Risk Factors for Eating Disorders
Ruth H. Striegel-Moore
Cynthia M. Bulik
University of North Carolina at Chapel Hill
The authors review research on risk factors for eating
disorders, restricting their focus to studies in which clear
precedence of the hypothesized risk factor over onset of the
disorder is established. They illustrate how studies of so-
ciocultural risk factors and biological factors have pro-
gressed on parallel tracks and propose that major ad-
vances in understanding the etiology of eating disorders
require a new generation of studies that integrate these
domains. They discuss how more sophisticated and novel
conceptualizations of risk and causal processes may inform
both nosology and intervention efforts.
the highest mortality rate of all mental disorders (Millar et
al., 2005; Sullivan, 1995; Zipfel, Lowe, Reas, Deter, &
Herzog, 2000). Fueled by these ominous indicators of their
clinical significance, efforts to identify risk or causal fac-
tors for eating disorders are indicated for at least four
critical reasons. First, identification of causal mechanisms
satisfies the need to understand why certain people develop
the problem in question and others do not. Indeed, some
experts believe that such an understanding helps decrease
the stigma associated with a mental disorder: If the cause is
seen as out of the individual’s control, less blame is as-
signed than if the disorder is seen as “volitional” (Crisp,
Gelder, Rix, Meltzer, & Rowlands, 2000). A Newsweek
magazine story titled “Fighting Anorexia: No One to
Blame” stressed recent findings on genetic vulnerability to
explain risk for the development of anorexia nervosa (Tyre,
Second, ideally, nosology is based on etiology, yet the
current classification schema for eating disorders, as artic-
ulated in the Diagnostic and Statistical Manual of Mental
Disorders (4th ed. [DSM–IV]; American Psychiatric Asso-
ciation, 1994), is based solely on the observed clustering of
signs and symptoms. The eating disorder criteria remain
the subject of considerable debate, in large part because
they fail to result in clearly defined subgroups or to account
for changing symptomatology over the course of the ill-
ness. Most individuals who experience a clinically signif-
icant eating disorder do not meet diagnostic criteria for
anorexia nervosa or bulimia nervosa but, rather, meet cri-
teria for eating disorder not otherwise specified (EDNOS),
a diagnosis intended to capture a residual group (Hoek &
Keywords: eating disorders, epidemiology, cultural risk
factors, genetic risk factors
ating disorders rank among the 10 leading causes of
disability among young women (Mathers, Vos,
Stevenson, & Begg, 2000), and anorexia nervosa has
van Hoeken, 2003; Hudson, Hiripi, Harrison, & Kessler,
2005; Striegel-Moore et al., 2005). Binge-eating disorder
(BED) is the most widely studied specific example of an
EDNOS (for review, see M. J. Devlin, Goldfein, & Do-
brow, 2003). Also, diagnostic crossover is common, espe-
cially from anorexia nervosa to bulimia nervosa (Tozzi et
al., 2005) or from bulimia nervosa to BED (Fichter, Quad-
flieg, & Hedlund, 2005). Risk-factor studies present an
untapped source of information of potential value for re-
vising the current classification system.
Third, treatment is best accomplished when we know
the causes of a disorder. The current evidence base for
treatment of anorexia nervosa, in particular, is weak (Berk-
man, Bulik, Brownley, & Lohr, in press). A classic exam-
ple from the history of psychiatry is the treatment of
neurosyphilis. As recently as the mid-19th century, ad-
vanced neurosyphilis with psychiatric manifestations was a
ticket to treatment in an asylum. With the discovery of the
Spirochaeta pallida (Treponema pallidum; Schaudinn &
Hoffman, 1905), the search for biological cures ultimately
led to the discovery of the efficacy of penicillin in the
treatment of this sexually transmitted disease, leading to a
rapid decline in incidence and changing treatment forever.
Although the story with anorexia nervosa is unlikely to be
so dramatic, this transformation of syphilis treatment from
asylums to penicillin illustrates the power of understanding
etiology in the search for effective interventions.
Fourth, identification of risk factors is important for
determining high-risk groups for targeted interventions,
designing prevention program content, and informing
public policy. For example, a growing literature on cross-
generational transmission of eating disorders, termed cy-
cles of risk (Bulik, Reba, Siega-Riz, & Reichborn-Kjenne-
rud, 2005), suggests that targeted prevention strategies
should be tested that focus on the offspring of women with
eating disorders. Through the lens of sociocultural models,
many prevention programs feature media literacy as a key
component (Stice & Shaw, 2004). Finally, legislative ef-
forts have included the introduction of laws prohibiting
false advertising by the diet industry.
Ruth H. Striegel-Moore, Department of Psychology, Wesleyan Univer-
sity; Cynthia M. Bulik, Department of Psychiatry, University of North
Carolina at Chapel Hill.
Correspondence concerning this article should be addressed to Ruth
H. Striegel-Moore, Department of Psychology, Wesleyan University, 207
High Street, Middletown, CT 06459. E-mail: email@example.com
181April 2007 ● American Psychologist
Copyright 2007 by the American Psychological Association 0003-066X/07/$12.00
Vol. 62, No. 3, 181–198 DOI: 10.1037/0003-066X.62.3.181
The single best predictor of risk for developing an
eating disorder is being female, prompting the question
why women? And indeed, most studies have been restricted
to girls or women; yet, clearly, female sex is not a sufficient
condition for explaining risk, prompting a second question:
Which women in particular? (Striegel-Moore, Silberstein
& Rodin, 1986). In the present review, we describe the
state of knowledge of risk and causal factors for eating
disorders as gleaned from studies on human populations.
This illustrates that the “prototypical” eating disorder case
is a young, White, middle- or upper-middle class woman
residing in Europe or North America, reflecting in part the
legacy of defining eating disorders on the basis of White
girls or women and the common practice in the field of
relying on patient samples (biasing samples toward White,
educated, and more affluent individuals). Our understand-
ing of risk factors will remain woefully incomplete until
research definitions and sampling strategies accommodate
diversity in the population within and across nations. We
also address how risk-factor knowledge contributes to de-
stigmatization of eating disorders, suggests revisions for
the next DSM and International Classification of Diseases
(World Health Organization, 1992), and informs treatment
and prevention interventions. We conclude with recom-
mendations for future studies and future thought about
Changing Perspectives on Risk
Factors for Eating Disorders
Eating disorders (compared with many other psychiatric
disorders) are newcomers to the official psychiatric nomen-
clature. Since their earliest appearances in the literature, the
field has been bifurcated in the search for etiological ex-
planations. In this section, we review briefly the history of
our understanding of anorexia nervosa and bulimia ner-
Anorexia nervosa was introduced as a new illness in the
late 19th century in separate yet almost simultaneous ac-
counts by British psychiatrist William Gull (1874, 1888)
and French physician Charles Lase `gue (1873). Although
both Gull and Lase `gue characterized anorexia nervosa as a
“nervous” disease, each man emphasized different aspects
of his patients’ clinical presentation. Gull’s clinical de-
scription elaborated on the physiological correlates that
resulted from a “perversion of the will” and attributed them
to “simple starvation” without detailed discussion of what
might have caused this “perversion.” Lase `gue described
anorexia nervosa as a “hysteria of the gastric center” and
paid considerable attention to the psychological or social
factors that he believed were involved in the development
of this disorder (cited in Brumberg, 2000, pp. 118–119). At
the risk of oversimplification, Gull focused more on bio-
logical processes and disruptions, whereas Lase `gue fo-
cused more on psychosocial and psychological roots. In
both cases, however, the treatment was somatic, involving
nutritional restoration. Nearly a century later, Hilde Bruch
(1973, 1979) introduced a biopsychosocial conceptualiza-
tion of anorexia nervosa that emphasized developmental
factors and family dynamics. Theoretical models prolifer-
ated in the 20th century ranging from the purely biological
(Kaye, Frank, et al., 2005) to the biopsychosocial (Connan,
Campbell, Katzman, Lightman, & Treasure, 2003) to the
purely cultural (Bordo, 1993; Orbach, 1986), yet studies of
risk factors typically have not tested comprehensive etio-
logic models that incorporate biological, psychosocial, and
environmental factors (for reviews, see Bulik et al., 2005;
Jacobi, Hayward, de Zwaan, Kraemer, & Agras, 2004;
Striegel-Moore & Cachelin, 2001).
Russell (1979) described bulimia nervosa as “an ominous
variant of anorexia nervosa,” and although he widely has
been credited with introducing this disorder into the no-
menclature, a few years prior, Boskind-Lodahl (1976) of-
fered a feminist formulation of the binge–purge syndrome
as a culture-bound syndrome that arose from Western cul-
ture’s obsession with female thinness in particular and the
restrictions of female gender role stereotypes in general. As
with anorexia nervosa, numerous theoretical models pro-
liferated, yet most risk-factor studies have tested variables
representing various risk domains rather than testing a
particular theoretical model (Jacobi et al., 2004; Stice,
2002; Striegel-Moore et al., 1986; for review, see Striegel-
Moore & Cachelin, 2001). Nevertheless, too often, discus-
sion of the etiology of eating disorders becomes polarized
into “cultural” versus “biological” explanations that ignore
the fact that biological and environmental variables are
182 April 2007 ● American Psychologist
Advances in Conceptualizing Risk
Fundamentally, risk-factor research seeks to understand the
factors that cause an outcome of interest (a full discussion
of the epistemological and methodological challenges of
such research is beyond the scope of this article; see, e.g.,
Haynes, 1992). A risk factor is a characteristic (e.g., allele),
event (e.g., teasing), or experience (e.g., growing up in a
culture that values extreme thinness) that precedes the
onset of the outcome of interest (e.g., an eating disorder)
and that, “if present, is associated with an increase in the
probability (risk) of a particular outcome over the base rate
of the outcome in the general (unexposed) population”
(Kazdin, Kraemer, Kessler, Kupfer, & Offord, 1997, p.
377). For causality to be inferred, it further needs to be
shown that the association between the risk factor and the
outcome is not due to confounding influences, that the
results are replicable, and that there are plausible explana-
tions for the processes mediating the relation between the
hypothesized factor and the outcome (Kazdin et al., 1997).
No one study can meet all of these requirements; rather,
risk-factor research involves piecing together the puzzle by
drawing on multiple studies using a range of designs and
As discussed in previous comprehensive reviews (Ja-
cobi et al., 2004; Stice & Shaw, 2002; Striegel-Moore &
Cachelin, 2001), the state of knowledge concerning the risk
and causal factors of eating disorders is frustratingly in-
complete. Notwithstanding the fact that they are central to
advancing etiological models, most epidemiological stud-
ies have not included eating disorders among the psychi-
atric disorders to be assessed in the population (Wittchen &
Jacobi, 2005). In the United States, the first epidemiolog-
ical study of a nationally representative sample was con-
ducted only in 2001–2003 (Hudson, Hiripi, Pope, &
Kessler, 2007). Few studies have moved beyond the first
(important, yet preliminary) step of demonstrating statisti-
cal association between the factor and the outcome to the
second step of establishing the factor’s precedence, and
fewer studies yet have used an experimental manipulation
as the ultimate test of causal hypotheses (Jacobi et al.,
2004). For example, anorexia nervosa has been shown to be
associated with abnormalities in the serotonergic system
during the acute illness stage as well as after recovery
(Kaye, Bailer, Frank, Wagner, & Henry, 2005). This re-
search suggests that the serotonin system is a potentially
fruitful area of further study, yet before they can be con-
sidered to be of etiological significance, it needs to be
established whether these abnormalities simply represent
concurrent symptoms or consequences (biological scars) of
the eating disorder. Similarly, measuring personality char-
acteristics or family functioning in acutely ill or recovered
patients does not permit disaggregation of risk factors from
clinical correlates or consequences of experiencing the
disorder. We caution that in decades past, researchers pro-
posed the now-debunked hypotheses that risk for schizo-
phrenia and autism arose from particular mothering styles
(Caplan & Hall-McCorquodale, 1985) on the basis of data
gathered with designs ill-suited for testing risk-factor hy-
potheses. Retrospective assessment of putative risk factors
(e.g., asking about an individual’s history of weight-related
teasing) is fraught with methodological problems such as
difficulty with accurately timing the exposure relative to
the age of onset of the disorder and inaccurate or selective
recall of critical events. We focus our review on the second
generation of research, which comprises genetic studies,
studies with prospective and experimental designs, and
evidence concerning fixed markers. We do not review the
voluminous literature of cross-sectional or retrospective
studies of personality characteristics or parenting styles and
family functioning, a literature that has been critically
discussed in numerous reviews (e.g., Jacobi et al., 2004;
Ward, Ramsay, & Treasure, 2000; Wonderlich, Lilenfeld,
Riso, Engel, & Mitchell, 2005).
Research Approaches to Uncovering Risk
Factors for Eating Disorders
The core features of eating disorders include disturbance in
body image (e.g., overvaluation of thinness, weight or
shape concerns), over- or undercontrol of eating (e.g.,
severe dietary restriction, binge eating), and extreme be-
haviors to control weight or shape (e.g., compulsive exer-
cise, purging). This suggests a research focus on biological
structures and processes involved in appetite, satiety, and
weight regulation and on cultural factors that shape atti-
tudes and behaviors related to body image and eating. For
decades, the primary focus of risk-factor research has been
sociocultural and family influences on etiology of eating
disorders, yet very few specific, replicated candidate envi-
ronmental risk factors have emerged (Jacobi et al., 2004).
In contrast, studies over the past decade have consistently
detected genetic effects. Furthermore, our ability to mea-
183 April 2007 ● American Psychologist
sure genes has outpaced our ability to measure environ-
ments that might influence eating disorder risk. In this
article, we ask what is known about risk factors for the
development of anorexia nervosa and bulimia nervosa from
research addressing the cultural and biological origins of
risk. Most research studies of these two risk domains have
progressed on separate tracks, with biological factors being
explored mostly in genetic studies and cultural factors
explored mostly in longitudinal or experimental studies.
We conclude with an illustration of how an integration of
research approaches will help overcome the bifurcation of
the field and advance understanding of the causes of eating
Culture and Risk for Eating Disorders
Sociocultural models of eating disorders have emphasized
“Western” culture’s female beauty ideal of extreme thin-
ness and objectification of the female body as specific risk
factors for the development of an eating disorder. The
cultural models describe these steps: exposure to the thin
ideal; internalization of the ideal; and experience of a
discrepancy between self and ideal, which in turn leads to
body dissatisfaction, dietary restraint, and restriction. In
some individuals, restraint and/or restriction leads to over-
eating, in turn amplifying body image concerns and, thus,
precipitating further restraint and/or purging (Polivy &
Herman, 1985; Striegel-Moore et al., 1986). Objectification
of the female body contributes to risk by teaching girls and
women that they are valued primarily for their looks,
reinforcing the need to pursue attractiveness (Moradi,
Dirks, & Matteson, 2005).
To explain why some but not all girls or women
develop an eating disorder in this cultural climate, addi-
tional variables have been proposed that serve to amplify or
mitigate against risk arising from the thin beauty ideal
(Striegel-Moore et al., 1986). These include social pressure
to be thin (this may take the form of being exposed to
media images, peer teasing, or admonishments to lose
weight, to name a few), high social class (with, presum-
ably, more attention being paid to and more resources
being available for working toward the beauty ideal), per-
sonality traits such as perfectionism (making one more
eager to comply with the social norms), high social anxiety
(increasing one’s susceptibility to social feedback), ele-
vated weight or obesity (moving one’s body further away
from the ideal), high impulsivity (making maintenance of
restrictive eating more challenging and amplifying risk for
binge eating), individual differences in biological response
to starvation, and individual differences in the reward value
of starvation or eating. These models cannot explain why
some individuals go on to develop binge eating whereas
others engage only in extreme dietary restriction and other
forms of inappropriate weight-control behaviors (e.g., ex-
Four lines of evidence have been considered as sup-
porting the cultural models: (a) the preponderance of fe-
male cases of anorexia nervosa and bulimia nervosa; (b) the
rising incidence of anorexia nervosa and bulimia nervosa in
girls or women coinciding with the decreasing body-size
ideal for women; (c) cross-cultural differences in the inci-
dence or prevalence of eating disorders, with higher inci-
dence–prevalence in cultures that value extreme female
thinness; and (d) the significant prospective relationship
between internalization of the thin ideal and disordered
Eating Disorders: Primarily a Female
Worldwide, females with an eating disorder outnumber
males by a sizeable margin in every study (Hoek, 2006;
Wittchen & Jacobi, 2005). For example, the National Co-
morbidity Survey Replication (Kessler et al., 2004;
Kessler, Chiu, Dernier, & Walters, 2005), which examined
eating disorders in a subset of this representative sample of
household residents in the United States ages 18 years and
older, found lifetime prevalence rates of 0.3% in men and
0.9% in women for anorexia nervosa and 0.5% in men and
1.5% in women for lifetime bulimia nervosa. In a repre-
sentative sample of Oregon high school students (ages
14–18 years), none of the boys and 0.74% of the girls met
criteria (current or past) for anorexia nervosa, and 0.14% of
boys and 1.6% of girls met criteria for bulimia nervosa
(Lewinsohn, Hops, Roberts, Seeley, & Andrews, 1993).
Sex differences are far less pronounced in BED or
when eating disorders are defined more broadly to include
partial syndromes (Hudson et al., 2007; John, Meyer,
Rumpf, & Hapke, 2006; Woodside et al., 2001). Indeed,
recurrent binge eating has been shown to be as common in
men as in women (Hay, 1998; Lewinsohn, Seeley, Moerk,
& Striegel-Moore, 2002; Reagan & Hersch, 2005; Wood-
side et al., 2001). Men who binge eat are significantly less
likely than women to report extreme weight-control behav-
iors such as purging (Hay, 1998), and they often use
different compensatory methods with different goals (e.g.,
reducing body fat and increasing muscularity; Anderson &
Bulik, 2004). This may account in part for the lower
prevalence of bulimia nervosa in males compared with
females and also suggests that the diagnostic criteria them-
selves may be sex-biased. Hence, the eating disorders for
which weight concerns are defining features are consider-
ably more common among females than among males. In
contrast, sex appears to be a less potent marker of risk for
eating disturbances that are not marked by weight and
shape concerns (as currently defined) and extreme compen-
Adolescence: The period of greatest vul-
With remarkable consistency, research has
shown that anorexia nervosa and bulimia nervosa typically
occur during adolescence and that onset thereafter is un-
common (Garfinkel et al., 1995; Hudson et al., 2005; Ken-
dler et al., 1991; Striegel-Moore et al., 2005; Woodside et
al., 2001). It is of note that onset of BED does not seem to
follow this pattern: Onset has been reported to occur well
into adulthood (Hudson et al., 2005, 2007; Kinzl,
Traweger, Trefalt, Mangweth, & Biebl, 1999).
184April 2007 ● American Psychologist
shown that in affluent countries, higher status individuals
on average are thinner than lower status individuals (Sobal
& Stunkard, 1989). On the basis of these observations,
anorexia nervosa has long been described as a disease of
affluence (Bruch, 1973), and a few studies have found
anorexia nervosa to be more common among individuals of
high socioeconomic status (Lindberg & Hjern, 2003; Mc-
Clelland & Crisp, 2001. In contrast, no relationship was
found between parental education and bulimia nervosa in
the only epidemiological study examining this association
(Kendler et al., 1991). Studies that combined anorexia
nervosa and bulimia nervosa (Favaro, Ferrara, & Santonas-
taso, 2003; Lewinsohn, Striegel-Moore, & Seeley, 2000;
Moya, Fleitlich-Bilyk, & Goodman, 2005; Wittchen, Nel-
son, & Lachner, 1998) found no association between so-
cioeconomic status and eating disorders; yet in combining
all eating disorders, the possible differences between an-
orexia nervosa and bulimia nervosa concerning socioeco-
nomic status were obscured.
Males with an eating disorder.
models emphasize the female beauty ideal and gender role
socialization in explaining the sex imbalance in the risk for
eating disorders; accordingly, homosexual males may be at
elevated risk because of gay culture’s increased emphasis
on physical appearance relative to that of heterosexual male
culture (Boroughs & Thompson, 2002; Silberstein, Mish-
kind, Striegel-Moore, Timko, & Rodin, 1989). We were
able to locate only one risk-factor study that addressed this
issue (omitting several studies with inadequate comparison
groups). Specifically, a survey of 4,374 adolescent boys
(mean age ? 14.3 years) found that boys who described
themselves as gay or bisexual reported making more efforts
to look like boys or men in magazines than did boys who
described themselves as heterosexual. There were no dif-
ferences in the frequency of dieting efforts reported across
sexual orientation, but the gay–bisexual boys were more
likely to binge eat than the heterosexual boys (Austin et al.,
2004). Given that trying to look like boys or men in
magazines does not necessarily represent a causal continu-
ity with eating disorders, and given the young age of this
sample, little can be concluded regarding the nature of
homosexuality as a risk factor for the development of
eating disorders in males.
It long has been assumed that
eating disorders are rare among ethnic minority popula-
tions, in part because in clinical practice or in treatment
trials, few ethnic minority individuals have been found
(Smolak & Striegel-Moore, 2001). Regardless of types of
psychiatric disorders, patient samples are biased toward an
overrepresentation of White women (Kessler et al., 2005).
Studies in the United States have found that ethnic minority
women compared with White women are disproportion-
ately less likely not only to seek care but, when they do
seek care, to receive treatment for the eating disorder
(Becker, Franko, Speck, & Herzog, 2003; Cachelin &
Striegel-Moore, 2006; Striegel-Moore et al., 2003; Wilfley,
Pike, Dohm, Striegel-Moore, & Fairburn, 2001).
Worldwide, studies have
We were able to locate only one study in the United
States that examined race/ethnicity as a marker of eating
disorders in a community sample that used a rigorous
diagnostic screening and assessment procedure. In a cohort
of 2,054 young adult African American (Black) and White
American women (mean age ? 21 years), all eating disor-
ders were less common among the Black women, and there
were no Black women with anorexia nervosa (compared
with 1.5% of the White women; Striegel-Moore et al.,
2003). However, the two groups differed in parental socio-
economic status, making it difficult to determine whether
the results reflected the fact that few of the Black girls came
from affluent households and accounted for the differences
in prevalence of anorexia nervosa. In the same sample, an
empirically based classification of eating disorders found
that the clustering of eating disorder symptoms varied by
ethnicity: Purging behaviors in the absence of binge eating
were significantly more common among the White women,
whereas binge eating in the absence of purging was more
common among the Black women (Striegel-Moore et al.,
2005). Other studies have found no racial/ethnic differ-
ences in the prevalence of recurrent binge eating (Reagan
& Hersch, 2005; Smith, Marcus, Lewis, Fitzgibbon, &
Schreiner, 1998; Striegel-Moore, Wilfley, Pike, Dohm, &
Fairburn, 2000). The lack of epidemiological data captur-
ing the population diversity in the United States is a sig-
nificant gap in our knowledge about eating disorders. On
the basis of the preliminary evidence, White race/ethnicity
may be a marker for eating disorders involving severely
restrictive or compensatory behaviors but not for binge
In conclusion, female sex is a potent and well-repli-
cated fixed marker for anorexia nervosa and bulimia ner-
vosa (Jacobi et al., 2004), but it appears to be less strongly
a predictor of BED. Adolescence marks the period of
greatest risk for onset. Few studies offer clues about the
importance of other demographic characteristics, yet there
are hints that variables such as socioeconomic status or
race/ethnicity may differentially signify risk for anorexia
nervosa, bulimia nervosa, and BED. If confirmed, this
would support a nosological distinction of syndromes in-
volving severe dietary restriction or purging from syn-
dromes involving binge eating without compensatory be-
Secular Trends in the Incidence of Eating
Ideal female body size significantly decreased during the
20th century, with marked decreases in media images hav-
ing been documented for the period between 1958 and
1988 (e.g., Wiseman, Gray, Mosimann, & Ahrens, 1992).
To examine whether there has been a corresponding in-
crease in eating disorder incidence (absent epidemiological
data), experts have examined changes in the number of new
patients being treated. Hoek and van Hoeken (2003) found
that the incidence of anorexia nervosa increased markedly
from 1930 through 1970 and has remained unchanged since
then. Similarly, the prevalence of anorexia nervosa in Swe-
185 April 2007 ● American Psychologist
den, studied in 31,406 twins, was significantly higher in
individuals born between 1945 and 1958 than in individu-
als born between 1935 and 1944 (Bulik et al., 2006).
Likely, this increased incidence is not simply the result of
greater public awareness or availability of specialized treat-
ment resources for anorexia nervosa in recent years: An-
orexia nervosa did not receive much public attention, nor
were there many eating disorder treatment facilities or
experts, until the latter quarter of the 20th century (Brum-
Bulimia nervosa was not officially recognized until
1979, precluding an exploration of changes in incidence
across the period of time when the female body ideal
drastically shrank in size (1950–1980). Epidemiological
studies suggest a secular increase in the incidence of bu-
limia nervosa during the latter half of the past century:
Lifetime prevalence was significantly lower among age
cohorts born before 1944 (Hudson et al., 2007), 1950
(Bushnell, Wells, Hornblow, Oakley-Browne, & Joyce,
1990), or 1960 (Kendler et al., 1991) than among more
recent age cohorts. Moreover, studies identifying new pa-
tients receiving medical care in the Netherlands (Hoek et
al., 1995), the United Kingdom (Treasure et al., 1996), and
the United States (Soundy, Lucas, Suman, & Melton, 1995)
reported significant increases in the incidence of bulimia
nervosa between 1985 and 1995.
The evidence of increased incidence of eating disor-
ders points to the importance of cultural factors in their
etiology, but it does not preclude the important role of
biological factors. A parallel example in a related field is
the rapid escalation of the prevalence of obesity. Although
the genetic underpinnings for obesity are undisputable
(Maes, Neale, & Eaves, 1997; Perusse et al., 2005), the
rapid increase in prevalence can only be attributable to
environmental shifts, because the gene pool cannot change
that quickly. Intriguingly, this argues for careful consider-
ation of other mechanisms of gene–environment interplay
rather than genetic main effects—such as genetic sensitiv-
ity to changes in the environment—which, as yet, remain
unstudied in eating disorders.
Some have described eating disorders as “culture-bound
syndromes,” either in the sense that they occur uniquely in
a limited number of cultures (Prince, 1985) or in the sense
that they represent the culturally shaped (i.e., culture-spe-
cific) expression of an underlying (culturally universal)
disease (Swartz, 1985). Within this framework, anorexia
nervosa and bulimia nervosa, as defined in the DSM–IV,
should not be found in cultures that do not subscribe to the
social norms about female thinness and the importance that
women pursue beauty to affirm their sense of femininity
and secure interpersonal or vocational success (Rodin, Sil-
berstein, & Striegel-Moore, 1985).
We have already noted the dearth of epidemiological
studies; consequently, the data needed to answer the ques-
tion of whether risk for eating disorders varies across
cultures are incomplete at best. Eating disorders have been
shown to occur across the globe (Becker & Fay, 2006; Keel
& Klump, 2003; Makino, Tsuboi, & Dennerstein, 2004),
yet few studies have used designs suitable for testing the
hypothesis that eating disorders are less common in non-
thin-ideal cultures than in thin-ideal cultures. We caution
that with one notable exception (Hoek et al., 2005; Hoek,
van Harten, van Hoeken, & Susser, 1998), these studies
have relied on samples of convenience, used diagnostic
assessments that were not validated for use in the popula-
tion under investigation, and failed to take socioeconomic
status into account. Given these limitations, it is not sur-
prising that prevalence estimates vary considerably across
studies (Keel & Klump, 2003; Makino et al., 2004).
Consistent with the cultural models, Hoek et al. (1998,
2005) found that the overall incidence of anorexia nervosa
was much lower on Curac ¸ao, an island on which the
majority population is Black and values large female bod-
ies, than in the Netherlands or the United States, but the
incidence among White or mixed-race women was on par
with that in the comparison countries. Specifically, all of
the Curac ¸ao cases were of mixed race (and, as such, were
navigating two cultures) or were White. The authors noted
that all mixed-race cases had been abroad, were more
affluent than the population average, and described (in
in-depth qualitative interviews) how they were aspiring to
lead a “Western” lifestyle (Katzman, Hermans, van
Hoeken, & Hoek, 2004).
Experts have emphasized that globalization has
brought the thin female beauty ideal and related social
norms to ever larger numbers of cultures and peoples and
that, as a consequence, eating disorders ought to be ex-
pected to increase worldwide (Catina & Joja, 2001; Gor-
don, 2001). When, after 51 years of unsuccessful Nigerian
participation in the Miss World beauty pageant, a Nigerian
contestant finally won the title in 2001, her success was
attributed to the fact that Nigeria for the first time had sent
a contestant who was not considered beautiful by local
standards because she was too thin (Onishi, 2002). Whether
this introduction of the thin ideal in a country that has long
cherished fat women will result in an increase in eating
disorders is yet to be seen; the findings from Curac ¸ao
suggest that this may happen. Research has lagged behind
in capturing the impact of the increasing penetration of the
thin beauty ideal into cultures that traditionally have valued
ample female bodies. Although ethnographic accounts of-
fer intriguing examples of adverse effects of exposure to
the thin beauty ideal on body-image concerns (Becker,
Burwell, Gilman, Herzog, & Hamburg, 2002), the few
studies that have explored the impact of cultural transition
of subpopulations (e.g., comparing individuals who moved
from a nonthin-ideal culture to a thin-ideal culture with
those who remained behind) or of entire populations
through acculturation on body image and eating behavior
are methodologically limited in much the same ways as the
aforementioned cross-cultural studies and have produced
conflicting results (for review, see Becker & Fay, 2006).
In conclusion, the literature on cross-cultural differ-
ences has accumulated clear evidence that eating disorders
186 April 2007 ● American Psychologist
do occur across the globe, yet it has been less successful in
providing unambiguous evidence for the role of culture in
risk, because of methodological limitations. Accelerating
globalization offers the perfect opportunity to study the
impact of changing body ideals on eating disorders risk as
well as the potential to elucidate mechanisms whereby such
an effect would occur.
Internalization of the Thin Beauty Ideal
Increases Risk for Eating Disorder Symptoms
The cultural theories of eating disorders have excellent face
validity, yet a critical question is by what mechanism(s) the
cultural factor of thin ideal contributes to eating disorder
risk. Recognizing the near ubiquitous exposure to images
of and social norms regarding the importance of attaining
the thin ideal in Western cultures, Rodin et al. (1985)
proposed internalization of the thin ideal as one such mech-
anism. Thin-ideal internalization encompasses an aware-
ness of the ideal and its social meaning and adoption both
of the ideal and belief in its personal relevance (Cafri,
Yamamiya, Brannick, & Thompson, 2005; Striegel-Moore
et al., 2004).
Longitudinal studies and experiments have been used
to test the relation between thin-ideal internalization and
eating disorders. In both designs, various outcome mea-
sures have been used to accommodate the low incidence of
full-syndrome eating disorders. Indeed, we found no study
with any new-onset cases of anorexia nervosa in girls, and
the literature documents only one incident case of bulimia
nervosa in the context of a longitudinal risk-factor study
(McKnight Investigators, 2003). Consequently, thus far the
literature is silent concerning the contribution of thin-ideal
internalization, body dissatisfaction, or dieting to risk for
the development of full-syndrome anorexia nervosa or bu-
Some investigators have coped with the challenge of
low incidences by broadening the case definition by com-
bining full- and partial-syndrome cases, either by disorder
(Kotler, Cohen, Davies, Pine, & Walsh, 2001) or across
anorexia nervosa and bulimia nervosa (Ghaderi & Scott,
2001; Martinez-Gonzalez et al., 2003; McKnight Investi-
gators, 2003; Patton, Selzer, Coffey, Carlin, & Wolfe,
1999). Although there is some evidence of etiological
continuity between partial and full syndromes within dis-
orders (Garfinkel et al., 1996; Kendler et al., 1991; Walters
& Kendler, 1995), as we illustrated earlier in the case of
fixed markers, etiological continuity should not be assumed
across the eating disorders. Another approach involves
using a continuous outcome measure that is derived by
adding various affective, cognitive, and behavioral symp-
toms of all eating disorders in a composite score (Stice &
Shaw, 2002). A meta-analysis of prospective and experi-
mental risk-factor studies found that effects were weaker
when outcome was defined using continuous composite-
symptom scores than when outcome was defined categor-
ically (Stice & Shaw, 2002).
A third, more granular approach disassembles diag-
nostic categories into component symptoms (which invari-
ably are more common than full syndromes) and identifies
risk factors associated with one or more particular compo-
nent parts of a syndrome (e.g., binge eating; Field, Ca-
margo, Taylor, Berkeley, Frazier, et al., 1999; Field et al.,
2002; Johnson & Wardle, 2005; Killen et al., 1994; Stice,
Killen, Hayward, & Taylor, 1998; Stice, Presnell, & Span-
gler, 2002). This approach is of interest not only for the
pragmatic reason of increased sample size but because it is
perhaps fallacious to assume that the risk factors for all of
the symptoms of our a priori defined syndromes are nec-
essarily the same. By the same token, however, it cannot be
assumed that the risk profile for a symptom necessarily
reflects the risk profile for the entire syndrome. Results
therefore need to be interpreted within the context of the
Longitudinal studies, consistently, have shown that
thin-ideal internalization, body dissatisfaction, elevated
body weight, and dieting predict risk for onset or worsen-
ing of eating pathology and that the effects of these risk
factors are considerable (McKnight Investigators, 2003;
Stice, 2002). For example, in a large cohort of 14–15-year-
old Australian children, girls reporting severe dieting were
18 times more likely to develop partial-syndrome bulimia
nervosa at a 6-month follow-up than were girls who did not
diet (Patton et al., 1999). A study of 1,177 adolescent girls
found that body dissatisfaction and dieting predicted in-
creased bulimic symptoms at a 12-month follow-up (John-
son & Wardle, 2005). The Growing Up Today Study,
which followed over 11,000 boys and girls (ages 9–14
years at study entry), reported that a composite measure of
thin-ideal internalization, social pressures or teasing about
weight, and dieting was predictive of onset of purging in
girls at the one-year follow-up (Field, Camargo, Taylor,
Berkey, & Colditz, 1999) and of onset of binge eating from
the one-year to the two-year follow-up (Field et al., 2002).
A meta-analysis (Groesz, Levine, & Murnen, 2002) of
25 experimental studies of the effect of exposure to media
images of thin women on female participants (most of them
college students) found that body dissatisfaction signifi-
cantly increased after exposure (in within-group designs) or
relative to women who were exposed to control images (in
between-groups designs). Overall, effect sizes were mod-
est, and effects were stronger in studies of high school girls
compared with college women and stronger among partic-
ipants who reported great body dissatisfaction prior to the
experimental exposure than those who were satisfied with
their body image. Experimental studies also showed that
female students reported significant increases in body dis-
satisfaction when they were exposed to peer modeling of
thin-ideal internalization or social pressure about being thin
(Krones, Stice, Batres, & Orjada, 2005; Stice, Maxfield, &
Wells, 2003). Such studies have typically involved no
follow-up to determine whether the effects on body image
were transient or lasting. Only one experimental study has
examined the longer term effects of exposure to media
images (receiving a year-long subscription to a fashion
magazine), and it found no long-term effects on body
dissatisfaction, dieting, or bulimic behavior (Stice, Span-
187 April 2007 ● American Psychologist
gler, & Agras, 2001). Stice, Trost, and Chase (2003) dem-
onstrated, however, that an intervention designed to reduce
thin-ideal internalization produced significant decreases in
thin-ideal internalization and significant improvements in
negative affect and bulimic symptoms. This work is prom-
ising in that it suggests that the adverse effects of exposure
to the thin ideal may be countered with a psychological
Taken together, the experimental evidence suggests
that media exposure to the thin ideal, or social pressure
about thin-ideal internalization, increases body-image con-
cerns at least in the short run. Experimental studies offer a
more rigorous test of etiological hypotheses than longitu-
dinal studies and permit a more clear separation of the
elements in the hypothesized causal sequence from expo-
sure to the thin ideal to thin-ideal internalization and so on.
Indeed, longitudinal studies that combine elements of this
sequence may yield inflated estimates of the role of the thin
ideal as a risk factor, because composite predictors con-
found predictor and outcome variables (e.g., body dissat-
isfaction and dieting are both links in the risk chain and
symptoms of an eating disorder). Exposure to the thin
ideal and social pressures to internalize it are nearly
ubiquitous, as exemplified by the extraordinarily high
number of hours spent with electronic media (Escobar-
Chaves et al., 2005), making it difficult to demonstrate
the effect of such exposure on eating disorder risk in
short-term studies. Future experimental studies need to
test whether repeated exposure to interventions that
counter the cultural messages of the importance of thin-
ness are protective against the onset of eating disorder
symptoms and to examine the impact of such interven-
tions over longer time periods.
The advantages of experimental designs notwithstand-
ing, we see a need also for future longitudinal studies. Our
review echoes the conclusions reached by others that the
complex etiology of eating disorders calls for multifactorial
risk models that accommodate risk factors from multiple
domains. Experimental designs can only test a small num-
ber of hypothesized risk factors at a given time. In contrast,
longitudinal studies permit exploration of multiple factors.
Stice et al. (2002), using signal detection analysis (a meth-
odology that permits identification of subgroups with dis-
tinct risk profiles), found that a subset of girls developed
binge eating in the absence of significant body-image con-
cerns; these girls’ path to binge eating involved significant
elevation of depressive symptoms and low self-esteem. The
role of culture in increasing risk for the development of low
self-esteem has not yet been examined empirically as it
relates to eating disorders. Conversely, another subgroup
was characterized by high thin-ideal internalization and
elevated body mass index (BMI). This work supports a
more complex understanding of risk that describes multiple
risk pathways toward eating pathology and helps explain
why a given risk factor, when tested at the population level,
may only be linked weakly or inconsistently with risk yet
potent when experienced in combination with other risk
The Role of Genetic Factors
After reviewing the plethora of research on sociocultural
factors and their influence on the development of eating
disorders, we are still left with one pressing unanswered
question. Namely, if all young girls are exposed to these
sociocultural pressures, why does only a small fraction go
on to develop anorexia nervosa and bulimia nervosa? The
methods we have described thus far are capable of identi-
fying patterns and trajectories, but they have not yet
evolved sufficiently methodologically to identify actual
mechanisms of risk. In contrast, genetic research is well
positioned to identify and explicate mechanisms. As we
review the state of knowledge, we are faced with three
First, understanding the genetic underpinnings of an-
orexia nervosa and bulimia nervosa may answer this vexing
question in much the same way it was stated—by helping
us identify why some individuals, by virtue of their genetic
legacy, are more vulnerable to sociocultural pressures to
attain a thin ideal. This would be a Gene ? Environment
interaction model whereby varying genotypes would render
individuals differentially sensitive to environmental events.
For example, an individual with Genotype A might exper-
iment with her first extreme diet, find the experience aver-
sive and uncomfortable, and reject the behavior on the
basis of it not being at all reinforcing. In contrast, an
individual with Genotype B might experience that first
episode of severe caloric restriction to be highly reinforcing
by reducing her innate dysphoria and anxiety, providing
her with a sense of control over her own body weight and
resulting in her receiving positive social attention for
weight-loss attempts. That individual might then adopt the
behavior in a persistent manner because of its multiple
reinforcing effects, which would then set the stage for the
development of anorexia nervosa.
A second model would be that we could, theoretically,
discover genetic main effects. We could find that the so-
ciocultural theories of eating disorders represent mere illu-
sory correlations—convenient and highly face valid yet
temporally and culturally limited explanations for a per-
plexing phenomenon, the plausibility of which obscures the
contribution of much stronger genetically driven processes
of appetite and weight dysregulation.
Third, we might uncover what could best be described
as a mixed model. This hypothetical model would reflect an
artifact of our diagnostic system that may obscure our
ability to detect genes by clustering together a grab bag of
symptoms of varying degrees genetic and environmental
etiology to create the syndromes we know today as an-
orexia nervosa and bulimia nervosa. Genetic main effects
could primarily account for the core symptoms we see in
eating disorders that have persisted thoughout history—
such as maintenance of low body weight, binge eating, and
self-induced vomiting—but the pervasive culture of the
times may have “filled in the gaps” by providing an ex-
planatory context and padding the definition of syndromes
with environmentally mediated and contextually plausible
188 April 2007 ● American Psychologist
symptoms. For example, the maintenance of low body
weight seen in anorexia nervosa has been observed for
centuries, and indeed, the core phenotype of persistent low
body weight appears to have genetic underpinnings (Grice
et al., 2002), yet the psychological “fillers” that have been
added to create the syndrome of anorexia nervosa have
changed over time. Historically, in European cultures, the
core symptom of low weight was cradled in an explanatory
system of saintliness, purity, and asceticism (Bell, 1985). In
current European culture, the core symptom is couched
with more temporally and contextually relevant criteria
which reflect thin-ideal internalization. The core symptom
has persisted over the centuries, but the psychological and
contextual factors in which we embed the symptom have
changed. Also supporting this model is the presentation of
anorexia nervosa in many Asian cultures in which the core
symptoms of low weight and food refusal exist in the
absence of fear of fatness (S. Lee, 1995; Ngai, Lee, & Lee,
2000). This mixed model suggests that our diagnostic cat-
egories may be heterogeneous mixtures of genetically in-
fluenced symptoms and cultural overlays that may not
accurately reflect underlying biology. This third model
could have major implications for methodological ap-
proaches to genetic research and contribute to furthering
our refinement of psychiatric nosology of the eating disor-
First Steps: Family Studies of Eating
Despite a late start relative to study of other psychiatric
disorders, considerable advances have been made in eluci-
dating the role of genetic factors both independently and in
concert with environment in the etiology of eating disor-
ders. Extensive family history studies have focused on the
basic question of whether eating disorders aggregate in
families. With familial transmission of anorexia nervosa,
bulimia nervosa, and BED established (Fowler & Bulik,
1997; Hudson et al., in press; Hudson, Pope, Jonas, &
Yurgelun-Todd, 1983; Hudson, Pope, Jonas, Yurgelun-
Todd, & Frankenburg, 1987; Y. Lee et al., 1999; Lilenfeld
et al., 1998; Strober, Freeman, Lampert, Diamond, & Kaye,
2000, 2001), more recent studies have focused on the
extent to which genes play a role, which genes most likely
are involved in conferring vulnerability, and their mecha-
nism of influence. Finally, new designs are emerging that
couple genetic and environmental risk factors to unveil risk
Twin Studies of Eating Disorders
adoption studies are the most effective ways to determine
the patterns of influence of genetic and environmental
factors on disease liability. In the absence of adoption
studies, the field of eating disorders has relied heavily on
twin studies to elucidate these factors. The fundamental
principles of twin methodology use the similarities and
differences between monozygotic (MZ) and dizygotic (DZ)
twin pairs to identify and delineate genetic and environ-
mental causes for a particular trait. Twin analyses are based
on the liability-threshold model (Falconer, 1965; Pearson,
1901), which assumes that an unobserved or latent variable
that indexes liability to a trait is fundamental to the ob-
served trait. Moreover, the twin model is based on the equal
environments assumption (EEA)—namely, that MZ twins
are not treated more similarly than DZ twins on factors of
etiological relevance to the trait of interest. For example,
although MZ twins might share the same bedroom more
frequently than do DZ twins, sharing a bedroom is unlikely
to be a factor of major etiological relevance to eating
disorders. To date, no notable violations of the EEA have
been observed, lending further credence to the observed
results (Bulik, Sullivan, Wade, & Kendler, 2000; Kendler,
Neale, Kessler, Heath, & Eaves, 1993; Klump, Holly, Ia-
cono, McGue, & Willson, 2000).
Because twin study methodology can be complex, a
brief primer is in order: The variance in liability to any trait
can be partitioned into additive genetic, shared environ-
mental, and unique environmental factors. Additive genetic
effects refer to the cumulative effects of many genes of
small-to-moderate effect (i.e., heritability). Shared envi-
ronmental factors contribute to twin similarity and reflect
environmental factors influencing both members of a twin
pair. Unique environmental factors, which include error of
measurement, refer to those environmental events to which
only one member of a twin pair is exposed. Although rarely
acknowledged, it is critical to note that any heritability
estimate is a product of the prevalence of the trait under
question—MZ twin concordance and DZ twin concor-
dance—and is specific to a given population at a particular
point in time. Critical to understanding twin studies is the
notion that there is not one definitive heritability of any trait
or disorder. A classic example of the effect of prevalence
on heritability estimates of a trait was reported by Kendler,
Thornton, and Pedersen (2000). In this study, regular to-
bacco use was studied in male and female twins born
between 1890 and 1958 in Sweden. In men, over time, both
the prevalence and heritability (?61%) of regular tobacco
use remained constant across birth cohorts. For women,
tobacco use was rare in early cohorts because of social
restrictions. Thus, in women born before 1925, rates of
tobacco use were low, and twin resemblance was environ-
mental in origin. In later cohorts, as social restrictions were
lifted, the prevalence of regular tobacco use increased in
women, and the heritability estimates mirrored those of
males (?63%). Functionally, social restrictions inhibited
the expression of underlying genetic predispositions to
regular tobacco use in women.
Twin and genetic studies of eating disorders have
approached the task of quantifying genetic and environ-
mental contributions to liability using categorical defini-
tions of illness (e.g., diagnostic categories like anorexia
nervosa, bulimia nervosa, and BED), subphenotypes (e.g.,
binge eating, purging, undue influence of self-evaluation on
shape and weight), or purported endophenotypes (e.g., tem-
perament or personality factors believed to be relevant to
189 April 2007 ● American Psychologist
the etiology of the disorders). One major shortcoming of
family and twin studies of eating disorders is that they have
virtually all been conducted on primarily European popu-
lations. We know little about the heritability of these dis-
orders and traits in other races and ethnic groups.
Twin studies of anorexia nervosa.
ies that have used multiple strategies to boost statistical
power to overcome the problem that anorexia nervosa is an
uncommon disorder, the heritability estimates from an-
orexia nervosa have been 48% (Kortegaard, Hoerder, Jo-
ergensen, Gillberg, & Kyvik, 2001), 58% (Wade, Bulik,
Neale, & Kendler, 2000), and 76% (Klump, Miller, Keel,
McGue, & Iacono, 2001). The contribution of the shared
environment was found to be negligible, and the remaining
variance was primarily attributable to unique environmen-
tal factors. Only recently has a sufficiently powerful study
reported heritability estimates for the narrow DSM–IV def-
inition of anorexia nervosa. In 31,406 Swedish twins born
between 1935 and 1956, Bulik et al. (2006) identified all
cases of anorexia nervosa by clinical interview of the
Swedish Twin Registry, hospital discharge diagnosis of
anorexia nervosa, or cause-of-death certificate. They re-
ported a heritability estimate of 56% (95% confidence
interval [CI]: .00–.87), with a small contribution (5%) of
shared environment (95% CI: .00–.64) and 38% of vari-
ance in liability attributable to unique environment (95%
CI: .13–.84). Despite varying definitions and wide confi-
dence intervals, all of these studies point to a substantial
contribution of additive genetic effects to anorexia nervosa.
Twin studies of bulimia nervosa.
studies of varyingly broad definitions of bulimia nervosa
using univariate, bivariate, and measurement model tech-
niques (Bulik, Sullivan, & Kendler, 1998; Kendler et al.,
1991; Kortegaard et al., 2001; Walters et al., 1992, 1993)
also have consistently yielded high heritability estimates,
ranging from 50% (Walters et al., 1992) to 83% (Bulik et
al., 1998), with unique environmental factors accounting
for the remaining variance. In line with the third model
presented above (the mixture model), bulimia nervosa has
also been dissected into its component symptoms, reveal-
ing substantial genetic effects on the symptoms of self-
induced vomiting (73%) and binge eating (49%–51%;
Reichborn-Kjennerud et al., 2003; Sullivan, Bulik, & Ken-
dler, 1998) but suggesting no genetic contributions to the
symptom of placing undue emphasis on shape and weight
where shared and unique environment were the sole con-
tributors to variance in liability in the best fitting models
(Reichborn-Kjennerud et al., 2004).
Twin studies of BED.
ported substantial heritability of the symptom of binge
eating (Bulik et al., 1998; Bulik, Sullivan, & Kendler,
2003) with the presence of purging behaviors not con-
trolled for statistically. One population-based study of Nor-
wegian twins between 18 and 31 years of age reported a
heritability estimate of 41% for a syndrome that approxi-
mated BED, termed binge eating in the absence of com-
pensatory behaviors, with the remaining variance attribut-
able to nonshared environment.
Twin studies have re-
Molecular Genetic Studies
of molecular genetic designs have been applied to eating
disorders: association studies and linkage studies. Associ-
ation studies compare cases displaying a trait of interest
with controls who do not display the trait. All individuals
are genotyped for the relevant candidate gene or genes.
Statistical analysis is used to compare allele or genotype
frequencies (Sasieni, 1997) in cases versus controls (Sham,
1998). Association studies are optimal when the patho-
physiology of a trait points to specific candidate genes. The
second approach, linkage analysis, requires a large sample
of multiplex pedigrees or extreme sibling pairs (Allison,
Heo, Schork, Wong, & Elston, 1998). Anonymous genetic
markers across the genome are used to identify chromo-
somal regions that may contain genes that influence the
trait of interest. Linkage approaches narrow the focus on
the genome. Genes located under the linkage peaks are then
further explored using association approaches to determine
whether they may indeed be associated with the trait of
Genetic association studies can be dizzying to the
reader unfamiliar with genetic research. The parade of
initially exciting and later nonreplicated findings has been
dubbed the Proteus effect (Ioannidis & Trikalinos, 2005)
and underscores the methodological and statistical chal-
lenges of finding a needle in a haystack while dealing with
issues of multiple comparisons and changing prior proba-
bilities. To focus the research, those involved in association
studies of eating disorders have homed in on systems
known to influence feeding, appetite, and mood as well as
genes that have been identified as potentially contributory
to other psychiatric disorders.
Molecular genetic studies of anorexia ner-
The palette of association studies conducted to
date is rich and far too detailed to review here. Several
comprehensive reviews and updates of association studies
in eating disorders have been published (Gorwood, Kip-
man, & Foulon, 2003; Hinney, Remschmidt, & Hebebrand,
2000; Klump & Gobrogge, 2005; Mazzeo, Slof-Op ‘t
Landt, van Furth, & Bulik, 2006; Slof-Op ‘t Landt et al.,
2005). Briefly, given the known involvement in both mood
and appetite, genes in the serotonergic system (e.g., sero-
tonin receptor 2A, 2C, the serotonin transporter gene) and
the dopaminergic system (e.g., D3 receptor, D4 receptor,
dopamine transporter) as well as several other genes in-
volved in functions believed to be central to the etiology of
eating disorders (e.g., brain-derived neurotrophic factor,
been explored, with associations observed and frequently
nonreplicated and interpretation clouded by the impact of
small sample sizes.
Linkage studies for anorexia nervosa (Bacanu et al.,
2005; B. Devlin et al., 2002; Grice et al., 2002; Kaye et al.,
2000) have yielded significant results and underscored the
importance of detailed phenotyping. A linkage study of a
heterogeneous sample of individuals with broadly defined
190 April 2007 ● American Psychologist
eating disorders yielded absolutely no signals of interest
across the genome. However, restricting that sample to
relative pairs exhibiting the classic restricting subtype an-
orexia nervosa in the absence of binge-eating behavior
yielded evidence for the presence of a susceptibility locus
on chromosome 1 (Grice et al., 2002). Additional ap-
proaches that enhanced the focus of the linkage analysis by
incorporating key behavioral covariates into linkage anal-
yses (B. Devlin et al., 2002)—namely, drive for thinness
and obsessionality—isolated several regions of interest on
chromosomes 1, 2, and 13. The second step in this analysis
involves exploring the identified regions of interest to de-
termine whether genes exist in those regions that could
plausibly be related to the disorder and testing them for
association. Two genes under these linkage peaks, seroto-
nin 1D (HTR1D) and delta opioid (OPRD1) receptor, ex-
hibited significant association with anorexia nervosa (Ber-
gen et al., 2003). The subsequent step is to determine the
actual functions of identified genes and how they might
contribute to risk for anorexia nervosa.
Molecular genetic studies of bulimia ner-
In association studies, the choices of candidate
genes in bulimia nervosa have closely paralleled those for
anorexia nervosa (Gorwood et al., 2003; Hinney et al.,
2000; Klump & Gobrogge, 2005; Mazzeo et al., 2006;
Slof-Op ‘t Landt et al., 2005). One intriguing advance that
again shows the importance of detailed phenotyping has
emerged from the laboratories of Steiger et al. (2005). This
group examined factors associated with the serotonin trans-
porter (5-HTTPLR) gene in 59 women with eating disor-
ders involving binge eating and purging (e.g., bulimia
nervosa; anorexia nervosa, binge–purging subtype). De-
tailed personality information was also available on these
women. In this sample, the S allele was not associated with
eating disorder symptoms but was associated with border-
line personality disorder and related symptoms such as
impulsivity, affective instability, and insecure attachment.
Individuals with the S allele also had a significantly lower
density of paroxetine-binding sites, suggesting that they
might not respond as well to selective serotonin reuptake
inhibitors—which are commonly prescribed to treat bu-
limia nervosa. The authors also speculated that the parox-
etine-binding densities could reflect Gene ? Environment
interactions, because chronic food restriction in animals is
associated with 5-HT dysregulation. The authors suggested
that chronic dieting typical of patients with these syn-
dromes could trigger the expression of this genetic poly-
morphism. This emerging body of research presages the
potential impact of pharmacogenetics in the treatment of
eating disorders and highlights another manner in which
genes and environment may interact to influence ultimate
Only one linkage study of bulimia nervosa has been
reported (Bulik, Devlin, et al., 2003). Significant linkage
was achieved on chromosome 10p13, and suggestive evi-
dence for linkage was reported for 10p14 and 14q22-23.
Again, working toward the most refined phenotype for
linkage analysis and focusing on information from twin
studies that highlighted the high heritability of self-induced
vomiting (Sullivan, Bulik, & Kendler, 1998), the authors
performed a second linkage analysis in a subset of 133
families, in which at least two affected individuals reported
regular vomiting. This refinement led to the narrowing of
the linkage peak on chromosome 10p13, which enabled a
more focused search for loci of interest.
Molecular genetic studies of BED.
tion studies have also been initiated to shed light on genetic
mechanisms underlying binge eating, with one study re-
porting BED to be associated with mutations in the mela-
nocortin 4 receptor gene (Branson et al., 2003), a gene
implicated in the development of overeating and obesity
(Farooqi et al., 2003; List & Habener, 2003); however, a
subsequent study failed to replicate this finding (Hebebrand
et al., 2004).
Genetic Epidemiology and Risk: Questions
for the Future
It is intriguing to reevaluate the existing genetic literature
on the basis of the three models forwarded. Most notably,
Reichborn-Kjennerud et al. (2004) suggested that there
may be distinct sources of familial resemblance (e.g., ge-
netic and environmental contributions) for different symp-
toms of bulimia nervosa as codified in the DSM–IV. Both
binge eating and vomiting, which comprise Criteria A and
B of DSM–IV bulimia nervosa, appear to represent more
genetically mediated symptoms, with the heritability of
binge eating reported to be between 49% and 51% (Reich-
born-Kjennerud et al., 2003; Sullivan, Bulik, & Kendler,
1998) and that of vomiting at 72%. In contrast, Criterion C
of DSM–IV bulimia nervosa, undue influence of shape and
weight concerns on self-evaluation, does not appear to be
heritable and shows substantially greater shared environ-
mental effects. Most notably, weight concerns (Wade, Mar-
tin, & Tiggemann, 1998) and placing undue importance on
weight as an indicator of self-evaluation are best accounted
for by models that include only shared and unique envi-
ronmental effects. Moreover, sex differences may also exist
in genetic and environmental contributions to individual
symptoms, as illustrated by Keski-Rahkonen et al. (2005),
who showed differences in patterns of heritability between
males and females on drive for thinness and body-dissat-
isfaction scores. Their results suggest that the heritability
patterns of eating disorder–related attitudes are highly sex
specific. Thus, a DSM–IV diagnostic category such as bu-
limia nervosa might actually represent an occasionally co-
occurring yet etiologically diverse mixture of genetically
and environmentally influenced symptoms that differ by
sex. From a genetic perspective, focusing on compound
syndromes that include multiple symptoms of varying ge-
netic etiology could impede searches for susceptibility loci.
Focused attention on heritable endo- and subphenotypes
could assist with isolating genetic factors that influence the
core behaviors, and such behaviors could then be rewoven
into more complex designs that elucidate gene–environ-
ment interaction and correlation.
191 April 2007 ● American Psychologist
Neonatal and Neurodevelopmental
Variables and Anorexia Nervosa
Nonetheless, the future of genetic research in eating disor-
ders may well rest with sophisticated approaches to
Gene ? Environment interplay. One theory has been for-
warded as an example of such interplay (Bulik et al., 2005),
and we present one prototype methodological example
from the affective disorders literature to illustrate one way
in which genes and environment may interact.
The theory involves the role of neonatal complications
and neurodevelopmental challenges in anorexia nervosa
and how genetically mediated maternal variables can in-
fluence intrauterine environment. The basis of this theory is
the observation that neonatal complications increase risk
for anorexia nervosa. Cnattingius, Hultman, Dahl, and
Sparen (1999) linked the Swedish birth registry with the
Swedish psychiatric inpatient registry and found that girls
born prematurely (especially if they were small for gesta-
tional age [SGA]) and those born with cephalhematoma
were at increased risk for developing anorexia nervosa later
in life. Similar results were reported in a different study by
Favaro, Tenconi, and Santonastaso (2006) in 114 individ-
uals with anorexia nervosa, 73 individuals with bulimia
nervosa, and 554 controls in Padua, Italy. Favaro et al.
(2006) reported that maternal anemia, diabetes mellitus,
preeclampsia, placental infarction, neonatal cardiac prob-
lems, and hyporeactivity were all significant independent
predictors of the later development of anorexia nervosa. In
addition, the more neonatal events, the higher the risk of
developing anorexia nervosa.
In both studies, the authors suggested that subtle brain
damage at birth could result in early feeding difficulties and
increased risk for anorexia nervosa. However, alternative
mechanisms, related to genetically mediated maternal eat-
ing behavior, could also be at play. For example, Bloom-
field et al. (2003) demonstrated that moderate maternal
food restriction in sheep around the time of conception
results in precocious fetal cortisol surge and preterm birth.
Human females with prolonged food-deprivation episodes
are also more likely to deliver at a shorter gestational age,
which is probably mediated through higher corticotrophin-
releasing hormone levels (Herrmann, Siega-Riz, Hobel,
Aurora, & Dunkel-Schetter, 2001).
Notably, in follow-up studies of women with anorexia
nervosa, even those who no longer met diagnostic criteria
tended to maintain relatively low body weight and cogni-
tive features characteristic of anorexia nervosa (perfection-
ism and cognitive restraint; Sullivan, Bulik, Fear, & Pick-
ering, 1998). This could reflect lingering subthreshold
symptoms and continuing efforts toward food restriction
and weight control. It is possible that the preterm births and
SGA babies in these women observed in these studies are
secondary to the persistence of genetically mediated eating
disorder symptoms that “fly under the radar” diagnostically
yet are sufficient to impact fetal growth and development.
Along these lines, although few data exist, the wide avail-
ability of fertility treatments may increase the likelihood
that individuals with eating disorders who have experi-
enced reproductive complications of the eating disorder
will conceive. The shame and secrecy associated with an
eating disorder, as well as the fear of being turned away by
fertility specialists, may result in underestimates of the
prevalence of eating disorders in fertility clinics (Norre,
Vandereycken, & Gordts, 2001). This could mean that
more individuals in partial recovery will become pregnant
and, tragically, not receive adequate perinatal counseling to
ensure adequate nutrition during pregnancy. Indeed, sev-
eral studies have confirmed that women with eating disor-
ders have higher rates of pregnancy complications, cesar-
ean deliveries, and postpartum depression (Bulik et al.,
1999; Franko et al., 2001; Franko & Spurrell, 2000; Franko
& Walton, 1993). In summary, women with histories of
anorexia nervosa tend to maintain low BMIs even after
recovery and tend to give birth to lower birth-weight ba-
bies, potentially increasing their offspring’s risk for the
development of later chronic disease (Barker, 1992; Barker
et al., 1993), including possibly anorexia nervosa (Cnattin-
gius et al., 1999). Thus, an intricate cycle of genetic factors
(influencing weight gain during pregnancy) and environ-
mental factors (fetal undernutrition in utero) coupled with
the direct heritability of eating disorders could be acting in
concert to influence offspring eating disorders risk.
How Genes Can Help Us Understand
We have no doubt that the remarkable historical changes in
traits such as eating disorders, fertility, and obesity reflect
environmental changes. However, individuals are differen-
tially genetically susceptible to environmental shifts. How
can discovering “liability genes” help researchers to under-
stand the impact of environment? Caspi et al. (2002, 2003)
reported two examples involving genetic variants that alter
gene expression, a variant in the gene MAOA encoding the
neurotransmitter-metabolizing enzyme monoamine oxi-
dase A and a variant in the promoter region of the gene
SLC6A4 encoding the serotonin transporter. These authors
showed that a child’s response to maltreatment early in life
depended critically on variation at MAOA: Maltreated
children were stochastically more likely to develop behav-
ior problems when they had low levels of MAOA expres-
sion than when expression was high. For SLC6A4 varia-
tion, they showed that individuals carrying one or two
copies of the “short” allele of the promoter polymorphism,
which produces lower expression of SLC6A4, were more
likely to exhibit more symptoms of depression and suicid-
ality after experiencing stressful life events than were in-
dividuals carrying two copies of the “long” allele. With
appropriate caution, this model may provide a beacon for
the future. This approach will be most appropriate in the
presence of clearly defined a priori hypotheses and selec-
tions of environmental risk factors and genetic variants.
Given the abundance of potential environmental factors
from which to choose, as well as the number of genes likely
to be implicated, the dangers of multiple testing yielding
false-positive results are considerable. If we were to iden-
192 April 2007 ● American Psychologist
tify similar examples of Gene ? Environment interactions
in the field of eating disorders, it would be the first step in
unraveling the manner in which genes and environment act
together in eating disorders—a definitive step away from
what has been a field bifurcated by the nature versus
nurture dichotomy for far too long.
Evidence has accumulated in support of both biological
(genetic and early developmental trauma) and cultural fac-
tors contributing to the increased risk for the development
of eating disorders or associated behaviors and attitudes.
Research on biological factors and cultural factors has
progressed largely along parallel tracks. Future studies
must explore these two classes of risk factors in tandem
while remaining cognizant of the broader cultural context
in which the disorders emerge. Entire classes of risk factors
(e.g., personality, familial environment factors) have not
yet been studied prospectively. Multimethod research ap-
proaches are needed to advance our understanding of the
etiology of eating disorders. Comprehensive epidemiolog-
ical studies are needed that capture more fully the clinical
presentation of eating disorders in demographically diverse
populations. Empirically based classification systems
should be validated using hypothesized risk factors. Re-
searchers need to exploit more fully the availability of
longitudinal data that have been collected in samples that
have been followed from birth or early childhood to gen-
erate hypotheses about the contribution of risk variables
like personality feature or early family environment to the
development of eating pathology. In addition, new longi-
tudinal studies need to be initiated that are designed to test
etiological hypotheses. Clearly, samples sizes numbering
in the tens of thousands will be required to ensure adequate
power for examining risk for the onset of full-syndrome
disorders. The existing literature also points to the promise
of experimental studies with high-risk populations (e.g.,
offspring of mothers with eating disorders) for testing the
contribution of certain risk factors.
Our review points to several conclusions about
stigma, nosology, treatment, and prevention of eating dis-
orders. The evidence shows that we live in a culture that
values thinness and that exposure or social pressure to
conform to this norm contributes to body image concerns.
The cultural context of thin idealization provides an all-
too-easy explanation of eating disorders as the consequence
of pursuit of beauty, contributing to a perception that these
problems are self-inflicted and undeserving of serious con-
sideration. The evidence is fairly strong that biological
factors contribute to risk factors for anorexia nervosa. The
dissemination of such findings may finally dispel the dam-
aging and disrespectful myth that anorexia nervosa is van-
ity run amok. Moreover, the almost wholesale exclusion
from research of individuals from racial or ethnic minority
groups and the marginalization of males cannot be justified
with (unsubstantiated) arguments that eating disorders af-
fect only White girls or women and contribute to stigma-
tization of members of these underresearched groups when
they present with an eating disorder.
This review also points to significant flaws in our
nosology. With the majority of individuals seeking treat-
ment being captured under an umbrella of a residual diag-
nosis (EDNOS), we have failed to characterize adequately
the core pathology profiles that comprise the eating disor-
ders. In part, this may be a result of our need to find
satisfying and plausible explanations for perplexing symp-
tom clusters. For decades, our patients with anorexia ner-
vosa have said “it’s not about looking like a model.” We
nonetheless persist with the explanatory framework of the
thin-ideal internalization regardless of eating disorder type.
Although there is no question that thin-ideal internalization
is damaging, the mechanism whereby it influences risk for
eating disorders remains unknown. Perhaps an example of
effort after meaning (Bartlett, 1932), we have created, for
example, a composite picture of anorexia nervosa that
includes low body weight (which may be more biologically
mediated) and undue influence of weight on self-evaluation
(which may be more environmentally mediated) under one
diagnostic label. Similarly, bulimia nervosa includes binge
eating and self-induced vomiting (both apparently geneti-
cally mediated) and undue influence of weight on self-
evaluation (apparently more environmentally mediated).
Our hodgepodge diagnoses may not reflect underlying bi-
ological processes, may not adequately capture the popu-
lation of interest, and may impair our ability to identify
either genetic or environmental risk factors for disease.
Thus, we encourage a critical reappraisal of our current
nosology as both biological and sociocultural research un-
The findings also point to population groups at high
risk (e.g., offspring of mothers with anorexia nervosa,
children with certain neonatal complications) and suggest
the need to test targeted preventive interventions for these
groups. The genetic branch of eating disorders research is
in its infancy. Extensions of genetic research exploring not
only the genetics of risk but also the genetics of course of
illness and treatment response (both biological and psycho-
logical interventions), as well as more sophisticated models
of Gene ? Environment interplay, will launch the next
generation of genetic investigations. Moreover, although
not reviewed here, greater cross-talk between animal and
human researchers will help us unveil new biological
mechanisms that influence eating disorders, and greater
cross-talk between obesity and eating disorders researchers
could only serve to enrich and inform both fields.
The corpus of findings from the sociocultural theory
of eating disorders literature underscores the importance of
preventive and policy interventions designed to decrease
exposure to or attenuate the impact of thin-ideal messages.
Even if we cannot prove that these factors cause eating
disorders, we can safely say that they negatively influence
the self-perceptions of young women. This fact has become
even more critical in the face of the obesity epidemic,
around which television shows, prevention programs, com-
munity and workplace interventions, and school-based pro-
193 April 2007 ● American Psychologist
grams designed for the explicit purpose of weight loss or
weight control have arisen rapidly without adequate testing
for their impact on individuals who are vulnerable to eating
disorders. Public health interventions countering over-
weight and obesity can be carried out in a manner that
addresses simultaneously the needs of those individuals at
risk for overweight and obesity and those individuals at risk
for eating disorders (Neumark-Sztainer, 2005). Yet the
rapidity with which such programs have arisen has out-
paced our ability to evaluate both their beneficial effects
and their potentially adverse side effects.
Perhaps most critical, as a field, we have also been a
victim of marginalization. The U.S. Centers for Disease
Control has failed to collect rigorous epidemiologic data
regarding eating disorders and disordered eating behavior.
The World Health Organization has not published facts on
disability-adjusted life years (DALYs) for anorexia nervosa
or bulimia nervosa, whereas DALYs for similarly prevalent
conditions (e.g., obsessive–compulsive disorder) have
been reported. We attribute much of this marginalization to
pervasive misperceptions about the volitional nature of
eating disorders, which has impacted research; third-party
reimbursement; and most tragically, families and sufferers
who have known all along that eating disorders are far
more grave than merely a choice to pursue thinness.
Allison, D. B., Heo, M., Schork, N. J., Wong, S. L., & Elston, R. C.
(1998). Extreme selection strategies in gene mapping studies of oligo-
genic quantitative traits do not always increase power. Human Hered-
ity, 48, 97–107.
American Psychiatric Association. (1994). Diagnostic and statistical
manual of mental disorders (4th ed.). Washington, DC: Author.
Anderson, C., & Bulik, C. (2004). Gender differences in compensatory
behaviors, weight and shape salience, and drive for thinness. Eating
Behaviors, 5, 1–11.
Austin, S. B., Ziyadeh, N., Kahn, J. A., Camargo, C. A., Jr., Colditz,
G. A., & Field, A. E. (2004). Sexual orientation, weight concerns, and
eating-disordered behaviors in adolescent girls and boys. Journal of the
American Academy of Child & Adolescent Psychiatry, 43, 1115–1123.
Bacanu, S., Bulik, C., Klump, K., Fichter, M., Halmi, K., Keel, P., et al.
(2005). Linkage analysis of anorexia and bulimia nervosa cohorts using
selected behavioral phenotypes as quantitative traits or covariates.
American Journal of Medical Genetics Part B: Neuropsychiatric Ge-
netics, 139, 61–68.
Barker, D. (1992). Fetal and infant origins of adult disease. London:
British Medical Journal Publishing.
Barker, D., Gluckman, P., Godfrey, K., Harding, J., Owens, J., & Rob-
inson, J. (1993). Fetal nutrition and cardiovascular disease in adult life.
Lancet, 341, 938–941.
Bartlett, F. (1932). Remembering: A study in experimental and social
psychology. London: Cambridge University Press.
Becker, A., Burwell, R. A., Gilman, S. E., Herzog, D. B., & Hamburg, P.
(2002). Eating behaviours and attitudes following prolonged exposure
to television among ethnic Fijian adolescent girls. British Journal of
Psychiatry, 180, 509–514.
Becker, A., & Fay, K. (2006). Sociocultural issues and eating disorders. In
S. Wonderlich, J. Mitchell, M. de Zwaan, & H. Steiger (Eds.), Annual
review of eating disorders 2006 (pp. 35–63). Oxon, England: Radcliffe.
Becker, A., Franko, D. L., Speck, A., & Herzog, D. B. (2003). Ethnicity
and differential access to care for eating disorder symptoms. Interna-
tional Journal of Eating Disorders, 33, 205–212.
Bell, R. (1985). Holy anorexia. Chicago: University of Chicago Press.
Bergen, A. W., van den Bree, M. B. M., Yeager, M., Welch, R., Ganjei,
J. K., Haque, K., et al. (2003). Candidate genes for anorexia nervosa in
the 1p33–36 linkage region: Serotonin 1D and delta opioid receptor loci
exhibit significant association to anorexia nervosa. Molecular Psychi-
atry, 8, 397–406.
Berkman, N., Bulik, C., Brownley, K., & Lohr, K. (in press). Eating
disorders treatment and outcomes. Rockville, MD: Agency for Health-
care Research and Quality.
Bloomfield, F., Oliver, M., Hawkins, P., Campbell, M., Phillips, D.,
Gluckman, P., et al. (2003, April 25). A periconceptional nutritional
origin for noninfectious preterm birth. Science, 300, 606.
Bordo, S. (1993). Unbearable weight: Feminism, Western culture, and the
body. Berkeley: University of California Press.
Boroughs, M., & Thompson, J. K. (2002). Exercise status and sexual
orientation as moderators of body image disturbance and eating disor-
ders in males. International Journal of Eating Disorders, 31, 307–311.
Boskind-Lodahl, M. (1976). Cinderella’s stepsisters: A feminist perspec-
tive on anorexia nervosa and bulimia. Signs, 2, 342–356.
Branson, R., Potoczna, N., Kral, J., Lentes, K., Hoehe, M., & Horber, F.
(2003). Binge eating as a major phenotype of melanocortin 4 receptor
gene mutations. New England Journal of Medicine, 348, 1096–1103.
Bruch, H. (1973). Eating disorders: Obesity, anorexia nervosa, and the
person within. New York: Basic Books.
Bruch, H. (1979). Island in the river: The anorexic adolescent in treat-
ment. In S. C. Feinstein & P. L. Giovacchini (Eds.), Adolescent psy-
chiatry: Vol. 7. Developmental and clinical studies (pp. 26–40). Chi-
cago: University of Chicago Press.
Brumberg, J. J. (1988). Fasting girls: The emergence of anorexia nervosa
as a modern disease. Cambridge, MA: Harvard University Press.
Brumberg, J. J. (2000). Fasting girls: The history of anorexia nervosa
(Rev. ed.). New York: Vintage Books.
Bulik, C. M., Devlin, B., Bacanu, S. A., Thornton, L., Klump, K. L.,
Fichter, M. M., et al. (2003). Significant linkage on chromosome 10p in
families with bulimia nervosa. American Journal of Human Genetics,
Bulik, C. M., Reba, L., Siega-Riz, A. M., & Reichborn-Kjennerud, T.
(2005). Anorexia nervosa: Definition, epidemiology, and cycle of risk.
International Journal of Eating Disorders, 37(Suppl.), S2–S9.
Bulik, C. M., Sullivan, P., Fear, J., Pickering, A., Dawn, A., & McCullin,
M. (1999). Fertility and reproduction in women with a history of
anorexia nervosa: A controlled study. Journal of Clinical Psychiatry,
Bulik, C. M., Sullivan, P. F., & Kendler, K. (1998). Heritability of
binge-eating and broadly defined bulimia nervosa. Biological Psychia-
try, 44, 1210–1218.
Bulik, C. M., Sullivan, P. F., & Kendler, K. S. (2003). Genetic and
environmental contributions to obesity and binge eating. International
Journal of Eating Disorders, 33, 293–298.
Bulik, C. M., Sullivan, P. F., Tozzi, F., Furberg, H., Lichtenstein, P., &
Pedersen, N. L. (2006). Prevalence, heritability, and prospective risk
factors for anorexia nervosa. Archives of General Psychiatry, 63, 305–
Bulik, C. M., Sullivan, P. F., Wade, T., & Kendler, K. (2000). Twin
studies of eating disorders: A review. International Journal of Eating
Disorders, 27, 1–20.
Bushnell, J. A., Wells, J. E., Hornblow, A. R., Oakley-Browne, M. A., &
Joyce, P. (1990). Prevalence of three bulimia syndromes in the general
population. Psychological Medicine, 20, 671–680.
Cachelin, F. M., & Striegel-Moore, R. H. (2006). Help seeking and
barriers to treatment in a community sample of Mexican American and
European American women with eating disorders. International Jour-
nal of Eating Disorders, 39, 154–161.
Cafri, G., Yamamiya, Y., Brannick, M., & Thompson, J. K. (2005). The
influence of sociocultural factors on body image: A meta-analysis.
Clinical Psychology: Science and Practice, 12, 421–433.
Caplan, P. J., & Hall-McCorquodale, I. (1985). Mother-blaming in major
clinical journals. American Journal of Orthopsychiatry, 55, 345–353.
Caspi, A., McClay, J., Moffit, T., Mill, J., Martin, J., Craig, I., et al. (2002,
August 2). Role of genotype in the cycle of violence in maltreated
children. Science, 297, 851–854.
Caspi, A., Sugden, K., Moffitt, T., Taylor, A., Craig, I., Harrington, H., et
194April 2007 ● American Psychologist
al. (2003, July 18). Influence of life stress on depression: Moderation by
a polymorphism in the 5-HTT gene. Science, 301, 386–389.
Catina, A., & Joja, O. (2001). Emerging markets: Submerging women. In
M. Nasser, M. A. Katzman, & R. A. Gordon (Eds.), Eating disorders
and cultures in transition (pp. 111–119). New York: Brunner-Rout-
Cnattingius, S., Hultman, C., Dahl, M., & Sparen, P. (1999). Very preterm
birth, birth trauma, and the risk of anorexia nervosa among girls.
Archives of General Psychiatry, 56, 634–638.
Connan, F., Campbell, I. C., Katzman, M., Lightman, S. L., & Treasure,
J. (2003). A neurodevelopmental model for anorexia nervosa. Physiol-
ogy and Behavior, 79, 13–24.
Crisp, A. H., Gelder, M. G., Rix, S., Meltzer, H. I., & Rowlands, O. J.
(2000). Stigmatisation of people with mental illnesses. British Journal
of Psychiatry, 177, 4–7.
Devlin, B., Bacanu, S., Klump, K., Bulik, C., Fichter, M., Halmi, K., et al.
(2002). Linkage analysis of anorexia nervosa incorporating behavioral
covariates. Human Molecular Genetics, 11, 689–696.
Devlin, M. J., Goldfein, J. A., & Dobrow, I. (2003). What is this thing
called BED? Current status of binge eating disorder nosology. Inter-
national Journal of Eating Disorders, 34(Suppl.), S2–S18.
Escobar-Chaves, S. L., Tortolero, S. R., Markham, C. M., Low, B. J.,
Eitel, P., & Thickstun, P. (2005). Impact of the media on adolescent
sexual attitudes and behaviors. Pediatrics, 116, 303–326.
Falconer, D. S. (1965). The inheritance of liability to certain diseases,
estimated from the incidence among relatives. Annals of Human Ge-
netics (London), 29, 51–76.
Farooqi, I., Keogh, J., Giles, S., Yeo, S., Lank, E., Cheetham, T., &
O’Rahilly, S. (2003). Clinical spectrum of obesity and mutations in the
melanocortin 4 receptor gene. New England Journal of Medicine, 348,
Favaro, A., Ferrara, S., & Santonastaso, P. (2003). The spectrum of eating
disorders in young women: A prevalence study in a general population
sample. Psychosomatic Medicine, 65, 701–708.
Favaro, A., Tenconi, E., & Santonastaso, P. (2006). Perinatal factors and
the risk of developing anorexia nervosa and bulimia nervosa. Archives
of General Psychiatry, 63, 82–88.
Fichter, M. M., Quadflieg, N., & Hedlund, S. (2005). Twelve-year course
and outcome predictors of anorexia nervosa. International Journal of
Eating Disorders, 39, 310–322.
Field, A. E., Austin, S. B., Frazier, A. L., Gillman, M. W., Camargo,
C. A., Jr., & Colditz, G. A. (2002). Smoking, getting drunk, and
engaging in bulimic behaviors: In which order are the behaviors
adopted? Journal of the American Academy of Child & Adolescent
Psychiatry, 41, 846–853.
Field, A. E., Camargo, C. A., Jr., Taylor, C. B., Berkey, C. S., & Colditz,
G. A. (1999). Relation of peer and media influences to the development
of purging behaviors among preadolescent and adolescent girls. Ar-
chives of Pediatrics and Adolescent Medicine, 153, 1184–1189.
Field, A. E., Camargo, C. A., Jr., Taylor, C. B., Berkey, C. S., Frazier,
A. L., Gilman, M. W., & Colditz, G. A. (1999). Overweight, weight
concerns, and bulimic behaviors among girls and boys. Journal of the
American Academy of Child & Adolescent Psychiatry, 38, 754–760.
Fowler, S., & Bulik, C. (1997). Family environment and psychiatric
history in women with binge-eating disorder and obese controls. Be-
haviour Change, 14, 1.
Franko, D. L., Blais, M., Becker, A., Delinsky, S., Greenwood, D., Flores,
A., et al. (2001). Pregnancy complications and neonatal outcomes in
women with eating disorders. American Journal of Psychiatry, 158,
Franko, D. L., & Spurrell, E. (2000). Detection and management of eating
disorders during pregnancy. Obstetrics and Gynecology, 95, 942–946.
Franko, D. L., & Walton, B. E. (1993). Pregnancy and eating disorders: A
review and clinical implications. International Journal of Eating Dis-
orders, 13, 41–48.
Garfinkel, P. E., Lin, E., Goering, P., Spegg, C., Goldbloom, D., Kennedy,
S., et al. (1995). Bulimia nervosa in a Canadian community sample:
Prevalence and comparison of subgroups. American Journal of Psychi-
atry, 152, 1052–1058.
Garfinkel, P. E., Lin, E., Goering, P., Spegg, C., Goldbloom, D. S.,
Kennedy, S., et al. (1996). Purging and nonpurging forms of bulimia
nervosa in a community sample. International Journal of Eating Dis-
orders, 20, 231–238.
Ghaderi, A., & Scott, B. (2001). Prevalence, incidence and prospective
risk factors for eating disorders. Acta Psychiatrica Scandinavica, 104,
Gordon, R. A. (2001). Eating disorders East and West: A culture-bound
syndrome unbound. In M. Nasser, M. A. Katzman, & R. A. Gordon
(Eds.), Eating disorders and cultures in transition (pp. 1–16). New
Gorwood, P., Kipman, A., & Foulon, C. (2003). The human genetics of
anorexia nervosa. European Journal of Pharmacology, 480, 163–170.
Grice, D. E., Halmi, K. A., Fichter, M. M., Strober, M., Woodside, D. B.,
Treasure, J. T., et al. (2002). Evidence for a susceptibility gene for
anorexia nervosa on chromosome 1. American Journal of Human
Genetics, 70, 787–792.
Groesz, L. M., Levine, M. P., & Murnen, S. K. (2002). The effect of
experimental presentation of thin media images on body satisfaction: A
meta-analytic review. International Journal of Eating Disorders, 31,
Gull, W. W. (1874). Anorexia nervosa (apepsia hysterica, anorexia hys-
terica). Transactions of the Clinical Society of London, 7, 22–28.
Gull, W. W. (1888). Anorexia nervosa. Lancet, i, 516–517.
Hay, P. (1998). The epidemiology of eating disorder behaviors: An
Australian community-based survey. International Journal of Eating
Disorders, 23, 371–382.
Haynes, S. (1992). Models of causality in psychopathology: Toward
dynamic, synthetic, and nonlinear models of behavior disorders. Need-
ham Heights, MA: Allyn & Bacon.
Hebebrand, J., Geller, F., Dempfle, A., Heinzel-Gutenbrunner, M., Raab,
M., Gerber, G., et al. (2004). Binge-eating episodes are not character-
istic of carriers of melanocortin-4 receptor gene mutations. Molecular
Psychiatry, 9, 796–800.
Herrmann, T., Siega-Riz, A., Hobel, C., Aurora, C., & Dunkel-Schetter,
C. (2001). Fasting during pregnancy increases risk for elevated mater-
nal corticotrophin releasing hormone concentrations. American Journal
of Obstetrics and Gynecology, 185, 402–412.
Hinney, A., Remschmidt, H., & Hebebrand, J. (2000). Candidate gene
polymorphisms in eating disorders. European Journal of Pharmacol-
ogy, 410, 147–159.
Hoek, H. W. (2006). Incidence, prevalence and mortality of anorexia
nervosa and other eating disorders. Current Opinion in Psychiatry, 19,
Hoek, H. W., Bartelds, A., Bosveld, J., van der Graaf, Y., Limpens, V.,
Maiwald, M., & Spaaij, C. J. (1995). Impact of urbanization on detec-
tion rates of eating disorders. American Journal of Psychiatry, 152,
Hoek, H. W., van Harten, P. N., Hermans, K. M., Katzman, M. A.,
Matroos, G. E., & Susser, E. S. (2005). The incidence of anorexia
nervosa on Curac ¸ao. American Journal of Psychiatry, 162, 748–752.
Hoek, H. W., van Harten, P. N., van Hoeken, D., & Susser, E. (1998).
Lack of relation between culture and anorexia nervosa—Results of an
incidence study on Curac ¸ao. New England Journal of Medicine, 338,
Hoek, H. W., & van Hoeken, D. (2003). Review of the prevalence and
incidence of eating disorders. International Journal of Eating Disor-
ders, 34, 383–396.
Hudson, J. I., Hiripi, E., Harrison, G., & Kessler, R. (2005, September).
The epidemiology of eating disorders: Results from the National Co-
morbidity Survey Replication. Paper presented at the 11th Annual
Meeting of the Eating Disorders Research Society, Toronto, Ontario,
Hudson, J. I., Hiripi, E., Pope, H. G., Jr., & Kessler, R. C. (2007). The
prevalence and correlates of eating disorders in the National Comor-
bidity Survey Replication. Biological Psychiatry, 61, 348–358.
Hudson, J. I., Lalonde, J., Pindyck, L., Bulik, C., Crow, S., McElroy, S.,
et al. (in press). Familial aggregation of binge-eating disorder. Archives
of General Psychiatry.
Hudson, J. I., Pope, H. G., Jr., Jonas, J. M., & Yurgelun-Todd, D. (1983).
195April 2007 ● American Psychologist
Family history study of anorexia nervosa and bulimia. British Journal
of Psychiatry, 142, 133–138.
Hudson, J. I., Pope, H. G., Jr., Jonas, J. M., Yurgelun-Todd, D., &
Frankenburg, F. R. (1987). A controlled family history study of bu-
limia. Psychological Medicine, 17, 883–890.
Ioannidis, J., & Trikalinos, T. (2005). Early extreme contradictory esti-
mates may appear in published research: The Proteus phenomenon in
molecular genetics research and randomized trials. Journal of Clinical
Epidemiology, 58, 543–549.
Jacobi, C., Hayward, C., de Zwaan, M., Kraemer, H. C., & Agras, W. S.
(2004). Coming to terms with risk factors for eating disorders: Appli-
cation of risk terminology and suggestions for a general taxonomy.
Psychological Bulletin, 130, 19–65.
John, U., Meyer, C., Rumpf, H. J., & Hapke, U. (2006). Psychiatric
comorbidity including nicotine dependence among individuals with
eating disorder criteria in an adult general population sample. Psychi-
atry Research, 141, 71–79.
Johnson, F., & Wardle, J. (2005). Dietary restraint, body dissatisfaction,
and psychological distress: A prospective analysis. Journal of Abnor-
mal Psychology, 114, 119–125.
Katzman, M. A., Hermans, K. M., van Hoeken, D., & Hoek, H. W. (2004).
Not your “typical island woman”: Anorexia nervosa is reported only in
subcultures in Curac ¸ao. Culture Medicine and Psychiatry, 28, 463–492.
Kaye, W. H., Bailer, U. F., Frank, G. K., Wagner, A., & Henry, S. E.
(2005). Brain imaging of serotonin after recovery from anorexia and
bulimia nervosa. Physiology and Behavior, 86, 15–17.
Kaye, W. H., Frank, G. K., Bailer, U. F., Henry, S. E., Meltzer, C. C.,
Price, J. C., et al. (2005). Serotonin alterations in anorexia and bulimia
nervosa: New insights from imaging studies. Physiology and Behavior,
Kaye, W. H., Lilenfeld, L., Berretini, W., Strober, M., Devlin, B., Klump,
K., et al. (2000). A genome-wide search for susceptibility loci in
anorexia nervosa: Methods and sample description. Biological Psychi-
atry, 47, 794–803.
Kazdin, A. E., Kraemer, H. C., Kessler, R. C., Kupfer, D. J., & Offord,
D. R. (1997). Contributions of risk-factor research to developmental
psychopathology. Clinical Psychology Review, 17, 375–406.
Keel, P. K., & Klump, K. L. (2003). Are eating disorders culture-bound
syndromes? Implications for conceptualizing their etiology. Psycholog-
ical Bulletin, 129, 747–769.
Kendler, K. S., MacLean, C., Neale, M. C., Kessler, R. C., Heath, A. C.,
& Eaves, L. J. (1991). The genetic epidemiology of bulimia nervosa.
American Journal of Psychiatry, 148, 1627–1637.
Kendler, K. S., Neale, M. C., Kessler, R. C., Heath, A. C., & Eaves, L. J.
(1993). A test of the equal environment assumption in twin studies of
psychiatric illness. Behavior Genetics, 23, 21–27.
Kendler, K. S., Thornton, L. M., & Pedersen, N. L. (2000). Tobacco
consumption in Swedish twins reared apart and reared together. Ar-
chives of General Psychiatry, 57, 886–892.
Keski-Rahkonen, A., Bulik, C. M., Neale, B. M., Rose, R. J., Rissanen,
A., & Kaprio, J. (2005). Body dissatisfaction and drive for thinness in
young adult twins. International Journal of Eating Disorders, 37,
Kessler, R. C., Berglund, P., Chiu, W. T., Demler, O., Heeringa, S., Hiripi,
E., et al. (2004). The US National Comorbidity Survey Replication
(NCS-R): Design and field procedures. International Journal of Meth-
ods in Psychiatric Research, 13(2), 69–92.
Kessler, R. C., Chiu, W. T., Dernier, O., & Walters, E. E. (2005).
Prevalence, severity, and comorbidity of 12-month DSM-IV disorders
in the National Comorbidity Survey Replication. Archives of General
Psychiatry, 62, 617–627.
Kessler, R. C., Demler, O., Frank, R. G., Olfson, M., Pincus, H. A.,
Walters, E. E., et al. (2005). Prevalence and treatment of mental
disorders, 1990 to 2003. New England Journal of Medicine, 352,
Killen, J., Taylor, C., Hayward, C., Wilson, D., Haydel, K., Hammer, L.,
et al. (1994). Pursuit of thinness and onset of eating disorder symptoms
in a community sample of adolescent girls: A three-year prospective
analysis. International Journal of Eating Disorders, 16, 227–238.
Kinzl, J. F., Traweger, C., Trefalt, E., Mangweth, B., & Biebl, W. (1999).
Binge eating disorder in males: A population-based investigation. Eat-
ing and Weight Disorders, 4, 169–174.
Klump, K. L., & Gobrogge, K. L. (2005). A review and primer of
molecular genetic studies of anorexia nervosa. International Journal of
Eating Disorders, 37(Suppl.), S43–48.
Klump, K. L., Holly, A., Iacono, W. G., McGue, M., & Willson, L. E.
(2000). Physical similarity and twin resemblance for eating attitudes
and behaviors: A test of the equal environments assumption. Behavior
Genetics, 30, 51–58.
Klump, K. L., Miller, K. B., Keel, P. K., McGue, M., & Iacono, W. G.
(2001). Genetic and environmental influences on anorexia nervosa
syndromes in a population-based twin sample. Psychological Medicine,
Kortegaard, L. S., Hoerder, K., Joergensen, J., Gillberg, C., & Kyvik,
K. O. (2001). A preliminary population-based twin study of self-
reported eating disorder. Psychological Medicine, 31, 361–365.
Kotler, L. A., Cohen, P., Davies, M., Pine, D. S., & Walsh, B. T. (2001).
Longitudinal relationships between childhood, adolescent, and adult
eating disorders. Journal of the American Academy of Child & Ado-
lescent Psychiatry, 40, 1434–1440.
Krones, P. G., Stice, E., Batres, C., & Orjada, K. (2005). In vivo social
comparison to a thin-ideal peer promotes body dissatisfaction: A ran-
domized experiment. International Journal of Eating Disorders, 38,
Lase `gue, E.-C. (1873). On hysterical anorexia. Medical Times and Ga-
zette, 2, 265–266, 367–369.
Lee, S. (1995). Self-starvation in context: Towards a culturally sensitive
understanding of anorexia nervosa. Social Science and Medicine, 41,
Lee, Y., Abbott, D., Seim, H., Crosby, R., Monson, N., Burgard, M., &
Mitchell, J. E. (1999). Eating disorders and psychiatric disorders in the
first-degree relatives of obese probands with binge eating disorder and
obese non-binge eating disorder controls. International Journal of
Eating Disorders, 26, 322–332.
Lewinsohn, P. M., Hops, H., Roberts, R. E., Seeley, J. R., & Andrews,
J. A. (1993). Adolescent psychopathology: I. Prevalence and incidence
of depression and other DSM–III–R disorders in high school students.
Journal of Abnormal Psychiatry, 102, 133–144.
Lewinsohn, P. M., Seeley, J. R., Moerk, K. C., & Striegel-Moore, R. H.
(2002). Gender differences in eating disorder symptoms in young
adults. International Journal of Eating Disorders, 32, 426–440.
Lewinsohn, P. M., Striegel-Moore, R. H., & Seeley, J. R. (2000). Epide-
miology and natural course of eating disorders in young women from
adolescence to young adulthood. Journal of the American Academy of
Child & Adolescent Psychiatry, 39, 1284–1292.
Lilenfeld, L., Kaye, W., Greeno, C., Merikangas, K., Plotnikov, K.,
Pollice, C., et al. (1998). A controlled family study of restricting
anorexia and bulimia nervosa: Comorbidity in probands and disorders
in first-degree relatives. Archives of General Psychiatry, 55, 603–610.
Lindberg, L., & Hjern, A. (2003). Risk factors for anorexia nervosa: A
national cohort study. International Journal of Eating Disorders, 34,
List, J., & Habener, J. (2003). Defective melanocortin 4 receptors in
hyperphagia and morbid obesity. New England Journal of Medicine,
Maes, H., Neale, M., & Eaves, L. (1997). Genetic and environmental
factors in body mass index. Behavioral Genetics, 27, 325–351.
Makino, M., Tsuboi, K., & Dennerstein, L. (2004). Prevalence of eating
disorders: A comparison of Western and non-Western countries. Med-
scape General Medicine, 6(3), 49.
Martinez-Gonzalez, M. A., Gual, P., Lahortiga, F., Alonso, Y., de Irala-
Estevez, J., & Cervera, S. (2003). Parental factors, mass media influ-
ences, and the onset of eating disorders in a prospective population-
based cohort. Pediatrics, 111, 315–320.
Mathers, C. D., Vos, E. T., Stevenson, C. E., & Begg, S. J. (2000). The
Australian Burden of Disease Study: Measuring the loss of health from
diseases, injuries and risk factors. Medical Journal of Australia, 172,
Mazzeo, S., Slof-Op ‘t Landt, M., van Furth, E., & Bulik, C. (2006).
Genetics of eating disorders. In S. Wonderlich, J. Mitchell, M. de
196April 2007 ● American Psychologist
Zwaan, & H. Steiger (Eds.), Annual review of eating disorders 2006
(pp. 17–33). Oxon, England: Radcliffe.
McClelland, L., & Crisp, A. (2001). Anorexia nervosa and social class.
International Journal of Eating Disorders, 29, 150–156.
McKnight Investigators. (2003). Risk factors for the onset of eating
disorders in adolescent girls: Results of the McKnight longitudinal risk
factor study. American Journal of Psychiatry, 160, 248–254.
Millar, H. R., Wardell, F., Vyvyan, J. P., Naji, S. A., Prescott, G. J., &
Eagles, J. M. (2005). Anorexia nervosa mortality in Northeast Scotland,
1965–1999. American Journal of Psychiatry, 162, 753–757.
Moradi, B., Dirks, D., & Matteson, A. (2005). Roles of sexual objectifi-
cation experiences and internalization of standards of beauty in eating
disorder symptomatology: A test and extension of objectification the-
ory. Journal of Counseling Psychology, 52, 420–428.
Moya, T., Fleitlich-Bilyk, B., & Goodman, R. (2005). Brief report: Young
people at risk for eating disorders in Southeast Brazil. Journal of
Adolescence, 29, 313–317.
Neumark-Sztainer, D. (2005). Can we simultaneously work toward the
prevention of obesity and eating disorders in children and adolescents?
International Journal of Eating Disorders, 38, 220–227.
Ngai, E. S., Lee, S., & Lee, A. M. (2000). The variability of phenome-
nology in anorexia nervosa. Acta Psychiatrica Scandinavica, 102, 314–
Norre, J., Vandereycken, W., & Gordts, S. (2001). The management of
eating disorders in a fertility clinic: Clinical guidelines. Journal of
Psychosomatic Obstetrics and Gynecology, 22, 77–81.
Onishi, N. (2002, October 3). Globalization of beauty makes slimness
trendy. The New York Times, p. A4.
Orbach, S. (1986). Fat is a feminist issue. New York: Penguin.
Patton, G. C., Selzer, R., Coffey, C., Carlin, J. B., & Wolfe, R. (1999).
Onset of adolescent eating disorders: Population based cohort study
over 3 years. British Medical Journal, 318, 765–768.
Pearson, K. (1901). Mathematical contributions to the theory of evolution.
VIII.—On the correlation of characters not quantitatively measurable.
Proceedings of the Royal Society of London, 66, 241–244.
Perusse, L., Rankinen, T., Zuberi, A., Chagnon, Y. C., Weisnagel, S. J.,
Argyropoulos, G., et al. (2005). The human obesity gene map: The
2004 update. Obesity Research, 13, 381–490.
Polivy, J., & Herman, C. P. (1985). Dieting and binging: A causal
analysis. American Psychologist, 40, 193–201.
Prince, R. (1985). The concept of culture-bound syndromes: Anorexia
nervosa and brain-fag. Social Science and Medicine, 21, 197–203.
Reagan, P., & Hersch, J. (2005). Influence of race, gender, and socioeco-
nomic status on binge eating frequency in a population-based sample.
International Journal of Eating Disorders, 38, 252–256.
Reichborn-Kjennerud, T., Bulik, C., Kendler, K., Roysamb, E., Maes, H.,
Tambs, K., & Harris, J. (2003). Gender differences in binge-eating: A
population-based twin study. Acta Psychiatrica Scandinavica, 108,
Reichborn-Kjennerud, T., Bulik, C., Kendler, K., Roysamb, E., Tambs,
K., Torgersen, S., & Harris, J. (2004). Undue influence of weight on
self-evaluation: A population-based twin study of gender differences.
International Journal of Eating Disorders, 35, 123–132.
Rodin, J., Silberstein, L., & Striegel-Moore, R. (1985). Women and
weight: A normative discontent. In T. Sonderegger (Ed.), Psychology
and gender: Nebraska Symposium on Motivation (pp. 267–307). Lin-
coln: University of Nebraska Press.
Russell, G. F. M. (1979). Bulimia nervosa: An ominous variant of an-
orexia nervosa. Psychological Medicine, 9, 429–448.
Sasieni, P. D. (1997). From genotypes to genes: Doubling the sample size.
Biometrics, 53, 1253–1261.
Schaudinn, F., & Hoffman, E. (1905). Vorla ¨ufiger Bericht u ¨ber das
Vorkommen von Spirochaeten in syphilitschen Krankheitsprodukten
und bei Papillomen [English translation]. Berlin: Springer.
Sham, P. (1998). Statistics in human genetics. London: Arnold.
Silberstein, L. R., Mishkind, M. E., Striegel-Moore, R. H., Timko, C., &
Rodin, J. (1989). Men and their bodies: A comparison of homosexual
and heterosexual men. Psychosomatic Medicine, 51, 337–346.
Slof-Op ‘t Landt, M., van Furth, E., Meulenbelt, I., Slagboom, P., Bartels,
M., Boomsma, D., & Bulik, C. (2005). Eating disorders: From twin
studies to candidate genes and beyond. Twin Research and Human
Genetics, 16, 467–482.
Smith, D. E., Marcus, M. D., Lewis, C. E., Fitzgibbon, M., & Schreiner,
P. (1998). Prevalence of binge eating disorder, obesity, and depression
in a biracial cohort of young adults. Annals of Behavioral Medicine, 20,
Smolak, L., & Striegel-Moore, R. H. (2001). Challenging the myth of the
golden girl: Ethnicity and eating disorders. In R. H. Striegel-Moore &
L. Smolak (Eds.), Eating disorders: Innovative directions in research
and practice (pp. 111–132). Washington, DC: American Psychological
Sobal, J., & Stunkard, A. J. (1989). Socioeconomic status and obesity: A
review of the literature. Psychological Bulletin, 105, 260–275.
Soundy, T., Lucas, A., Suman, V., & Melton, L. (1995). Bulimia nervosa
in Rochester, Minnesota from 1980 to 1990. Psychological Medicine,
Steiger, H., Joober, R., Israe ¨l, M., Young, S., Ng Ying Kin, N., Gauvin,
L., et al. (2005). The 5HTTLPR polymorphism, psychopathological
symptoms, and platelet [3H-] paroxetine binding in bulimic syndromes.
International Journal of Eating Disorders, 37, 57–60.
Stice, E. (2002). Risk and maintenance factors for eating pathology: A
meta-analytic review. Psychological Bulletin, 128, 825–848.
Stice, E., Killen, J. D., Hayward, C., & Taylor, C. B. (1998). Support for
the continuity hypothesis of bulimic pathology. Journal of Consulting
and Clinical Psychology, 66, 784–790.
Stice, E., Maxfield, J., & Wells, T. (2003). Adverse effects of social
pressure to be thin on young women: An experimental investigation of
the effects of “fat talk.” International Journal of Eating Disorders, 34,
Stice, E., Presnell, K., & Spangler, D. (2002). Risk factors for binge eating
onset in adolescent girls: A 2-year prospective investigation. Health
Psychology, 21, 131–138.
Stice, E., & Shaw, H. (2002). Role of body dissatisfaction in the onset and
maintenance of eating pathology: A synthesis of research findings.
Journal of Psychosomatic Research, 53, 985–993.
Stice, E., & Shaw, H. (2004). Eating disorder prevention programs: A
meta-analytic review. Psychological Bulletin, 130, 206–227.
Stice, E., Spangler, D., & Agras, W. S. (2001). Exposure to media-
portrayed thin-ideal images adversely affect longitudinal experiment.
Journal of Social and Clinical Psychology, 20, 270–288.
Stice, E., Trost, A., & Chase, A. (2003). Healthy weight control and
dissonance-based eating disorder prevention programs: Results from a
controlled trial. International Journal of Eating Disorders, 33, 10–21.
Striegel-Moore, R. H., & Cachelin, F. M. (2001). Etiology of eating
disorders in women. Counseling Psychologist, 29, 635–661.
Striegel-Moore, R. H., Dohm, F., Kraemer, H., Taylor, C., Daniels, S.,
Crawford, P., & Schreiber, G. (2003). Eating disorders in White and
Black women. American Journal of Psychiatry, 160, 1326–1331.
Striegel-Moore, R. H., Franko, D. L., Thompson, D., Barton, B., Schrei-
ber, G. B., & Daniels, S. R. (2004). Changes in weight and body image
over time in women with eating disorders. International Journal of
Eating Disorders, 36, 315–327.
Striegel-Moore, R. H., Franko, D. L., Thompson, D., Barton, B., Schrei-
ber, G. B., & Daniels, S. R. (2005). An empirical study of the typology
of bulimia nervosa and its spectrum variants. Psychological Medicine,
Striegel-Moore, R. H., Silberstein, L., & Rodin, J. (1986). Toward an
understanding of risk factors for bulimia. American Psychologist, 41,
Striegel-Moore, R. H., Wilfley, D. E., Pike, K. M., Dohm, F. A., &
Fairburn, C. G. (2000). Recurrent binge eating in Black American
women. Archives of Family Medicine, 9, 83–87.
Strober, M., Freeman, R., Lampert, C., Diamond, J., & Kaye, W. (2000).
Controlled family study of anorexia nervosa and bulimia nervosa:
Evidence of shared liability and transmission of partial syndromes.
American Journal of Psychiatry, 157, 393–401.
Strober, M., Freeman, R., Lampert, C., Diamond, J., & Kaye, W. (2001).
Males with anorexia nervosa: A controlled study of eating disorders in
first-degree relatives. International Journal of Eating Disorders, 29,
197April 2007 ● American Psychologist
Sullivan, P. F. (1995). Mortality in anorexia nervosa. American Journal of Download full-text
Psychiatry, 152, 1073–1074.
Sullivan, P. F., Bulik, C. M., Fear, J. L., & Pickering, A. (1998). Outcome
of anorexia nervosa: A case-control study. American Journal of Psy-
chiatry, 155, 939–946.
Sullivan, P. F., Bulik, C. M., & Kendler, K. S. (1998). The genetic
epidemiology of binging and vomiting. British Journal of Psychiatry,
Swartz, L. (1985). Anorexia nervosa as a culture-bound syndrome. Social
Science and Medicine, 20, 725–730.
Tozzi, F., Thornton, L., Klump, K., Fichter, M., Halmi, K., Kaplan, A., et
al. (2005). Symptom fluctuation in eating disorders: Correlates of
diagnostic crossover. American Journal of Psychiatry, 162, 732–740.
Treasure, J., Schmidt, U., Troop, N., Tiller, J., Todd, G., & Turnbull, S.
(1996). Sequential treatment for bulimia nervosa incorporating a self-
care manual. British Journal of Psychiatry, 168, 94–98.
Tyre, P. (2005, December 5). Fighting anorexia: No one to blame. News-
week, 146, 50–59.
Wade, T., Bulik, C. M., Neale, M., & Kendler, K. S. (2000). Anorexia
nervosa and major depression: Shared genetic and environmental risk
factors. American Journal of Psychiatry, 157, 469–471.
Wade, T., Martin, N., & Tiggemann, M. (1998). Genetic and environ-
mental risk factors for the weight and shape concerns characteristic of
bulimia nervosa. Psychological Medicine, 28, 761–771.
Walters, E. E., & Kendler, K. S. (1995). Anorexia nervosa and anorexic-
like syndromes in a population-based female twin sample. American
Journal of Psychiatry, 152, 64–71.
Walters, E. E., Neale, M. C., Eaves, L. J., Heath, A. C., Kessler, R. C., &
Kendler, K. S. (1992). Bulimia nervosa and major depression: A study
of common genetic and environmental factors. Psychological Medicine,
Walters, E. E., Neale, M. C., Eaves, L. J., Heath, A. C., Kessler, R. C., &
Kendler, K. S. (1993). Bulimia nervosa: A population-based study of
purgers versus nonpurgers. International Journal of Eating Disorders,
Ward, A., Ramsay, R., & Treasure, J. (2000). Attachment research in
eating disorders. British Journal of Medical Psychology, 73, 35–51.
Wilfley, D. E., Pike, K. M., Dohm, F. A., Striegel-Moore, R. H., &
Fairburn, C. G. (2001). Bias in binge eating disorder: How represen-
tative are recruited clinic samples? Journal of Consulting and Clinical
Psychology, 69, 383–388.
Wiseman, C. V., Gray, J. J., Mosimann, J. E., & Ahrens, A. H. (1992).
Cultural expectations of thinness in women: An update. International
Journal of Eating Disorders, 11, 85–89.
Wittchen, H. U., & Jacobi, F. (2005). Size and burden of mental disorders
in Europe–A critical review and appraisal of 27 studies. European
Neuropsychopharmacology, 15, 357–376.
Wittchen, H. U., Nelson, C. B., & Lachner, G. (1998). Prevalence of
mental disorders and psychosocial impairments in adolescents and
young adults. Psychological Medicine, 28, 109–126.
Wonderlich, S. A., Lilenfeld, L. R., Riso, L. P., Engel, S., & Mitchell, J. E.
(2005). Personality and anorexia nervosa. International Journal of
Eating Disorders, 37(Suppl.), S68–S71.
Woodside, D. B., Garfinkel, P. E., Lin, E., Goering, P., Kaplan, A. S.,
Goldbloom, D. S., & Kennedy, S. H. (2001). Comparisons of men with
full or partial eating disorders, men without eating disorders, and
women with eating disorders in the community. American Journal of
Psychiatry, 158, 570–574.
World Health Organization. (1992). The ICD-10 classification of mental
and behavioral disorders: Clinical descriptions and diagnostic guide-
lines. Geneva, Switzerland: World Health Organization.
Zipfel, S., Lowe, B., Reas, D. L., Deter, H. C., & Herzog, W. (2000).
Long-term prognosis in anorexia nervosa: Lessons from a 21-year
follow-up study. Lancet, 355, 721–722.
198 April 2007 ● American Psychologist