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Coming to Terms With Risk Factors for Eating Disorders: Application of Risk
Terminology and Suggestions for a General Taxonomy

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2004, Vol. 130, No. 1, 19 – 65 0033-2909/04/$12.00 DOI: 10.1037/0033-2909.130.1.19

Coming to Terms With Risk Factors for Eating Disorders: Application of

Risk Terminology and Suggestions for a General Taxonomy

Corinna Jacobi Chris Hayward

University of Trier Stanford University

Martina de Zwaan Helena C. Kraemer and W. Stewart Agras

University of Vienna Stanford University

The aims of the present review are to apply a recent risk factor approach (H. C. Kraemer et al., 1997)
to putative risk factors for eating disorders, to order these along a timeline, and to deduce general
taxonomic questions. Putative risk factors were classified according to risk factor type, outcome
(anorexia nervosa, bulimia nervosa, binge-eating disorder, full vs. partial syndromes), and additional
factor characteristics (specificity, potency, need for replication). Few of the putative risk factors were
reported to precede the onset of the disorder. Many factors were general risk factors; only few
differentiated between the 3 eating disorder syndromes. Common risk factors from longitudinal and
cross-sectional studies were gender, ethnicity, early childhood eating and gastrointestinal problems,
elevated weight and shape concerns, negative self-evaluation, sexual abuse and other adverse experi-
ences, and general psychiatric morbidity. Suggestions are made for the conceptualization of future risk
factor studies.

Although the field of risk factor research in psychology has
grown rapidly during the past 15 years and the term risk factor has
been much used, precise definitions for risk factor terminology
have only recently been proposed (Kazdin, Kraemer, Kessler,
Kupfer, & Offord, 1997; Kraemer et al., 1997). In the scientific
literature, the terms used for the same potential risk factors still
vary from terms such as vulnerability factor, predisposing factor,
preceding factor, diathesis, causal factor, or etiology factor and
have been used interchangeably with the term risk factor.
Specifically, more than 30 variables have been reported as
putative risk factors for the development of an eating disorder (for
a list of factors, see Appendix A, not to be considered a definitive
compilation). Among these variables, risk has been assessed from
different perspectives: reported risk factors include social factors,
familial, psychological, developmental, and biological factors. Be-
cause for many of these factors (e.g., depression, low self-esteem,
altered serotonin levels) it is unclear whether they precede the
Corinna Jacobi, Department of Psychology, University of Trier, Ger-
many; Chris Hayward, Helena C. Kraemer, and W. Stewart Agras, De-
partment of Psychiatry and Behavioral Sciences, Stanford University;
Martina de Zwaan, Department of Psychology, University of Vienna,
Vienna, Austria.
Martina de Zwaan is now at the Department of Psychosomatic Medicine
and Psychotherapy, Friedrich Alexander University of Erlangen-
Nuremberg, Erlangen, Germany.
This research was supported by German Research Foundation Grant JA
635/2-1 to Corinna Jacobi. We would like to thank Lisette Morris for
careful editing and proofreading of an early version of the article and
Melanie Kupsch for assistance in preparation of figures and tables.
Correspondence concerning this article should be addressed to Corinna
Jacobi, Department of Psychology, University of Trier, 54286 Trier, Ger-
many. E-mail: jacobi@uni-trier.de
19
onset of the eating disorder, it is impossible to determine whether
they are symptoms of the disorder, maintaining factors, or conse-
quences or “scars” of the disorder.
The inconsistent use of the term risk factor as well as the lack
of precise definitions led Kraemer and colleagues in two recent
articles to set out a conceptual basis for a typology of risk factors
(Kazdin et al., 1997; Kraemer et al., 1997). To our knowledge, the
proposed definitions and classification of risk factors have not yet
been applied to the putative risk factors for a specific disorder. Yet,
the application of this theoretical risk framework may have im-
portant implications for future risk research for specific disorders
(Jacobi & de Zwaan, 1998). Such an application may also help to
develop more general guidelines to classify putative risk factors
across a range of different disorders.
In the past, risk and etiological factors for psychiatric disorders
have either been proposed from one specific theoretical perspec-
tive (e.g., biological, cognitive– behavioral, psychodynamic) or
from an integrative perspective (e.g., biopsychosocial model). In
both cases, the underlying theoretical model leads to a (smaller or
wider) range of factors considered to be important for the devel-
opment of a disorder. Factors in these models can be based on both
clinical experience and empirical data, but the empirical founda-
tion can vary from very strong to very weak and can comprise a
wide range of methods and definitions for risk and etiological
factors. In contrast, the risk factor approach applied here for eating
disorders is primarily descriptive and data oriented and should be
regarded as a precursor to a more complex model. Its atheoretical
nature allows for the inclusion of putative risk factors from a
variety of theoretical perspectives, while relying on consistent
definitions, but refraining from making “dynamic” assumptions
about the interactions of factors. Furthermore, this approach does
not address the proximity of factors to the outcome (e.g., predis-
20 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
posing vs. precipitating, distal vs. proximal factors) often covered
by previous models but delegates it to the next step provided the
status of a factor as a risk factor has been established.
Therefore, the aims of the present review are to clarify some of
the inconsistencies in the field by (a) stringently applying the risk
factor approach outlined by Kraemer et al. (1997) to a specific
psychiatric disorder, thereby establishing the status of each of the
reported putative risk factors for eating disorders (anorexia ner-
vosa, bulimia nervosa, and binge-eating disorder) as a correlate or
noncorrelate, a fixed or variable marker, a variable risk factor, or
a causal risk factor; (b) comparing risk factors derived from
longitudinal research with factors from cross-sectional research
and ordering them along a timeline according to their chronolog-
ical emergence; and (c) placing the specific findings regarding the
classification of risk factors for eating disorders within a broader
context by deducing general taxonomic questions for the classifi-
cation of risk factors for psychiatric disorders in general.
Summary of Risk Factor Terminology
In the conceptual articles previously noted (Kazdin et al., 1997;
Kraemer et al., 1997), a risk factor is considered to be a measurable
characteristic of each subject in a specified population which
precedes the outcome of interest and which can be shown to divide
the population into two groups: a high- and a low-risk group. The
probability of the outcome in the high-risk group must be shown to
be greater than in the low-risk group. Beyond a statistically sig-
nificant association between risk factor and outcome, the clinical
significance of a risk factor should be indicated by the magnitude
of the association, called the potency of the factor.
If in the defined population, an association between a potential
risk factor and the outcome can be shown, the factor is called a
correlate (see Table 1 for a summary of the definitions and
identification methods). Any characterization measured concomi-
tantly with or after the outcome may potentially be a concomitant
or consequence of the outcome (i.e., a symptom or a scar). Only if
a correlate can be demonstrated to precede the outcome, is the term
risk factor justified. To establish a factor’s status as a risk factor,
Table 1
Risk Factor Typology and Identification Methods
Term Definition
Noncorrelate No significant association between
factor and outcome (onset)
Correlate Statistically significant association
between factor and outcome
Risk factor Significant statistical and clinical
association between factor and
outcome; precedence
Fixed marker Risk factor that cannot be changed or
change spontaneously
Variable risk factor Risk factor that can be changed or can
change spontaneously
Variable marker Variable risk factor, manipulation does
not change the risk of outcome
Causal risk factor Variable risk factor, manipulation
changes the risk of outcome
precedence is a crucial criterion. A risk factor that can be shown to
change spontaneously within a subject (e.g., age, weight) or to be
changed by an intervention (e.g., medication or psychotherapy) is
called a variable risk factor. A risk factor that cannot be demon-
strated to change or be changed (e.g., race, gender, year of birth)
is called a fixed marker. A variable risk factor for which it can be
shown that manipulation changes the risk of the outcome (e.g.,
onset of disorder) is called a causal risk factor. If that cannot be
shown, it is called a variable marker.
The label that is used for a given factor always reflects the
current state of scientific knowledge about the factor. Thus, a
factor can change its status during its scientific life. In addition, the
status of some factors (e.g., pubertal timing, specific biological or
endocrine parameters) may also change depending on the period of
assessment. A factor may be variable prior to a certain event (e.g.,
developmental phase, infection) and therefore be classified as a
variable risk factor or marker but become immutable after the
event and consequently be classified as a fixed marker.
Study Designs for the Identification of Risk Factors
We suggest dividing study designs that have been applied for
the identification of potential risk factors into two main categories:
preliminary risk studies and definitive risk studies.
The first category of preliminary risk studies comprises cross-
sectional studies, which—with few exceptions— only permit one
to assess correlates (Kazdin, 1998; Kazdin et al., 1997). They
constitute, however, an important and necessary first step before
testing specific risk (or causal) factors in subsequent longitudinal
studies (Kazdin, 1998; Rutter, 1994). Cross-sectional risk studies
can be subdivided into (a) population-based epidemiological stud-
ies, (b) cross-sectional and retrospective case-control studies, and
(c) family or family history studies. These studies usually compare
certain characteristics of the affected (or patient) group with an
unaffected control group, but the majority do not allow conclu-
sions about the sequence of the assessed characteristics and onset
of the disorder to be drawn. Precedence, however, is given when
fixed markers such as race, gender, or certain birth characteristics
Study design
Cross-sectional and longitudinal studies
Cross-sectional studies: epidemiological
studies, case-control studies, family or
family history studies
Longitudinal studies
Cross-sectional studies using data from
medical records or birth registers,
longitudinal studies (including twin and
genetic studies)
Longitudinal studies
Randomized clinical trial (preventive or
therapeutic intervention study)
Randomized clinical trial (preventive or
therapeutic intervention study)
 RISK FACTORS FOR EATING DISORDERS
(e.g., birth complications, preterm birth) are assessed within
population-based epidemiological or other cross-sectional risk
studies.
In cross-sectional case-control studies, subjects are selected and
assessed in relation to factors that are currently associated with a
particular characteristic. Because all measures are obtained at the
same point in time, these studies are useful for identifying asso-
ciated features or correlates. Retrospective case-control studies
compare subjects with a specific disorder to healthy control sub-
jects with respect to past exposure to certain potential risk factors,
which are retrospectively assessed. In family history or family
studies, rates of disorders in the families (usually in first-degree
relatives) of the affected group are (directly or indirectly) assessed
and compared with rates in the families of a nonaffected group.
The assessment of the familial disorders is again retrospective.
Retrospective assessment of risk factor information is problem-
atic because the information may be biased by retrospective recall
or the subject’s inaccurate memory. Therefore, Kraemer et al.
(1997) and Kazdin et al. (1997) strongly recommended establish-
ing the risk factor status within a prospective, longitudinal design.
If risk factors are assessed retrospectively, they should be assessed
before the outcome—for example, at the onset of a disorder—to
avoid further biasing the recall by possible reinterpretation in light
of the subject having the disorder. Thus, the only risk factors that
can be identified in cross-sectional studies are fixed markers and
factors from medical records or birth registers recorded before the
onset of the disorder (Table 1). However, because of the enormous
time and cost requirements associated with longitudinal studies,
the majority of putative risk factors are in fact assessed within
cross-sectional designs comparing affected versus nonaffected
subjects.
For the purpose of the present review we decided—instead of
categorizing the whole body of putative risk factors from cross-
sectional research as correlates—to differentiate between those
cross-sectional studies that assessed putative risk factors retrospec-
tively and those that did not. Although it seems plausible that
retrospective risk factor assessment of fixed markers and medical
record information (e.g., birth weight) is more valid than that of
other retrospectively assessed factors (e.g., self-esteem, family
functioning), no systematic comparisons of the respective biases
have been carried out so far. However, it is probable that the
reliability and likelihood of measurement error are far lower in, for
example, birth weight records, as compared with retrospective
self-reports about historical dieting behavior. The latter category of
retrospectively assessed factors, which predated the onset of the
disorder according to the subjects’ self-report, are summarized
within a separate category of “retrospective correlates”.1 This
procedure at least allowed us to compare these results with the
results of studies with the most stringent application of risk factor
terminology (reliance on prospectively assessed factors only).
The second category of study designs for the identification of
risk factors are definitive risk studies. These comprise (a) the
identification of genes or genetic markers and (b) longitudinal
studies.
The interest in trying to identify genes or genetic markers for
psychiatric disorders has increased considerably over the past
decade. Of the different types of genetic studies, single gene or
candidate gene studies are the only ones allowing definitive risk
factor identification. At present, there is agreement that the ma-
21
jority of psychiatric disorders are not likely to be conceivable as
single gene conditions, and specific candidate genes for specific
psychiatric disorders have as yet not been replicated (Plomin &
Rutter, 1998; Rende, 1996; Rutter et al., 1997).
The first step in identifying definitive risk factors, according to
hypotheses from preliminary studies, should be an exploratory
longitudinal study. On the basis of hypotheses from exploratory
longitudinal studies and from cross-sectional research, factors
should then be included for a stronger test within a confirmatory
longitudinal study. An example of this type of study would be the
prospective comparison of the natural course of a previously
identified “high-risk” group (subjects affected with the risk factor)
and a “low-risk” group (nonaffected subjects) to determine which
risk factors are risk factors for the full disorder and which are risk
factors for initial symptoms or precursors of the disorder. Risk
factors that turn out to predict the full disorder should finally be
tested within randomized controlled trials to establish their status
as causal factors (Kraemer et al., 1997).
Method
Identification of Studies
Empirical studies of potential risk factors reputed to correlate with the
onset (see below) of eating disorders were identified as follows. First,
literature searches of MEDLINE and PsycLIT identified studies published
through April 2002. Index terms used in a Boolean search together with the
words eating disorders were risk factors, prospective studies, longitudinal
studies, and etiology. As previous reviews suggested that only few factors
are able to discriminate between anorexia nervosa and bulimia nervosa (Z.
Cooper, 1995; Striegel-Moore, 1997) and risk factor research for the
proposed criteria for binge-eating disorder is still at its beginning, we
deliberately chose broad index terms (i.e., eating disorders) for the liter-
ature search. Second, in addition to abstracts found this way, related
articles were checked for potential factors. Third, reference lists from
identified studies as well as recent reviews on eating disorders were
searched to identify additional factors and studies. Fourth, for factors that
had been identified in cross-sectional studies, search strategies were re-
peated for the identified factor, this time in conjunction with each of the
individual diagnostic categories for eating disorders as search terms (e.g.,
sexual abuse AND anorexia nervosa, sexual abuse AND bulimia nervosa,
sexual abuse AND binge-eating disorder; self-esteem AND anorexia ner-
vosa, self-esteem AND bulimia nervosa, self-esteem AND binge-eating
disorder). On the basis of these search criteria a total of about 5,000
abstracts on potential psychosocial and biological risk factors were
screened for inclusion by two of the authors (psychosocial factors by
Corinna Jacobi, biological factors by Martina de Zwaan). About 320
studies and reviews were finally included.
Inclusion and Exclusion Criteria for Studies
The present review focuses on psychosocial and biological risk factors
for the onset of the disorder. Studies dealing with factors for remission or
relapse were therefore not included. For the majority of factors examined,
only studies with a control group (e.g., healthy nonclinical control group)
were included in the review; studies comparing different eating disorder
1
Factors that have been assessed retrospectively but recorded before the
onset of a disorder (e.g., birth trauma) are considered to fulfill precedence
and are classified as (prospective) risk factors. These are often assessed as
part of longitudinal study together with some concurrently assessed factors
and followed further on.
22 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
groups alone were excluded. To establish specificity, an additional clinical
group was required. Sample size of studies had to contain a minimum of 10
subjects per cell, both for the measurement of the predictors and the
outcome variables (“case” or “risk group”), to be included; case reports
were excluded. The follow-up interval for longitudinal studies had to be at
least 1 year to allow enough time for (full or partial) syndromes of eating
disorders to emerge. If both univariate and multivariate analyses were
carried out in the original studies with the same predictors, results of both
analyses are reported separately, and the significance level for the univar-
iate differences was set at p ⱕ .05. This bears a risk of including false
positive results because of multiple testing, collinearity of the predictors, or
both. On the other hand, the studies often differ in the extent to which they
adjust significance levels and usually do not give information on the
intercorrelations of predictors. We therefore felt the basis for an exclusion
of individual studies at present too vague. In longitudinal studies, ques-
tionnaires (e.g., Eating Attitudes Test; EAT-26; Garner, Olmsted, Bohr, &
Garfinkel, 1982) were only accepted for outcome assessment if sufficient
sensitivity and specificity for diagnostic (or eating disorder syndrome)
assessment had been established beforehand (see Jacobi, Abascal, & Tay-
lor, in press). Longitudinal studies addressing (dimensional) eating distur-
bances or eating disorder symptoms using questionnaires (e.g., Eating
Disorders Inventory; EDI, Body Shape Questionnaire; BSQ) or selected
subscales (e.g., EDI subscales) were not included. In cross-sectional stud-
ies, outcome was restricted to full Diagnostic and Statistical Manual of
Mental Disorders (DSM; 3rd ed.; DSM–III; American Psychiatric Associ-
ation, 1980; 3rd ed., rev.; DSM–III–R; American Psychiatric Association,
1987; 4th ed.; DSM–IV; American Psychiatric Association, 1994) syn-
dromes of eating disorders. Longitudinal studies that did not control for full
or partial eating disorder syndromes or “caseness” were not included.
Finally, if any further specific exclusion criteria had to be imposed, they
are reported at the beginning of the respective Results subsections.
Because of the extremely large number of studies that had to be screened
initially, only longitudinal studies were reviewed separately for inclusion/
exclusion criteria by Corinna Jacobi and Chris Hayward for the purpose of
consensus. In two cases, in which initial eating disorder symptomatology
had not been controlled for or had not been reported, there was disagree-
ment on inclusion. Though it was finally decided to include the studies,
when reporting the results, this is considered a limitation. In two other
studies, in which the number of new cases at Time 2 was not clearly
reported, one of us had reservations about the study inclusion. This was
finally resolved by a consensus decision.
Classification of Risk Factors Included
Factors from the studies meeting the above-mentioned criteria were
classified according to three levels: risk factor type, outcome status, and
additional risk factor characteristics (specificity, potency, need for
replication).
Factors were first classified according to the Kraemer et al. (1997)
typology as outlined above. To establish a factor’s status as a risk factor (or
retrospective correlate), a statistically significant association between fac-
tor and outcome had to be demonstrated in at least half of the studies
without limitations. Factors were also classified with regard to outcome
status; that is, they were categorized according to whether they were
associated with or predicted (a) the full syndrome of anorexia nervosa,
bulimia nervosa, or binge-eating disorder or (b) partial syndromes or
symptoms of one of the diagnostic categories, otherwise defined as case-
ness or mixed outcomes of syndromes and symptoms. A third level of
classification was finally applied to establish additional risk factor charac-
teristics (specificity, potency, need for replication).
We classified a factor as a specific risk factor for one of the three
diagnostic categories of eating disorders if it predicted the outcome only
for this group but not for the comparison (clinical) group. When no
differences between clinical groups (eating disorders and psychiatric dis-
orders) could be found but both groups differed in comparison to the
healthy control group, we classified these factors as general risk factors. If
the question of specificity had not been addressed in the study, factors were
classified as “specificity not tested.” Specificity was not addressed for
factors that had been classified as correlates.
To assess the potency of a risk factor, we calculated and presented
indicators of the magnitude of the difference between the high- and
low-risk groups, provided a significant relationship between risk factor and
outcome had been established. As Kraemer et al. (1999) pointed out in a
recent article, no universal measure of potency is interpretable and mean-
ingful for every clinical and policy decision. Not only are different mea-
sures of association between risk factor and outcome preferred in different
fields of research, but potency measures available for ordinal risk factors
(e.g., Cohen’s, 1988, delta) are different and not necessarily comparable to
measures available for binary risk factors (weighted kappa coefficient,
odds ratio [OR], risk ratio [RR], phi coefficient). Some measures range
between ⫺1 and 1, some between 0 and 1, some from 0 to infinity.
Although rescaling can—at least for some of the measures—solve this
problem, the remaining measures do not necessarily lead to the same
conclusions.
The area under the curve (AUC) statistic estimates the probability that a
person with eating disorders will have a higher value on an ordinal risk
factor or be more likely to have a binary risk factor than a person without
eating disorders (ties randomly allocated; e.g., McGraw, & Wong, 1992).
Where Cohen’s delta (effect size; ES) is used, AUC ⫽ ⌽(ES/公2), where
⌽(ES/公2) is the cumulative standard normal distribution. Where P1 and
P0 are the proportion of subjects with the binary risk factor in the high- and
low-risk subgroups, AUC ⫽ .5 (P1 ⫺ P0 ⫹ 1). The standards used to
categorize the AUC reflect Cohen’s standards for ES. Thus, AUC ⬍ 55.6%
is very low (ES ⬍ 0.2), 55.6% ⱕ AUC ⬍ 63.8% is low (0.2 ⬍ ES ⬍ 0.5);
63.8% ⱕ AUC ⬍ 71.4% (0.5 ⬍ ES ⬍ 0.8) is medium, and AUC ⱖ 71.8%
(ES ⬎ 0.8) is large. Use of the AUC fosters comparability of potency
measures for ordinal and binary outcomes.
Where it was not possible to compute AUC (e.g., when only ORs,
standardized or unstandardized beta weights, or correlations were pre-
sented), we reported these values. However, these could not be categorized
because no standards comparable to the ones above have been established.
No potency information is presented for factors classified as correlates.
Regardless of the potency measure, it must be remembered that potency
varies from one clinical population to another. In particular, for populations
in which the prevalence of the disorder or of the risk factor is very low (in
general, very homogeneous populations), AUC will tend to be low,
whereas ORs and RRs may be very inflated. For this reason, we chose,
whenever possible, to report (or calculate from available data) the preva-
lence (percentage) of subjects affected with the factor in the high-risk
group (e.g., anorexia nervosa group) versus the prevalence affected with
the factor in the low-risk (control) group, as well as measures of potency.
For several reasons, we decided not to assess the potency of the risk
factors using a meta-analysis but to describe it qualitatively: First of all, as
we point out in the Results section, different outcome measures have been
used in longitudinal and cross-sectional studies. In addition, outcome
measures for the assessment of risk also vary within longitudinal studies.
Secondly, the number and assessment of predictors varies widely within
longitudinal and cross-sectional studies. Finally, because of variation and
inconsistency in the reported raw data, only a minority of longitudinal and
cross-sectional studies would have allowed the calculation of the same
effect size measure (e.g., Cohen’s delta) for comparisons across studies.
In addition to specificity and potency, we address whether a factor is in
need of replication, that is, has been confirmed as a risk factor in one study
only, or when results yielded in several studies were inconsistent with only
one more study, confirming rather than rejecting risk factor status.
 RISK FACTORS FOR EATING DISORDERS
Results of Risk Factor Classification From Cross-
Sectional and Longitudinal Studies
Psychosocial Factors
In the beginning of the article we pointed to limitations of
cross-sectional studies for risk factor assessment and suggested
that longitudinal risk studies represent the “gold standard” for the
identification of risk factors. Before we report the classification
results from both types of studies, we want to summarize the main
characteristics of longitudinal studies (see Table 2), as these will
affect the evaluation of the factor classification.
The results of risk factor classification from longitudinal studies
are presented in Table 3. Results of fixed and variable markers,
retrospective correlates, and correlates from cross-sectional studies
are presented in Tables 4 – 6, for the DSM syndromes anorexia
nervosa, bulimia nervosa, and binge-eating disorder, respectively.2
For both study types, risk factor classification is presented together
with potency and specificity information. Because of the large
number of cross-sectional studies, we present only a few examples
of studies for correlates in Tables 4 – 6. However, studies identi-
fying retrospective correlates are listed entirely in Tables 4 – 6,
together with the respective potency and specificity information.
Of the about 320 studies and reviews included, 103 cross-sectional
studies identifying fixed and variable markers and retrospective
correlates served as a basis for the classification of these factors
(psychosocial and biological factors).
Description of Longitudinal Studies
Twenty-eight longitudinal studies were found. For classification
of risk factors, 10 of these were excluded because of too few cases,
insufficient information on risk factors and reported methodology,
or too broad outcome measures (Gardner, Stark, Friedman, &
Jackson, 2000; Jacobi, Agras, & Hammer, 2001; King, 1989;
Martin et al., 2000; Rathner & Messner, 1993; Santonastaso,
Friederici, & Favaro, 1999; Schleimer, 1983; Stice, Agras, &
Hammer, 1999; Vohs, Heatherton, & Herrin, 2001; Wlodarczyk-
Bisaga & Dolan, 1996). An additional 3 studies were excluded
because the follow-up interval was shorter than 1 year (Leung &
Steiger, 1991; Rosen, Compas, & Tracy, 1993; Stice, 1998).
Although the sample sizes in the majority of longitudinal studies
are relatively large, the majority of the studies have only been able
to identify risk factors for a mixture of full DSM syndromes of
anorexia nervosa and bulimia nervosa as well as partial syndromes
or eating disorders not otherwise specified (EDNOS; Ghaderi &
Scott, 2001; J. G. Johnson, Cohen, Kasen, & Brook, 2002; Killen
et al., 1994, 1996; Kotler, Cohen, Davies, Pine, & Walsh, 2001;
Marchi & Cohen, 1990; Patton, Johnson-Sabine, Wood, Mann, &
Wakeling, 1990; Patton, Selzer, Coffey, Carlin, & Wolfe, 1999;
Vollrath, Koch, & Angst, 1992). In six studies, the outcome
samples were high-risk samples, mostly defined as scoring above
the EAT-26 cutoff (Attie & Brooks-Gunn, 1989; Button, Sonuga-
Barke, Davies, & Thompson, 1996; Calam & Waller, 1998; Gra-
ber, Brooks-Gunn, Paikoff, & Warren, 1994; Leon, Fulkerson,
Perry, & Early-Zald, 1995; Leon, Fulkerson, Perry, Keel, &
Klump, 1999). Given the low prevalence rates for anorexia and
bulimia nervosa (e.g., Fairburn & Beglin, 1990; Fombonne, 1995),
a sample size of at least 3,000 subjects would probably have been
23
necessary for detection of a larger number of (DSM) cases within
a community-based study.
Table 2 summarizes the main characteristics of the 15 longitu-
dinal studies included. The primary aims of these studies vary from
explicitly identifying risk factors (e.g., Killen et al., 1996; Leon et
al., 1995) to addressing broader epidemiological questions (e.g.,
Vollrath et al., 1992). Accordingly, the number and broadness of
potential risk factors varies significantly. Twelve studies include
broader independent variables, such as personality or temperamen-
tal factors, family relationships, general psychopathological dis-
turbances, or self-esteem, in addition to weight- and eating-related
variables. In 2 studies, measures based on maternal report were
also included as possible risk factors.
Samples in the studies consist mostly of adolescents between 12
and 15 years old; three studies assessed infants or younger children
(J. G. Johnson et al., 2002; Kotler et al., 2001; Marchi & Cohen,
1990), and two studies assessed young adults (Ghaderi & Scott,
2001; Vollrath et al., 1992). In eight studies the samples included
females only; in seven studies the samples consisted of both males
and females. The duration of follow-ups varied from 1 to 18 years.
Risk status or definition of caseness (symptomatic, asymptom-
atic; cases, noncases; high, moderate, low risk) is defined differ-
ently in the studies: seven studies assessed eating disorder symp-
toms and syndromes with structured diagnostic interviews, eight
studies relied solely on questionnaire cutoffs or score combina-
tions. In addition, the majority of studies excluded subjects with or
controlled for any initial eating disorders or risk status at Time 2
in the longitudinal analyses. Two studies did not control for outcome
status (EAT-26 scores) at Time 1 (Button et al., 1996; Calam &
Waller, 1998), and in one further study the procedure was not made
clear (Vollrath et al., 1992). Two of the child studies (Kotler et al.,
2001; Marchi & Cohen, 1990) explicitly analyzed the relationship
between early childhood eating problems (e.g., eating conflicts, picky
eating, pica) and eating disorders in adolescence. Finally, Graber et al.
(1994) divided their total sample into four groups, two of which
already had an EAT-26 score above the cutoff at Time 1. One of these
two groups remained stable above the cutoff until Time 2 (chronic
group), the other group dropped below the cutoff at Time 2 (early-
transient risk group). We therefore did not include the results of these
two groups but restrict the reported results to the comparison between
the low-risk group (subjects below the cutoff at both times) and the
late-transient group (subjects below the cutoff at Time 1 but above it
at Time 2 or Time 3).
As expected, a wide range of different indicators of potency for
risk factors was found in longitudinal studies, depending on the
methodology used to discriminate between high- and low-risk
groups in the respective studies. The statistical analyses comprise
simple correlation coefficients of a set of Time 1 predictors and
Time 2 outcome variables (Calam & Waller, 1998), multivariate
procedures such as multiple regression analyses (Attie & Brooks-
Gunn, 1989; Button et al., 1996; Leon et al., 1995), structural
equation modeling (Leon et al., 1999), multivariate analysis of
(text continues on page 32)
2
Reported numbers and statistical measures in the tables reflect what
was reported in the original articles. If certain measures (e.g., standard
deviations) are missing or certain statistics could not be calculated, this is
due to missing data in the original articles.
 24
Table 2
Characteristics of Longitudinal Studies on Risk Factors for Eating Disorders

Age at baseline Follow-up

Study Sample (N) (years) interval (years) Outcome (dependent variables) Predictors (independent variables)

Attie & Brooks-Gunn 193 female adolescents and
(1989) their mothers; initial
symptoms controlled for
Marchi & Cohen 659 children and mothers;
(1990) 326 girls and 333 boys
Patton et al. (1990) 734 adolescent girls; initial
symptoms controlled for
by subgrouping
Vollrath et al. (1992) 292 males and 299 females
of representative young
adult sample (N ⫽ 4,567),
divided into high- and
low-risk groups according
to SCL-90 scores;
controlling for initial
symptoms not reported
Killen et al. (1994) 967 adolescent girls,
community sample;
subjects with initial
symptoms excluded from
analysis
13.9 2 Emergence of eating problems, EAT-26 scores
Interviewed at 10 Problematic eating behaviors and disorders
three ages, (modified Diagnostic Interview Schedule for
depending on Children; DISC)
subgroup: 1–10
(6), 9–19 (14),
and 11–21 (16)
15 1 Eating disorder (risk group selected EAT-26
cut-off: 20/21), General Health
Questionnaire (GHQ) ⱖ 5/6; subsequent
semistructured interview for assessment of
clinical status or caseness (categories: cases,
dieters, nondieters)
27–28 2 (out of 9-year Eating problems (binge eating, vomiting,
follow-up) dieting, weight, etc.) as part of the
Structured Psychological Interview and
Rating of the Social Consequences for
Epidemiology; diagnosis: computerized
algorithms
12.4 3 Eating disorder symptoms and partial
syndromes, classification as symptomatic
based on binge eating, compensatory
behaviors, overconcern with weight and
body shape, loss of control
Height; weight; body fat; pubertal timing; body
image; personality: psychopathology,
emotional tone, impulse control (SIQYA);
family relationships, EAT-26
Eating behaviors (struggle over eating, amount
eaten, picky eater, speed of eating, interest
in food, pica, digestive problems)
EAT-26; GHQ; putative risk factors: family
background, reported family weight and
eating pattern, personal background, weight
history, perceived current social stress,
personality (Cattell Personality
Questionnaire); attitudes toward eating,
weight, and shape; menstrual history; current
weight and shape (clinical interview)
Same as dependent variables
Weight concerns, EDI, dietary restraint,
pubertal development, height, weight, BMI,
Behavior Problem Scales (Youth Self-Report
Inventory; YSRI)
JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS

Graber et al. (1994) 116 female adolescents,
recruited from private
schools; grouped into four
groups (low to chronic
risk)
Leon et al. (1995) Community sample (852
girls, 815 boys); initial
symptoms controlled for
14.3 8 Subclinical or clinical eating problems (cutoff:
EAT-26 ⱖ 20)
Grades 7–10 3 Disordered eating (risk status: 18 items from
Eating Disorders Checklist, BMI ⬍ 17 or ⬎
30, abnormal range scores on EDI Drive for
Thinness and Bulimia subscales)
EAT-26; physical development (body fat, age
at menarche); body image, self-image,
psychopathology; emotional tone; family
relationships (SIQYA); EDI: Perfectionism,
Ineffectiveness; affective states (YSRI);
family organization and functioning (FES)
Demographic variables; Eating Disorders
Checklist; EDI; Health Behavior Survey;
Pubertal Development Scale; personality
(MMPI): Negative and Positive
Emotionality, Constraint; General Behavior
Inventory (GBI) autonomy; attitudes about
sexuality
Table 2 (continued )

Age at baseline Follow-up

Study Sample (N) (years) interval (years) Outcome (dependent variables) Predictors (independent variables)

Killen et al. (1996) 877 high school girls
(community sample);
initial symptoms
controlled for
Button et al. (1996) 594 girls; initial symptoms
not controlled for
Calam & Waller 92 girls and their mothers
(1998) (part of study of family
management of children’s
eating habits); initial
symptoms not controlled
for
Leon et al. (1999) 726 girls, 698 boys, high- Grades 7–10 to 9–12
risk subjects were
excluded from prospective
analysis at t1
Patton et al. (1999) 1,947 male and female
students, recruited in
cohorts; initial symptoms
controlled for
Ghaderi & Scott 1,157 women, random
(2001) general population sample;
initial symptoms
controlled for by
14.9 4 Eating disorder symptoms and partial Weight concerns, EDI, dietary restraint, height,
syndromes (EDE—Interview Adaptation) weight, BMI, temperament (emotionality,
activity, sociability), drinking frequency
(baseline and follow-up), EDE—Adaptation
11–12 4 EAT-26 score; EAT-26 score ⱖ 20; EATpath; Self-esteem; perceived health status, fatness
eating behavior and concerns, weight concern, family relationships, school
variables; self-esteem; Hospital Anxiety and problems, general worrying/nervousness
Depression Scale (five questions)
12.8 7 EAT-26, BITE scores EAT-26, BITE, Setting Conditions for
Anorexia Questionnaire (including 14 self-
esteem and 8 perfectionism items), BMI,
Family Assessment Device
3–4 Eating Disorder Risk Factor Index, Kiddie- Personality and temperament (MPQ, GBI),
SADS: expanded eating disorders module Eating Disorders Checklist, EDI, health
behaviors, physical and pubertal
development, psychopathology (Kiddie-
SADS)
14–15 3 Branched Eating Disorders Test to assess Dieting (Adolescent Dieting Scale), exercise,
symptoms and partial syndromes weight and height, psychiatric morbidity
(computerized interview)
18–30 2 Survey for Eating Disorders, questionnaire to Self-Concept Questionnaire, Body Shape
assess DSM–IV eating disorders Questionnaire, perceived social support from
family, Ways of Coping Questionnaire
RISK FACTORS FOR EATING DISORDERS

subgrouping
Kotler et al. (2001) 976 (t1) to 776 (t4) children, 6.1 (range ⫽ 1–10.9) 17 Eating behaviors based on maternal interviews Early childhood eating problems (unpleasant
45%–50% female (t1–t3); parent (t2, t3) and youth (t2–t4) meals, struggles over eating, amount eaten,
versions of the DISC picky or choosy eating, interest in food)
assessed by maternal interview
J. G. Johnson et al. 782 children, 397 males, 385 6 16–18 Parent (t2, t3) and youth (t2–t4) versions of the Childhood temperament, parental psychiatric
(2002) females; initial symptoms DISC problems, maladaptive parental behavior,
controlled for childhood maltreatment, other childhood
adversities (all assessed by the
Disorganizing Poverty Interview)

Note. EAT-26 ⫽ Eating Attitudes Test; SIQYA ⫽ Self-Image Questionnaire for Young Adolescents; SCL-90 ⫽ Symptom Checklist–90; EDI ⫽ Eating Disorders Inventory; BMI ⫽ body mass index;
FES ⫽ Family Environment Scale; MMPI ⫽ Minnesota Multiphasic Personality Inventory; EDE ⫽ Eating Disorder Examination; EATpath ⫽ EAT-26 ⱖ 20 plus one or more of the following: vomiting,
laxatives, or diuretics; BITE ⫽ Bulimic Investigatory Test; Kiddie-SADS ⫽ Schedule for Affective Disorder and Schizophrenia; MPQ ⫽ Multidimensional Personality Questionnaire; DSM–IV ⫽
Diagnostic and Statistical Manual of Mental Disorders (4th ed.; American Psychiatric Association, 1994); t1 ⫽ Time 1; t4 ⫽ Time 4; t3 ⫽ Time 3; t2 ⫽ Time 2.
25
26 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS

Table 3
Classification, Potency, and Specificity of Risk Factors for Eating Disorders (EDs)

Study Risk factor classification Indications of potency AUC (%) Specificity

Fixed markers
Leon et al. (1995) Race ␤ ⫽ .08 (R2 in Step 4 ⫽ .55; ⌬R2 ⫽ .02) NT

Variable risk factors

Attie & Brooks-Gunn Eating problems: NT
(1989) t1 EAT-26 ␤ ⫽ .436; ⌬R2 ⫽ .19, F⌬R2(F) ⫽ 32.55
Body image ␤ ⫽ ⫺.166; ⌬R2 ⫽ .02, F⌬R2(F) ⫽ 3.79
Marchi & Cohen Bulimic symptoms: NT
(1990) Digestive problems B ⫽ 0.781
Pica B ⫽ 1.715
Reducing concerns and behavior B ⫽ 0.667
Bulimia nervosa (BN):
Pica in early childhood OR ⫽ 6.66 (SE ⫽ 2.20)
Anorexic symptoms:
Digestive problems B ⫽ 0.778
Picky eating in early and later childhood B ⫽ 0.258, 0.496
Anorexia nervosa (AN):
Elevation on measure of anorexic symptoms
(DISC)
Patton et al. (1990) Factors predictive of caseness (BN): NT
General psychiatric morbidity change score GHQ cases: 2.3; dieters: ⫺1.6
(GHQ)a,b
Dieting/weight control RR for dieters developing on ED 7.9 times 63.75
that of nondieters; 50% (13 of 26) of
cases and 22.5% (25 of 111) of noncases
were dieters at t1
Vollrath et al. (1992) Binge eaters: Mbinge eaters ⫽ 22.6, Mweight concerned ⫽ 22.2, NT
Higher BMI Mcontrols ⫽ 20.7
Graber et al. (1994) Eating problems (differences between low- NT
and late-transient risk groups):
Body image (young adolescence) Cohen’s ␦ ⫽ ⫺0.47 63.02
Body image (midadolescence) Cohen’s ␦ ⫽ ⫺0.49 63.55
EAT-26 (late adolescence) Cohen’s ␦ ⫽ 0.70 68.47
Killen et al. (1994) Partial syndrome and/or ED symptoms vs. NT
asymptomatic:
Weight concernsa Cohen’s ␦ ⫽ 0.75 70.21
EDI Drive for Thinness/Body Dissatisfactiona Cohen’s ␦ ⫽ 0.83 72.14
EDI Bulimiaa Cohen’s ␦ ⫽ 0.33 59.23
EDI Perfectionisma Cohen’s ␦ ⫽ 0.50 63.82
EDI Ineffectiveness/Interpersonal Distrust/ Cohen’s ␦ ⫽ 0.25 57.02
Interoceptive Awarenessa
BMIa Cohen’s ␦ ⫽ 0.39 60.86
Restraint (CD)a Cohen’s ␦ ⫽ 0.66 67.96
Restraint (WF)a Cohen’s ␦ ⫽ 0.42 61.68
YSRI—Unpopulara Cohen’s ␦ ⫽ 0.37 60.32
YSRI—Aggressivea Cohen’s ␦ ⫽ 0.36 60.05
Weight concernsb Cox parameter estimate ⫽ .03 ⫾ .01
Leon et al. (1995) Disordered eating: NT
Year 1 risk score ␤ ⫽ .18
Year 2 risk score ␤ ⫽ .54
Poor interoceptive awareness ␤ ⫽ .15 (R2 in Step 4 ⫽ .55; ⌬R2 ⫽ .02)
Button et al. (1996) Low self-esteem B ⫽ 0.17
Concern about fatness B ⫽ 0.19
Killen et al. (1996) Partial syndrome vs. asymptomatic: NT
Weight concernsa Cohen’s ␦ ⫽ 1.06 77.32
EDI Drive for Thinnessa Cohen’s ␦ ⫽ 0.93 74.46
EDI Bulimiaa Cohen’s ␦ ⫽ 0.48 63.28
EDI Body Dissatisfactiona Cohen’s ␦ ⫽ 0.57 65.65
EDI Ineffectivenessa Cohen’s ␦ ⫽ 0.39 60.86
EDI Interoceptive Awarenessa Cohen’s ␦ ⫽ 0.64 67.46
Temperament: distressa Cohen’s ␦ ⫽ 0.56 65.39
Temperament: feara Cohen’s ␦ ⫽ 0.71 69.22
Restraint (CD)a Cohen’s ␦ ⫽ 1.07 77.54
Restraint (WF)a Cohen’s ␦ ⫽ 0.76 70.45
No. of alcoholic drinks (past 30 days)a 56% vs. 39% 57.50
Weight concernsb ␹2(1, N ⫽ 734) ⫽ 19.10
 RISK FACTORS FOR EATING DISORDERS 27

Table 3 (continued )

Study Risk factor classification Indications of potency AUC (%) Specificity

Variable risk factors (continued)

Calam & Waller High EAT-26 score: NT
(1998) EAT-26 Bulimia Cohen’s ␦ ⫽ 3.76 99.61
BITE Cohen’s ␦ ⫽ 1.38 83.54
High BITE score:
EAT-26 Bulimia, EAT-26 total Cohen’s ␦ ⫽ 1.74 89.07
BITE Cohen’s ␦ ⫽ 1.80 89.85
Leon et al. (1999) Negative affect, attitudes Girls: R2 ⫽ .22 (.11)c NT
Boys: R2 ⫽ .14 (.04)c
Patton et al. (1999) Unadj./adj. hazard ratios: NT
Intermediate dieting 9.1 (3.1, 26.0), 4.9 (1.7, 15.0)
Severe dieting 66.0 (20.0, 211.0), 18.0 (4.9, 67.0)
Psychiatric morbidity 16.0 (6.8, 36.0), 6.6 (2.6, 17.0)
Kotler et al. (2001) AN: eating conflicts OR ⫽ 6.20 NT
AN: struggles around meals OR ⫽ 7.30
AN: unpleasant meals OR ⫽ 6.20
BN: eating too little OR ⫽ 0.40
(all assessed in early childhood)
Ghaderi & Scott Self-esteem Cohen’s ␦ ⫽ 0.86 72.84 NT
(2001) Body concern Cohen’s ␦ ⫽ ⫺1.33 82.65
Escape–avoidance coping Cohen’s ␦ ⫽ ⫺0.73 69.71
Perceived social support Cohen’s ␦ ⫽ 0.88 73.31
J. G. Johnson et al. Physical neglect ED: 11.2% (6 of 54), non-ED: 2.7% (18 of 681) 54.25 NT
(2002) Sexual abuse ED: 12% (6 of 50), non-ED: 2.9% (18 of 618) 54.55

Correlates
Attie & Brooks-Gunn Internalizing dimensions of psychopathology
(1989)
Graber et al. (1994) Depressive affect

Factors not shown to be risk factors

Attie & Brooks-Gunn Pubertal timing,b family functioning,b
b
(1989) psychopathology
Patton et al. (1990) Family and personal background variables,
family weight and eating patterns, weight
history, social stress, personality
Graber et al. (1994) Family relationships,b Psychopathology,b
percentage of body fat,b age at menarche
Killen et al. (1994) Pubertal status,a EDI Maturity Fearsa
Leon et al. (1995) Self-concept,b pubertal status,b EDI 3–6, 8b;
personality,b negative emotionalityb
Button et al. (1996) Family relationshipsb
Killen et al. (1996) EDI (Maturity Fears, Interpersonal Distrust,
Perfectionism),a temperament (anger,
activity, sociability),a BMIa
Kotler et al. (2001) AN/BN: Pica, digestive problems, not eating,
not interested in food, picky eater, eating
too little and too slowly; BN: eating
conflicts, struggles around meals,
unpleasant meals
J. G. Johnson et al. ED: Maladaptive maternal behavior,
(2002) environmental risk factors
Calam & Waller High EAT-26 scores: EAT-26 Total, EAT-26
(1998) Dieting, EAT-26 Oral Control, BMI
High BITE scores: EAT-26 Dieting, EAT-26
Oral Control, BMI
Leon et al. (1999) Substance-related impulsivity (smoking and
drinking frequency, MPQ Constraint)
Development (pubertal level, grade, EDI Body
Dissatisfaction)
Shoebridge & Gestational age (AN)
Gowers (2000)

Note. Data in the table are organized by risk factor classification. AUC ⫽ area under the curve; Exponent ␤ ⫽ percentage change in hazard; NT ⫽
specificity not tested; t1 ⫽ Time 1; EAT-26 ⫽ Eating Attitudes Test; OR ⫽ odds ratio; DISC ⫽ Diagnostic Interview Schedule for Children; GHQ ⫽
General Health Questionnaire; RR ⫽ risk ratio; BMI ⫽ body mass index; EDI ⫽ Eating Disorders Inventory; CD ⫽ concern for dieting; WF ⫽ weight
fluctuation; YSRI ⫽ Youth Self-Report Inventory; BITE ⫽ Bulimic Investigatory Test; Unadj./adj. ⫽ unadjusted and adjusted hazard ratios; MPQ ⫽
Multidimensional Personality Questionnaire.
a
Univariate comparisons. b Multivariate comparisons. c Explained variance for three latent variables; numbers in parentheses represent the replication sample.
Table 4 28
Classification, Potency, and Specificity of Fixed and Variable Markers, Retrospective Correlates, and Correlates for Anorexia Nervosa (AN)

Study Risk factor classification Indications of potency AUC (%) Specificity

Fixed markers
Cnattingius et al. (1999), Hultman Very preterm birth OR ⫽ 3.2; AN: 1.8% (14 of 781), CG: 0.6% (23 of 3,905) 50.60 S
et al. (1999) Cephalhematoma (birth trauma) OR ⫽ 2.4; AN: 2.4% (19 of 781), CG: 1.1% (41 of 3,905) 50.65
Schotte & Stunkard (1987), Nielsen Female 10:1 female to male ratio G
(1990), Whitaker et al. (1990),
Vollrath et al. (1992), Lewinsohn
et al. (1993), Wittchen et al.
(1998), Patton et al. (1999)
Chen et al. (1993), Ohzeki et al. Not Asian
(1990)
Holland et al. (1984) Genetic effects CCR (MZ/DZ): 55% vs. 7% NT
Holland et al. (1988) Genetic effects CCR (MZ/DZ): 56% vs. 5%; A for EDI 1 & 3: almost 100% NT
Treasure & Holland (1989) Genetic effects CCR (MZ/DZ): 67% vs. 0%; A: 88%, E: 12% NT
Walters & Kendler (1995) Genetic effects CCR (MZ/DZ): 10% vs. 22% NT
Wade et al. (2000) Genetic effects CCR (MZ/DZ): 18% vs. 14%; A: 58%, E: 42% NT
Klump et al. (2001) Genetic effects CCR (MZ/DZ): 40% vs. 0%; A: 76%, E: 24% NT
Graber et al. (1997) Early pubertal timinga Hazard ratio ⫽ 2.7 G
Hayward et al. (1997) Early pubertal timinga 3.5% (of 172) for early maturers, 0.8% (of 629) for on time

Retrospective correlates (case-control, family history, comorbidity studies)

Hooper & Garner (1986), Davis & Acculturation NT
Katzman (1999), Gowen et al.
(1999), Lee & Lee (2000)
Rastam (1992) OCPD AN: 35% (18 of 51), CG: 4% (2 of 51) 65.50 NT
Early feeding and severe AN: 90% (46 of 51), CG: 55% (28 of 51) 67.50 NT
gastrointestinal problems
Bulik et al. (1997) OCD OR ⫽ 11.8 S
Overanxious disorder OR ⫽ 13.4 G
Any preceding lifetime anxiety disorder: AN: 54% (37 of 68), MD CG: 34% (19
of 56)
Fairburn, Cooper, et al. (1999)b Comparison with healthy CG: G
Greater level of exposure to AN (N ⫽ 64), CG (N ⫽ 204):
personal, 52% vs. 12%; OR ⫽ 16.7 70.00
environmental, and 46% vs. 11%; OR ⫽ 15.3 67.50
JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS

dieting risk domains 15% vs. 6%; OR ⫽ 11.3 54.50

Comparison with psyCG: AN, psyCG (N ⫽ 102), CG:
Negative self-evaluation 55% vs. 30% vs. 13%; OR in comparison with psyCG ⫽ 3.1 AN–CG: 71.00 S
psyCG–CG: 58.50
Premorbid perfectionism 61% vs. 26% vs. 24%; OR in comparison with psyCG ⫽ 4.1 AN–CG: 68.50 S
psyCG–CG: 51.00
Comparison with BN group:
Less exposure to parental obesity 11% vs. 34% vs. 11% AN–CG: 50.00 S
psyCG–CG: 61.50
Vize & Cooper (1995) Sexual abuse AN: 42.9% (of 28), MD: 40.0% (of 35), CG: 6.7% (of 30) AN–CG: 68.10 G
MD–CG: 66.65
Rastam & Gillberg (1992) Adverse life events AN: 14% (7 of 51), CG: 0% (0 of 51) 57.00 NT
Horesh et al. (1995) Adverse life events AN vs. CG: Cohen’s ␦ ⫽ 1.45 84.74 NT
Horesh et al. (1996)c Adverse life events (inappropriate AN/BN vs. CG: Cohen’s ␦ ⫽ 1.57, 86.65 S
parental pressures) AN/BN vs. psyCG: Cohen’s ␦ ⫽ 0.69 68.72
Table 4 (continued )

Study Risk factor classification Indications of potency AUC (%) Specificity

Retrospective correlates (case-control, family history, comorbidity studies) (continued)

Gowers et al. (1996) Adverse life events (extremely AN: 26% (9 of 35), psyCG: 34% (12 of 35), CG: 8% (3 of 35) AN–CG: 59.00 G
negative events) psyCG–CG: 63.00
Schmidt et al. (1997) Adverse life events (“major AN: 22% (16 of 76), CG: 4% (1 of 28) 59.00 NT
difficulties”)
Davis et al. (1994) High-level exercise MEAT-26 (age 13) ⫽ 1,695.4 (2,161.8), MCG ⫽ 966.8 (819.2); Cohen’s ␦ ⫽ 0.889 73.54 NT
Rabe-Jablonska & Tomasz (2000) Body dysmorphic disorder AN: 25% (9/36), CG: 7.5% (3 of 40) 58.75 NT
Shoebridge & Gowers (2000) High-concern parenting, two or AN: 57.5% (23 of 40), CG: 15% (6 of 40) 71.25 NT
more factors:
Baby and infant care almost AN: 37.5% (15 of 40), CG: 12.5% (5 of 40) 62.50
exclusively by mother
Distress when first leaving AN: 30% (12 of 40), CG: 10% (4 of 40) 60.00
daughters in nursery
Age when daughter first spent a AN significantly older than CG
weekend with other adults
Infant sleep pattern difficulties AN: 47.5% (19 of 40), CG: 20% (8 of 40) 63.75
Foley et al. (2001) Pregnancy complications OR ⫽ 1.4 S
Gestational age OR ⫽ 0.8 S

Variable markers
Woodside & Garfinkel (1992), Adolescent agea
Mitrany et al. (1995), Stice et al.
(1998)

(e.g., Garfinkel et al., 1983; Waller
et al., 1989; McNamara &
Loveman, 1990; Shisslak et al.,
1990)
(e.g., Strober et al., 1985, 1990,
2000)
Correlates
Family functioning/interaction
styles, attachment styles
Familial psychopathology (eating
disorders, depression, anxiety
RISK FACTORS FOR EATING DISORDERS

disorders, SUD, etc.)

(e.g., Kaye et al., 1991; Bastiani et Perfectionism
al., 1995; Srinivasagam et al.,
1995)
(e.g., Jacobi, 1999, 2000) Low self-esteem, negative self-
concept
(e.g., Garner & Garfinkel, 1978; Participation in weight-related
Sundgot-Borgen, 1994; Fulkerson subculture
et al., 1999; C. Johnson et al.,
1999)

Note. Data in the table are organized by risk factor classification. AUC ⫽ area under the curve; OR ⫽ odds ratio; CG ⫽ control group; S ⫽ specific risk factor; G ⫽ general risk factor (generic);
NT ⫽ specificity not tested; CCR (MZ/DZ) ⫽ concordance rates for monozygotic versus dizygotic twins (A ⫽ additive genetic effects, E ⫽ individual environmental effects); EDI ⫽ Eating Disorders
Inventory; NT ⫽ specificity not tested; OCPD ⫽ obsessive– compulsive personality disorder; OCD ⫽ obsessive– compulsive disorder; MD ⫽ major depression; psyCG ⫽ psychiatric control group;
BN ⫽ Bulimia nervosa; SUD ⫽ substance use disorder.
a
The status of these factors may change from variable to fixed depending on the period of assessment. b Because of the large number of significant differences between patients with eating disorders
and nonpsychiatric controls in this study, only specific significant differences are listed individually in the table. c Mixed (AN, BN) but predominantly anorexic sample; the only specific factor listed
in table.
29
Table 5 30
Classification, Potency, and Specificity of Fixed and Variable Markers, Retrospective Correlates, and Correlates for Bulimia Nervosa (BN)

Study Risk factor classification Indications of potency AUC (%) Specificity

Fixed markers
Schotte & Stunkard (1987), Female OR ⫽ 10.00 G
Fairburn & Beglin (1990),
Nielsen (1990), Whitaker et al.
(1990), Vollrath et al. (1992),
Lewinsohn et al. (1993),
Wittchen et al. (1998), Patton et
al. (1999)
Chen et al. (1993), Ohzeki et al. Not Asian NT
(1990), Crago et al. (1996)
Treasure & Holland (1989) Genetic effects CCR (MZ/DZ): 35% vs. 29% NT
Fichter & Nögel (1990) Genetic effects CCR (MZ/DZ): 83.3% vs. 26.7% NT
Kendler et al. (1991) Genetic effects CCR (MZ/DZ): 22.9% vs. 8.7%; A: 50%–55%, E: 50% NT
Walters et al. (1992) Genetic effects A: 50%, E: 50% NT
Rutherford et al. (1993) Genetic effects CCR (MZ/DZ) for EAT-26 ⬎ 20: 9.5% vs. 17% NT
A: 41% (EAT-26 total score); A: 25%–52% (EDI subscales); A: 64% (BMI)
Kendler et al. (1995) Genetic effects A: 30%, E: 29%, C: 41% NT
Bulik et al. (1998) Genetic effects A: 83%, E: 17% NT
Sullivan et al. (1998) Genetic effects Bingeing: A: 46%, E: 54%; vomiting: A: 72%, E: 28% NT
Wade et al. (1998) Genetic effects Shape concern: A: 62%, E: 38%; weight concern: C: 52%, E: 48% NT
Wade et al. (1999) Genetic effects Disordered eating: A: 60%, E: 40% NT
Graber et al. (1997) Early pubertal timinga Hazard ratio ⫽ 2.7 G
Hayward et al. (1997) Early pubertal timinga 3.5% (of 172) for early maturers, 0.8% (of 629) for on time

Retrospective correlates (case-control, family history, comorbidity studies)

Bulik et al. (1997)
Fairburn et al. (1997)b
Social phobia OR ⫽ 15.54 G
Overanxious disorder OR ⫽ 4.86 G
Any preceding lifetime anxiety disorder: BN: 53% (62 of 116)
MD CG: 34% (19 of 56)
Comparison with healthy CG: BN (N ⫽ 102), CG (N ⫽ 204) G
Greater level of exposure to
personal, 65% vs. 13%; OR ⫽ 35.30 76.00
environmental, and 60% vs. 11%; OR ⫽ 42.48 74.50
dieting risk domains 42% vs. 6%; OR ⫽ 30.80 68.00
JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS

Comparison with psyCG: BN, psyCG (N ⫽ 102), CG:

Negative self-evaluation 54% vs. 30% vs. 13%; OR in comparison with psyCG ⫽ 2.80 BN–CG: 70.50 S
psyCG–CG: 58.50
Parental alcoholism 20% vs. 6% vs. 3%; OR in comparison with psyCG ⫽ 4.50 BN–CG: 58.50 S
psyCG–CG: 51.50
Low parental contact 34% vs. 14% vs. 18%; OR in comparison with psyCG ⫽ 3.20 BN–CG: 58.00 S
psyCG–CG: 48.00
High parental expectations 51% vs. 25% vs. 21%; OR in comparison with psyCG ⫽ 3.40 BN–CG: 65.00 S
psyCG–CG: 52.00
Critical comments by family 65% vs. 31% vs. 25%; OR in comparison with psyCG ⫽ 5.90 BN–CG: 70.00 S
about weight and shape psyCG–CG: 53.00
Childhood obesity 40% vs. 13% vs. 15%; OR in comparison with psyCG ⫽ 4.50 BN–CG: 62.50 S
psyCG–CG: 49.00
Parental obesity 34% vs. 20% vs. 11%; OR in comparison with psyCG ⫽ 2.40 BN–CG: 61.50 S
psyCG–CG: 54.50
Table 5 (continued )

Study Risk factor classification Indications of potency AUC (%) Specificity

Retrospective correlates (case-control, family history, comorbidity studies) (continued)

Welch & Fairburn (1994) Sexual abuse OR for BN vs. CG ⫽ 3.16, BN: 26% (13 of 50), CG: 24% (12 of 50); OR for BN vs. BN–CG: 51.00 G
psyCG ⫽ 1.11 (ns); psyCG: 16% (8 of 50); OR for BN vs. BNclinic ⫽ 1.93 (ns) psyCG–CG: 46.00
Vize & Cooper (1995) Sexual abuse BN: 27.1% (of 48), MD: 40.0% (of 35), CG: 6.7% (of 30) BN–CG: 60.20 G
MD–CG: 66.65
Garfinkel et al. (1995) Sexual abuse BN: 32.7% (18 of 55), partial BN: 36.4% (8 of 22), CG: 13.9% (585 of 4,208) BN–CG: 59.40 NT
partialBN–CG: 61.25
Dansky et al. (1997) Sexual abuse BN: 26.6% (of 72), CG: 13.3% (of 29) 56.65 NT
Steiger et al. (2000) Sexual abuse, prior to age 13 BN/BPD: 50% (7 of 14), BN/non-BPD: 23.1% (6 of 26), CG: 16% (4 of 25) BN, BDP–CG: 67.00 NT
BN, non-BDP–CG:
53.55
Welch et al. (1997) Adverse life events (three or more BN: 18% (18 of 102), CG: 5% (11 of 204) 56.50 NT
events)
Schmidt et al. (1997) Adverse life events (“major BN: 34% (10 of 29), CG: 4% (1 of 28) 65.00 NT
difficulties”)
Webster & Palmer (2000) Adverse family experiences
Parental indifference BN: 34% (11 of 32), DEP: 40% (16 of 40), CG: 13% (5 of 40) BN–CG: 60.50 G
DEP–CG: 63.50
Discord in the family BN: 53% (17 of 32), DEP: 50% (20 of 40), CG: 23% (9 of 40) BN–CG: 65.00 G
DEP–CG: 63.50
Lack of care BN: 47% (15 of 32), DEP: 43% (17 of 40), CG: 23% (9 of 40) BN–CG: 62.00 G
DEP–CG: 60.00
High adversity BN: 53% (17 of 32), DEP: 50% (20 of 40), CG: 28% (11 of 40) BN–CG: 62.50 G
DEP–CG: 61.00
Hooper & Garner (1986), Davis & Acculturation NT
Katzman (1999), Gowen et al.
(1999), Lee & Lee (2000)
Raffi et al. (2000) Prodomal symptoms: NT
Subclinical mood disturbance NT
Low self-esteem BN: 63% (19 of 30), CG: 3% (1 of 30) 80.00
Depressed mood BN: 60% (18 of 30), CG: 13% (4 of 30) 73.50
Anhedonia BN: 57% (17 of 30), CG: 0% (0 of 30) 78.50
RISK FACTORS FOR EATING DISORDERS

Irritability BN: 47% (14 of 30), CG: 17% (5 of 30) 65.00

Impaired work performance BN: 43% (13 of 30), CG: 0% (0 of 30) 71.50
Anorexia/strict diet BN: 77% (23 of 30), CG: 3% (1 of 30) 87.00
Generalized anxiety BN: 50% (15 of 30), CG: 17% (5 of 30) 66.50
Reactivity BN: 33% (10 of 30), CG: 3% (1 of 30) 65.00
Phobic avoidance BN: 33% (10 of 30), CG: 7% (2 of 30) 63.00
Guilt BN: 37% (11 of 30), CG: 10% (3 of 30) 63.50
Foley et al. (2001) Pregnancy complications OR ⫽ 1.21 S

Variable markers
Woodside & Garfinkel (1992), Adolescent agea G
Mitrany et al. (1995), Stice et al.
(1998)

Correlates
(e.g., Garfinkel et al., 1983; Waller Family functioning/interaction
et al., 1989; McNamara & styles, attachment styles
Loveman, 1990; Shisslak et al.,
1990; Friedmann et al., 1997)
31

(table continues)
32 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS

variance group comparisons of different risk groups (Ghaderi &

EDI ⫽ Eating Disorders Inventory; MD ⫽ major depression; CG ⫽ control group; psyCG ⫽ psychiatric control group; S ⫽ specific risk factor; BPD ⫽ borderline personality disorder; DEP ⫽
Note. Data in the table are organized by risk factor classification. AUC ⫽ area under the curve; G ⫽ general risk factor (generic); OR ⫽ odds ratio; NT ⫽ specificity not tested; CCR (MZ/DZ) ⫽
concordance rates for monozygotic versus dizygotic twins (A ⫽ additive genetic effects, E ⫽ individual environmental effects, C ⫽ shared environmental effects); EAT-26 ⫽ Eating Attitudes Test;

The status of these factors may change from variable to fixed depending on the period of assessment. b Because of the large number of significant differences between patients with eating disorders
Specificity Scott, 2001; Graber et al., 1994), a mixture of descriptive univar-
iate risk group comparisons, and multivariate (Cox proportional
hazard model or logistic regression analysis) testing (Killen et al.,
1994, 1996; Patton et al., 1990), or a combination of multivariate
(regression) analyses and risk parameters such as odds or risk
AUC (%)

ratios (Kotler et al., 2001; J. G. Johnson et al., 2002; Marchi &

Cohen, 1990; Patton et al., 1990).
Finally, in some of the studies (e.g., Attie & Brooks-Gunn,
1989; Graber et al., 1994; Leon et al., 1995; Patton et al., 1990,
1999), both longitudinal and cross-sectional analyses were per-
formed to identify factors predicting the outcome and factors
concurrently associated with the outcome. For the purpose of the
present review we limit the following summary of results from
longitudinal studies to factors assessed before the onset of the
disorder or to fixed markers (e.g., gender), and we exclude factors
concurrently associated with the disorder.

Potential Risk Factors and Classification

Indications of potency

Gender. One of the most consistent findings in the eating

disorder literature is the preponderance of females with eating
disorders compared with males. The greater prevalence of eating
disorders in females compared with males has been frequently
observed in clinical samples as well as nonclinical populations
(Lewinsohn, Hops, Roberts, Seeley, & Andrews, 1993; Nielsen,
and nonpsychiatric controls in this study only specific significant differences are listed individually in the table.
Correlates (continued)

1990; Patton et al., 1999; Schotte & Stunkard, 1987; Vollrath et al.,
1992; Whitaker et al., 1990). The female to male ratio from
population-based studies is estimated to be in the range of 10:1 for
both anorexia and bulimia nervosa (American Psychiatric Associ-
ation, 1994; Hsu, 1996; Wittchen, Nelson, & Lachner, 1998).
Preliminary estimates suggest a 2.5:1 female to male ratio for
binge-eating disorder (Spitzer et al., 1992). Because gender is, for
the most part, an immutable characteristic, this factor is catego-
rized as a fixed marker according to the taxonomy of Kraemer et
al. (1997). Because of the large effect size (10:1) female status is
a highly potent fixed marker for eating disorders, although non-
specific in that rates of major depression and anxiety disorders are
Familial psychopathology (eating
disorders, depression, anxiety

Low self-esteem, negative self-

Risk factor classification

also higher in females compared with males (Blazer, Kessler,

Participation in weight related

McGonagle, & Swartz, 1994; Kessler et al., 1994).

Ethnicity. Historically, eating disorders have been character-
disorders, SUD, etc.)

ized as affecting primarily Caucasian females (see review by

Striegel-Moore & Smolak, 1996). Recent studies reveal a more
Perfectionism

complex pattern. In one survey of the literature Hispanics were

subculture

noted to have equal rates of eating disturbances compared with

concept

Caucasians, and Native Americans had higher rates, and Blacks

depression; SUD ⫽ substance use disorder.

and had Asians lower rates, than did Caucasians (Crago, Shisslak,
& Estes, 1996). Black females in South Africa, however, have
Sundgot-Borgen, 1994; Fulkerson
(e.g., Lilenfeld et al., 1997; Stein et

higher rates of eating disorder symptoms than do Caucasian fe-

al., 1999; Strober et al., 2000)

et al., 1999; C. Johnson et al.,

(e.g., Garner & Garfinkel, 1978;

males (Le Grange, Telch, & Tibbs, 1998; Szabo & Hollands,
1997). Blacks in the United States have lower rates of body
(e.g., Jacobi, 1999, 2000)

dissatisfaction and weight concerns, but equal or higher rates of

Table 5 (continued )

bingeing behavior compared with a Caucasian sample (Striegel-

Study

Moore et al., 2000). Thus, simple generalizations regarding eth-

Kaye et al. (1998)

nicity are difficult to make. Asians appear to have lower rates of

bulimia and anorexia nervosa (Chen et al., 1993; Ohzeki et al.,
1990), and African Americans have higher rates of binge eating
1999)

(Striegel-Moore et al., 2000). To the extent that ethnicity does

influence risk, it is classified as a fixed marker in the Kraemer
a
 RISK FACTORS FOR EATING DISORDERS 33

Table 6
Classification, Potency, and Specificity of Fixed Markers, Retrospective Correlates, and Correlates for Binge-Eating Disorder (BED)

Study Risk factor classification Indications of potency AUC (%) Specificity

Fixed markers
Spitzer et al. (1992) Female 2.5:1 female to male ratio G
Striegel-Moore & African American, Caucasian NT
Smolak (1996)

Retrospective correlates (case-control, family history, comorbidity)

Fairburn et al. (1998) Comparison with healthy CG: BED (N ⫽ 52), CG (N ⫽ 104) G
Greater level of exposure to
personal, 42.3% vs. 11.5%; OR ⫽ 7.25 65.40
environmental, and 48.1% vs. 11.5%; OR ⫽ 21.40 68.30
dieting risk domains 28.8% vs. 11.5%; OR ⫽ 5.98 58.65
Comparison with psyCG: BED, psyCG (N ⫽ 102), CG
Low parental contact 38.5% vs. 13.7% vs. 20.2%; OR in BED–CG: S
comparison with psyCG ⫽ 6.00 59.15
psyCG–CG:
46.75
Critical comments about weight, shape, and 53.8% vs. 31.4% vs. 25%; OR in comparison BED–CG: S
eating with psyCG ⫽ 2.70 64.40
psyCG–CG:
53.20
Childhood obesity 30.8% vs. 12.7% vs. 19.2%; OR in BED–CG: S
comparison with psyCG ⫽ 3.30 55.80
psyCG–CG:
46.75
Comparison with BN subjects:
Less exposure to subdomains,
childhood characteristics, and S
obesity risk S
Dominy et al. (2000) Perception of paternal rejection BED (N ⫽ 32), nonobese CG (N ⫽ 30): 64.34 NT
Cohen’s ␦ ⫽ 0.52
BED (N ⫽ 32), obese CG (N ⫽ 51): Cohen’s 64.61
␦ ⫽ 0.53
Perception of paternal neglect BED (N ⫽ 32), nonobese CG (N ⫽ 30): 69.71
Cohen’s ␦ ⫽ 0.73
BED (N ⫽ 32), obese CG (N ⫽ 51): Cohen’s 60.59
␦ ⫽ 0.38

Correlates
Friedmann et al. Family functioning/interaction styles,
(1997) attachment styles
Jacobi (1999, 2000) Low self-esteem, negative self-concept
Dominy et al. (2000) Higher level of depression
Lower satisfaction with life
Pratt et al. (2001) Higher self-oriented perfectionism

Note. Data in the table are organized by risk factor classification. AUC ⫽ area under the curve; G ⫽ general risk factor (generic); NT ⫽ specificity not
tested; CG ⫽ control group; OR ⫽ odds ratio; S ⫽ specific risk factor; psyCG ⫽ psychiatric control group; BN ⫽ bulimia nervosa.

schema. Its potency varies depending on the cultural context and
outcome of interest. The specificity of association between ethnic-
ity and eating disorders has not been well studied.
Acculturation. Within-ethnic-groups differences among mi-
norities are also related to acculturation, with the more accultur-
ated subjects having higher rates of eating disorder symptoms
(Davis & Katzman, 1999; Gowen, Hayward, Killen, Robinson, &
Taylor, 1999; Hooper & Garner, 1986). In addition, within ethnic
groups, in China for example, differences are related to urbaniza-
tion and industrialization, with higher rates among more industri-
alized cities (Lee & Lee, 2000). Generalizations regarding accul-
turation and risk of developing an eating disorder therefore depend
on the cultural context and outcome of interest. Acculturation is
measured cross-sectionally in these studies but is classified as a
retrospective correlate, as it presumably predates onset of the
symptoms. Its potency is not known, nor has its specificity been
tested.
Age. Another consistent finding from both clinic- and
population-based samples is the peak in incidence of eating dis-
orders during adolescence and early adulthood (Mitrany, Lubin,
Chetrit, & Modan, 1995; Stice, Killen, Hayward, & Taylor, 1998;
Wittchen et al., 1998; Woodside & Garfinkel, 1992). The increase
in risk associated with age depends on which ages are compared,
and direct comparisons of eating disorder rates in latency age
samples versus later adolescent samples have, as yet, not been
reported. Thus, the potency of the age effect is difficult to estimate
even though it is likely to be large between childhood and late
adolescence. In the Kraemer typology age is classified as a vari-
34 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
able marker, and because age is related to other psychiatric disor-
ders age effects are categorized as nonspecific.
Weight concerns, dieting, and negative body image. The as-
sociation between dieting and eating disorders is probably one of
the most often quoted in theories on the etiology of eating disor-
ders. Dieting has been considered to be an important precursor, if
not cause, of eating disorders, especially bulimia nervosa (Hsu,
1990; Polivy & Herman, 1985). When limited to cross-sectional
research, primarily two lines of evidence have linked dieting to
anorexia and bulimia nervosa: (a) clinical descriptions of factors
associated with the onset of the syndromes in samples of patients
requesting treatment and (b) laboratory studies (including animal
studies) examining the effect of attempted manipulation of re-
strained eating or dieting.
It is interesting to note that the majority of clinical studies
addressing the chronology of dieting and bingeing behavior date
back almost 20 years. The number of these studies is relatively
small, and more recent reports related to the temporal association
of the two behaviors are scarce. For example, in one of the earliest
reports, Russell (1979) observed that in 22 of 30 (73%) bulimic
patients, weight loss began sometime during the calendar year
prior to the onset of bulimia. In the study by Garfinkel, Modolfsky,
and Garner (1980), 91% of the patients with bulimic anorexia
developed bulimia after the onset of weight loss. Pyle, Mitchell,
and Eckert (1981) reported that in 30 of the 34 (88%) bulimic
patients “the onset of their bulimic behavior started during a period
of voluntary dieting” (p. 61). Similarly, Mitchell, Hatsukami, Pyle,
and Eckert (1986) stated that 84% of their bulimic sample “indi-
cated that they had started binge-eating during a period of volun-
tary dieting” (p. 166). Although the latter two reports remain
somewhat vague in their description of the exact nature of the
temporal sequence of the two behaviors, Mussell et al. (1997)
recently reported that a total of 69.9% of the cases included in their
study had been categorized as “dieted first,” on the basis of
definitions obtained from the Eating Disorders Questionnaire
(Mitchell, Hatsukami, Eckert, & Pyle, 1985). Finally, Haiman &
Devlin (1999) also reported that in 83.5% of bulimic subjects, the
onset of dieting occurred at an earlier age than the onset of binge
eating based on information obtained with the Diagnostic Survey
for Eating Disorders (C. Johnson, 1984). Onset of bulimia ner-
vosa—although not always consistent across studies—is usually
defined as the onset of binge eating. Dieting as a potential risk
factor can therefore be clearly distinguished from binge eating as
a symptom of the disorder. For anorexia nervosa, however, the
potential risk factor (dieting) and the onset of the disorder—
usually defined as a longer period of dieting and by considerable
weight loss— can be confounded, and drawing the line between the
exposure to a risk factor and the beginning of a disorder can be
much more difficult.
The second line of evidence is derived from experimental and
laboratory-based studies on restrained eating and diet-induced
binge eating. One of the earliest, albeit uncontrolled, studies dem-
onstrating the effects of prolonged dieting in a nonclinical popu-
lation was reported by Keys, Brozek, Hentschel, Mickelsen, and
Taylor (1950). Besides a variety of emotional, physical, and social
changes following a period of semistarvation and average weight
loss of 25%, bingeing was one of the behavioral changes reported,
which had never been observed in the subjects prior to the exper-
iment. In addition, so-called counterregulation or behavioral dis-
inhibition of “restrained eaters” under laboratory conditions has
been regarded as an experimental analog of binge eating (Polivy &
Herman, 1985; Ruderman, 1986; Tuschl, 1990). Although the
concepts of restrained eating and disinhibition following condi-
tions that disrupt the dieter’s restrained eating pattern (e.g., exper-
imental preload, anxiety or stress induction, alcohol consumption)
resemble the behavioral pattern displayed by bulimic patients, they
have been developed in laboratory settings with nonclinical pop-
ulations. Their generalizability to clinical populations of eating
disordered patients has—to our knowledge—not been tested so far.
Taken together, cross-sectional research related to the temporal
sequence of dieting and the onset of eating disorders provides
some evidence for the precedence of dieting in clinical popula-
tions. The relationship seems to be particularly strong for patients
who binge, that is, patients with bulimia nervosa and anorexia
nervosa bingeing–purging subtype, and to a much lesser extent for
restricting anorexic patients. However, the potency of dieting in
these studies is not clear because of the absence of general popu-
lation control groups. In addition, anorexia or strict dieting as-
sessed by an interview was found to be significantly more frequent
in bulimic patients than in controls 6 months before the onset of
bulimia nervosa in the study by Raffi, Rondini, Grandi, and Fava
(2000). The potency of dieting as one of several prodromal symp-
toms (see below) assessed in this study was high. Based on
cross-sectional studies, dieting behavior is classified as a retro-
spective correlate of eating disorders. Replication studies are
needed to confirm the potency of dieting. Its specificity is unclear,
since other clinical comparison groups have not been included.
Turning to results of longitudinal studies, a factor best labeled as
“weight concerns” has been the most often assessed factor (12 of
15 studies). It predicted the development of eating disturbances
most consistently, namely, in 9 of the 10 studies controlling for
initial eating symptomatology (Attie & Brooks-Gunn, 1989; Gha-
deri & Scott, 2001; Graber et al., 1994; Killen et al., 1994, 1996;
Leon et al., 1995, 1999; Patton et al., 1990, 1999; Vollrath et al.,
1992). The factor comprises fear of weight gain, dieting behavior,
negative body image, and specific eating disorder symptoms and
attitudes such as bulimic behavior. Two studies explicitly used the
Weight Concerns Scale developed by Killen et al. (1994) together
with other measures such as the EDI and the Restraint Scale
(Herman, Polivy, Pliner, & Threlkeld, 1978). In three studies, the
EAT-26 was used to assess weight concerns, one study addressed
fatness concern via a single item, one study used a combined risk
score, and two other studies used other questionnaires. Three
studies found that negative adolescent body image or higher body
concern predicted later eating disturbances (Attie & Brooks-Gunn,
1989; Ghaderi & Scott, 2001; Graber et al., 1994), and two other
studies found the EDI Drive for Thinness, Body Dissatisfaction,
and Bulimia subscales as well as the two Restraint subscales
(univariately) to be related to subsequent partial eating syndromes
(Killen et al., 1994, 1996). Body dissatisfaction was also one of the
variables that formed the latent variable negative affect, which
significantly predicted eating disorder risk in the study by Leon et
al. (1999). Subjects initially classified as dieters in the study by
Patton et al. (1990) had an almost eight times higher risk of
becoming cases (mixed bulimic and partial syndromes) than those
initially classified as nondieters. In their more recent study, sub-
jects who dieted at a severe level had an even higher risk (18
 RISK FACTORS FOR EATING DISORDERS
times) of developing an eating disorder than those who did not diet
(Patton et al., 1999).
Five longitudinal studies allowed for the calculation of effect
sizes from raw data. Large AUCs were found for weight concerns
in one study (Killen et al., 1996) and for related constructs such as
EDI Drive for Thinness and Body Dissatisfaction (Killen et al.,
1994, 1996), EAT-26 changes (Patton et al., 1990), the Concern
for Dieting subscale of the Restraint Scale (Killen et al., 1994) and
the BSQ (Ghaderi & Scott, 2001), respectively (range ⫽ 71.66%–
77.54%) in four studies. In addition, four studies yielded medium
AUCs for weight concerns, the Concern for Dieting subscale of the
Restraint Scale (Killen et al., 1994), Body Image (Graber et al.,
1994), EDI Body Dissatisfaction (Killen et al., 1996), as well as
dieting behavior or food restriction (Patton et al., 1990). The
remaining AUCs for the Weight Fluctuation subscale of the Re-
straint Scale and for EDI Bulimia were of small to medium
potency.
Taken together, weight concerns, negative body image or diet-
ing, as assessed in longitudinal research, seems to be a very potent,
well-supported factor which is classified as a variable risk factor in
the Kraemer typology. Again, with the exception of one study,
which did not control for initial symptoms (Button et al., 1996),
none of the reported studies addressed the specificity of weight
concerns by including other outcomes than eating disorders (e.g.,
depression, anxiety disorders).
General psychiatric disturbance and negative emotionality.
Previous theories on the development of eating disorders have
stressed the role of other psychiatric disorders as the “primary
underlying conditions.” Affective disturbances, for example, have
been proposed as underlying disorders for bulimia nervosa, and a
similar relationship has been proposed between anorexia nervosa
and obsessive– compulsive disorders (Casper, 1998; P. J. Cooper,
1995; Fornari et al., 1992; Hsu, Kaye, & Weltzin, 1993; Laessle,
Wittchen, Fichter, & Pirke, 1989). The notion of a third disorder
“causing” eating disorders has also been discussed in the context
of a large body of research on comorbidity, as eating disorders
have been found to be highly comorbid with affective disorders,
substance abuse disorders, anxiety disorders, and predominantly
Cluster B and C personality disorders (for reviews see Casper,
1998; Holderness, Brooks-Gunn, & Warren, 1994; Mitchell,
Specker, & de Zwaan, 1991; Skodol et al., 1993; Wonderlich &
Mitchell, 1997). All of these studies are cross-sectional in nature.
Of specific interest here are comorbid disorders occurring prior to
the onset of the eating disorder. Chronology of onset, however, has
only been explicitly addressed in a very small number of cross-
sectional comorbidity studies. Of these, only half had included a
control group to control for baseline rates of disorders in healthy
individuals. We found two studies fulfilling both the criteria of
chronology and the inclusion of a control group.
Rastam (1992) examined premorbid problems (physical and
developmental problems) and premorbid personality disorders di-
agnosed with a semistructured interview carried out with the
mothers of an adolescent sample of patients with anorexia and
control probands. The total number of premorbid personality dis-
orders was significantly higher in the patients with anorexia (66%
vs. 27%). Of the individual personality disorder diagnoses, only
premorbid obsessive– compulsive personality disorder (OCPD) oc-
curred significantly more often in patients with anorexia than in
the control probands (35% vs. 4%). Personality disorder diagnoses
35
in this study were assigned according to DSM–III–R but not by
structured clinical interviews.
Bulik, Sullivan, Fear, and Joyce (1997) compared prevalence
and onset of comorbid childhood anxiety disorders in two eating
disordered groups (women with anorexia and bulimia nervosa), a
clinical control group (women with major depression), and a
healthy control group (N ⫽ 98). Rates of lifetime anxiety disorders
were highest in the three clinical groups (48%– 60%) but they were
also found in control group (30%). The prevalence of panic dis-
order was highest in the anorexia nervosa and major depression
groups, social phobia was highest in the bulimia nervosa group,
obsessive– compulsive disorder (OCD) was highest in the anorexic
group, overanxious disorder was highest in the anorexic and bu-
limic groups, and separation anxiety disorder was highest in the
anorexic group. Of those individuals with lifetime anxiety disor-
ders, 90% of women with anorexia, 94% of women bulimia, and
71% of women with major depression reported that the onset of
their anxiety disorder predated the onset of their other respective
disorder.
Logistic regression showed that the risk for anorexia nervosa
was significantly increased given the presence of OCD (OR ⫽
11.8) and overanxious disorder (OR ⫽ 13.4) relative to controls.
The risk for bulimia nervosa and major depression was increased
given the presence of social phobia (ORbulimia nervosa ⫽ 15.5;
ORmajor depression ⫽ 6.4) and overanxious disorder (ORbulimia nervosa ⫽
4.9; ORmajor depression ⫽ 6.1) relative to controls. The authors
interpret their findings as supporting the hypothesis that overanx-
ious disorder of childhood is a nonspecific risk factor for later
psychopathology (eating or affective disorders) and that the rela-
tionship with anorexia nervosa is particularly strong. Similarly,
social phobia may represent a nonspecific risk factor for eating and
affective disorders but its association with bulimia nervosa was
particularly strong. In addition to identifying overanxious disorder
of childhood, it has also been shown that OCD may be a specific
risk factor for anorexia nervosa (Bulik et al., 1997).
No information could be obtained as to the rates of the specific
anxiety disorders preceding the eating disorders in this study.
When the rates of any lifetime anxiety disorder were compared in
the three patient groups, the rates in patients with anorexia nervosa
and in patients with bulimia nervosa versus patients with depres-
sion were almost twice as high: 54% of anorexic patients, 53% of
bulimic patients, and 34% of depressed patients endorsed the
presence of any lifetime anxiety disorder predating the onset of the
eating disorder. The potency of lifetime anxiety disorders in both
eating disordered groups cannot be specified; the potency of
OCPD in anorexia nervosa based on AUC is medium.
In an attempt to explore mood and anxiety related prodromal
symptoms of bulimia nervosa, Raffi et al. (2000) found the fol-
lowing symptoms to be significantly more common in patients
with bulimia than in controls 6 months before the onset of the
disorder: low self-esteem (see below), depressed mood, anhedonia,
irritability, impaired work performance, generalized anxiety, psy-
chophysiological reactivity, phobic avoidance, guilt, and strict
dieting. Prodromal symptoms were assessed using a modified
version of Paykel’s Clinical Interview for Depression. Unfortu-
nately, anorexia or strict dieting was the most frequent and highly
potent prodromal symptom. Because the exact sequence of the
individual prodromal symptoms was not assessed, both the mood-
and anxiety-related symptoms observed before the onset of the
36 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
bulimia could be confounded with strict dieting. The potency of
the mood-related symptoms and of dieting has to be considered
high; AUCs for the other symptoms were small and medium.
Although specificity has not been tested in this study, it seems
unlikely that these symptoms are specific prodromal symptoms of
eating disorders because they also present themselves as typical
prodromal symptoms of depressive disorders.
Taken together, cross-sectional evidence for comorbid disorders
is limited to childhood overanxious disorder, social phobia, OCD,
and OCPD. These disorders are therefore classified as retrospec-
tive correlates for either anorexia or bulimia nervosa. As the
evidence for the correlate status of these anxiety disorders is
limited to one study only, further studies are needed to replicate
these results and also to examine the role of other comorbid
disorders (e.g., affective and substance use disorders). In addition,
prodromal mood- and anxiety-related symptoms are classified as
retrospective correlates for bulimia nervosa. However, their exact
interaction with more specific prodromal symptoms of eating
disorders needs to be clarified.
Seven longitudinal studies included general psychiatric morbid-
ity, psychopathology, or, more specifically, negative emotionality
as a predictor (Attie & Brooks-Gunn, 1989; Graber et al., 1994;
Killen et al., 1996; Leon et al., 1995, 1999; Patton et al., 1990,
1999). The change score in general psychiatric morbidity in the
study by Patton et al. (1990) turned out to be the only predictor of
caseness in the multivariate testing, although it explained only
3.8% of diagnostic variance. In the study by Patton et al. (1999),
psychiatric morbidity predicted the onset of eating disorders (in-
cluding partial syndromes) independently of dieting status. In this
study, psychiatric morbidity turned out to be a strong predictor,
with subjects in the highest morbidity category exhibiting an
almost sevenfold risk of developing an eating disorder. Leon et al.
(1999) found negative affectivity to be the only significant (though
moderate) predictor of eating disorder risk measured 3– 4 years
later. The negative affect variable consisted of the measures of
negative emotionality, depression, ineffectiveness, and body dis-
satisfaction. In four other studies (Attie & Brooks-Gunn, 1989;
Graber et al., 1994; Killen et al., 1996; Leon et al., 1995), negative
emotionality or psychopathology did not predict the outcome in
the multivariate analyses; in two of these, internalizing dimensions
of psychopathology were only concurrently associated with eating
disturbances (Attie & Brooks-Gunn, 1989; Graber et al., 1994).
However, two of the temperament scales (distress, fear) used in the
study by Killen et al. (1996) discriminated asymptomatic from
symptomatic girls in the univariate comparisons, at medium and
large AUC effect sizes.
Prior psychiatric morbidity and negative emotionality are vari-
able risk factors of unclear potency, as, apart from the tempera-
ment scales, no other AUCs could be calculated. None of the
longitudinal studies addressed the specificity of this risk factor.
However, longitudinal studies in other fields indicate that premor-
bid anxiety disorders and negative affectivity are risk factors for
the development of other psychiatric conditions including affective
disorders and substance abuse (Hayward, Killen, Kraemer, &
Taylor, 2000; Ingram & Price, 2000; Pine, Cohen, Gurley, Brook,
& Ma, 1998). They can therefore be considered as nonspecific risk
factors.
Sexual abuse. The role of sexual abuse, especially childhood
sexual abuse, as a risk factor for eating disorders has been widely
discussed in many studies as well as in several early (e.g., Connors
& Morse, 1993; Everill & Waller, 1995; Pope & Hudson, 1992) or
more recent reviews (e.g., Wonderlich, Brewerton, Jocic, Dansky,
& Abbott, 1997). All but one study are cross-sectional in nature.
For a comprehensive examination of the role of sexual abuse as a
risk factor for eating disorders, studies included here were not
restricted to childhood sexual abuse but rather dealt with any kind
of sexual abuse reported. For sexual abuse to be considered a risk
factor it did not necessarily have to occur in childhood but did have
to occur before the onset of the eating disorder. In addition,
because methodological inconsistencies in the definitions of child-
hood versus adolescent abuse in the included studies (e.g., over-
lapping criteria and required ages for classification as childhood or
adolescent abuse), a distinction between these different types of
abuse did not seem valid.
We found 10 studies fulfilling the inclusion criteria, 3 of these
with community samples and 7 with clinical samples. Considering
studies with clinical samples, L. Brown, Russell, Thornton, and
Dunn (1997) found that patients with eating disorders (mixed
groups with anorexia and bulimia nervosa) had significantly higher
rates (34% vs. 20%) of child sexual abuse compared with a control
group of general practice patients. Unfortunately, the analyses
were not carried out separately for individual eating disorder
diagnoses. No information was given on the onset of the eating
disorder or first occurrence of sexual abuse. Bulimic patients in
Casper and Lyubomirsky’s (1997) study reported higher rates of
rape, sexual harassment, and molestation after age 17, but not of
childhood sexual abuse, compared with controls. Information on
the onset of the eating disorder was not presented. Folsom et al.
(1993) compared their mixed anorexic and bulimic clinical sample
with a general psychiatric group and found no significant differ-
ences in the rates for sexual abuse between the two groups. Steiger
and Zanko (1990) compared four groups of eating disordered
samples (anorexic restricted eaters, anorexic binge eaters, bulimic
individuals with an anorexic history, and bulimic individuals with
no prior anorexia) with a group of psychiatric controls and a group
of nonpsychiatric controls. Frequencies of any kind of abuse were
highest in the anorexic binge eaters, both bulimic groups, and the
psychiatric control group, and frequencies of any kind of abuse
were lowest in anorexic restricted eaters and in the nonpsychiatric
control group. The majority of the sexual trauma occurred between
the ages of 5 and 15, but no eating disorder onset information was
given. Webster and Palmer (2000) found no differences in the rates
of sexual abuse occurring before age 16 when comparing four
clinical groups (anorexia nervosa, bulimia nervosa, mixed an-
orexia and bulimia nervosa, major depression) to a nonmorbid
comparison group. However, significant differences were found
when comparing overall childhood sexual experience rates for the
anorexia nervosa and the major depression groups and when
comparing sexual experiences before age 13 between the bulimia
nervosa and the major depression groups. In both cases, the pa-
tients who had eating disorders showed lower rates than the
patients who had major depression. In 74% of the patients with
eating disorders, age of onset of the eating disorder was after the
age of 16. In the study by Steiger et al. (2000), significantly
elevated rates of childhood sexual abuse prior to age 13 in bulimic
patients were only found in the presence of borderline personality
disorder; in its absence only nonsignificantly elevated rates were
found.
 RISK FACTORS FOR EATING DISORDERS
Although it seems very likely that the abuse occurred prior to
the onset of the eating disorder in the latter two studies, only one
study with clinical samples explicitly assessed the precedence of
the abuse relative to the eating disorders (Vize & Cooper, 1995).
Comparing three patient groups (anorexia nervosa, bulimia ner-
vosa, and depression) and a control group, the authors found that
the rates of abuse did not differ significantly between the three
patient groups (42.9%, 27.1%, 40.0%, respectively) but that all of
the clinical groups had significantly higher rates of sexual abuse
than did the control group (6.7%).
Examining sexual abuse in a community sample, Dansky, Brew-
erton, Kilpatrick, and O’Neal (1997) found that bulimic respon-
dents had a significantly higher prevalence of rape, sexual moles-
tation, aggravated assault, direct victimization, and current and
lifetime history of posttraumatic stress disorder (PTSD) compared
with controls. The odds of having bulimia nervosa were 1.86 times
higher among victims of direct assault than among women of the
nonvictim group, controlling for PTSD status (26.0% vs. 13.3%).
In contrast, respondents with binge-eating disorder did not differ
from control subjects (11.5%). Garfinkel et al. (1995), in a large
epidemiological study, found that bulimic subjects had experi-
enced childhood sexual abuse at almost three times the rate of the
female comparison group. Finally, Welch and Fairburn (1994)
found sexual abuse to be significantly more common in the
community-based bulimic group than in the comparison subjects
without an eating disorder (OR ⫽ 3.16; 26% vs. 10%) but found
no differences between bulimic subjects and general psychiatric
patients (26% vs. 24%). Both in Welch and Fairburn’s study and
in Dansky et al.’s study, the abusive experiences occurred before
the onset of the eating disorder, whereas Garfinkel et al. (1995) did
not report age of onset or age of first occurrence of sexual abuse.
Taken together, in five studies (two with community samples,
three with clinical samples) evidence of sexual abuse predating the
eating disorder was reported or was highly probable. All but one
found higher rates of sexual abuse for both patients with bulimia
and anorexia nervosa but not for patients with binge-eating disor-
der. In the studies that did not address precedence the findings are
similar. However, the evidence is much stronger for bulimia ner-
vosa than for anorexia nervosa. With one exception (Webster &
Palmer, 2000), no differences were found when comparing people
with anorexia and bulimia nervosa with other psychiatric patient
groups. Furthermore, the results did not vary with respect to the
type of sample examined, that is, clinical or community. Thus,
sexual abuse was classified as a nonspecific, retrospective corre-
late for anorexia and bulimia nervosa. In the majority of studies,
the potency of sexual abuse according to the AUC is low.
To date, only one longitudinal study investigated the association
between childhood adversities including sexual abuse and prob-
lems with eating or weight during adolescence and early adulthood
in a large community-based sample of mothers and offspring (J. G.
Johnson et al., 2002). Individuals who had experienced sexual
abuse or physical neglect during childhood were at elevated risk
for eating disorders and some eating problems (e.g., weight fluc-
tuations, strict dieting) during adolescence or early adulthood.
Information on sexual abuse and physical neglect had been ob-
tained from a central registry and, for a subgroup of the sample,
from maternal interviews. Sexual abuse and physical neglect in
this study is classified as a nonspecific, variable risk factor of
37
medium potency. However, additional prospective replication
studies are needed.
Adverse life events. Although the association between stressful
life events and psychopathology in general has been studied ex-
tensively (G.W. Brown & Harris, 1978; Dohrenwend & Dohren-
wend, 1981), only a few studies have investigated the relationship
between stressful life events and the onset of an eating disorder.
All of these studies are again cross-sectional in nature. Among
studies comparing patients with eating disorders solely with non-
psychiatric controls, the results are not consistent. Welch, Doll,
and Fairburn (1997) found that their community sample of patients
with bulimia nervosa reported more life events during the year
before onset of disordered eating in comparison with age-matched
healthy controls (18% vs. 5% for three or more events). In contrast,
the percentages of (recovered) anorexic and bulimic patients who
had experienced a severe event before the onset of their eating
disorder did not differ markedly from the percentage of controls
who had experienced severe events in the study by Troop and
Treasure (1997). The authors, however, did not explicitly test the
differences for significance.
Schmidt, Tiller, Blanchard, Andrews, and Treasure (1997),
comparing anorexic and bulimic patients as well as community
controls, found no differences in the proportion of patients with at
least one severe event but found that significantly more anorexia
and bulimia patients had experienced what was called a “major
difficulty” and “pudicity” problems. Also, Rastam and Gillberg
(1992), comparing a mixed clinical and population sample of 51
anorexic patients with a matched control group, found differences,
not with respect to chronic life events, but with respect to recent (3
months before onset of the disorder) major life events such as loss
of first-degree relatives (14% of anorexic patients vs. 0% of controls).
Among studies that also included a psychiatric control group,
the studies by Horesh and colleagues found that adverse life events
differentiated significantly between anorexic patients and healthy
controls (Horesh et al., 1995) and between a mixed group of
anorexic and bulimic patients and healthy controls (Horesh et al.,
1996). More distinct differences in comparison to psychiatric
controls could be found only for one of the subcategories (i.e.,
inappropriate parental pressures; Horesh et al., 1996). Gowers,
North, and Byram (1996) found an intermediate rate of negative
life events for anorexic patients between that of psychiatric pa-
tients and community controls.
Taken together, there is some evidence that bulimic and an-
orexic patients experience more severe life events before the onset
of their eating disorder than healthy control subjects, although the
evidence for this is not as consistent as it is for the role of sexual
abuse. There is also some evidence that this relationship is not
specific to patients with eating disorders but true for psychiatric
patients in general. In all of the studies investigating the role of life
events in precipitating eating disorders, the events were reported to
have occurred prior to the onset of the eating disorders. Therefore,
general adverse life events are classified as nonspecific retrospec-
tive correlates. The potency of adverse life events has to be
considered as small, with consistent AUC classification results
both across studies and eating disorder diagnoses (anorexia ner-
vosa, bulimia nervosa).
Body mass index (BMI) and other weight-related variables.
Childhood obesity was one of the risk factors assessed retrospec-
tively for the time span prior to the eating disorder in the studies
38 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
by Fairburn and colleagues (Fairburn, Cowen, & Harrison, 1999;
Fairburn et al., 1998; Fairburn, Welch, Doll, Davies, & O’Connor,
1997). Three patient groups of people with eating disorders (those
with histories of anorexia nervosa, of bulimia nervosa, and of
binge-eating disorder) were separately compared in three
community-based, case-control studies with a group of general
psychiatric patients and a group of nonpsychiatric controls. A large
number of putative risk factors (N ⫽ 59) were assessed by an
interview focusing on the period before the onset of the eating
disorders. Childhood obesity specifically differentiated subjects
with bulimia nervosa and binge-eating disorder from the psychi-
atric control group. Almost a third of the subjects with binge-
eating disorder and 40% of the subjects with bulimia nervosa in
these studies reported childhood obesity as compared with 13% to
19% of the control groups. In addition, in bulimic patients parental
obesity was reported to occur more often than in both control
groups. On the basis of these cross-sectional studies, childhood
and parental obesity are classified as a specific retrospective cor-
relate of low potency. Although these studies do have some im-
portant methodological strengths such as large sample sizes and
community-based samples, the large number of putative risk fac-
tors tested increases the risk of false positive results. Also, no
information concerning validity and reliability of the risk factor
interview was provided. Given these limitations and the fact that
only one study for bulimia nervosa and one study for binge-eating
disorder supported the status of childhood obesity as a retrospec-
tive correlate, a replication of these findings is necessary.
Weight-related variables were assessed in seven longitudinal
studies, three of which found positive relations with subsequent
eating disturbances or disorders. Higher BMI or higher degree of
body fat was positively correlated with subsequent Bulimic Inves-
tigatory Test (BITE) total scores in the study by Calam and Waller
(1998), although it did not significantly predict risk status (defined
by high BITE and EAT-26 scores) 7 years later. However, in this
study initial levels of EAT-26 and BITE scores had not been
controlled for. Higher BMI or higher degree of body fat was also
predictive of being symptomatic (Killen et al., 1994), or a partial
diagnosis, of binge eating (Vollrath et al., 1992). In the study by
Killen et al. (1994), higher BMI was predictive in the univariate
comparisons only, not in the multivariate testing. In four other
studies, BMI or percentage of body fat at Time 1 was not related
to subsequent eating disturbances or caseness (Attie & Brooks-
Gunn, 1989; Graber et al., 1994; Killen et al., 1996; Patton et al.,
1999), although in one of these studies BMI had not been entered
separately in the analyses but as part of a set of physical maturation
variables. If the aforementioned studies with limitations were not
taken into consideration (or counted), two longitudinal studies
found higher BMI to be predictive of partial syndromes, whereas
three other studies did not support this relationship. Accordingly,
higher BMI cannot be classified as a risk factor.
Early childhood eating and digestive problems. One case-
control study found retrospectively assessed early feeding and
severe gastrointestinal problems to be extremely frequent in ano-
rectic patients (together, found in 90%). Rates were almost two
times higher than in the matched control group (Rastam, 1992).
Early childhood eating problems were addressed prospectively
in two studies: The first longitudinal study including a sample of
younger children found pica, early digestive problems, and reduc-
ing efforts related to later bulimic symptoms. Digestive problems
and picky eating were prospectively related to subsequent anorexic
symptoms. An elevation on a measure of anorexic symptoms was
related to later full diagnoses of anorexia nervosa, and pica in early
childhood was related to a full diagnosis of bulimia nervosa in
adulthood (Marchi & Cohen, 1990). The risk of bulimia nervosa
was found to be almost seven times higher in those with pica in
early childhood; however, no information on base rates in both
groups was presented.
The second longitudinal study also found a range of early
childhood eating problems assessed between 1 and 10 years of age
to predict eating disorder diagnoses in early and late adolescence
and young adulthood: Eating conflicts, struggles around meals,
and unpleasant meals in childhood predicted later diagnosis of
anorexia nervosa, whereas eating too little was modestly protective
for the future diagnosis of bulimia nervosa (Kotler et al., 2001).
Pica, digestive problems, not eating, not being interested in food,
picky eating, and eating too slowly predicted neither anorexia nor
bulimia nervosa in adolescence or adulthood. Although eating
conflicts, struggles around meals, and unpleasant meals are usually
correlated with picky eating, the OR for picky eating failed to
reach significance (5.1). Also, the respective confidence interval
was very large (0.4, 56.3), possibly indicating outliers (e.g., a low
prevalence of the predictors).
On the basis of the results of the case-control study, early
childhood feeding and digestive problems are classified as retro-
spective correlates of medium potency. On the basis of the results
of the longitudinal studies, pica, picky eating, digestive and other
early eating-related problems as well as eating conflicts, struggles
around meals, and unpleasant meals are classified as variable risk
factors of unclear potency. Given the small number of studies and
the methodological limitations mentioned above, replication stud-
ies are needed. Specificity has not been tested in either type of
study.
Low interoception. Low interoception or low interoceptive
awareness is—in line with ineffectiveness and body image distur-
bances— one of the three core psychopathological features of
patients with eating disorders, as originally suggested by Bruch
(1962). The construct of low interoception addresses difficulties in
the interpretation of internal (emotional and gastrointestinal) stim-
uli. Its correlate status has been confirmed in numerous cross-
sectional studies using the corresponding EDI subscale. In con-
trast, longitudinal evidence on the role of interoception is much
more scarce. Low interoceptive awareness was predictive of Year
3 disordered eating in one longitudinal study (Leon et al., 1995). In
three other studies in which it was assessed, it did not turn out to
be predictive when considered in a multivariate model (Killen et
al., 1994, 1996; Leon et al., 1999). Differences were, however,
found in univariate comparisons between the group that turned out
to be symptomatic and the asymptomatic group (Killen et al.,
1994, 1996). In these studies, the AUCs were small and medium,
respectively. Low interoceptive awareness is therefore classified as
a variable risk factor of unclear potency and specificity.
Family interaction, family functioning, and attachment styles.
Historically, the role of dysfunctional family interaction styles was
put forward in theories on the development of eating disorders
(Bruch, 1973; Minuchin, Rosman, & Baker, 1978). Characteristics
of the patient–family relationships of patients with eating disorders
include problematic family structures, interaction or communica-
tion styles (e.g., overprotection, enmeshment), and attachment
 RISK FACTORS FOR EATING DISORDERS
styles. Although the total number of cross-sectional studies exam-
ining these factors is relatively large, the number of studies using
nonpsychiatric control groups is small, and there is a striking lack
of studies including psychiatric or other psychologically disturbed
control groups.
In the majority of studies (e.g., Friedmann, Wilfley, Welch, &
Kunce, 1997; Garfinkel et al., 1983; McNamara & Loveman,
1990; Shisslak, McKeon, & Crago, 1990; Strober & Humphrey,
1987; Waller, Calam, & Slade, 1989) anorexic and bulimic pa-
tients describe different aspects of their family structure (e.g.,
interaction, communication, cohesion, affective expression) as
more disturbed, conflictual, pathological, or dysfunctional than do
controls across different family assessment measures. A more
recent study also found similar levels of family dysfunction for
obese binge eaters as for normal-weight bulimic patients compared
with normal-weight and overweight controls (Friedmann et al.,
1997). Also, patients with eating disorders seem to be more likely
than controls to report attachment disturbances, such as insecure,
anxious attachment styles and deactivating defensive strategies
(Cole-Detke & Kobak, 1996; O’Kearney, 1996).
Besides a number of methodological limitations, for example,
reliance on patient or (more rarely) parent self-report measures and
limited number of studies including observational measures of
family functioning, the more crucial limitation with regard to the
aim of the present review is the issue of precedence. The onset of
the eating disorder relative to the family dysfunction has not been
taken into consideration. Accordingly, in the majority of these
cross-sectional studies, variables of family interaction, family
functioning, or attachment are classified as correlates. Further-
more, patterns of family interaction or family functioning in other
disorders (noneating disorders) resemble those found in eating
disorders (e.g., Woodside, Swinson, Kuch, & Heinmaa, 1996),
indicating a possible nonspecific nature of these disturbances.
To date, in four studies family variables for the time span prior
to onset of the eating disorders were assessed retrospectively. In
the studies by Fairburn and colleagues (Fairburn, Cowen, & Har-
rison, 1999; Fairburn et al., 1997, 1998) some parental variables
(high expectations, low contact, and critical comments about
weight and shape by the family) were found to be specifically
predictive for bulimia nervosa when compared with the psychiatric
comparison group. The last two of the parental variables were also
specifically predictive for patients with binge-eating disorder.
These factors are classified as retrospective correlates of low to
medium potency, depending on factor and outcome.
The childhood and family background as well as the specificity
of these possible characteristics were also addressed retrospec-
tively in the study by Webster and Palmer (2000). Three groups of
eating disorder patients (anorexia nervosa, bulimia nervosa, mixed
anorexia and bulimia nervosa) were compared with a group of
women with major depression and a nonmorbid comparison group
using a semistructured interview measure of childhood care before
the age of 17. When compared with the nonmorbid group, patients
with anorexia nervosa showed no significant differences on any of
the variables studied (e.g., parental indifference, control and care,
antipathy, discord in family). By contrast, women with bulimia
nervosa reported significantly more indifference, discord, lack of
care, and overall adversity than the women of the nonmorbid
comparison group. The pattern of the women with major depres-
sion did not differ significantly from that of the women with
39
bulimia nervosa, pointing to the nonspecific nature of these expe-
riences. Variables of troubled family background as assessed in
this study are classified as nonspecific retrospective correlates.
With one exception (discord in family), the AUCs are indicative of
low potency.
The individual’s perception of parental acceptance versus rejec-
tion during childhood was the focus of the study by Dominy,
Johnson, and Koch (2000). Women with binge-eating disorder
were compared with obese and nonobese women without eating
disorders on their perception of parents. Women with binge-eating
disorder reported greater paternal (not maternal) neglect and re-
jection than did nonobese women, whereas the obese women
without binge-eating disorder did not differ significantly from the
other two groups. Perceived paternal neglect and rejection are
therefore classified as retrospective correlates of medium potency.
Because no clinical control groups had been included, their spec-
ificity is not known.
Shoebridge and Gowers (2000) addressed overprotection or
high-concern parenting in anorexia nervosa as part of a cross-
sectional case-control study. High-concern parenting was assessed
by a structured clinical interview carried out with the mothers
covering the first 5 years of the child’s life. A wide range of
high-concern attitudes and behaviors was found to be significantly
more frequent in mothers of anorexic patients compared with
mothers of controls. Two or more high-concern attitudes and
behaviors were almost four times as frequent in mothers of an-
orexic patients than in mothers of controls. In addition, infant sleep
pattern difficulties were significantly more frequent in anorexic
patients than in controls. In the same sample, a more than threefold
higher frequency of obstetric losses was found prior to the birth of
the future anorexic patients compared with controls. The findings
concerning parenting may therefore also reflect an adaptive paren-
tal behavior to a severe life event and may not be generalizable to
a different sample or different (e.g., adolescent) age group. The
presence of two or more variables of high-concern parenting is
classified as a retrospective correlate of medium potency and
unclear specificity.
Four longitudinal studies included family structure or family
functioning variables as potential risk factors for later eating
problems (Attie & Brooks-Gunn, 1989; Button et al., 1996; Calam
& Waller, 1998; Graber et al., 1994). The Family Relationships
Scale used in the longitudinal analyses of the study by Attie and
Brooks-Gunn (1989) did not contribute further to the prediction of
EAT-26 scores 2 years later once initial EAT-26 scores and body
image had been taken into account. In the study by Graber et al.
(1994), family relationships assessed by the Family Environment
Scale (Moos, 1974) did not differentiate the low-risk group from
the higher risk group 4 and 8 years later, nor did the question
regarding family relationships in the study by Button et al. (1996)
predict different EAT-26 outcome scores 4 years later. Calam and
Waller (1998) found moderate correlations (r ⫽ .21–.36) between
some of the Family Assessment Device Scales (Communication,
Roles, General Function) at Time 1 and EAT-26 and BITE scores
at Time 2, 7 years later, but initial eating disturbances were not
controlled for. Because evidence for family relationship factors
was found in only one longitudinal study, which did not control for
initial eating disturbance symptoms, they are not classified as risk
factors but remain correlates.
40 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
Family history and family psychopathology. This section deals
with the role of familial psychiatric disorders as a potential risk
factor for eating disorders. All of the studies falling into this
category are cross-sectional in nature. In addition to the inclusion
criteria outlined above, only studies using the family study method
were included here. In earlier studies comparing the family study
method (direct interviews of family members to obtain the psy-
chiatric family history) with the family history method (assessment
of the psychiatric family history via interviewing the patient), the
family history method had been shown to underestimate preva-
lences of psychiatric disorders in relatives (Andreasen, Rice, En-
dicott, Reich, & Coryell, 1986; Gershon et al., 1983; Orvaschel,
Thompson, Belanger, Prusoff, & Kidd, 1982). Also, a recent
review on familial aggregation of eating disorders (Lilenfeld et al.,
1997) suggests that some of the inconsistencies of the results might
be related to the use of a family history design.
To avoid additionally biasing the retrospective assessment of the
putative risk factors by relying on patient information solely, we
decided to include only studies that had obtained the risk factor
information (psychiatric disorder or any other familial factors) by
direct examination of the relatives (family study design). As it is
generally not possible to interview all of the family members
directly, a family study design very often also includes a certain
number of family members whose family history has been ob-
tained through other available relatives using family history
interviews.
Blind assessment of information about relatives of eating dis-
order patients is another methodologically crucial criterion. Blind-
ness of interviewers was not reported in almost half of the studies
reviewed below. As the total number of studies is still relatively
small, we decided to not use blindness as an additional inclusion
criterion but to consider it carefully in the interpretation and
summary of the results.
We found seven studies comparing familial psychopathology of
anorexic patients with relatives of either a healthy or psychiatric
control group. The study by Gershon et al. (1983) was one of the
first to apply a methodologically rigorous family study approach
including a blind analysis of family interview data. The combined
rates of anorexia and bulimia nervosa in first-degree relatives of
anorexic probands were six times higher than in relatives of
controls.
Rivinus et al. (1984) also found that anorexic patients had
significantly more first-degree relatives with psychiatric disorders
than the healthy control group (morbid risk: 36.6% vs. 18.2%).
Comparisons of individual diagnoses indicated that only the dif-
ferences in the combined frequencies of depression or substance
abuse were significantly elevated in patients’ first- and second-
degree relatives in comparison to controls (morbid risk for first-
degree relatives: 29.5% vs. 12.9%; for second-degree relatives:
23.3% vs. 13.8%). Differences in the frequency of depression
alone and substance abuse disorders alone failed to attain signifi-
cance. A limitation of this early study is the assessment of psy-
chiatric histories while nonblind to the patients’ clinical diagnosis.
Also, the family history information gathered in this study using
the Family History Research Diagnostic Criteria did not include
categories of eating disorders.
Strober, Morrell, Burroughs, Salkin, and Jacobs (1985) com-
pared anorexic probands with psychiatrically ill control probands.
They found a threefold greater risk of anorexia nervosa and a
2.5-fold greater risk of bulimia nervosa in female first- and second-
degree relatives compared with relatives of control probands.
Pooling all eating disorder diagnoses (anorexia nervosa, bulimia
nervosa, subclinical anorexia), female relatives of anorexic pa-
tients had a fivefold increased risk compared with relatives of
controls (unadjusted OR ⫽ 5.46).
In a subsequent study, which included the sample from the first
study, patients with anorexia nervosa, patients with major affective
disorder, and mixed nonaffective disorders, Strober, Lampert,
Morrell, Burroughs, and Jacobs (1990) again found significantly
elevated lifetime rates for anorexia nervosa and eating disorders in
general, but not for bulimia nervosa, when compared with both
control groups. The risk of an eating disorder in relatives of
patients with anorexia nervosa was fivefold as compared with the
mixed patient group and tenfold as compared with relatives of
affective disorder probands. Stratification by presence or absence
of coexisting depression did not lead to significantly different rates
of eating disorders in relatives of patients with anorexia nervosa,
whereas the risk for affective disorder was markedly increased in
relatives of depressed anorexic patients as compared with relatives
of nondepressed anorexic patients and relatives of the mixed
proband group. Also, the risk for affective disorder in relatives of
depressed anorexic patients did not differ from relatives of pure
affective disorder probands.
In a combined comorbidity and family history study, Halmi et
al. (1991) found only OCD and psychosexual dysfunction to be
significantly more prevalent in the directly interviewed mothers of
the anorexic patients compared with mothers of controls. Diag-
noses were determined blind to proband status.
Stern et al. (1992) assessed personal as well as family psychi-
atric history in one parent of patients with anorexia nervosa and
matched controls. Lifetime prevalence and morbid risk of psycho-
active substance use disorder did not significantly differ between
the relatives of the two groups, nor did the total number of eating
disorders.
Finally, Nilsson, Gillberg, and Rastam (1998) interviewed
mothers and patients of a mixed group of anorexic clinical and
community probands and matched control probands with a (non-
standardized) semistructured family– genetic interview. The only
significant differences between the groups were for history of
major depression and for two or more social impairment symptoms
of autism in relatives of anorexic patients. Limitations of the study
are that diagnoses of anxiety and depression were only assigned to
individuals who had been treated for these diagnoses, that insuf-
ficient information was provided about the final assignment of
diagnoses, and that the family background information was not
analyzed fully blind.
Seven studies examined the family history of bulimic patients in
comparison with normal controls. In three of these, the eating
disorder patient groups had, in addition to generally looking at
rates of psychiatric disorders in the families, either been stratified
by presence or absence of one specific (major depression, sub-
stance abuse) or any of the respective comorbid disorders.
In one of the earliest studies fulfilling the inclusion criteria,
Stern et al. (1984) could not find significant differences between
the relatives of DSM–III-bulimic probands and matched control
probands with regard to either the lifetime prevalence of affective
disorder or morbid risk for major affective disorder.
 RISK FACTORS FOR EATING DISORDERS
Kasset et al. (1989), in contrast, found a significantly higher risk
for major affective disorder, bulimia nervosa, total eating disor-
ders, and alcoholism in relatives of bulimic patients as compared
with relatives of controls. The rates for major affective disorder
and bipolar disorder alone were still significantly elevated when
relatives of bulimic patients who themselves had no history of a
major affective disorder were compared with relatives of bulimic
patients with such a history, indicating a familial relationship
between bulimia and major affective disorder. No information
regarding blindness to proband diagnosis when assessing the fam-
ily history was given.
The study by Carney, Yates, and Cizadlo (1990) is one of the
few studies examining parental personality psychopathology.
DSM–III–R personality traits in first-degree family members of
bulimic probands were assessed using a self-report personality
inventory (Personality Diagnosis Questionnaire—Revised). No
differences in mean scores could be found when compared with
control families. Bulimic probands in this study, however, had not
been stratified according to their own comorbid personality
disorder.
Boumann and Yates (1994) found both the rates for any psy-
chiatric disorder, major depression, and personality disorder sig-
nificantly more frequent in parents of bulimia nervosa patients
compared with parents of matched controls (respective ORs: 4.8,
3.5, and 6.1). Although the rates for alcoholism were higher in
parents of the bulimic group (10%) than in the control parents
(4%), the difference was not statistically significant. The study is,
similar to the study by Carney et al. (1990), limited by the
self-report assessment of personality disorders (which may lead to
increased rates of false positive personality disorder diagnoses)
and the mixture of interview and self-report techniques for the
assessment of the other psychiatric illnesses.
Kaye et al. (1996) found that the prevalence of both alcohol and
drug dependence was increased only among the first-degree rela-
tives of bulimic women who themselves had alcohol or drug
dependence, whereas the first-degree relatives of bulimic probands
without alcohol or drug dependence did not have increased rates,
suggesting an independent transmission of these two disorders in
families.
Lilenfeld et al. (1997) also found elevated rates of alcohol and
drug dependence, drug abuse, social phobia, panic disorder, and
Cluster B personality disorders among first-degree relatives of
bulimic women with comorbid substance dependence compared
with the relatives of bulimic women without comorbid substance
dependence and relatives of a community control group. In rela-
tives of both bulimic groups, rates of EDNOS and of overanxious
disorder were also significantly higher compared with relatives of
the control group. OCD and generalized anxiety disorder were
significantly more common among relatives of bulimic women
without substance dependence, whereas major depressive disorder
was significantly elevated among relatives of women with bulimia
nervosa and comorbid substance dependence. The authors there-
fore suggested an independent familial transmission of bulimia
nervosa and substance dependence.
Stein et al. (1999) found in both the sisters and the mothers of
bulimic probands significantly higher lifetime rates of eating dis-
orders, especially EDNOS when compared with sisters and moth-
ers of controls. Finally, four studies included either an mixed
bulimic–anorexic sample (Logue, Crowe, & Bean, 1989; Pasquale,
41
Sciuto, Cocchi, Ronchi, & Bellodi, 1994) or separate groups of
anorexic and bulimic patients each (Lilenfeld et al., 1998; Strober,
Freeman, Lampert, Diamond, & Kaye, 2000).
Logue et al. (1989) compared psychiatric illnesses in the fami-
lies of a mixed bulimic and anorexic eating disorder patient group,
the families of a group with major depression, and the families of
a nonpsychiatric control group. For all diagnoses, they found that
relatives of the eating disorder probands had higher rates of illness
than the relatives of the controls. Only major depression, however,
was significantly higher among the relatives of the eating disorder
probands (adjusted OR ⫽ 3.51), whereas alcoholism or drug abuse
did not significantly aggregate among the eating disorder families.
The results of the study are limited by the nonblind assessment of
diagnoses in relatives, the relatively small sample sizes of both the
major depression and the control groups, and the mixture of
bulimic and anorexic diagnoses in the eating disorder group, which
might have resulted in samples sizes too small for meaningful
comparisons.
In a comparison of families of patients with eating disorders,
OCD patients, and patients with mood disorders, Pasquale et al.
(1994) found among all diagnoses evaluated a significantly ele-
vated morbidity risk only for OCD in the families of OCD pro-
bands when compared with the other two groups.
Comparing purely restricting anorexic probands, bulimic pro-
bands, and community controls, Lilenfeld et al. (1998) found
similar (unadjusted) lifetime rates of EDNOS and any eating
disorder in first-degree relatives of anorexic and bulimic probands.
These rates were significantly greater than among relatives of
control probands. Relatives of bulimic probands had significantly
higher rates, and relatives of anorexic probands a trend toward
higher rates, of major depressive disorder than did relatives of
control probands. Unadjusted rates of substance disorders did not
differ between groups, the (adjusted) risk for alcohol and drug
dependence was, however, half as much among relatives of an-
orexic probands as among relatives of bulimic probands. Relatives
of both anorexic and bulimic patients had significantly increased
rates of generalized anxiety disorder and panic disorder compared
with relatives of control probands. Relatives of anorexic probands
had increased rates of social phobia and OCD compared with
relatives of controls and increased rates of OCPD compared with
relatives of both bulimic and control probands. Relatives of bu-
limic probands had significantly elevated rates of PTSD and Clus-
ter B personality disorders compared with relatives of control
probands. After stratification by proband comorbidity status, there
were elevated adjusted RRs for major depressive disorder only
among relatives of anorexic and bulimic probands who themselves
suffered from major depressive disorder, suggesting independent
familial transmission. Similar results were found for OCD. Rates
of OCPD among relatives of anorexic probands with and without
OCPD were almost identical and significantly greater than among
relatives of control probands, suggesting shared familial transmis-
sion of anorexia nervosa and OCPD.
The most recent study determined lifetime rates of full and
partial anorexia and bulimia nervosa in first-degree relatives of
diagnostically pure proband groups of female anorexic and bulimic
patients and relatives of matched never-ill probands (Strober et al.,
2000). Whereas anorexia was rare in the families of the compar-
ison subjects, full and partial syndromes of anorexia aggregated in
female relatives of both anorexic and bulimic probands. For the
42 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
full syndrome of anorexia nervosa, the relative risks were 11.3 and
12.3 in female relatives of anorexic and bulimic probands, respec-
tively. The corresponding relative risks for bulimia nervosa were
4.2 and 4.4 for female relatives of anorexic and bulimic probands,
respectively. Anorexia nervosa also transmitted in families of
males with the disorder (Strober, Freeman, Lampert, Diamond, &
Kaye, 2001). The authors concluded that the cross-transmission of
both anorexia and bulimia nervosa in families suggest a common
or shared familial diathesis.
Taken together, the majority of these studies suggest elevated
rates of eating disorders, affective disorders, and some anxiety
disorders (panic disorder, generalized anxiety disorder, OCD) in
relatives of anorexic and bulimic patients. Whereas the evidence
for elevated rates of substance use disorder in the families of
anorexia patients is inconsistent and rather weak, rates of sub-
stance use disorder seem to be consistently elevated in families of
bulimic patients. The studies also suggest elevated rates of social
phobia, overanxious disorder, PTSD, and Cluster B personality
disorders, especially in relatives of bulimic patients, and elevated
rates of OCD and OCPD primarily in relatives of anorexic patients
compared with controls. Whereas the nature of the transmission for
substance abuse disorders, major depression (with the contradic-
tory findings for major depression by Kasset et al., 1989), and
OCD seems to be independent of the eating disorder, OCPD and
anorexia nervosa seem to share a path of transmission.
In spite of many methodological strengths, these studies also
have a number of limitations: Although all of the studies reported
here used a family study design, the majority of them additionally
relied on family history information for those family members that
could not be interviewed directly. The diagnostic information
reported for the families therefore usually represents a mixture of
direct and indirect family history information obtained from one
family member.
With two exceptions, the eating disorder samples in all of the
studies summarized are clinical samples. Nilsson et al. (1998) had
examined a mixed community and clinical sample; the sample in
the studies by Lilenfeld et al. (1998) and Stein et al. (1999) had
also been recruited partially from in- and outpatient programs and
via advertisements. While the results of these studies do not differ
from the results of purely clinical samples, it is conceivable that
clinical samples in general have higher rates of family psychopa-
thology than community samples of eating disorders.
A stratification of the eating disorder group according to a
comorbid disorder has been carried out more often in studies with
bulimic patients; only one study with anorexic patients stratified
the group by comorbid depression. Future studies with anorexic
patients might achieve more consistent results regarding family
history factors by stratifying them according to comorbidity status.
Also, with the exception of some recent studies, sample sizes in
most of the studies are relatively small, at least when subgroups are
compared. Therefore, in some of the studies nonsignificant group
differences might have been due to power problems.
Finally, only four studies (Logue et al., 1989; Pasquale et al.,
1994; Strober et al., 1985, 1990) compared the psychiatric family
history of eating disorder patients with the family history of other
psychiatric patient groups, and only one of them (Logue et al.,
1989) also included a healthy control group. Therefore, little is
known about the specificity of the rates reported above. Many of
the disorders that seem to aggregate in families of patients with
eating disorders also aggregate in families of other psychiatrically
ill patient groups (Dunner, Gershon, & Barrett, 1988; Ingram &
Price, 2000).
Another more serious limitation with regard to the aims of the
present review is the fact that none of the studies described above
reported the time of onset of the different familial psychiatric
disorders assessed. Although it seems probable that parental psy-
chiatric disorders did in fact precede the onset of the eating
disorders in the child, they may have emerged subsequently.
Because the exact timing of the aggregation of certain psychiatric
disorders in families is unclear, family history or family psycho-
pathology factors from these studies are classified as correlates.
Parental psychiatric disorders prior to the onset of the child’s
eating disorder, however, were tested retrospectively in the risk
factor studies by Fairburn and colleagues (Fairburn, Cooper, Doll,
& Welch, 1999; Fairburn et al., 1997, 1998) as part of the envi-
ronmental domain risk factors in patients with bulimia nervosa,
anorexia nervosa, and binge-eating disorder in comparison with
healthy and psychiatric controls. In bulimic patients only, parental
depression, parental alcoholism, and parental drug abuse predating
the onset of the eating disorder was significantly more frequent
compared with healthy controls (19% vs. 3%; 20% vs. 3%; 9% vs.
1%, respectively). In addition, rates of parental alcoholism were
specifically more frequent in bulimic patients compared with psy-
chiatric controls. On the basis of these studies, parental alcoholism
is classified as a specific retrospective correlate, whereas parental
depression and drug abuse are classified as nonspecific retrospec-
tive correlates of low potency.
Low self-esteem, negative self-concept, and ineffectiveness.
Low self-esteem or a negative self-concept has assumed a central
role in many clinically derived theories of eating disorders. Bruch
(1962) first described disturbances in self-concept in terms of a
“paralyzing sense of ineffectiveness” (p. 191) as one of three
characteristic psychopathological features of patients with eating
disorders and suggested that these might be more basic than the
disturbances in body image and the interpretation of internal
stimuli. The fact that the self-evaluation of anorexic and bulimic
patients is “highly” or “unduly” influenced by their body weight
and shape has also been explicitly addressed in a diagnostic feature
in the latest revision of the diagnostic criteria in the DSM–IV
(American Psychiatric Association, 1994).
Low self-esteem, ineffectiveness (operationalized by the EDI
subscale Ineffectiveness), or negative self-concept has been exam-
ined in many cross-sectional studies using different constructs as
well as different methods of operationalization. The results of
these different constructs and measures for patients with anorexia
nervosa, bulimia nervosa, and binge-eating disorder have been
summarized recently by Jacobi (1999, 2000): For anorexia ner-
vosa, 24 studies had been included, in 21 of which the anorexic
patients exhibited lower self-esteem, a more negative self-concept
or higher levels of ineffectiveness in comparison with control
groups; in only 3 studies were they comparable to the control
groups. Only 7 of these studies included clinical or psychiatric
control groups with inconsistent results. Twenty-two studies were
found in which self-concept, self-esteem, or ineffectiveness had
been examined in patients with bulimia nervosa. The results also
consistently confirmed the negative self-concept of bulimic pa-
tients (cross-sectionally). Again, only 4 studies included psychiat-
ric control groups also with inconsistent results. The results for the
 RISK FACTORS FOR EATING DISORDERS
only two studies including more narrowly defined criteria for
binge-eating disorder (de Zwaan et al., 1994; Telch & Agras,
1994) are in accordance with results for the other eating disorder
groups, showing lower self-esteem or a more negative self-concept
in patients with binge-eating disorder. In summary, with the ex-
ception of binge-eating disorder, where the number of studies in
general is still small, these studies confirm self-concept deficits for
patients with anorexia and bulimia nervosa regardless of the kind
of construct and operationalization used.
Major limitations concern the selection of healthy control
groups (mostly college students with higher prevalences of eating
disorder symptoms) as well as the almost complete absence of
psychiatric control groups (Jacobi, 1999, 2000). In addition, none
of these studies controlled for patients’ depressive symptomatol-
ogy. As low self-esteem and depression are highly correlated, it is
unclear whether the self-esteem deficits were confounded with
patients’ possible depressive symptomatology. Moreover, none of
the studies analyzed in the review assessed self-concept or self-
esteem before the onset of the eating disorder. The retrospective
assessment of self-concept and its temporal relation to onset of the
eating disorder has only been considered in two cross-sectional
studies: For both the (previously) anorexic and the (currently)
bulimic subjects in the risk factor studies by Fairburn and col-
leagues (Fairburn, Cooper, et al., 1999; Fairburn et al., 1997,
1998), but not the binge-eating disorder subjects, negative self-
evaluation before the onset of the eating disorder was more com-
mon in comparison to healthy controls, and specifically more
common in comparison to psychiatric controls. However, the rates
between the psychiatric patients and the healthy controls, although
not tested for significance, were also different (30% vs. 13%).
Furthermore, the aforementioned methodological problems con-
cerning family interaction and family functioning variables also
apply for these variables. Low self-esteem was also reported as one
of several prodromal symptoms of bulimic patients compared with
controls occurring prior to the onset of their bulimia nervosa by
Raffi et al. (2000). Self-esteem was assessed by a modified version
of Paykel’s Clinical Interview for Depression. Although low self-
esteem in this study would have to be considered as a highly potent
retrospective correlate, the most potent prodromal symptom re-
ported was anorexia or strict dieting. Thus, it remains unclear how
the two prodromal symptoms were interrelated before the onset of
the bulimia.
Taken together it seems that, although self-esteem has been
assessed in a large number of studies with different groups of
eating disorder patients and the use of different operationaliza-
tions, the majority of this research has neither addressed the
precedence of low self-esteem to the eating disorder nor a possible
confounding depressive symptomatology nor specificity. In these
studies, self-concept deficits in patients with eating disorders are
classified as correlates. Negative self-evaluation as assessed in the
studies by Fairburn and colleagues (Fairburn, Cooper, et al., 1999;
Fairburn et al., 1997, 1998) and by Raffi et al. (2000) would have
to be classified as a specific retrospective correlate of medium
potency.
Four longitudinal studies included measures of self-concept
(Button et al., 1996; Calam & Waller, 1998; Ghaderi & Scott,
2001; Leon et al., 1995). In the study by Leon et al. (1995) they did
not prove to be important in risk prediction and were therefore
dropped from the analyses. Calam and Waller (1998) also could
43
not find significant relations between self-esteem and subsequent
disordered eating. On the other hand, low self-esteem predicted
elevated EAT-26 scores 4 years later in the study by Button et al.
(1996). Girls in the lowest self-esteem range (Rosenberg Scale
scores ⫽ 4 – 6) had an eightfold increased risk for a high EAT-26
(ⱖ 20) compared with those with high self-esteem. However,
although self-esteem in this study was assessed at ages 11–12, the
authors pointed out that it is unclear whether low self-esteem
predated the onset of eating disturbances as these had not been
assessed and controlled for at baseline. Finally, Ghaderi and Scott
(2001) reported significantly lower self-esteem at Time 1 for the
incidence group that developed an eating disorder 2 years later.
The EDI Ineffectiveness subscale was included in four of the
studies at baseline (Killen et al., 1994, 1996; Leon et al., 1995,
1999), but it turned out to be predictive of disturbed eating patterns
or caseness in only one of the multivariate analyses as part of the
latent variable negative affectivity (Leon et al., 1999). Significant
differences, however, were found in the univariate comparisons of
the subsequent symptomatic and the asymptomatic groups (Killen
et al., 1994, 1996). In both studies, the ESs were small; in addition,
in one study Ineffectiveness had been used in combination with
three intercorrelated EDI subscales.
On the basis of longitudinal assessment, there seems to be a
slight superiority of studies confirming the presence of a negative
self-concept, low self-esteem, or higher ineffectiveness prior to the
onset of an eating disorder. Low self-esteem and ineffectiveness
are therefore classified as variable risk factors, with potency rang-
ing from low to high. On the basis of existing studies, their
specificity is unclear, although it seems reasonable to assume that
they are not highly specific for eating disorders. Because AUCs
were only available for two of the studies without limitations, and
their results were contradictory, a potency classification seems
premature. Replication studies are needed for further confirmation
of risk factor status and potency.
Perfectionism. From a clinical point of view, it is well recog-
nized that patients with anorexia nervosa often display rigid,
stereotypic, ritualistic, or perfectionistic behaviors. Most recently,
these characteristics have been examined in a psychobiological
light, connecting perfectionistic traits with alterations in serotonin
activity supported by a number of cross-sectional studies (see CNS
Serotonin Activity section). These studies found elevated scores for
perfectionism in remitted anorexic and bulimic patients, even
when using different measures of perfectionism (Bastiani, Rao,
Weltzin, & Kaye, 1995; Kaye et al., 1998; Kaye, Gwirtsman,
George, & Ebert, 1991; Srinivasagam et al., 1995). Both acutely ill
bulimic patients and patients with binge-eating disorder also
scored significantly higher on a measure of self-oriented perfec-
tionism than controls (Pratt, Telch, Labouvie, Wilson, & Agras,
2001). None of the studies addressed premorbid perfectionism. To
our knowledge, again only Fairburn and colleagues’ risk factor
studies (Fairburn, Cooper, et al., 1999; Fairburn et al., 1997, 1998)
included perfectionism in their retrospective assessment of puta-
tive risk factors. They found that in (recovered) patients with
anorexia nervosa, premorbid perfectionism was more common
than in the psychiatric controls and in the healthy controls but not
when compared with patients with bulimia. Perfectionism in these
studies is therefore classified as a specific, retrospective correlate
of medium potency. Perfectionism as assessed in the former stud-
ies would have to be classified as a correlate.
44 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
Four longitudinal studies used the EDI subscale Perfectionism
as a measure of perfectionism (Killen et al., 1994, 1996; Leon et
al., 1995, 1999). In the studies by Killen et al. (1994, 1996),
perfectionism at Time 1 was not related to subsequent eating
disturbances in the multivariate analyses but was found to differ-
entiate between symptomatic and asymptomatic girls at baseline in
the univariate comparisons, with a medium ES (Killen et al.,
1994). In both the studies by Leon et al. (1995, 1999) EDI
Perfectionism did not turn out to be predictive in the multivariate
comparison. No other measures of perfectionism have been used in
any of the longitudinal studies. On the basis of these results,
perfectionism is classified as a correlate.
Athletic competition, participation in weight-related subculture,
and exercise. Members of professions that overemphasize a cer-
tain (low) weight and shape and athletes from particular sport
disciplines (ballet dancers, gymnasts, wrestlers, swimmers, jock-
eys, etc.) were originally proposed as high-risk groups for the
development of eating disorders more than 20 years ago (Garner &
Garfinkel, 1978). A recent review of eating disorders (e.g.,
Striegel-Moore, 1997) confirmed the current belief in the high-risk
status of these groups. The interest in the past few years has
focused primarily on the examination of eating disorder symptoms
in athletes and a phenomenon called the female athlete triad
(eating disorders, amenorrhea, osteoporosis), which a considerable
number of elite athletes seem to develop (e.g., Brownell, 1995;
Putukian, 1998; West, 1998). Another major focus has been on the
role of physical activity or high-level exercise in general in the
development and maintenance of eating disorders (Davis, Fox,
Cowles, Hastings, & Schwass, 1990; Davis et al., 1997).
A major limitation of these cross-sectional studies is that rates of
eating disorders in these high-risk groups are often reported to be
elevated without including a control group. Definitions of eating
disorders vary and are often based on questionnaire scores or other
rather broad criteria. Although the few controlled studies generally
show symptomatic elevations (e.g., on EDI subscales), rates for the
full syndromes of eating disorders (anorexia and bulimia nervosa)
are, when assessed, not higher than in the control groups. Consid-
ering the relatively small samples sizes for the assessment of
prevalence rates in these studies, this is not surprising.
Although the sample sizes in studies with elite athletes are much
larger, the results are less consistent. In one of the most compre-
hensive surveys covering six different sport disciplines, Sundgot-
Borgen (1994) surveyed 522 female elite athletes. Of the sample,
1.3% met DSM–III–R criteria for anorexia nervosa, 8.0% met
criteria for bulimia nervosa, and 8.2% for a category defined as
anorexia athletica. Slightly more conservative but comparable
results were obtained from a more recent national survey of male
and female student athletes (C. Johnson, Powers, & Dick, 1999):
1.1% of the female athletes met DSM–IV criteria for bulimia
nervosa versus none of the male athletes; none of the student
athletes met stringent criteria for anorexia nervosa. When less
stringent criteria were used, 2.85% of the females and none of the
males were classified as having subclinical anorexia, and 9.2% of
females versus 0.005% of males were classified as having subclin-
ical bulimia nervosa, whereas rates for “self-identified” eating
disorders were even lower. On the other hand, Fulkerson, Keel,
Leon, and Dorr (1999), comparing 318 high school athletes to 360
nonathletes on the EDI, the Restraint Scale, and the Eating Dis-
orders Checklist, could not find significant differences between the
groups.
A severe limitation for the classification of high-level exercise
in an athletic– competitive context as a risk factor for the devel-
opment of eating disorders is the almost complete absence of
longitudinal research addressing precedence of these factors to the
eating disorders. To our knowledge, high-risk groups such as
dancers or athletes have only once been assessed prospectively in
a noncontrolled study. Garner, Garfinkel, Rockert, and Olmsted
(1987) followed 35 ballet students 2 or 4 years after their first
assessment and classified 25.7% as having DSM–III-based an-
orexia nervosa, 2.8% as having bulimia nervosa according to
Russell’s criteria, and 11.4% as having “partial syndromes.” Un-
fortunately, subjects had not been interviewed at initial testing.
Self-report data indicated that a considerable percentage of the
group assessed at follow-up already had some eating and weight-
related difficulties at first assessment. Also, no information was
given regarding the temporal relation of these difficulties to sub-
jects’ participation in ballet.
Of all the studies examining the impact of physical activity or
exercise in a noncompetitive context on the development of eating
disorders, we found only one that retrospectively assessed the
amount of physical activity before the onset of the eating disorder.
Davis, Kennedy, Ravelski, and Dionne (1994) compared a mixed
eating disorder sample of anorexic, previously anorexic, and bu-
limic patients with control subjects on the amount of physical
activity predating the eating disorder using a structured interview.
The results indicated that the eating disorder patients were signif-
icantly more physically active than controls from adolescence (age
13) onwards and also prior to the onset of the disorder. As
indicated by the AUC for this factor (see Table 4), its potency
would have to be considered as high.
The results of the above cross-sectional studies are consistent in
their findings of elevated rates of eating disorder symptoms or—
however defined— broader “subclinical eating disorders” in fe-
male dancers and other groups of athletes, primarily aesthetic and
weight-related sports (Fulkerson et al., 1999; Sundgot-Borgen,
1994). For the full syndromes of eating disorders they are much
less clear. To estimate prevalence rates more precisely, studies
with even larger sample sizes as well as longitudinal studies
addressing precedence are needed. Athletic competition or partic-
ipation in a competitive weight-related subculture is therefore
classified as a correlate. A high level of exercise, however, is
classified as a retrospective correlate of high potency.
Other Factors
Cross-sectional studies. In addition to the specific retrospec-
tive correlates reported above, in Fairburn and colleagues’ studies
(Fairburn, Cooper, et al., 1999; Fairburn et al., 1997, 1998) a
greater level of exposure to all three risk domains (personal,
environmental, dieting) was found in all three groups of patients
with eating disordered when compared with healthy controls but
not in comparison with psychiatric controls. The exposure to the
three risk domains thus seems to be a nonspecific effect. The potency
of these factors varies depending on the domain and outcome.
Body dysmorphic disorder (BDD) was assessed retrospectively
for a period of at least 6 months prior to the onset of the eating
disorder in samples of anorexic and bulimic patients as well as in
 RISK FACTORS FOR EATING DISORDERS
controls. BDD belongs to the somatoform disorder spectrum ac-
cording to both the ICD-10 (World Health Organization, 1992) and
the DSM–IV (American Psychiatric Association, 1994), but simi-
larities with OCDs are also stressed by some authors. Symptoms of
BDD were found to be more than three times higher in anorexic
patients than in controls and were not observed at all in bulimic
patients. BDD is therefore classified as a retrospective correlate of
low potency and unclear specificity.
Finally, some of the factors discussed in the literature have not
been mentioned so far, as they did not meet inclusion criteria (e.g.,
Expressed Emotion, as a measure of impaired family interaction)
or did not address precedence in the way other cross-sectional
studies did. Male homosexuality, for example, has been suggested
to be a risk factor for eating disorders on the basis of a number of
cross-sectional findings showing that homosexual men exhibit
higher body dissatisfaction and weight concerns, higher ideal and
lower real BMI, a greater number of binge-eating symptoms, and
so forth, when compared with heterosexual men (e.g., Carlat,
Camargo, & Herzog, 1997; French, Story, Remafedi, Resnick, &
Blum, 1996; Siever, 1994). Because rates of full eating disorders
have not been found to be elevated, male homosexuality is clas-
sified as a noncorrelate.
Apart from parental critical comments on weight and shape, a
history of shape and weight-related teasing by peers has also been
postulated as increasing the risk for eating disturbances or disor-
ders (e.g., Thompson & Heinberg, 1993). However, teasing has not
yet been assessed in longitudinal studies, and studies with clinical
groups of patients with eating disorders are also scarce. Current
evidence, therefore, does not even support a significant association
between clinical eating disorders and a history of peer-related
teasing.
Longitudinal studies. Girls who later turned out to be symp-
tomatic in the study by Killen et al. (1994) had higher scores on the
Youth Self-Report Inventory Aggressive and Unpopular subscales
when (univariately) compared with asymptomatic girls, although
the effect sizes for the two subscales were rather low. Girls who
developed a partial syndrome in the study by Killen et al. (1996)
had (univariately tested) higher 30-day prevalences of alcohol
consumption. Thus, these factors thus are classified as nonspecific
variable risk factors of low potency.
High use of escape–avoidance coping as well as low perceived
social support were found to be prospective risk factors for sub-
sequent eating disorders in the study by Ghaderi and Scott (2001).
These factors are also classified as variable risk factors of medium
and high potency, respectively. All of the factors classified as
retrospective correlates or variable risk factors in this section are in
need of replication.
Biological Factors
Research on biological risk factors for eating disorders has
focused mainly on genetic factors and neurobiological distur-
bances (e.g., altered serotonin levels). This section therefore con-
centrates on the evidence currently available on the importance of
genetic factors in the liability to eating disorders and on the
possible role of central nervous system (CNS) serotonin activity in
the etiopathogenesis of eating disorders. In addition, research on
factors related to pubertal development and pre- and perinatal
complications is reviewed.
45
Genetic Factors and Genes
It must be kept in mind that genes, environment, and neurobi-
ology interact and are inseparable. Many of the psychological risk
factors for eating disorders may ultimately be a reflection of
genetic predisposition and gene– environment interactions (Fair-
burn, Cowen, & Harrison, 1999). There is, for example, evidence
that some character traits, which are highly attributable to genetic
make-up, may function as risk factors for eating disorders (Lilen-
feld et al., 1998). In addition, the genetic basis for eating disorders
is likely to be polygenic, with a multitude of genetic traits con-
tributing to their development. The prevailing hypothesis assumes
that an accumulation of various genes of small effect, together with
adverse environmental factors increases the risk to develop an
eating disorder in those carrying the greatest genetic and environ-
mental loading (Devlin et al., 2002).
Family studies. Family studies provide a necessary first step in
determining whether a disorder is genetic by establishing whether
it clusters among biologically related individuals. These studies
generally have found an increased rate of eating disorders in
anorexia and bulimia nervosa relatives compared with control
relatives (see above). However, given that first-degree relatives
share genes and environments, these studies are unable to differ-
entiate genetic versus environmental causes for familial clusters.
Adoption studies for eating disorders are thus far lacking.
Twin studies. Statistical analyses of differences in concor-
dance between monozygotic (MZ) and dizygotic (DZ) twins allow
one to tease apart the variance in risk for illness into independent
genetic (additive genetic) and environmental sources (shared and
individual) and give estimates of their relative magnitude. Twin
studies corroborate the observed familiality for both eating disor-
ders, with MZ twins (being genetically identical) having a signif-
icantly higher concordance of eating disorders than DZ twins in
most but not all studies (for recent reviews, see Bulik, Sullivan,
Wade, & Kendler, 2000; Kipman, Gorwood, Mouren-Simeoni, &
Ades, 1999; Klump, Wonderlich, Lehoux, Lilenfeld, & Bulik,
2002; see also Tables 4 and 5). Early twin studies included only
small clinical and volunteer samples, and selection effects cannot
be ruled out (Fichter & Nögel, 1990; Holland, Hall, Murray,
Russell, & Crisp, 1984; Holland, Sicotte, & Treasure, 1988; Hsu,
Chesler, & Santhouse, 1990; Rutherford, McGuffin, Katz, & Mur-
ray, 1993; Treasure & Holland, 1989).
Although more recent twin studies used population-based twin
registries and applied sophisticated statistical analyses (Bulik, Sul-
livan, & Kendler, 1998; Hettema, Neale, & Kendler, 1995; Ken-
dler et al., 1991, 1995; Klump, Miller, Keel, McGue, & Iacono,
2001; Wade, Bulik, Neale, & Kendler, 2000; Wade et al., 1999;
Wade, Martin, & Tiggeman, 1998; Walters & Kendler, 1995;
Walters et al., 1992), the methods and results of these studies have
not remained without criticism (Fairburn, Cowen, & Harrison,
1999). Overall, however, there is evidence that a reasonable pro-
portion of the observed familial aggregation for anorexia and
bulimia nervosa is due to both additive genetic effects and unique
environmental factors. For anorexia nervosa, the contribution of
additive genetic effects to risk has been estimated at between 58%
and 88%. Even though these numbers are intriguing, the small
number of studies precludes definite conclusions. In addition, in
one study (Walters & Kendler, 1995) the concordance rates of the
DZ twins were higher than those of the MZ twins. The contribution
46 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
of additive genetic effects to liability to bulimia nervosa has been
found to vary between 28% and 83%. The remaining variance is
explained mainly by unique environmental factors. The magnitude
of the contribution of shared environment is less clear, but it
appears to be less prominent than additive genetic factors (Bulik et
al., 2000). However, in one study (Hettema et al., 1995), an equal
environment assumption (EEA) violation (twin resemblance) ac-
counted for all of the variance otherwise attributed to additive
genetic effects. The EEA is central to the twin method and assumes
that MZ and DZ twins are exposed to equivalent environmental
influences of etiological importance. The low lifetime prevalence
of eating disorders severely restricts the power for the statistical
analyses. Hence, different definitions of phenotypes ranging from
narrow categorical definitions of eating disorders to various
broader definitions for anorexia and bulimia nervosa have been
used. Attempts have also been made to quantify the contribution of
genes and environment to continuous measures of disordered
eating and related attitudes (Klump, McGue, & Iacono, 2000;
Rutherford et al., 1993; Wade et al., 1998). One such effort
generated heritability estimates for binge eating and vomiting of
46% and 70%, respectively (Sullivan, Bulik, & Kendler, 1998).
Taken together, genetic effects on the basis of both early and
more recent twin studies are classified as fixed markers for an-
orexia and bulimia nervosa. However, the limited number of
studies, the inconsistent findings and the differences in the meth-
odologies used preclude definitive conclusions about the relative
contribution of genes and environment in the etiology of eating
disorders. Replication studies applying more strict methodological
criteria are needed to confirm the genetic effects.
Gene mapping. As in many other fields, there is much enthu-
siasm regarding the possibility of locating the specific genes that
influence the risk of eating disorders. This task falls in the domain
of molecular genetics research. Advances in molecular and statis-
tical technology have made the possibility of locating specific
genes that might influence the risk of eating disorders more fea-
sible than it was in the past. At the moment, relevant genes might
be seen as fixed markers because they precede the onset of the
eating disorder but cannot be manipulated.
Researchers have begun directly examining genetic influences
through candidate genes and linkage studies. The first approach
examines the relative influence of a specific gene, called a candi-
date gene, on the development of a specific phenotype (i.e., eating
disorders). The candidate gene approach involves the selection of
a gene on the basis of its perceived relevance to the suspected
pathophysiology of the disorder under study. Association studies
measure the difference in allele frequency between patients and
controls (case-control studies). Transmission disequilibrium stud-
ies use family trios consisting of an index patient and both parents
and measure the frequency of parental transmission of a given
allele to the affected child. Candidate gene studies in eating dis-
orders have so far focused on genes encoding proteins implicated
in the regulation of feeding and body composition, and genes
involved in neurotransmitter pathway regulating behavior. Poly-
morphisms and variations in genes have been assessed for associ-
ation and transmission disequilibrium pertaining to anorexia
and/or bulimia nervosa. Thus far, only a few polymorphisms have
been found to be associated with anorexia nervosa and there is
only a small number of studies investigating candidate genes in
bulimia nervosa (for a review, see Hinney, Remschmidt, & Hebe-
brand, 2000). However, the literature in this area is growing
rapidly. Studies examining candidate genes in eating disorders are
summarized in Table 7. A polymorphism (⫺1438G/A) within the
promoter region of the 5-HT2A gene has been examined in 11
studies. Five studies revealed an association of the A allele to
anorexia nervosa with an increased frequency of the ⫺1438/A
allele in anorexia nervosa compared with controls (Collier, Arranz,
Mupita, Brown, & Treasure, 1997; Enoch et al., 1998; Nacmias et
al., 1999; Ricca et al., 2002; Sorbi et al., 1998). The association
seems to be stronger in anorexia nervosa restricting type than
binge-eating/purging type. However, 6 studies could not confirm
this result (Ando et al., 2001; Campbell, Sundaramurthy,
Markham, & Pieri, 1998; Gorwood et al., 2002; Hinney, Ziegler,
Nothen, Remschmidt, & Hebebrand, 1997; Nishiguchi et al., 2001;
Ziegler et al., 1999). Both genotype and allele frequencies vary
substantially between the individual studies resulting in dissimilar
ORs. Stratification effects, genetic heterogeneity (U.S., English,
German, Japanese samples), and false-positive and false-negative
findings may account for these discrepant results. In a meta-
analysis of 6 studies no association between the ⫺1438G/A pro-
moter polymorphism and anorexia nervosa could be detected
(Ziegler et al., 1999). The studies are listed in Table 8.
Studies performing genome-wide screenings in a collection of
affected families are underway to find the rough location of
susceptibility gene(s) involved in eating disorders. So-called link-
age analyses identify contributing genetic loci by examining allele
sharing among family members at several genetic markers across
the genome. This approach does not focus on one particular gene.
A first study in 196 families with two or more family members
with anorexia nervosa, bulimia nervosa, or EDNOS has been
published (Grice et al., 2002). Overall, analyses showed only
modest evidence for linkage. However, linkage analysis in a more
homogeneous subgroup of 37 families in which at least two
affected relatives had diagnoses of restricting anorexia nervosa
suggests evidence for the presence of an anorexia nervosa-
susceptibility locus on chromosome 1p. Genes that play a role in
feeding behaviors and that map to this linkage region are now
being analyzed for association with anorexia nervosa. A narrower
diagnosis may reduce heterogeneity, but it makes it harder to find
multiply affected families, thereby reducing statistical power.
Larger genome-wide linkage studies are underway.
Rather than using purely clinical characteristics, a phenotype
can be further defined using neurobiological data (endophenotype).
Future studies will combine neurobiological findings with genetic
findings.
Even though the literature is growing rapidly, molecular genetic
research of eating disorders is still in infancy. So far, the majority
of the studies yielded negative results, and single positive findings
have not yet been confirmed. Overall, the results of the molecular
genetic studies have not yet identified alleles that can be safely
labeled as fixed markers. Most of the examined candidate genes
are noncorrelates. However, promising areas for future research
have already been identified and large-scale linkage studies are
underway.
CNS Serotonin Activity
From a neurobiological perspective, research suggests that the
serotonin system may play an important role in the pathophysiol-
 RISK FACTORS FOR EATING DISORDERS 47

Table 7
Candidate Genes Investigated in Anorexia Nervosa (AN) and Bulimia Nervosa (BN;
Polymorphisms Not Stated)

Results of association tests or

TDT (allele and genotype
frequencies)

Candidate gene Reference AN BN

Serotonin transporter (5- Hinney et al. (1997) ⫺ 0

hydroxytryptamine, 5-HT)
Tryptophan hydroxylase
5-HT1B receptor
5-HT1D␤ receptor
5-HT2C receptor
5-HT7 receptor
Uncoupling protein 2,3
␤3-adrenergic receptor
Dopamine D4 receptor
Dopamine D3 receptor
Estrogen receptor 2
Estrogen receptor 1
Leptin
Melanocortin MC4 receptor
Neuropeptide Y Y1 receptor
Neuropeptide Y Y5 receptor
Pro-opiomelanocortin
Agouti-related protein
Catechol-O-methyltransferase
Tumor necrosis factor-␣
Potassium channel hSKCa3
Norepinephrine transporter
Di Bella et al. (2000) ⫺ ⫹
Sundaramurthy et al. (2000) ⫺ 0
Fumeron et al. (2001) ⫹ 0
Han et al. (1999) ⫺ 0
Levitan et al. (2001) 0 ⫾
(min. BMI)
Hinney et al. (1997) ⫺ 0
Hinney et al. (1997) ⫺ ⫺
Burnet et al. (1999) 0 ⫺
Nacmias et al. (1999) ⫺ ⫺
Hinney et al. (2000) ⫺ 0
Westberg et al. (2002) ⫹ 0
(weight loss)
Hinney et al. (1999) ⫺ 0
Campbell et al. (1999) ⫹ 0
Hu et al. (2002) ⫺ 0
Hinney et al. (1997) ⫺ 0
Hinney et al. (1999) ⫺ 0
Bruins-Slot et al. (1998) ⫺ 0
Rosenkranz et al. (1998) ⫹a ⫺
Eastwood et al. (2002) ⫹a 0
Eastwood et al. (2002) ⫺ 0
Hinney et al. (1998) ⫺ ⫺
Hinney et al. (1999) ⫺ ⫺
Rosenkranz et al. (1998) ⫺ 0
Rosenkranz et al. (1998) ⫺ 0
Hinney et al. (1998) ⫺ 0
Vink et al. (2001) ⫹ 0
Frisch et al. (2001) ⫹ 0
Ando et al. (2001) ⫺ 0
Koronyo-Hamaoui et al. (2002) ⫹ 0
Urwin et al. (2002) ⫹ 0

Note. Results for 5-HT2A receptor are shown in Table 8. TDT ⫽ transmission disequilibrium test; ⫺ ⫽ not
significant; 0 ⫽ not assessed; ⫹ ⫽ significant; ⫾ ⫽ unclear; min. BMI ⫽ minimum body mass index;
hSKCa3 ⫽ small-conductance calcium-activated potassium channel type 3.
a
Discrepant results.

ogy and perhaps etiopathogenesis of eating disorders. The seroto-
nergic system is not the only neurotransmitter system potentially
implicated in the physiopathology of eating disorders but it is the
most extensively studied system. Disturbances of brain serotonin
activity have been described in acutely ill as well as long-term
recovered patients with both anorexia and bulimia nervosa. Re-
search methods for the assessment of serotonin activity include
neuroendocrine and behavioral responses to pharmacological chal-
lenge studies (using methyl-chlorophenylpiperazine, fenfluramine,
or tryptophan), tryptophan depletion, tryptophan availability in
plasma, serotonergic parameters in platelets (3H-imipramine bind-
ing, uptake of serotonin, serotonin-amplified platelet aggregation,
serotonin-induced platelet calcium mobilization), and release and
metabolism of serotonin in the CNS as reflected by levels of the
serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in ce-
rebrospinal fluid (CSF). More recently, brain-imaging studies us-
ing single photon emission computed tomography and positron
emission tomography were used to characterize binding of sero-
tonin transporters and 5-HT2A receptors (Kaye et al., 2001; Kuikka
et al., 2001; Tauscher et al., 2001). The studies have to be classi-
fied as preliminary risk studies because they all use a case-control
design. Because neurobiological abnormalities cannot be assessed
retrospectively, some of the studies included a recovered study
design. The rationale in these studies is that individuals who have
achieved stable remission from a disorder provide an opportunity
to identify trait-related characteristics that may be risk factors for
the development of the disorder. Nevertheless, it is not possible to
determine whether alterations are the cause of a disorder, a revers-
ible consequence of the disorder (which might contribute to the
perpetuation of the disorder), or a scar caused by the abnormal
behavior using this design. Accordingly, this type of study was not
included in the present review. In anorexia nervosa, CNS seroto-
nergic responsiveness is substantially reduced in low-weight pa-
tients, which could be secondary to a diet-induced reduction of
48 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS

Table 8
⫺1438G/A 5-HT2A Promotor Polymorphism, A Allele Frequency

Authors, sample Frequency of A

ethnicity Sample (n) allele (% alleles) Chi square

Collier et al. (1997), AN (81) 83 (51) p ⫽ .023, OR ⫽ 1.52

British sample CG (226) 185 (41)
Hinney et al. (1997), AN (100) 79 (40) ns, OR ⫽ 0.89
German sample CG (254) 215 (42)
Campbell et al. (1998), AN (152) 146 (48) ns, OR ⫽ 1.26
British sample CG (160) 127 (42)
Sorbi et al. (1998), AN (77) 87 (57) p ⬍ .0001, OR ⫽ 2.36
Italian sample Anr (43) (66) p ⬍ .0001
Anp (34) (44) ns
CG (107) 76 (36)
Enoch et al. (1998), AN (68) 69 (51) p ⬍ .005, OR ⫽ 1.81
American sample BN (22) 15 (34) ns
CG (69) 50 (36)
Italian sample AN (20) 26 (65) p ⬍ .005
BN (37) 28 (38) ns
Ziegler et al. (1999), AN (78) 53 (34) ns, OR ⫽ 0.98
German sample BN (99) 91 (46)
CG (170) 131 (39) ns
Nacmias et al. (1999), AN (109) 119 (55) p ⬍ .0001
Italian sample ANr (57) (63) p ⬍ .0001
ANp (52) (45) ns
BNp (59) 55 (47) ns
CG (107) 76 (35)
Ricca et al. (2002), AN (148) (52) p ⬍ .0001
extended sample of ANr (74) (60) p ⬍ .0001
Nacmias et al. (1999) ANp (74) (44) ns
BNp (86) (54) p ⬍ .0001
CG (115) (36)
Nishiguchi et al. AN (62) 57 (46) ns, OR ⫽ 1.37
(2001), Japanese
BN (110) 96 (44) p ⬍ .01, OR ⫽ 1.51
sample
CG (374) 403 (54)
Ando et al. (2001), AN (75) (55) ns
Japanese sample ANr (37) (53) ns
ANp (38) (55) ns
CG (127) (50)
Gorwood et al. (2002), AN (316) 253 (40) ns
mixed sample (six CG 244 (43) Family-based transmission disequilibrium
European centers) approach: A allele transmitted 133
times, not transmitted 148 times

Note. 5-HT ⫽ 5-hydroxytryptamine; AN ⫽ anorexia nervosa; OR ⫽ odds ratio; CG ⫽ control group; ANr ⫽
anorexia nervosa, restricting type; Anp ⫽ anorexia nervosa, binge eating-purging type; BN ⫽ bulimia nervosa;
BNp ⫽ bulimia nervosa, purging type.

availability of the amino acid, tryptophan, the precursor of sero-
tonin (e.g., Brewerton & Jimerson, 1996; Hadigan, Walsh, Butt-
inger, & Hollander, 1995; Kaye, Ebert, Raleigh, & Lake, 1984;
Kaye, Gwirtsman, George, Jimerson, & Ebert, 1988; Monteleone,
Brambilla, Bortolotti, La Rocca, & Maj, 1998; Ward, Brown,
Lightman, Campbell, & Treasure, 1998). There is some evidence
that reduced brain serotonin activity persists after short-term
weight recovery (Frank et al., 2001). In contrast, neuroendocrine
responses to serotonin-stimulating drugs have been reported to be
normalized (O’Dwyer, Lucey, & Russell, 1996) and CSF concen-
trations of 5-HIAA even to be elevated (Kaye et al., 1991) in
women who were long-term weight recovered from anorexia ner-
vosa, suggesting that hyperserotonergic function might be a trait
marker in anorexia nervosa. In bulimia nervosa, there is also
considerable evidence for an impaired serotonergic responsiveness
during the acute illness state (e.g., Brewerton et al., 1992; Gold-
bloom, Garfinkel, Katz, & Brown, 1990; Jimerson et al., 1997;
Kaye et al., 1998; Kaye, Gendall, et al., 2000; Levitan, Kaplan,
Joffe, Levitt, & Brown, 1997; McBride, Anderson, Khait, Sunday,
& Halmi, 1991; Monteleone, Brambilla, Bortolotti, Ferraro, &
Maj, 1998; Oldman, Walsh, Salkovskis, Fairburn, & Cowen, 1995;
Smith, Fairburn, & Cowen, 1999; Weltzin, Fernstrom, McConaha,
& Kaye, 1994; Weltzin, Fernstrom, Fernstrom, Neuberger, &
Kaye, 1995). Studies have shown an inverse relationship between
symptom severity and measures of serotonergic responsiveness
(Jimerson, Lesem, Kaye, & Brewerton, 1992). In addition, there is
evidence for an association between self-destructiveness, a history
of sexual abuse and impulsivity and reduced serotonin function
(Steiger, Gauvin, et al., 2001; Steiger, Koerner, et al., 2001;
Steiger, Young, et al., 2001). In long-term recovered patients with
bulimia nervosa, 5-HIAA levels were elevated in CSF in compar-
ison with those of controls (Kaye et al., 1998). The prolactin
 RISK FACTORS FOR EATING DISORDERS
response to fenfluramine was significantly larger than in patients
with current bulimia nervosa but not compared with healthy con-
trols (Wolfe et al., 2000). In addition, recovered individuals expe-
rienced a transient return of eating disorder-related symptoms after
tryptophan depletion (Smith et al., 1999). These results in recov-
ered bulimic patients suggest that dysregulation in some CNS
serotonergic pathways may persist after recovery from bulimia
nervosa. Given the results in recovered patients with anorexia and
bulimia nervosa it could be hypothesized that a disturbance of
serotonin activity may create a vulnerability for the development
of an eating disorder. However, as mentioned earlier, it cannot be
ruled out that the findings related to serotonergic functions in
patients who have recovered from eating disorders are long-term
consequences of the eating disorder rather than a premorbidly
existing trait.
In addition to affecting eating behavior directly, alterations in
CNS serotonin function may contribute to other psychological
symptoms associated with eating disorders. The diminished CNS
serotonin could play a role in the high prevalence of depressive
disorders in patients with bulimia nervosa. An impulsive–
aggressive behavioral style, which is frequently seen in bulimic
patients, may also be associated with diminished CNS serotonin
function. In addition, increased CNS serotonin has been shown to
be associated with obsessive– compulsive symptomatology. Ob-
sessive personality traits frequently persist after recovery from
anorexia nervosa. It has been hypothesized that increased serotonin
activity might contribute to symptoms such as anxiety, perfection-
ism, obsessions with symmetry and exactness, and harm avoid-
ance, which, when coupled with psychosocial influences, make
people vulnerable to developing anorexia nervosa.
Taken together, the available data cannot prove whether distur-
bances of serotonergic function as described above predate the
onset of eating disorder symptoms or result from dietary abnor-
malities or other changes characteristic of the disorders. Conse-
quently, they can only be regarded as correlates. Future studies
examining alterations in serotonin function in high-risk individuals
prior to the development of an eating disorder may be clarifying.
Pregnancy and Perinatal Complications
Whereas associations between pregnancy and perinatal compli-
cations and schizophrenia have been reported repeatedly (e.g.,
Geddes & Lawrie, 1995), the association with other psychiatric
disorders, especially eating disorders, has received relatively little
attention. Two studies carried out recently examined associations
between pregnancy and perinatal complications in eating disor-
ders. In one of these (Foley, Thacker, Aggen, Neale, & Kendler,
2001), data were obtained from medical records. Pregnancy and
perinatal complications were examined in a large population-based
sample of female twins. Information was obtained retrospectively
by an interview carried out with the parents. Shorter gestational
age was associated with an increased risk for anorexia nervosa, and
pregnancy complications were associated with an increased risk
for both anorexia and bulimia nervosa. Risk for alcoholism, major
depression, and most anxiety disorders was not significantly asso-
ciated with pregnancy complications or gestational age. Pregnancy
complications in this study are classified as a specific retrospective
correlate for anorexia and bulimia nervosa; gestational age is
classified as a specific retrospective correlate for anorexia nervosa.
49
Cnattingius, Hultman, Dahl, and Sparén (1999) reported a (pro-
spectively assessed) more than threefold increased risk of very
preterm birth in a large case-register sample of anorexic patients.
Also, the risk (OR) of severe birth trauma (cephalhematoma) was
increased between two- and threefold in anorectic patients. An
elevation of these obstetrical complications was not found in a
related study with patients with schizophrenia and patients with
affective or reactive psychosis (Hultman, Sparén, Takei, Murray,
& Cnattingius, 1999). Preterm birth and birth trauma are therefore
classified as specific fixed markers for anorexia nervosa of low
potency according to the AUC. However, the base rates of affected
cases versus controls are extremely low. When comparing this
factor with other low-potency risk factors, the fact that the OR is
overly sensitive to low prevalences becomes apparent (Kraemer et
al., 1999). In addition, replication studies are needed for further
confirmation of risk factor status.
Pubertal status. Two features of puberty that can be confused
are pubertal status and pubertal timing. Pubertal status refers to the
level or stage of pubertal development, whereas pubertal timing
refers to the age of a pubertal event and is often categorized as
early, on time, or late in comparison to a defined reference group.
Pubertal status cannot be considered a risk factor in the Kraemer
typology because everyone goes through puberty. However, cross-
sectional studies that isolated the frequency of eating disorder
symptoms by pubertal status indicate that during the peripubertal
time period eating disorder symptoms are more strongly associated
with sexual maturation than is age (Killen et al., 1992). Whether
the association between eating disorder symptoms and sexual
maturation is a function of increasing BMI at puberty or other
aspects of puberty is not clear. Because sexual maturation and BMI
are highly positively correlated, it is difficult to separate their
respective influence. Furthermore, the potency of pubertal stage as
a correlate appears to be weak, as it is not significantly related to
eating disorder symptoms in multivariate models (Smolak & Le-
vine, 1996). Perhaps the best way to regard the role of pubertal
status in relation to eating disorder risk is that pubertal status is
more related to when symptoms develop rather than whether
symptoms develop.
Pubertal timing. Pubertal timing effects are often confounded
with pubertal status effects in cross-sectional studies limited to one
age or grade. If more sexually mature fifth-grade girls have higher
depression scores it is impossible to know whether this is a status
effect or a timing effect. The less sexually mature girls may “catch
up” when they proceed through puberty, or they may not.
Although all girls pass through puberty, the age at which pu-
berty begins varies considerably. The association between early
pubertal timing and eating disorder symptomatology as well as
diagnosis has been observed in a number of studies (Graber,
Lewinsohn, Seeley, & Brooks-Gunn, 1997; Hayward et al., 1997).
These include studies of girls currently in the pubertal transition as
well as samples wherein all girls had completed puberty in which
the retrospective report of early puberty compared with peers is
associated with higher rates of eating disorders (Graber et al.,
1997; Hayward et al., 1997). Not all studies report a pubertal
timing effect, and as is the case for the effects of pubertal stage,
pubertal timing effects frequently fall out in multivariate modes
(Smolak & Levine, 1996).
In the five longitudinal studies in which different indicators of
pubertal timing were assessed, it was not associated with subse-
50 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
quent eating disturbances (Attie & Brooks-Gunn, 1989; Graber et
al., 1994; Killen et al., 1994; Leon et al., 1995) or not predictive in
the structural model (Leon et al., 1999). Graber et al. (1994) found
the timing of pubertal maturation to be related to eating distur-
bances already present at the beginning of the study, with the girls
in the chronic group having the earliest age of menarche. On the
basis of the longitudinal evidence, pubertal timing can neither be
classified as a risk factor nor as a correlate. With respect to the
Kraemer typology, early pubertal timing as assessed in the cross-
sectional studies is a nonspecific fixed marker.
Integrating Longitudinal and Cross-Sectional Findings
This section integrates findings from longitudinal and cross-
sectional studies and illustrates the result of the classification
process graphically. The empirically supported risk factors from
longitudinal studies and retrospective correlates, fixed and variable
markers from cross-sectional studies are shown along timelines
from birth to the respective onset of the eating disorder in Figures
1, 2, and 3 for eating disorders, anorexia nervosa, and bulimia
nervosa, respectively.3 Though it is our intention to emphasize the
developmental perspective with the timelines, the timelines are not
intended to illustrate a causal pathway to eating disorders, as
combinations and interactions between risk factors are not the
focus of this review. The age of the occurrence of each factor on
the timeline is the age as reported in the respective studies. If no
exact age of occurrence or onset was reported, we assumed that the
factor was present before age X, which was calculated by subtract-
ing mean illness duration from the lowest mean age of the respec-
tive sample. This does not necessarily reflect the actual age of
occurrence of a factor but rather the age of the included samples or
the time span of retrospective assessment of retrospective corre-
lates. In addition, some factors were predictive from early child-
hood to late adolescence. Fixed markers, such as ethnicity and
female gender are already present at or even before birth, irrespec-
tive of the study design.
Longitudinal studies (see Figure 1) have assessed risk factors for
adolescent eating disorders primarily in adolescence. Very few
studies included factors in early and later childhood. Early child-
hood gastrointestinal and other eating problems predicted subse-
quent eating disturbances. Pica in early childhood predicted full
diagnoses of bulimia nervosa, whereas elevated scores on a mea-
sure of anorexic symptoms, picky eating, eating conflicts, and
struggles around meals predicted full diagnoses of anorexia ner-
vosa. Experiences of sexual abuse or physical neglect during
childhood put individuals at elevated risk for eating disorders or
eating problems. During early and late adolescence (ages 13 and
15), low self-esteem or higher levels of ineffectiveness and low
interoceptive awareness was prospectively related to eating disor-
der syndromes. Subsequent eating disorder syndromes were also
predicted by change in psychiatric morbidity, general level of
psychiatric morbidity, negative affectivity, amount of alcohol con-
sumption over the last 30 days, elevations on two subscales (Un-
popular, Aggressive) of the Youth Self-Report Inventory, as well
as increased weight concerns. All of the latter risk factors had been
first assessed at about age 15. Finally, perceived low social support
from the family and an escape–avoidant style of coping with
stressful events of everyday life was prospectively related to eating
disorders in late adolescence. Weight concerns/dieting represents
the most frequently assessed, best confirmed, and most potent
variable risk factor from longitudinal studies. Sexual abuse and
physical neglect are variable risk factors of medium potency;
variable risk factors related to temperament and alcohol consump-
tion are of low potency. Female gender, ethnicity, low interocep-
tion, increased weight concerns/dieting behavior, negative self-
evaluation and psychiatric morbidity are factors confirmed in more
than one study, whereas the remaining factors need replication.
Perceived low social support, though also very potent, has only
been confirmed once in a sample of higher age (18 –30 years) than
most of the other samples. Its generizability to early adolescence is
therefore unclear. For none of these risk factors has specificity
been addressed. For many of them (e.g., gender, sexual abuse,
general psychiatric morbidity, low self-esteem, low social sup-
port), however, it seems highly probable that they are nonspecific
predictors of psychopathology.
Regarding fixed markers, variable markers, and retrospective
correlates for anorexia and bulimia nervosa from cross-sectional
studies (see Figures 2 and 3): A number of twin studies suggest a
genetic influence for anorexia and bulimia nervosa. Although this
influence is present at or even before birth, to date nothing is
known about the exact nature of the gene– environment interac-
tion. For anorexia nervosa, additional factors are present at or
around birth: Birth-related perinatal complications (e.g., cephalhe-
matoma) and premature delivery based on medical records specif-
ically predicted a diagnosis of anorexia nervosa in subjects as-
sessed 10 years later. However, the potency of these fixed markers
is very low. Similarly, although assessed retrospectively, preg-
nancy complications and shorter gestational age were confirmed as
specific retrospective correlates for anorexia nervosa.
Furthermore, feeding and gastrointestinal problems, infant sleep
difficulties, and a high-concern parenting style are retrospective
correlates during early childhood, followed by OCPDs and child-
hood anxiety disorders, both starting in childhood. During adoles-
cence, early pubertal timing represents a nonspecific fixed marker.
Retrospective correlates during early adolescence are a high level
of exercise, dieting behavior, the presence of BDD and OCD and
acculturation. Increased exposure to sexual abuse and other ad-
verse life events are retrospective correlates occurring before age
12 to 19, depending on the study. Adolescent age itself is consid-
ered a variable marker for both anorexia and bulimia nervosa.
Finally, a higher level of perfectionism, negative self-evaluation,
as well as premorbid OCD represent retrospective correlates spe-
cific for anorexia nervosa that could have occurred any time before
onset. Factors that have been found only once are early feeding and
gastrointestinal problems, high-concern parenting, infant sleep dif-
ficulties, childhood overanxious disorders, high level of exercise,
BDD and negative self-evaluation. Although OCPD, OCD, and
perfectionism are separate syndromes, we assume that they overlap
considerably.
For bulimia nervosa, in addition to the previously mentioned
factors, retrospective correlates reported to emerge in childhood
are childhood obesity and childhood overanxious disorder. Simi-
larly as for anorexia nervosa, adverse life events including sexual
3
Because of the very small number of risk factors and retrospective
correlates for binge-eating disorder, we felt it would be premature to
present these results in a similar way.
RISK FACTORS FOR EATING DISORDERS 51

abuse, some parental problems (alcoholism, depression, drug

abuse, obesity), a number of family environmental factors (e.g.,
critical comments on weight and shape, low contact), other adverse
family experiences, and negative self-evaluation could have oc-
curred at any time before the onset of the disorder. For sexual
abuse and adverse life events, occurrence before age 12 to 18 years
has been reported. Other retrospective correlates (and fixed mark-

Emergence of risk factors for eating disorders from longitudinal studies. YSR ⫽ Youth Self-Report Inventory; y. ⫽ year; ED ⫽ eating disorder.
ers) reported for early adolescence are social phobia, dieting, and
acculturation, as well as early pubertal timing. Finally, mood- and
anxiety-related prodromal symptoms including severe dieting were
found during late adolescence. Pregnancy complications, child-
hood obesity, parental alcoholism, family environmental factors,
and negative self-evaluation are specific retrospective correlates
for bulimia nervosa. The majority of retrospective correlates com-
prises factors that have been reported only once and thus are in
need of replication, namely, pregnancy complications, childhood
obesity, overanxious disorder, social phobia, parental problems,
family environmental factors, and prodromal symptoms.
The following factors constitute the “common denominator” of
factors, which have consistently been reported to predict eating
disturbances and disorders from both longitudinal and cross-
sectional studies. Female gender and ethnicity (except Asian) are
consistently reported fixed markers for eating disorders. For both
anorexia and bulimia nervosa, it can be assumed that genetic
factors increase the risk of developing the disorder, although to
date, the relative contribution of these factors in relation to other
factors is uncertain. In addition, early childhood problems con-
cerning feeding and eating and gastrointestinal problems are pre-
cursors of later adolescent syndromes. Furthermore, childhood
adversities comprising both adverse sexual and physical experi-
ences have to be considered as early precursors of anorexia and
bulimia nervosa. In adolescence, which itself constitutes a risk
period, both disorders seem to be foreshadowed by negative self-
evaluation or low self-esteem; by an increased risk of psychiatric
morbidity including mood- and anxiety-related syndromes; and—
probably most strongly— by heightened weight and shape con-
cerns, body dissatisfaction, and dieting behavior.

General Questions for the Classification of Risk Factors

for the Onset of a Disorder
Against the background of the application of the risk factor
typology and additional risk factor characteristics, we finally want
to suggest questions for the classification of risk factors for psy-
chiatric disorders in general. These questions could lead to the
development of a general taxonomy of risk factors for psycholog-
ical or psychiatric disorders (see Appendix B).
The first question concerns the precise definition of the risk
population and possible sampling limitations that have to be taken
into consideration. The examination of putative risk factors in a
Figure 1.

community sample might, for example, lead to different conclu-

sions compared with those found in clinical or subclinical samples.
Risk factors found in samples with children might differ from
those found in adolescent or adult samples, male and female
samples might differ in the range and emergence of putative risk
factors, as might different ethnic groups. Some risk factors might
be limited to specific developmental phases (e.g., early childhood,
puberty), whereas others might be active throughout the whole life
span. Risk factors for the full diagnostic (DSM) syndrome might
 52
JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS

Figure 2. Emergence of fixed markers, variable markers, and retrospective correlates for anorexia nervosa from cross-sectional studies. OCD ⫽
obsessive– compulsive disorder; BDD ⫽ body dysmorphic disorder; OCPD ⫽ obsessive– compulsive personality disorder; y. ⫽ year; AN ⫽ anorexia
nervosa.
 RISK FACTORS FOR EATING DISORDERS

Figure 3. Emergence of fixed markers, variable markers, and retrospective correlates for bulimia nervosa from cross-sectional studies. y. ⫽ year; BN ⫽
bulimia nervosa.
53
54 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
differ from those for partial syndromes, for symptoms of the full
disorder, or for prodromal or early symptoms of the disorder. From
a developmental perspective, the latter question is especially im-
portant for the timely discrimination between subjects at risk for
the full disorder and subjects with merely transient symptoms or
risk factors, thus establishing the developmental trajectories for a
disorder.
The next questions concern the association between the putative
risk factor and the disorder. As we have demonstrated for some of
the aforementioned factors for eating disorders, although an asso-
ciation might have been reported in the literature, a closer exam-
ination indicates that the methods used do not allow conclusions to
be made about risk factor status according to the Kraemer typol-
ogy. The most crucial question according to Kraemer et al. (1997)
in establishing risk factor status is the question of precedence of
the factor to the disorder. To assess precedence, the study design
(prospective longitudinal vs. cross-sectional) is most important.
Although we consider prospective longitudinal studies to be the
gold standard, cross-sectional studies are able to address prece-
dence for fixed markers and for some factors found in medical
records or case/birth registers. For the remaining cross-sectional
research, it seems at least reasonable to compare results of studies
in which the factors have been assessed retrospectively before the
onset of a disorder with the results of prospectively assessed
factors. Moreover, even if the status of a factor as a risk factor has
been established prospectively, it should be examined and repli-
cated in different populations.
Questions 5 and 6 address the variability or changeability of the
factor together with the effect of its manipulation on the onset of
a given disorder. This information is necessary to establish a causal
relationship. Additional important risk factor information (Ques-
tion 7) concerns the specificity of a factor for a disorder to
distinguish between generic factors, which play a role in the
development of a variety of psychiatric disorders, and (additional)
specific factors and (Question 8) the potency of the factor as
measure of the magnitude of its impact. Because of the use of
different measures of potency in psychological and psychiatric
research, which often are not directly transformable across studies,
and, moreover, the finding that reliance on some of them (e.g.,
ORs) can lead to misinterpretations regarding the magnitude of the
effect (Kraemer et al., 1999), we recommend including the
AUCs— based on the respective risks or Cohen’s delta—as indi-
cators of the magnitude of the effect, whenever possible. At least
for some factors, the question of a possible dose or necessary
intensity limit (or threshold) for the factor might be of additional
importance.
Finally, although not the subject of this article, the question of
a factor’s effectiveness alone or in interaction with other (psycho-
social or biological) factors is important to establish the pathway to
a distinct disorder. More specifically, this pathway can be charac-
terized by overlapping, moderating, and mediating effects of dif-
ferent factors (see Kraemer, Stice, Kazdin, Offord, & Kupfer,
2001).
Conclusion
The major purpose of this article was to apply a more rigorous
risk factor terminology to a selected psychiatric disorder, eating
disorders, to clarify the status of longitudinal versus cross-
sectional risk factor research in that field. Our second goal was to
place these specific findings into a broader theoretical context by
suggesting general taxonomic criteria for the classification of risk
factors for psychiatric disorders in general. These criteria are based
on theoretical considerations and methodological questions that
emerged when applying the risk factor terminology to eating
disorders.
The process of applying the risk factor criteria to research in the
area of eating disorders turned out to be a difficult balancing act
between stringent application of the taxonomy and “throwing the
baby out with the bath water.” Because the risk terminology
applied has only recently been published (Kazdin et al., 1997;
Kramer et al., 1997), previous “risk factor studies” had, of course,
not been designed with this concept in mind. For example, the
(predominantly cross-sectional) methods used in these studies did
not allow for the prediction of onset, initial symptoms were not
controlled for, and, in many cases, precedence was not addressed.
The majority of studies reviewed in this article is cross-
sectional, falling into the category of “preliminary risk studies”
and thus generating hypotheses concerning putative risk factors
that need to be confirmed in longitudinal studies. In comparison to
these, the number of “definitive” (longitudinal) studies is much
smaller. Most of the preliminary studies compared patients with
eating disorders with control subjects on one or several putative
risk factors assessed concurrently, thus only allowing for the
identification of correlates. A subset of cross-sectional studies,
however, addressed precedence by retrospectively assessing the
putative risk factor before onset of the eating disorder. Given the
novelty of the terminology applied here, the explicit consideration
of these retrospective correlates and their comparison with factors
from definitive risk studies seems important.
However, despite applying these more liberalized criteria, some
of the previously reported factors were not classifiable as retro-
spective correlates, or they yielded inconsistent results when com-
pared with other cross-sectional or longitudinal studies. As a
consequence, for example, family functioning variables, family
interaction styles, higher premorbid BMI, perfectionism, and par-
ticipation in weight-related subcultures, could not be confirmed as
risk factors. Other inconsistencies between results from longitudi-
nal and (retrospectively assessed) cross-sectional factors may be
related to the complexity behind the factor, that is, the fact that the
factor may be a proxy for or be associated with one or several other
interacting risk factors, or to differences in samples studied.
On the other hand, even the most rigorous studies had limita-
tions. The first limitation is related to the outcome criteria from
longitudinal studies. The majority of risk factors from longitudinal
studies predicted a mixture of full and partial (subclinical) DSM
syndromes of eating disorders. Furthermore, a closer examination
of the outcome criteria reveals that their focus is on bulimic and
binge-eating syndromes, whereas anorexic syndromes as outcomes
were much more rare. Although the majority of longitudinal stud-
ies included sample sizes of several hundred subjects, it is not
surprising that they were not able to purely predict full eating
disorder syndromes. Given the prevalence rates of bulimia nervosa
(1%–2% of the female population), and the average attrition during
the course of longitudinal studies, a sample size of 3,000 to 5,000
subjects would be needed to subsequently detect a number of cases
(30 –100) large enough for a meaningful risk factor prediction. It
should also be noted that most longitudinal studies only follow
 RISK FACTORS FOR EATING DISORDERS
subjects through high school. Because bulimia nervosa has a mean
onset of 19 years of age, this length of follow-up is not sufficient.
Because of the even lower prevalence rates of anorexia nervosa,
the sample size for an initial screening would probably have to
comprise 10,000 or more subjects.
An additional problem related to outcome criteria used in lon-
gitudinal studies is the differentiation between risk factors and
early symptoms of eating disorders. Although this could equally
apply to any of the factors proximal to the onset of the disorders,
the distinction is most crucial for one of the most potent factors,
that is, weight concerns. This factor usually represents a combi-
nation of attitudes and behaviors such as worrying about weight
and shape, dieting behavior, and fear of weight gain, and the exact
sequence of the emergence of these components is unknown.
Although it seems plausible that risk factors for the early symp-
toms of a disorder are the same as for the full syndrome, the
cut-offs for normative behaviors turning into risk factors and risk
behaviors turning into full syndromes are not clear. In addition,
information on the sensitivity and specificity of the respective
outcome measures (e.g., EAT-26 subscales or algorithms of EAT-
26, EDI subscales, and additional criteria) as diagnostic tests are
not known for all of the outcomes, partial syndromes in particular
(Jacobi et al., in press). To discriminate between early symptoms
and risk factors, it would be necessary to follow the natural course
of a group of subjects affected with the most potent factor, high
weight and shape concerns, over several years, to assess the
incidence rates of full eating disorder symptoms in this group and
to identify risk factors—in addition to the ones already present—
for the prediction of newly developed full cases. Such a high-risk
natural course study could help to clarify and differentiate risk
factors for weight concerns or early symptoms from those for the
full syndromes.
We were also not able to identify differential risk factors for
subgroups of eating disorder diagnoses (e.g., for restricting vs.
binge-eating/purging people with anorexia nervosa, for purging vs.
nonpurging people with bulimia nervosa, for people with bulimia
nervosa with or without a history of anorexia nervosa, or for early
vs. late-onset eating disorders). Again, to answer questions like
these, sample sizes of several thousand subjects would be
necessary.
The majority of risk factors for eating disorders has been as-
sessed in Caucasian samples of adolescents. With few exceptions,
research on potential early or late childhood risk factors is based
on retrospective correlates from cross-sectional studies. But even
when considering risk factors assessed during adolescence, repli-
cations with different populations (e.g., different ethnic popula-
tions) are needed for most factors to improve the generalization of
the results.
Another limitation of previous risk factor research is that none
of the longitudinal studies provided information on the specificity
of the risk factors with regard to the development of anorexia
nervosa, bulimia nervosa, or binge-eating disorder. Information on
specificity could only be obtained from those cross-sectional stud-
ies with retrospective factor assessment that also included a second
psychiatric comparison group. From these studies, factors specif-
ically predicting anorexia nervosa were pregnancy and birth-
related complications, OCD, perfectionism, and negative self-
evaluation. Factors specifically predicting bulimia nervosa were
pregnancy complications, childhood obesity, parental problems
55
(alcoholism and obesity), family environmental factors, such as
critical comments on weight and shape by the family, and negative
self-evaluation. With the exception of pregnancy complications,
the factors specifically predicting bulimia nervosa have all been
found in the same study (Fairburn et al., 1997). The fact that
negative self-evaluation was classified as a specific retrospective
correlate for both anorexia and bulimia nervosa highlights that a
factor may be specific when compared with other psychiatric
disorders without being able to discriminate between different
eating disorder syndromes. On the other hand, although perfec-
tionism was— on the basis of one study— classified as a specific
retrospective correlate for anorexia but for neither bulimia nor
other psychiatric disorders, results from other studies indicate that
perfectionism may be a precursor or retrospective correlate for
other psychiatric disorders, especially OCD (see, e.g., Frost &
Steketee, 1997). Once more, the necessity of replicating the results
in different populations becomes apparent.
The variability in both independent and dependent measures as
well as in methodologies applied did not allow us to carry out a
meta-analysis for the assessment of potency. It is not surprising,
though, that consistent indications of potency even across the
different measures used were found only for weight concerns/
dieting, which turned out to be the most potent factor. On the
basis of cross-sectional studies, the potency of sexual abuse and
adverse life events also consistently turned out to be low. For the
remaining factors, potency has to be considered either unclear or
unreplicated.
To date, the question of precedence has not been addressed for
most of the biological factors. In spite of the large body of research
on neurobiological disturbances, these have as yet not been exam-
ined prospectively. With the exception of genetic factors from twin
studies, preterm birth, birth trauma, and pubertal timing, biological
factors can be classified best as correlates. None of the studies
have allowed for the joint examination of psychosocial and bio-
logical risk factors. In addition, none of the studies have examined
biological factors in high-risk groups prior to the development of
eating disorders. Future study designs integrating psychosocial and
biological factors prospectively may lead to a better understanding
of the relative contribution of biology and environment.
The majority of the above-classified risk factors has been clas-
sified as variable risk factors; that is, they can change or be
changed spontaneously. None of the above-classified factors has
been classified as a causal risk factor. A causal risk factor was
defined as a variable risk factor that, when manipulated, can be
shown to change the risk of the outcome, that is, the onset of the
disorder. For some of the previously discussed variable risk fac-
tors, intentional manipulation is hardly conceivable or, for ethical
reasons, feasible: To test the role of dieting as a causal factor
would mean having women diet for several weeks or months and
then comparing them with a group of nondieting women with
regard to the onset of possible eating disturbances. To change
peoples’ social environment to watch the risk for the development
of an eating disorder change is similarly difficult. The impact of a
changing social environment can, however, be addressed within
migration studies, as has already been done for other disorders
(e.g., cardiovascular diseases). A limited number of early epide-
miological studies have addressed the question of changes in the
incidence of eating disorders in a population of women moving
from countries with low cultural emphasis on weight and shape
56 JACOBI, HAYWARD, DE ZWAAN, KRAEMER, AND AGRAS
into a Western culture with high cultural emphasis on weight and
shape (e.g., Fichter, Elton, Sourdi, Weyerer, & Koptagel-Ilal,
1988). However, these studies are extremely difficult to carry out
and need large sample sizes to detect meaningful differences.
Another way to manipulate a factor and thus establish its status
as a causal factor is to manipulate it within a randomized con-
trolled trial. So far, at least for bulimia nervosa (and, to a lesser
extent, for binge-eating disorder but not for anorexia nervosa) a
relatively large number of controlled treatment trials has been
carried out (Craighead & Agras, 1991; Jacobi, Dahme, & Rusten-
bach, 1997; Wilson & Fairburn, 1993). Usually, weight and shape
concerns are significantly decreased after treatment. The crucial
issue is, however, that different treatment approaches such as
cognitive– behavior therapy, interpersonal therapy, and antidepres-
sant treatment result in almost similar reductions of this risk factor,
thus raising questions about the mechanisms of these changes.
Another, and to date possibly the most realistic, way to manip-
ulate a potential causal factor would be to address the factor in a
high-risk group within a preventive approach and to show that by
reduction in exposure to the risk factor, the risk decreases. This,
however, only confirms the causal status of a risk factor, if the
natural course of these high-risk groups and the predictive value of
the risk factors for full syndromes of eating disorders have been
clarified in previous studies. To date, the results of the majority of
primary prevention outcome studies have been considered “disap-
pointing” (e.g., Smolak, Levine, & Schermer, 1998; Taylor &
Altman, 1997). Although these programs try to reduce the most
potent risk factor, weight and shape concerns, by providing de-
tailed information, their results indicate moderate changes in
knowledge but not in eating behaviors, such as eating patterns or
weight-reduction attempts. It has been argued that the programs
might be more effective if they focused on younger (elementary
school) children rather than adolescents (Smolak et al., 1998). This
could not, however, be supported by the findings from a controlled
evaluation of an elementary school primary prevention program
(Smolak et al., 1998).
More promising results have been achieved when the samples
were subdivided into high- and low-risk groups. For the high-risk
groups, the effects of the preventive interventions were much
stronger than for the low-risk group (Killen et al., 1993; Winzel-
berg et al., 2000), indicating the importance of secondary preven-
tive approaches. An alternative explanation is, given the diversity
of the above-classified variable risk factors, that the focus of
previous preventive interventions has been too narrow and that
some risk factors (e.g., general psychiatric comorbidity) might
need more intensive interventions (Taylor & Altman, 1997). Fi-
nally, some of the risk factors such as early eating and gastroin-
testinal problems and eating conflicts have been reported during
the first years of the child’s life. To manipulate these, preventive
interventions may also have to target parental attitudes and behav-
iors. To our knowledge, none of the prevention programs to date
has included parents in order to reduce the risk for their children.
The present review has tried to come to terms with risk factors
for eating disorders and thus to come to terms with risk factors for
psychiatric disorders in general. In addition to the differences
between this approach and previous reviews outlined above, the
classification of risk factors, as applied here, is also different in
terms of the “dynamic” element that is part of many etiological
models. Even by ordering risk factors for eating disorders on the
basis of precedence along a timeline, no conclusions about the
interaction of factors, about moderating and mediating influences
of factors, or about protective effects of factors can be drawn. The
timeline ordering can, however, help to generate hypotheses about
the way risk factors work together, which could then be tested in
subsequent studies.
The results of the application of risk factor criteria to eating
disorders represent the present “state of the art,” even in view of
the many limitations that we have pointed out. We do not claim to
provide a comprehensive understanding of the factors involved in
and necessary for the development of an eating disorder. Like in a
meta-analysis, the results obtained by approaches like ours are
often counterbalanced by newly emerging limiting factors to be
addressed and resolved by subsequent studies. We hope that the
influence of the approach outlined here will not be limited to the
clarification of the status of risk factor research for the domain of
eating disorders but will reach beyond to increase the awareness
for risk factor issues in general.
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Appendix A

Potential Risk Factors for Eating Disorders

General and social factors
Gender
Race/ethnicity
Participation in weight-related social or professional subculture
(dancer, model, athlete, gymnasts, etc.)
Sex role orientation; for males: homosexuality
Familial factors
Parental obesity
Parental psychopathology
Family interaction/communication style, expressed emotion
Developmental factors
Adolescent age
Premorbid obesity, higher body mass index
Childhood picky eating, problem eating, pica
Childhood feeding and digestive problems
Teasing/critical comments about weight and shape
Early pubertal maturation
Childhood anxiety disorders
Adverse life events
Sexual or physical abuse
Other stressful or adverse life events
Psychological and behavioral factors
Dieting, restrained eating
Overconcern with weight and shape, body dissatisfaction/negative
body image, high drive for thinness
Low interoceptive awareness
Low self-esteem
Perfectionism, obsessive–compulsiveness, obsessive–compulsive
personality disorder
Depression, anxiety disorders, substance and/or alcohol abuse
problems, affective instability
Attachment style
Self-awareness
High-level exercise
Biological factors
Genetic factors
Neuroendocrine and metabolic disturbances
Changes in receptor density
Electroencephalogram changes
Changes in regulation of hunger and satiety
 RISK FACTORS FOR EATING DISORDERS 65

Appendix B

General Questions for the Classification of Risk Factors for the Onset of a Disorder
1. How can the risk population be defined and what kind of sampling limitations have to be taken into
consideration (community sample vs. clinical or subclinical sample; follow-up sample of a longitudinal
study; specific age or ethnic group)?
Is the risk factor limited to specific developmental phases?
Is the factor a risk factor for the full diagnostic (DSM) syndrome, for a partial syndrome/partial
symptoms, or for prodromal symptoms/early signs of the disorder?
2. Is there a relationship between the putative risk factor and the disorder at all?
Has the factor’s association to the disorder been demonstrated consistently and repeatedly in different
samples or settings?
3. Does the factor precede the disorder?
4. How was the factor assessed, longitudinally or cross-sectionally? (Cross-sectional assessment could
include different study types such as epidemiological or prevalence studies, cross-sectional studies with
cross-sectional factor assessment, cross-sectional case-control studies with retrospective risk factor
assessment, family and family history studies, or genetic studies.
5. Is the factor manipulable/changeable?
6. Does manipulation of the factor affect the onset of the disorder?
7. Is the factor a specific risk factor for the disorder or a general risk factor (generic)?
8. How potent is the factor? How was this assessed?
9. Is there a dose–intensity limit to the factor (threshold)?
10. Is the factor effective alone or only in combination/interaction with other factors? How can the
interaction with the other factors be characterized (moderator–mediator, overlapping, proxy)?

Note. DSM ⫽ Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association,
1994).

Received October 16, 2002

Revision received June 10, 2003
Accepted June 10, 2003 䡲

Correction to Smith et al. (2003)

In the article “Religiousness and Depression: Evidence for a Main Effect and the Moderating
Influence of Stressful Life Events,” by Timothy B. Smith, Michael E. McCullough, and Justin Poll
(Psychological Bulletin, 2003, Vol. 129, No. 4, pp. 614 – 636) the description on p. 616 (Other
Potential Moderators of the Association section) of results from Burris’s (1994) previous study of
intrinsic and extrinsic religious orientations and their associations with depressive symptoms was
incorrect. Burris (1994) indeed found a positive association between extrinsic religious motivation
and symptoms of depression. However, this effect was qualified by a significant Intrinsic ⫻
Extrinsic interaction, such that persons who scored high on both orientations reported more
symptoms of depression than did persons who scored high on intrinsic orientation only, whereas
persons who scored low on intrinsic orientation reported a depression level that was between those
two groups.
Furthermore, the effect size (r) reported in Table 2 (p. 619) for this study should be .23, not ⫺.11,
and the sample size should be 200, not 100. These corrections result in a change in the reported
random effects weighted average effect size (r) across all 147 studies (reported on p. 623, Omnibus
Analysis section) from ⫺.096 to ⫺.094. All substantive conclusions of the review remain the same.

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