of appetite in the case of AN and apparently uncontrollable appetite
in the case of BN—there is an understandable temptation to look for biological
with EDs, some of which we review. Researchers in this area have for the most
part shown commendable reluctance to promote biological correlates of EDs into
candidate causes, probably because of repeated warnings that AN and BN both
biological anomalies may be just as likely to be effects as causes. Indeed, many
of the anomalies are well-known effects of starvation or stress, undermining their
causal candidacies. The preferred approach to identifying biological (or any other
class of potential) causes is to conduct prospective research in which a normal
(pre-symptomatic) sample is assessed, permitting the identification of differential
predictors of eventual ED, and avoiding the contaminating influence of the ED
on the predictor. As Leon et al. (1997, p. 407) note, however, “the assessment of
many types of biological risk factors is often too costly and invasive to be done
in prospective studies with large nonclinical samples.” (The same can be said for
many nonbiological risk factors as well.)
Because EDs so prominently involve appetite—
of EDs, although such evidence is not conclusive. For one thing, behavior genet-
ics currently emphasizes environmental factors as much as genetic factors. (The
Twin and family studies provide evidence for the genetic transmission
double irony of modern behavior genetics is that not only does it not necessarily
are only remotely related to actual behavior.) Family studies (see Spelt & Meyer
1995 for a review) indicate that EDs aggregate in families, but such studies cannot
coefficients—reflecting the relative importance of strictly genetic factors—have
been claimed for both AN and BN. Klump et al.’s (2000) reading of the literature
leads them to conclude that 50–83% of the variance in AN and BN is genetic.
These estimates are based on twin studies, which may yield artifactually high
heritability estimates, owing to contrast and assimilation effects and the skewing
effect of nonadditive genetic variance (Plomin et al. 1990). More troubling, in our
view, is the common finding that not only the disorder itself but also the associated
attitudes (concerns, fears, and preoccupations) are highly heritable (Klump et al.
2000). We are prepared to concede a role for genetics in the regulation of physio-
logical parameters that might in principle contribute to an ED; however, statistics
notwithstanding, it is difficult to understand how genes influence these attitudes,
which in turn influence the development of the disorder. We are confronted with
analyses that purport to show that genes have a major influence on EDs, but that
do not indicate how. A persuasive case for genetic influence awaits a clearer indi-
(Allison 1997). As Hewitt (1997, p. 355) concludes, “although there is consistent
are far from clear.”
“glandular” in origin, so current EDs are often seen as explicable in terms of neu-
dysfunction might be primary (i.e., a hormonal aberration triggers the disorder) or
sponsive to hormonal controls, a neuroendocrine explanation for EDs is attractive.
The major problem with such an explanation is that EDs are not simply disorders
of appetite. Almost everyone sees AN as principally attributable to the relentless
pursuit of thinness (RPT) that dictates restrictive food intake, which leads directly
sion could precede RPT (unless you wanted to construct a convoluted scenario in
which RPT develops as an ex post facto attitudinal justification for not eating). In
the most prevalent view of BN, RPT and restrictive intake precedes bingeing, and
bingeing is simply a breakdown of restraint (e.g., Polivy & Herman 1985, Stice
et al. 1998). An alternative view of BN regards bingeing as primary and restrictive
this minority view might possibly be compatible with a primary neuroendocrine
disorder, but it does not easily accommodate the centrality of RPT in BN.
Just as the former ED, obesity, was often explained as
CAUSES OF EATING DISORDERS
One notable feature of neuroendocrine accounts of EDs is that AN and BN are
seen as virtual opposites, whereas most other theories regard them as more alike
than different. The neuroendocrine approach emphasizes starving (AN) versus
bingeing (BN). What factors might go awry to produce the extremes of normal
One possibility would be primary dysfunction of the hypothalamus, the “seat”
of appetite. The evidence that AN is due to a disturbance of the hypothalamus,
either structural or functional, is weak. “Although structural lesions involving the
disorder in AN in general, although this possibility is not excluded” (Study Group
on Anorexia Nervosa [SGAN] 1995, p. 239). The SGAN indicates (p. 237) that “a
(arginine vasopressin) may have a key role in sustaining the reduced food intake
that is characteristic of the disorder,” but note the careful wording: the hormonal
abnormality is characterized as “sustaining” the reduced intake, not causing it.
Although tests of hormonal functioning and evidence of hormonal aberrations
in AN are both prevalent, the balance of opinion is that these aberrations are not
what cause the disorder (Leung et al. 1996). “In fact, refeeding alone, leading
to consistent weight gain and balanced nutrition, reverses the endocrine changes
observed in AN” (SGAN 1995, p. 238).
One popular neurochemical candidate cause for EDs is serotonin (Brewerton
1995). Might ANs suffer from increased 5-Hydroxytryptamine (HT) activity,
which would be consistent with their generally obsessive-compulsive approach
to life, even after recovery from AN (SGAN 1995)? Both AN and obsessive-
that AN might simply be a variant of OCD (Pryor et al. 1995). By contrast, BN
has been interpreted in terms of a 5-HT deficit (and a possible connection to both
impulsivity and seasonal affective disorder). Recovered BNs show persistent ab-
normalities related to serotonin function, suggesting that such abnormalities may
underlie the development of BN (Kaye et al. 1998). Serotonin imbalance has more
surface appeal than most other biological hypotheses of ED, but the case is not yet
strong. Recovered ANs do not show persistent 5-HT anomalies (O’Dwyer et al.
1996), leading Ward et al. (2000c) to conclude that “an abnormality of serotonin
for alternating restriction and bingeing, which occurs to some extent in BN and
more dramatically in bulimic-type AN.
Other biologically based factors
is that biological factors can act to perpetuate a disorder that might not initially
have been biological in origin. For instance, very-low-weight AN patients show
olfactory impairment; such impairment is in all probability a consequence of star-
One interesting theme in much of the research
food may not appeal to ANs because it loses its “incentive-value”; this decline in
deprived individuals (Pinel et al. 2000). Gastric distress and bloating, commonly
reported in EDs, may also make eating aversive (e.g., Krahn et al. 1996).
the emphasis is on craving. Just as an addict craves a drug, BNs are postulated to
responses to food cues and/or distress, which has been associated with overeating
in the past (e.g., Wilson 1991, Woods & Brief 1988). ANs may be “addicted” to
the body’s endogenous opioids, which are released in self-starvation accompanied
by excessive exercise (Davis & Claridge 1998). Wilson dismisses the addiction
model because of the lack of evidence for an addictive personality; the model does
not address the core clinical characteristics of EDs (such as RPT) or the identified
underlying psychopathology (such as low self-esteem, interpersonal distrust, and
between dieting and EDs. Like Wilson, we are reluctant to apply the addiction
metaphor to EDs.
Lack of internal awareness
inability to accurately identify internal states or feelings, including physiological
states (such as hunger and satiety) and emotional states (Garner et al. 1983).
(Note that the problem is not an inability to detect internal states, but rather an
inability to identify them.) It has long been argued (since at least Bruch 1969) that
defective interoceptive awareness may produce confusion, so that the individual
misinterprets her emotions as hunger, with the result that emotional arousal may
trigger eating or even bingeing. By the same token, it seems possible that genuine
when it is not there (BN?).
There is little question that ED patients suffer from LIA (as reflected in its
incorporation into the EDI). Questions remain, though, as to whether LIA is a
cause or a consequence of EDs, and whether it should be regarded as a biological,
perceptual, or cognitive problem. Bruch (1973) regarded LIA as a consequence of
faulty learning beginning in infancy, when caretakers do not provide food merely
to assuage hunger, but in response to all expressions of distress. Bruch further
theorized that such faulty learning undermines trust in one’s body and increases
the need to control both the body and the self, which are seen as intertwined.
Lack of interoceptive awareness (LIA) refers to an
Reviewing the literature on EDs leaves us with many questions about how these
disorders develop. To some extent, this may be unavoidable; research on clini-
cal syndromes is of necessity mostly nonexperimental, and nonexperimental data
preclude causal inferences. Unfortunately, many researchers lose sight of this
CAUSES OF EATING DISORDERS
limitation in their efforts to explain these syndromes. Moreover, the interaction
of etiological factors in a complex behavioral syndrome such as EDs is difficult
if not impossible to capture. There are so many possible influences that their
particular combination in any given individual becomes almost unique, and thus
retical attempts to measure and correlate particular researchers’ favorite variables,
rather than attempting to test etiological hypotheses about EDs. This is not to say
that there are not theoreticians doing systematic studies testing conceptual views
of the disorder, but such research is often overshadowed by the myriad studies in
this area that do not rely on theoretical underpinnings. The noise-to-signal ratio in
the literature is thus higher than one would like.
Eating disorders did not emerge as a serious problem until the late 1970s, so
perhaps it is not surprising that a mere 25 years later we still seem to be so far
from understanding their etiology. In fact, how much do we really know about the
causes of other, longer-studied disorders such as depression? As with the EDs, we
esteem also make a contribution. We are still incapable, though, of predicting who
will develop depression, when, and why other at-risk individuals will be spared.
The literature suggests that EDs result similarly from the convergence of several
facilitating factors, but the causal mechanisms are not yet identified. No single
agent seems to be sufficient, but we may perhaps distinguish among stronger and
weaker contributory factors.
What factors appear to be most necessary for the development of EDs? It is
although the majority of individuals who are dissatisfied with their bodies will
never go on to develop an ED. Similarly, negative emotion (such as depression
or anxiety) and markedly low self-esteem are prominent features of EDs, and
seem to be virtually invariant precursors of their development. Other elements that
stressors (usually the triggering factor) and cognitive distortions such as obsessive
thoughts (e.g., that one is too fat). Finally, personality features such as a need for
control (over oneself or one’s body) and inadequate identity formation have been
plausibly suggested as being necessary for the development of an ED.
Sociocultural pressure to be thin, family influences such as criticism or enmesh-
such as perfectionism, dissociation, maturity fears, and interpersonal distrust all
appear to contribute to the development of EDs, and the more of them impinging
on an individual, the greater the risk. Some or all of these may contribute to the
right. Although it may turn out that one or more of these factors will be shown
to be a prime cause of EDs, for the moment their connection seems less central,
although clearly this is a judgment call.
Establishing which factors are more tightly linked to EDs does not bring us
closer to understanding the mechanism underlying EDs. On the one hand, we are
left with the question of what produces these causal factors (e.g., body dissatisfac-
tion, identity deficits) in the first place; on the other, establishing the connection
does not explain the process of going from the cause (body dissatisfaction, iden-
tity deficits) to the effects (EDs). Arguably, effective treatment does not require
a full understanding of mechanisms. (We can treat headaches with aspirin with-
out understanding either where the headache came from or how aspirin works.)
Still, as scientists, our first obligation must be understanding. Our review indi-
cates that we are a long way from understanding EDs. Constraints on research
in this field will not make it easy to achieve empirical or conceptual progress.
As with other psychological problems, we may have to be satisfied with recog-
nizing contributory risk factors and devising therapies to help alleviate the dis-
comfort, without conclusive proof of exactly what causes the disorder in any
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