Stice Et Al (2017)

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J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.
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Published in final edited form as:

J Abnorm Psychol. 2017 January ; 126(1): 38–51. doi:10.1037/abn0000219.
Risk Factors that Predict Future Onset of Each DSM-5 Eating

Disorder: Predictive Specificity in High-Risk Adolescent Females
Eric Stice, Jeff M. Gau, Paul Rohde, and Heather Shaw
Oregon Research Institute
Abstract
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Objective—Because no single report has examined risk factors that predict future onset each
type of eating disorder and core symptom dimensions that crosscut disorders, we addressed these
aims to advance knowledge regarding risk factor specificity.
Method—Data from 3 prevention trials that targeted young women with body dissatisfaction
(N=1272; M age 18.5, SD 4.2) and collected annual diagnostic interview data over 3-year follow-
up were combined to identify predictors of subthreshold/threshold anorexia nervosa (AN), bulimia
nervosa (BN), binge eating disorder (BED), and purging disorder (PD).
Results—Negative affect and functional impairment predicted onset of all eating disorders. Thin-
ideal internalization, body dissatisfaction, dieting, overeating, and mental health care predicted
onset of subthreshold/threshold BN, BED, and PD; positive thinness expectations, denial of cost of
pursuing the thin ideal, and fasting predicted onset of 2 of these 3 disorders. Similar risk factors
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predicted core eating disorder symptom onset. Low BMI and dieting specifically predicted onset
of subthreshold/threshold AN or low BMI. Only a subset of factors showed unique predictive
effects in multivariate models, likely due to moderate correlations between the risk factors (M r = .
14).
Conclusions—Results provide support for the theory that pursuit of the thin ideal and the
resulting body dissatisfaction, dieting, and unhealthy weight control behaviors increase risk for
binge/purge spectrum eating disorders, but suggest that youth who are inherently lean, rather than
purposely pursuing the thin ideal, are at risk for AN. Impaired interpersonal functioning and
negative affect are transdiagnostic risk factors, suggesting these factors should be targeted in
prevention programs.
General Scientific Summary
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Findings suggest that pursuit of the thin beauty ideal and the resulting body dissatisfaction and
weight control behaviors increase risk for developing eating disorders involving binge eating and
unhealthy weight control behaviors, but that inherently lean young women, rather than those
purposely pursuing the thin ideal, are at risk for eating disorders involving a dangerously low body
weight. Findings also suggest that negative affect and impaired interpersonal functioning are
transdiagnostic factors that increase risk for the full spectrum of eating disorders.
*
Correspondence should be addressed to Eric Stice at Oregon Research Institute, 1776 Millrace Drive, Eugene, Oregon, 97403, USA.
estice@ori.org. Phone: 011-541-484-2123. Fax: 011-541-484-1108.
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Keywords
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risk factors; prospective; anorexia nervosa; bulimia nervosa; binge eating disorder; purging
disorder; eating disorder symptoms
Eating disorders affect 13% of females (Allen, Byrne, Oddy, & Crosby, 2013; Stice, Marti,
& Rohde, 2013a) and are marked by chronicity, relapse, distress, functional impairment, and
risk for future obesity, depression, suicide, substance abuse, and mortality (Arcelus,
Mitchell, Wales, & Nielsen, 2011; Swanson, Crow, Le Grange, Swendsen, & Merikangas,
2011). However, few studies have evaluated risk factors that predict future onset of each
DSM-5 (American Psychiatric Association, 2013) eating disorder using validated diagnostic
interviews, which is vital because this design provides definitive evidence that the risk
factors predate onset of the disorder (Kraemer, Stice, Kazdin, & Kupfer, 2001). Although
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prospective studies have predicted future increases in eating disorder symptom composite
measures (e.g., Stice, 2001; Vohs Bardone, Joiner, Abramson, & Heatherton, 2001), they
provide less definitive evidence of temporal precedence and can be challenging to interpret
because symptoms often decrease over time and it is not clear that the models are predicting
emergence of clinically significant eating pathology. Studies have also predicted future onset
of individual eating disorder symptoms (e.g., Pearson, Combs, Zapolski, & Smith, 2012;
Goldschmidt, Wall, Loth, Le Grange, & Neumark-Sztainer, 2012), which provides clear
evidence of temporal precedence, but the clinical significance of individual eating disorder
symptoms has not been well established. Another limitation of this literature is that many
studies have not used diagnostic interviews, which is concerning because many researchers
view diagnostic interviews as the gold standard. An improved understanding of risk factors
that predict onset of each DSM-5 eating disorder will inform etiologic theory for each
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disorder, inform content for prevention programs tailored for the various eating disorders,
which would be indicated if they have distinct risk factors, determine which high-risk
subgroups to target with selective prevention programs for each disorder, and potentially
identify transdiagnostic risk factors.
Only one study examined factors that predicted future onset of interview-assessed
subthreshold/threshold anorexia nervosa (sAN/AN) among participants confirmed to be
disorder-free at baseline. Low body mass index (BMI) and low dieting during early
adolescence predicted sAN/AN over 5-year follow-up in a community sample of females
who were in early adolescence at baseline, but early puberty, pressure for thinness, thin-ideal
internalization, body dissatisfaction, negative affect, or social support deficits did not (Stice
& Bohon, 2013). Findings from risk factor studies are summarized in Table 1.
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Five studies examined factors that predicted future onset of interview-assessed subthreshold/
threshold bulimia nervosa (sBN/BN), all of which involved community samples of
adolescent girls. Dieting predicted onset of sBN/BN onset over 1-year follow-up (Patton,
Johnson-Sabine, Wood, Mann, & Wakeling, 1990). Weight concerns, drive for thinness,
body dissatisfaction, ineffectiveness, negative affectivity, dieting, and alcohol use, and low
interoceptive awareness predicted onset of sBN/BN over 4-year follow-up, but
perfectionism, maturity fears, interpersonal distrust, and BMI did not (Killen et al., 1996).

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Dieting and psychiatric problems predicted BN onset over 3-year follow-up, but peer
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dieting, BMI, daily exercise, and parental separation did not (Patton, Selzer, Coffey, Carlin,
& Wolfe, 1999). Elevated BMI, social pressure for thinness, thin-ideal internalization,
dieting, fasting, negative affect, social support deficits, and early puberty predicted onset of
sBN/BN over 5-year follow-up, but body dissatisfaction did not (Stice, Davis, Miller, &
Marti, 2008a; Stice & Bohon, 2013). Social pressure to be thin and body dissatisfaction
predicted onset of sBN/BN over a longer 7-year follow-up in the same sample, but thin-ideal
internalization, dieting, negative affect, or depressive symptoms did not (Stice, Marti, &
Durant, 2011a).
Only one study each examined factors that predicted future onset of subthreshold/threshold
binge eating disorder (sBED/BED) and purging disorder (PD), both of which used the same
community sample of females who were in early adolescence at baseline. Social pressure for
thinness predicted onset of sBED/BED over 7-year follow-up, but thin-ideal internalization,
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body dissatisfaction, dieting, or negative affect did not (Stice et al., 2011a). Thin-ideal
internalization, body dissatisfaction, and dieting predicted PD onset over 7-year follow-up,
but social pressure to be thin, negative affect, and depressive symptoms did not (Stice et al.,
2011a).
Thus, no single report has investigated risk factors that predict future onset of each major
DSM-5 eating disorder, which limits knowledge about risk factor specificity. Indeed, only
four prospective studies have contributed to this literature, underscoring the need to expand
this evidence-base. Equally striking, only one prospective study investigated risk factors that
predict onset of AN, BED, and PD. The low incidence of certain eating disorders,
particularly AN, has contributed to this lacuna. For instance, one of the largest prospective
studies did not identify a single participant who showed AN onset (McKnight Investigators,
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2003). One solution is to use a high-risk design wherein participants at elevated risk for
mental health disorders are followed. Prospective high-risk designs have been used to
elucidate risk factors for a variety of disorders, such as depression (LeMoult, Ordaz,
Kircanski, Singh, & Gotlib, 2015), anxiety disorders (Schmidt, Lerew, & Jackson, 1999),
substance abuse (Chassin, Pitts, DeLucia, & Todd, 1999), and psychosis (Cannon et al.,
2008). One previous study used this approach for eating disorders (Jacobi et al., 2011),
though not all diagnoses were confirmed by interview and the small sample size precluded
the ability to examine risk factors for each type of eating disorder. Accordingly, the present
study combined data from three large randomized eating disorder prevention trials that used
parallel recruitment and assessment procedures, which increased sensitivity to detecting risk
factors that predict future onset of eating pathology. The goal was to test whether a set of
factors assessed at baseline predicted future onset of eating disorders and the core eating
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disorder symptom dimensions that crosscut different diagnostic categories over 3-year
follow-up.
We investigated a range of factors that have been theorized to increase risk for eating
disorders in several univariate and multivariate etiologic models (e.g., Hohlstein, Smith, &
Atlas, 1998; Lavender et al., 2016; McCarthy 1990; Stice, 2001). For instance, the dual
pathway model posits that elevated cultural pressure for thinness and internalization of the
thin ideal promotes body dissatisfaction, which in turn contributes to unhealthy weight

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control behaviors (e.g., meal skipping) and negative affect, which both increase risk for
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emergence of binge eating and compensatory weight control behaviors (Stice, 2001). We
hypothesized that baseline elevations in thin-ideal internalization, positive expectances
regarding thinness, denial of costs of pursuing the thin ideal, and body dissatisfaction would
increase risk for onset of disorders marked by use of weight loss behaviors, including AN,
BN, and PD. We further hypothesized that baseline elevations in weight control behaviors,
dieting, and negative affect would increase risk for onset of disorders characterized by binge
eating, including AN, BN, and BED. We hypothesized that functional impairment and
mental health care, which may represent proxy measures of general psychopathology, may
be transdiagnostic risk factors that increase risk for any eating disorder. Based on past
findings, we also hypothesized that a low BMI at baseline would increase risk for onset of
AN, but a high BMI at baseline would increase risk for BN and BED, as it might be a proxy
measure for a tendency toward dysregulated eating.
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We also investigated the predictive effects of prodromal eating disorder symptoms, based on
evidence that fasting predicted BN (Stice et al., 2008a). Specifically, we tested the
hypotheses that overeating, fasting, and excessive exercise would predict onset of syndromal
eating disorders. Such analyses are useful because it is possible that the emergence of one of
these prodromal symptoms reliably predicts emergence of eating disorders, serving as a
“gateway” to the full syndrome. However, it is important to consider the partial criterion
confounding when interpreting any predictive effects of prodromal symptoms.
We estimated models that predicted onset of subthrehold or threshold eating disorders, as

well as onset of threshold eating disorders, because individuals with threshold versus
subthreshold levels of BN and BED showed similar functional impairment, emotional
distress, and treatment care (Stice, Marti, Shaw, & Jaconis, 2009). This is also important
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because many individuals who seek treatment meet criteria for subthreshold rather than
threshold eating disorders (Eddy, Celio, Hoste, Herzog, & Le Grange, 2008). A related
lacuna is that only four studies reported descriptive data about progression from
subthreshold to threshold levels of an eating disorder, which should also advance knowledge
of etiologic processes; an average of 4% of young women with subthreshold AN progressed
to threshold AN during follow-up, 25% of young women with subthreshold BN progressed
to threshold BN during follow-up, and 21% of young woman with subthreshold BED
progressed to threshold BED over follow-up (Lewinsohn et al., 2000; Patton et al., 1990;
Stice et al., 2009, 2013). However, because those studies had small numbers of participants
with subthreshold eating disorders, we also reported diagnostic progression for each eating
disorder in the present study.
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Finally, scholars have called for research on behavioral and cognitive symptom dimensions
that crosscut psychiatric diagnoses (Sanislow et al., 2010), consistent with the Research
Domain Criteria (RDoC) perspective. Studies using a wide variety of analytic approaches
conducted over the last two decades suggest that eating pathology occurs along a continuum
(Luo, Donnellan, Burt, & Klump, in press; Olatunji et al., 2012; Stice, Killen, Hayward, &
Taylor, 1998; Tylka & Subich, 2003). Accordingly, we also investigated baseline factors that
predicted onset of core symptom dimensions that crosscut eating disorders, including binge

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eating, compensatory behaviors, overvaluation of weight and shape, fear of weight gain, and
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low body weight.
Methods
Participants and Procedures
We combined data from one efficacy trial (Trial 1; Stice, Marti, Spoor, Presnell, & Shaw,
2008b) and two effectiveness trials (Trial 2; Stice, Rohde, Shaw, & Gau, 2011b; Trial 3;
Stice, Rohde, Butryn, Shaw, & Marti, 2015) resulting in a sample of 1,272 participants.
Design of Randomized Prevention Trials

Mailings and fliers recruited female students for trials evaluating body acceptance
interventions at high schools (Trial 1 and 2) and colleges (Trial 1 and 3). There was only one
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inclusion criterion: that participants answer affirmatively when asked if they had body image
concerns during a phone screen. Regarding exclusion criteria, we sought to exclude
participants who met criteria for DSM-IV (American Psychiatric Association, 2000) AN or
BN, though analyses of the baseline diagnostic interview data indicated that we were not
entirely successful (see below). Informed consent was obtained from participants (and
parents if minors). Trial 1 participants were randomized to the Body Project eating disorder
prevention program, Healthy Weight eating disorder prevention program, an expressive
writing intervention, or assessment-only control condition. Trial 2 and 3 participants were
randomized to the Body Project or educational brochure control condition. Participants
completed surveys and interviews at baseline and at 1-, 6-, 12-, 24-, and 36-month follow-
up. Additional details can be found in Stice et al. (2008b, 2011b, 2015).
Measures
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Eating pathology—The semi-structured Eating Disorder Diagnostic Interview (EDDI;

Stice et al., 2013a) assessed eating disorder symptoms over the past 3 months at baseline and
since previous interview at follow-ups on a month-by-month basis. DSM-5 criteria for eating
disorders, as operationalized in Stice et al. (2013a), were used (see Table 2 for definitions).
However, we operationalized subthreshold AN following Stice et al. (2009) because it
represents a subthreshold version that more closely parallels AN (overweight and obese
participants can be diagnosed with atypical AN per DSM-5) and because we did not collect
data on weight loss history, making it impossible to diagnose atypical AN. We also predicted
onset of recurrent (2 or more episodes) binge eating, recurrent compensatory behaviors, and
diagnostic threshold levels of overvaluation of weight/shape and fear of weight gain/obesity.
With regard to prodromal symptoms, Overeating included counts of eating rapidly, eating
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until uncomfortably full, eating large amounts when not hungry, eating alone due to
embarrassment, feeling depressed or guilty after overeating, and feeling upset that you could
not control overeating, Fasting reflected the number of times per week in past three months
two meals in a row were skipped to “as a means of controlling your shape or weight” and
Excessive exercise reflected the number of times per week in the past 3 months of vigorous
exercise for more than an hour or moderate exercise for more than 2 hours was used “to
compensate for overeating”. EDDI eating disorder diagnoses have shown 1-week test-retest
reliability (κ = .79) and inter-rater agreement (κ = .75) for DSM-5 eating disorders,

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sensitivity to intervention effects, and participants with versus without EDDI-diagnosed

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eating disorders show greater functional impairment, emotional distress, and treatment care
(Stice et al., 2008b, 2009, 2013a, 2013b).
Thin ideal internalization—The Ideal-Body Stereotype Scale–Revised assessed thin-

ideal internalization (Stice et al., 2008b). It has shown internal consistency (α = .91), 2-week
test–retest reliability (r = .80), predictive validity for bulimic symptom onset, and sensitivity
to intervention effects (Stice et al., 2008b).
Positive thinness expectancies—The Thinness Expectancy scale (Hohlstein et al.,

1998) assessed expected social and psychological benefits of thinness. It has shown internal
consistency (α = .86) and predictive validity for body dissatisfaction onset (Stice &
Whitenton, 2002).
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Denial of costs of pursuing thin ideal—We created 5 items assessing denial of costs
associated with pursuing the thin ideal (sample item: The risks associated with severe
dieting are overrated). This scale has shown internal consistency (α = .82), 1-week test-
retest reliability (r = .87), and predictive validity for eating disorder onset (Stice, Rohde,
Gau, & Shaw, 2012).
Body dissatisfaction—The Body Dissatisfaction Scale (Stice et al., 2001) assessed

dissatisfaction with 9 body parts. It has shown internal consistency (α = .94), 3-week test–
retest reliability (r = .90), predictive validity for eating disorder onset, and sensitivity to
intervention effects (Stice et al., 2008b, 2011a).
Weight control behaviors—We used the Weight Control scale to assess reported dietary
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and exercise behaviors used to control weight (sample item: I have eaten more fruits and
vegetables). This scale showed internally consistent (α = .82), 4-week test-retest (r = .63),
and sensitivity to intervention effects (Stice, Presnell, Gau, & Shaw, 2007).
Dieting—The Dutch Restrained Eating Scale (van Strien, Frijters, van Staveren, Defares, &
Deurenberg, 1986) assesses the frequency of various dieting behaviors. It has shown internal
consistency (α = .95), 2-week test–retest reliability (r = .82), convergent validity with self-
reported (but not objectively measured) caloric intake, predictive validity for bulimic
symptoms, and sensitivity to intervention effects (Stice et al., 2008b; van Strien et al., 1986).
Negative affect—Different measures of negative affect were used in each trial and were
standardized to permit analyses of the combined data set. In Trial 1 negative affect was
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assessed with the sadness, guilt, and fear/anxiety subscales from the Positive Affect and
Negative Affect Scale-Revised (PANAS-X; Watson & Clark, 1992), which has shown
internal consistency (α = .95), 3-week test-retest reliability (r = .78), predictive validity for
bulimic symptom onset, and sensitivity to detecting intervention effects (Stice et al., 2008b).
In Trial 2 negative affect was assessed with the Center for Epidemiologic Studies-
Depression Scale (CESD; Radloff, 1977), which has shown internal consistency (α = .74 – .
91), temporal reliability (2- to 8-week test-retest r = .51 – .59), and convergent validity with
clinician ratings of depressive symptoms (M r = .88; Andrews, Lewinsohn, Hops, & Roberts,

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1993; Roberts, Lewinsohn, & Seeley, 1991). In Trial 3 negative affect was assessed with the
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21-item Beck Depression Inventory (Beck et al., 1988), which has shown internal
consistency (α = .73-.95), 1-week test-retest reliability (r = .93), convergent validity with
clinician ratings of depressive symptoms, and sensitivity to intervention effects (M r = .75;
Beck et al., 1988; Stice et al., 2015).
Functional impairment—Impairment in the family, peer group, romantic, and school

domains was measured with 17 items from the Social Adjustment Scale-Self Report for
Youth (Weismann & Bothwell, 1976). The original scale has shown convergent validity with
clinician and collateral ratings (M r = .72) and sensitivity to detecting treatment effects
(Weismann & Bothwell, 1976). The 17-item version has shown internal consistency (α = .
77), 1-week test–retest reliability (r = .83) and sensitivity to intervention effects (Stice et al.,
2008b).
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Mental health care—Use of mental health services was operationalized as the frequency
of visits to mental health care providers. Receipt of care in the last 6-months was coded “1”
and no health care coded “0”. This item showed 1-year test-retest reliability (r = .89) and
differentiate individuals with versus without eating disorders (Stice et al., 2008b; Stice et al.,
2013a).
Body mass—The BMI (kg/m2; Pietrobelli et al., 1998) was examined as a baseline
predictor of eating disorder onset and used to diagnose AN. Height was measured to the
nearest mm using portable stadiometers. Weight was assessed to the nearest 0.1 kg using
digital scales with participants wearing light indoor clothing without shoes or coats. Age-
and sex-adjusted BMI centiles were used to determine whether participants were
underweight for AN. Height and weight were measured twice at each assessment, to reduce
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errors, and averaged. BMI has shown convergent validity (r = .80 – .90) with direct measures
of body fat (Pietrobelli et al., 1998).
Statistical Methods
Cox proportional hazard models estimated with SAS PHREG (SAS Institute Inc., 2011)
tested which baseline risk factors predict onset of (a) subthreshold/threshold eating
disorders, (b) threshold eating disorders, and (c) eating disorder symptoms. Participants who
met criteria for the outcomes at baseline were excluded from the Cox models. Each risk
factor was first tested in separate models and then significant predictors were entered
simultaneously to assess unique effects. All risk factors were converted to z-scores so hazard
ratios could be interpreted as the difference in risk at each time point associated with a one
standard deviation change in the risk factor. To isolate risk factor effects from intervention
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effects, dummy coded vectors of intervention condition were included as covariates. The
Breslow (1974) method was used to handle tied event times in the hazard models. A
transform of the Martingale residuals evaluated the proportional hazards assumption. If this
assumption was not met models were re-estimated with covariate interactions with time
included as predictors. Missing onset data were accounted for with right-censoring in the
hazard models and 20 imputed data sets were used to account for missing risk factor data.
Sequential regression multiple imputation (SRMI; van Burren, 2007) was used to impute

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data sets using IVEware software V0.2 (Raghunathan, Solenberger, & Van Hoewyk, 2002).
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Model parameters and standard errors were combined following Rubin (1987) as
implemented in SAS PROC MIANALYZE (SAS Institute Inc., 2011).
Results
Preliminary Analyses
Table 3 provides demographic data for the present sample and compares it to a
representative sample of age-matched young women recruited from middle schools on
demographic factors and study variables that were assessed in both studies. The mean body
dissatisfaction score from our high-risk sample was 0.6 standard deviation (SD) higher than
the mean body dissatisfaction score from a representative sample of adolescent girls (Rohde
et al., 2015), mean thin-ideal internalization score was 0.6 SD higher, mean dieting score
was 0.7 SD higher, mean overeating score was 1.2 SDs higher, mean fasting score was 0.1
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SD higher, mean excessive exercise score was 0.1 SD higher, and mean functional
impairment was 0.2 SD lower. Data suggest that the sample used in the present study was at
moderately higher risk, suggesting that results may generalize to the broader population of
adolescent girls and young women. A related question is whether there was a restriction in
range for the risk factors, which could reduce sensitivity. Table 3 indicates that although
some variables had a smaller SD in the present high-risk sample compared to the
representative community-recruited sample, this was not the case for all variables examined.
Moreover, the fact that such a high percentage of risk factors exhibited significant predictive
effects (see below) implies we had sufficient sensitivity.
Attrition for diagnostic data, which are the only data examined from each follow-up
assessment, was 2% at posttest, 7% a 6-months, 6% at 1-year, 7% at 2-year, and 14% at 3-
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year follow-up. All but one case completed the full baseline assessment and 99% completed
at least one follow-up (M = 5.3 of 6 assessments, SD = 0.9). Incidence rates for subthreshold
and threshold levels of each disorder and core symptom dimensions over follow-up are
shown in Table 4. Incidence rates were 9% for any threshold level disorder, 15% for any
subthreshold disorder, and 52% for any core symptom dimension.
Rates of diagnostic progression, which is defined as a subthreshold level disorder that

escalates to threshold level at a later date, was 5% for AN, 40% for BN, 46% for BED, and
33% for PD. Participants who only experienced a subthreshold eating disorder after
experiencing a full threshold eating disorder are not included in these analyses.
We tested whether participants with subthrehold versus threshold levels of each eating
disorder differed significantly in terms of negative affect and functional impairment, as few
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studies have tested whether these groups show similar impairment. Negative affect and
functional impairment scores reported closest to onset of each disorder were compared.
Negative affect scores between subthreshold and threshold cases did not significantly differ
(all p-values > .214) and were associated with small effect sizes differences for BN (d = .07),
BED (d = 0.24), and PD (d = .01). Negative affect scores for subthreshold AN (Mean = 0.10,
SD = 1.07) versus threshold AN (Mean = 1.30, SD = 1.13) significantly differed (t-value =
2.54, p-value = .018, d = 1.11). Functional impairment scores between subthreshold and

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threshold cases did not significantly differ (all p-values > .134) and were associated with
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small effect size differences for AN, BN, BED, and PD (Cohen’s d’s .24, .27, .11, and .10,
respectively).
Correlations between baseline risk factors are shown in Table 5. The average correlation
among risk factors was r = .14 (range = .01 – .54).
Univariate Predictors of Specific Eating Disorders

We first tested in Cox proportional hazard moderation models whether the relation between
the risk factors targeted in the Body Project prevention program (thin-ideal internalization,
thinness expectancies, denial of thin-ideal costs) showed significantly different relations
with eating disorder onset among Body Project versus control participants. This was
necessary because an assumption of combining the data from these trials is that condition
did not moderate the predictive effects of the risk factors targeted in the prevention
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programs. We likewise tested whether the relation between the risk factor targeted in the
Healthy Weight prevention program (weight control behaviors) showed significantly
different relations with eating disorder onset among Healthy Weight versus control
participants. No significant interactive effects were found (all p-values > .098).
Table 6 reports results from the univariate Cox proportional hazard models predicting onset
of future subthreshold or threshold eating disorders. Functional impairment and lower BMI
at baseline predicted future onset of sAN/AN. Greater thin-ideal internalization, thinness
expectancy, denial of costs of pursuing the thin ideal, body dissatisfaction, dieting, negative
affect, overeating, fasting, functional impairment, and mental health care predicted future
onset of sBN/BN. Greater thin-ideal internalization, thinness expectancy, body
dissatisfaction, dieting, negative affect, overeating, functional impairment, and mental health
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care predicted future onset of sBED/BED. Greater thin-ideal internalization, thinness

expectancies, denial of costs of pursuing the thin ideal, body dissatisfaction, dieting,
negative affect, overeating, fasting, excessive exercise, functional impairment, and mental
health care predicted future onset of sPD/PD.
Table 7 reports results from univariate Cox proportional hazard models were also used to
predict future onset of threshold eating disorders. Significant baseline risk factors were
similar to those predicting onset of subthreshold/threshold eating disorders. Differences
were that negative affect was a predictor for onset of AN (p = .014), but not sAN/AN (p = .
534); denial costs was a predictor for onset BED (p = .007), but not sBED/BED (p = .143);
thinness expectancy was a predictor for onset of sBED/BED (p = .028), but not BED (p = .
056); and fasting and excessive exercise were predictors for onset of sPD/PD (p’s = .001
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and .017, respectively), but not for PD (p’s = .078 and .706). No differences in predictors for
sBN/BN versus BN were found.
Table 8 shows results from the univariate Cox proportional hazard models predicting future
onset of core eating disorder symptoms. Greater thin-ideal internalization, thinness
expectancy, denial costs of thin ideal pursuit, body dissatisfaction, dieting, negative affect,
overeating, excessive exercise, functional impairment, and mental health care predicted
binge eating onset. Similar risk factors predicted compensatory behavior onset, with the

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exception that the effect for denial of the costs of thin ideal pursuit was non-significant and
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weight control behaviors was significant. Similar risk factors also predicted onset of
overvaluation of weight or shape, except that thin ideal internalization, denial of costs of thin
ideal pursuit, and mental health care were non-significant, and fasting was significant.
Finally, similar risk factors predicted onset of fear of gaining weight, except fasting was
significant. Unlike the other symptoms, current BMI was only assessed at each assessment,
not on a month-by-month basis over follow-up. Thus, logistic regression models were used
to assess whether baseline risk factors predicted onset of low BMI at any follow-up
assessment. Lower baseline dieting scores (OR = 0.67, 95% CI [0.47, 0.97], p = .033) and
lower BMI (OR = 0.03, 95% CI [0.01, 0.10], p < .0001) predicted low BMI onset.
Multivariate Predictors of Specific Eating Disorders

Multivariate models predicting onset of future subthreshold or threshold eating disorders,
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which included risk factors with significant univariate effects, revealed that elevated
functional impairment (HR = 1.64, 95% CI [1.10, 2.44], p = .0142) and lower BMI (HR =
0.06, 95% CI [0.02, 0.14], p < .0001) remained unique predictors of sAN/AN onset.
Elevated dieting (HR = 1.45, 95% CI [1.12, 1.88], p = .0048), negative affect (HR = 1.46,
95% CI [1.19, 1.79], p = .0003), and overeating (HR = 1.78, 95% CI [1.48, 2.13], p < .0001)
showed unique predictive effects for sBN/BN onset. Elevated thin-ideal internalization (HR
= 1.36, 95% CI [1.05, 1.75], p = .0184), body dissatisfaction (HR = 1.71, 95% CI [1.31,
2.23], p < .0001), and functional impairment (HR = 1.31, 95% CI [1.04, 1.65], p = .0209)
showed unique predictive effects for sBED/BED onset. Elevated body dissatisfaction (HR =
1.63, 95% CI [1.21, 2.18], p = .0012), dieting (HR = 2.24, 95% CI [1.66, 3.03], p < .0001),
and overeating (HR = 1.25, 95% CI [1.03, 1.52], p = .0224) showed unique predictive effects
for sPD/PD onset.
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Multivariate models predicting onset of future threshold eating disorders, which included
risk factors that showed significant univariate effects, revealed that elevated negative affect
(HR = 2.24, 95% CI [1.25, 3.99], p = .0064) and lower BMI (HR = 0.63, 95% CI [0.44,
0.91], p < .0135) showed unique predictive effects for AN onset. Elevated body
dissatisfaction (HR = 1.50, 95% CI [1.08, 2.08], p = .0166), overeating (HR = 2.07, 95% CI
[1.65, 2.61], p < .0001), and fasting (HR = 1.29, 95% CI [1.08, 1.53], p = .0046) showed
unique predictive effects for BN onset. Elevated body dissatisfaction (HR = 1.49, 95% CI
[1.07, 2.06], p = .0167), overeating (HR = 1.99, 95% CI [1.59, 2.49], p < .0001), and
functional impairment (HR = 1.40, 95% CI [1.07, 1.83], p = .0142) showed unique
predictive effects for BED onset. Elevated body dissatisfaction (HR = 1.88, 95% CI [1.29,
2.72], p = .0009) and dieting (HR = 1.94, 95% CI [1.35, 2.79], p = .0003) showed unique
predictive effects for PD onset.
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Multivariate models predicting onset of future eating disorder symptoms, which included
risk factors that showed significant univariate effects, revealed that elevated dieting (HR =
1.26, 95% CI [1.08, 1.47], p = .0041), negative affect (HR = 1.34, 95% CI [1.17, 1.54], p < .
0001), and overeating (HR = 1.50, 95% CI [1.29, 2.76], p < .0001) showed unique predictive
effects for binge eating onset. Elevated thin-ideal internalization (HR = 1.16, 95% CI [1.01,
1.33], p = .0304), dieting (HR = 1.50, 95% CI [1.30, 1.73], p < .0001), negative affect (HR =

1.23, 95% CI [1.08, 1.39], p = .0019), overrating (HR = 1.31, 95% CI [1.15, 1.48], p < .
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0001), and excessive exercise (HR = 17.92, 95% CI [1.17, 275.55], p = .0385) showed
unique predictive effects for compensatory behavior onset. Elevated body dissatisfaction
(HR = 1.20, 95% CI [1.06, 1.37], p = .0048), negative affect (HR = 1.22, 95% CI [1.07,
1.40], p = .0037), fasting (HR = 1.17, 95% CI [1.01, 1.35], p = .0379), and excessive
exercise (HR = 1.29, 95% CI [1.15, 1.44], p < .0001) showed unique predictive effects for
onset of overvaluation of weight or shape. Elevated body dissatisfaction (HR = 1.44, 95% CI
[1.19, 1.74], p = .0002), dieting (HR = 1.58, 95% CI [1.32, 1.89], p < .0001), negative affect
(HR = 1.21, 95% CI [1.01, 1.45], p = .0343), overeating (HR = 1.24, 95% CI [1.08, 1.42], p
= .0017), fasting (HR = 1.16, 95% CI [1.03, 1.30], p = .0019) and functional impairment
(HR = 1.24, 95% CI [1.03, 1.49], p = .0220), showed unique predictive effects for onset of
fear of weight gain/obesity. Lower baseline BMI (HR = 0.03, 95% CI [0.01, 0.11], p < .
0001) showed a unique predictive effect for onset of low BMI.
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Discussion
Thin-ideal internalization, positive expectancies for thinness, body dissatisfaction, dieting,
overeating, and mental health care predicted onset of BN, BED, and PD, and denial of costs
of pursuing the thin ideal and fasting predicted onset of two of these three disorders. Results
for the first four risk factors largely converge with prior prospective studies that identified
predictors of future onset of subthreshold/threshold BN, BED, and PD (Table 1) and provide
support for the theory that pursuit of the culturally sanctioned thin ideal and the resulting
body dissatisfaction, dieting, and maladaptive weight control behaviors increase risk for
eating disorders involving binge eating and unhealthy compensatory behaviors. The overlap
in predictors of BN, BED, and PD is striking, as each of these risk factors predicted onset of
two or three of these eating disorders and no examined risk factor was specific to only one of
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these eating disorders classes.
Few studies have tested whether prodromal symptoms predict onset of syndromal eating
disorders. The predictive relation between fasting and onset of binge-spectrum eating
disorders converges with past findings (Stice et al., 2008a), but the effects for overeating and
excessive exercise are novel. When interpreting the prodromal effects, it should be noted that
there was partial criterion confounding, in that fasting and excessive exercise can be
diagnostic features of AN, BN, and PD, and that three of the six overeating questions must
be endorsed for a BED diagnosis. The former might have contributed to the relation of
fasting and excessive exercise to BN onset and the relation of fasting to PD onset, but could
not explain the relation of excessive exercise to BED onset. Moreover, if criterion
confounding were solely driving the results, fasting and excessive exercise should have
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predicted onset of AN, but they did not. The latter criterion confounding could have
contributed to the relation of overeating to BED onset, but could not explain why overeating
predicted onset of BN and PD, as those overeating features are not required for these two
diagnoses. The fact that it took 11.5 months on average to show onset of BED also implies
that participants did not simply show a small increase in binge eating to fulfill BED criteria.
Further, all of the participants at baseline who endorsed overeating did not met criteria for
the other symptoms of each of the eating disorders; as such participants were excluded from
survival models. Although effect sizes were generally small, overeating showed the largest

predictive effects for BN and BED. Data imply that it might be useful for indicated
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prevention programs to focus on individuals with prodromal eating disorder symptoms.
Negative affect and impaired psychosocial functioning were the only risk factors that
predicted onset of all four eating disorders. The former finding provides support for etiologic
models that posit that negative affect increases risk for binge eating and compensatory
weight control behaviors (Lavender et al., 2016; Stice, 2001). Theoretically, negative affect
increases the reward value of high-calorie foods and binge eating improves mood
(Lemmens, Rutters, Born, & Westerterp-Plantenga, 2011; Stice, 2001). Negative affect may
also increase the likelihood of unhealthy weight control behaviors because they reduce
anxiety about excess body fat. For others, negative affect may reduce appetite, contributing
to unhealthy weight loss. The finding that impaired psychosocial functioning increased risk
for all eating disorders is noteworthy because etiologic theory has not implicated this risk
factor. Yet this finding converges with evidence that social withdrawal predicted onset of any
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eating disorder (except AN) over 3–20 year follow-up (Allen, Byrne, Oddy, Schmidt, &
Crosby, 2014). Data suggest that impaired functioning precedes onset of the disorders
examined herein and thus may play a role in the development of the full spectrum of eating
disorders. Impaired functioning may contribute to negative affect, which could increase risk
for binge eating, compensatory behaviors, and under-nutrition for the reasons enumerated
above.
This is the first study to find that mental health care predicts onset of eating disorders. It is
unlikely that mental health care prompts eating disorder onset. Rather, receiving mental
health care may be a proxy risk factor for comorbid psychopathology (e.g., it is possible that
mood and anxiety disorders contribute to mental health care and also increase risk for eating
disorders).
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One striking findings is that low BMI, low dieting, negative affect, and functional
impairment predicted onset of AN and a low BMI, whereas the risk factors relating to
cultural pressures for thinness and resulting body dissatisfaction and weight control
behaviors did not. The evidence that a low BMI predicted onset of AN and a low BMI,
which was the largest effect, and the evidence that low dieting predicted onset of a low BMI,
converges with evidence that low BMI and low dieting predicted future onset of AN in the
only other prospective study of risk factors for AN onset (Stice & Bohon, 2013). The earlier
study used data from a community sample of adolescent girls followed over 5-years (early
puberty, perceived pressure for thinness, thin-ideal internalization, body dissatisfaction,
negative affect, and social support deficits did not predict AN onset). The evidence that low
BMI predicted AN onset in two studies converges with the finding from retrospective studies
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that lifetime diagnoses of AN correlated with a low BMI at age 6 (Tyrka, Waldron, Graber,
& Brooks-Gunn, 2002) and with low birth weight (Cnattingius, Hultman, Dahl, & Sparen,
1999), and low dieting, eating conflict, meal struggles, and unpleasant meals at age 6
(Kotler, Cohen, Davies, Pine, & Walsh, 2001). Contrary to accepted theorizing based on
case-control studies, which implicate dieting, perfectionism, and low self-esteem (e.g.,
Fairburn, Cooper, Doll, & Welch, 1999), results imply that youth who are ambivalent to food
or who undereat for other reasons, and therefore have lower BMIs and less need to diet, are
at risk for AN. Although low body weight during early adolescence might be construed as a

prodromal sign of incipit AN onset, fasting and excessive exercise did not predict AN onset.
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Negative affect and impaired psychosocial functioning also predicted AN onset, implying
that youth who have high negative affect and difficulty getting along well with their family,
friends, and peers are at risk for AN onset or that under-eating causes or exacerbates
affective disturbances and interpersonal conflict. The fact that thin ideal internalization and
body dissatisfaction did not predict AN implies that cultural pressure for thinness do not
increase risk for AN.
Risk factors that predicted onset of subthreshold or threshold eating disorders generally
predicted onset of threshold versions of the same eating disorder, implying that risk factors
for subthreshold and threshold variants of these eating disorders are more similar than
different. Further, the risk factors that predicted onset of binge eating and compensatory
behaviors were similar to those that predicted onset of subthreshold and threshold BN, BED,
and PD. There were only a few differences in risk factors identified in these analyses:
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whereas excessive exercise did not predict onset of subthreshold or threshold BN and BED,
it did predict binge eating onset; and fasting showed a stronger relation to onset of
subthreshold or threshold PD than compensatory behavior onset. Results suggest that these
forms of eating pathology have similar risk processes. In contrast, perhaps the largest
difference is that most of the examined risk factors predicted future onset of weight and
shape overvaluation and of fear of weight gain, whereas only two of these risk factors
predicted onset of subthreshold or threshold AN. These findings imply that sociocultural
factors and prodromal symptoms play a more potent role in the attitudinal components of
AN versus the low BMI component. These results also suggests that the etiologic processes
that give rise to a low BMI and AN are distinct from those that predict onset of the other
core behavioral and attitudinal symptoms.
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Many of the risk factors that showed significant univariate effects did not account for unique
variance in eating disorder onset in multivariate models, presumably because these factors
are functionally correlated; subscription to the thin ideal theoretically contributes to body
dissatisfaction, which motivates use of unhealthy weight control behaviors, and contributes
to negative affect (Stice, 2001). Body dissatisfaction and dieting showed unique effects for
onset of BN and BED, implying that these are cornerstone risk factors that should be
targeted in prevention programs. Negative affect and thin-ideal internalization also showed
unique predictive effects for onset of BN and BED respectively, implying that the effects of
these factors are somewhat distinct from those of body dissatisfaction and dieting. It was
noteworthy that overeating and functional impairment showed unique effects for onset of
these two eating disorders and that overeating showed a unique effect for onset of PD, as is
the first study to investigate these factors. Findings imply that these variables are tapping
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orthogonal risk processes that deserve greater attention in etiologic theories and prevention
programs.
Diagnostic progression from subthreshold to threshold levels of eating disorders was higher
in this high-risk sample (31%) than in studies of more representative samples (17%).
Diagnostic progression was lower for AN (4%) than for BN, BED, and PD (21–46%),
mirroring the pattern from community samples (AN = 4%, BN = 25%, BED = 21%).
Individuals with full threshold versus subthreshold levels of eating disorders generally had

similar deficits in functional impairment and negative affect, replicating past findings (Stice
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et al., 2009).
It is important to consider study limitations. First, most of the examined risk factors involved
variables implicated in sociocultural etiologic models of eating disorders. Future risk factor
studies should include biological variables. The evidence that a prevention program that
reduces pursuit of the thin ideal decreases fMRI-assessed brain reward region response to
thin models (Stice, Yokum, & Waters, 2015) suggests that this cornerstone sociocultural risk
factor has a biological basis that maps onto reward valuation from the RDoC matrix. There
may be value in examining biological processes that underlie other risk factors examined
herein. Second, the focus on body-dissatisfied women may have obscured detection of other
risk factors orthogonal to body dissatisfaction. However, the means and SDs for the risk
factors were similar to those from a community sample of aged-matched adolescent girls,
implying that this sample is representative and that there was no restriction in range that
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reduced sensitivity. Moreover, the risk factors identified in this high-risk study of adolescent
females were similar to those identified in community studies of adolescent females (Table
1), suggesting that the high-risk design did not bias results. Third, participants in this study
completed eating disorder prevention programs, though the effects of condition were
statistically controlled and the predictive effects of the risk factors were not affected by the
interventions. Fourth, we combined normalized responses to a negative affect measure and
depressive symptom measures, but the two constructs are not isomorphic and combining
them probably introduced error variance, though fortunately this did not prevent us from
detecting predictive effects of this risk factor. Fifth, it is possible that some of the results
could have emerged due to chance. We considered using a lower alpha, but decided against it
for three reasons. First, it is important to balance Type I error risk (false positive findings)
against Type II error risk (false negative findings); given that survival models that predict
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onset of low incident events have low sensitivity, we were more concerned about Type II
errors. Second, the fact that 62% of the tested effects were significant communicates that it
is unlikely that we are interpreting chance findings, which would have been closer to 5% of
the tested effects. Third, the fact that findings from this report converge with those from
prior studies also suggests it is unlikely that the present results are due to chance.
Nonetheless, we report the exact p-values of each of the tests so that readers can focus on the
effects that exceed more stringent alpha levels (e.g., p < .01) if they so desire.
With regard to implications, results suggest that examining high-risk samples is a useful way
to identify risk factors for specific mental disorders within a diagnostic cluster. Second, the
predictive role across eating disorders played by negative affect and functional impairment
suggests that these should be examined as potential risk factors for the onset of other mental
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disorders, as they may represent transdiagnostic risk factors for psychopathology, which if
targeted in prevention programs might reduce a range of mental health problems. Third,
findings suggest a distinct risk profile for AN versus eating disorders in the binge eating/
purging spectrum. Data imply it would be useful to target low BMI middle school students
to advance knowledge of risk factors for AN. Fourth, the overall similarity in risk factors
that predicted onset of threshold versus subthreshold or threshold eating disorders versus the
core symptom dimensions that crosscut eating disorders implies that eating pathology exists
along a continuum. Future research should focus on elucidating how best to model eating

pathology in etiologic studies to maximize sensitivity for detecting risk factors. Fifth, results
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imply that the yield of eating disorder prevention programs, which typically focus on thin-
ideal internalization and body dissatisfaction, might be improved by also targeting negative
affect, overeating, and functional impairment. The evidence that negative affect and
impaired interpersonal functioning predict a range of eating disorders implies that it might
be fruitful to target these high-risk populations with selective prevention programs if the
goal is to prevent the full spectrum of eating disorders. Also, existing prevention
interventions may be more effective in reducing future binge/purge behaviors than the
weight restriction present in AN, which should be investigated. Data suggest that
interventions aimed at preventing AN may need to target qualitatively different high-risk
populations (e.g., low weight middle school girls) and might need to focus on reducing
distinct risk processes for optimal success.
Author Manuscript
Acknowledgments
This research was supported by NIH grants MH/DK061957, MH070699, and MH086582.
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Table 1
Summary of Predictors for Specific Subthreshold/Threshold Eating Disorders from Previous Trials in which Participants were Confirmed to be Disorder-
free at Baseline.
Stice et al.
Potential Risk Factor AN BN BED PD
+ 0 - + 0 - + 0 - + 0 -
Pressure for thinness A CEF F F
Thin-ideal internalization AG EG F G F FG
Thinness expectancies G G G G
Denial of costs of pursuing thin ideal G G G G
Body dissatisfaction AG CFG E G F FG
BMI AG E CDG G G
Weight concerns C
Dieting G A BCDEG F G F FG
Weight control behaviors G G G G
Overeating G G G G
Daily exercise D
Excessive exercise G G G G
Fasting G EG G G
Peer dieting D
Negative affect AG EG F G F G F
Negative affectivity C
Depressive symptoms F F

Social support deficits A E
Early puberty A E
Ineffectiveness C
Alcohol use C
Low interoceptive awareness C
Perfectionism C
Maturity fears C
Interpersonal distrust C
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Potential Risk Factor AN BN BED PD
+ 0 - + 0 - + 0 - + 0 -
Psychiatric problems D
Stice et al.
Mental health care G G G G
Functional impairment G G G
Parental separation D
Note. AN = anorexia nervosa; BN = bulimia nervosa, BED = binge eating disorder; PD = purging disorder. The + column contains studies finding a significant positive relation for the risk factor; the 0
column contains studies finding a non-significant relation; and the – column contains studies finding a significant negative relation for the risk factor. The letters refer to the study that reported each
association: A = Stice & Bohon (2013); B = Patton, Johnson-Sabine, Wood, Mann, & Wakeling (1990); C = Killen et al. (1996); D = Patton, Selzer, Coffey, Carlin, & Wolfe (1999); E = Stice, Davis, Miller,
& Marti (2008a); F = Stice, Marti, & Durant (2011a); G = Present Study.

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Table 2
Diagnostic Criteria for DSM-5 Eating Disorders

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Anorexia nervosa Body mass index (BMI) less than 85% of the median expected for age and gender
Definite fear of weight gain more than 75% of the days for at least 3 months
Weight and shape were 1 of the main aspects of self-evaluation
Bulimia nervosa At least four uncontrollable binge-eating episodes per month for at least 3 months
At least 4 compensatory behavior episodes per month for at least 3 months
Weight and shape were definitely 1 of the main aspects of self-evaluation
Binge eating disorder At least four uncontrollable binge-eating episodes/days per month for at least 3 months
Less than 1 compensatory behavior on average per month during this period
Marked distress about binge eating
Binge eating characterized by 3 or more of the following: rapid eating; eating until uncomfortably full;
eating large amounts when not physically hungry; eating alone because of embarrassment; feeling
disgusted, depressed, or guilty after overeating
Subthreshold anorexia nervosa BMI between 90% and 85% of that expected for age and gender
Definite fear of weight gain more than 25% of the days for at least 3 months
Subthreshold bulimia nervosa At least 2 uncontrollable binge-eating episodes per month for at least 3 months or at least 6 episodes over a
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shorter period
At least 2 compensatory behavior episodes (i.e., self-induced vomiting, laxatives or diuretic use, fasting,
and excessive exercise to compensate for overeating) per month for at least 3 months or at least 6 episodes
over a shorter period
Weight and shape were definitely 1 of the main aspects of self-evaluation
Subthreshold binge eating At least 2 uncontrollable binge-eating episodes/days per month for at least 3 months or at least 6 episodes
disorder over a shorter period
Less than 1 compensatory behavior on average per month during this period
Marked distress about binge eating
Binge eating characterized by 3 or more of the following: rapid eating; eating until uncomfortably full;
eating large amounts when not physically hungry; eating alone because of embarrassment; feeling
disgusted, depressed, or guilty after overeating
Purging disorder At least 4 episodes of self-induced vomiting or diuretic/laxative use for weight control purposes per month
for at least 3 months
Less than 1 uncontrollable binge-eating episode on average per month during this period
Subthreshold purging disorder At least 2 episodes of self-induced vomiting or diuretic/laxative use for weight control purposes per month
for at least 3 months or at least 6 episodes over a shorter period
Less than 1 uncontrollable binge-eating episode on average per month during this period
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Note. Anorexia nervosa took diagnostic precedence over bulimia nervosa and binge eating disorder.
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Table 3
Demographic Data from a Representative Sample of Age-Matched Community-Recruited Young Women and
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the Present High-Risk Sample.
Community Sample High Risk Sample

Demographic Characteristics
Age [Mean, (SD)] 18.5 (1.4) 18.5 (4.2)
Race and Ethnicity [n, %]
American Indian or Alaskan Native 4 0.8 28 2.2
Asian 8 1.6 130 10.3
Black or African American 36 7.3 58 4.6
Native Hawaiian or other Pacific Islander 0 0.0 9 0.7
Hispanic 90 18.3 141 11.2
Caucasian 336 68.2 848 67.3

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Other or mixed heritage 19 3.9 46 3.7
Parental education [n, %]
High school graduate or less 67 14.1 137 11.0
Some college 71 15.0 223 17.8
College graduate 212 44.8 465 37.2
Advanced degree 123 26.0 425 34.0
Baseline Risk Factors [Mean, (SD)]

Thin ideal internalization 3.30 (0.71) 3.69 (0.53)
Thinness expectancy 2.64 (0.99) 3.23 (0.78)
Denial of thin-ideal costs NA NA 2.26 (0.70)
Body dissatisfaction 2.79 (0.96) 3.40 (0.79)

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Weight control behaviors NA NA 2.89 (0.70)
Dieting 2.07 (0.88) 2.66 (0.90)
Overeating 0.14 (0.74) 1.01 (2.00)
Fasting 0.62 (4.41) 1.08 (3.66)

Excessive exercise 0.70 (3.22) 1.11 (3.35)
Functional impairment 2.46 0.54 2.34 (0.53)
Mental health care NA NA 0.23 (0.42)
Body Mass Index 22.10 (4.58) 24.1 (5.11)
NA = not available.
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Table 4
Rates of DSM-5 Eating Disorders and Symptoms

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Cumulative 3-year
Study Prevalence Incidence
n % n %
Full-syndrome disorders
Anorexia nervosa 9 0.7 7 0.6
Bulimia nervosa 77 6.0 47 3.8
Binge eating disorder 69 5.5 51 4.1
Purging disorder 53 4.2 41 3.3
Subthreshold eating disorders
Anorexia nervosa 25 2.0 21 1.7
Bulimia nervosa 115 9.1 87 7.0
Binge eating 71 5.6 60 4.8
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Purging disorder 115 9.1 65 5.2

Eating disorder symptoms
Recurrent binge eating 367 29.0 177 16.5
Recurrent compensatory behaviors 722 32.9 266 32.9
Low body weight 65 5.1 33 2.7
Overvaluation of weight/shape 888 70.2 305 44.7
Fear of gaining weight 381 30.1 165 15.7
Note. Eating disorder classifications are not mutually exclusive across disorders. Study prevalence reflects the number of participants who met
criteria at baseline and those who showed onset during the follow-up period. Cumulative incidence reflects participants who showed onset during
the follow-up period, excluding those who met criteria at baseline.
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Table 5
Pearson Correlations for Baseline Risk Factors
1 2 3 4 5 6 7 8 9 10 11 12 13
Stice et al.
1. Thin ideal internalization 1.00

2. Thinness expectancy 0.31 1.00
3. Denial of thin-ideal costs 0.14 0.41 1.00
4. Body dissatisfaction 0.27 0.48 0.23 1.00
5. Weight control behaviors 0.10 0.13 0.08 0.10 1.00
6. Dieting 0.31 0.36 0.29 0.37 0.47 1.00
7. Negative affect 0.24 0.33 0.24 0.42 0.06 0.30 1.00
8. Overeating 0.14 0.31 0.15 0.27 0.06 0.21 0.35 1.00
9. Fasting 0.15 0.22 0.33 0.23 0.17 0.43 0.25 0.10 1.00
10. Excessive exercise 0.08 0.14 0.20 0.14 0.21 0.37 0.15 0.08 0.50 1.00
11. Functional impairment 0.07 0.22 0.14 0.29 -0.01 0.15 0.54 0.23 0.18 0.12 1.00
12. Mental health care 0.03 0.13 0.08 0.16 0.07 0.10 0.26 0.13 0.15 0.07 0.18 1.00
13. Body Mass Index -0.04 0.19 0.03 0.34 0.08 0.10 0.07 0.07 0.05 0.01 0.01 0.04 1.00

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Table 6
Results from Univariate Cox Regression Models Predicting Future Onset of Subthreshold/Threshold Eating Disorders.
Anorexia Nervosa Bulimia Nervosa

Stice et al.
95% CI 95% CI
HR LB UB p-value HR LB UB p-value
Thin ideal internalization 1.38 0.91 2.09 .1270 1.69 1.30 2.18 <.0001
Thinness expectancy 1.04 0.69 1.58 .8434 1.73 1.30 2.31 .0002
Denial costs 1.09 0.72 1.65 .6807 1.40 1.10 1.78 .0067
Body dissatisfaction 1.11 0.75 1.65 .5928 1.94 1.51 2.51 <.0001
Weight control behaviors 1.15 0.73 1.82 .5546 1.29 0.96 1.73 .0919
Dieting 1.15 0.78 1.69 .4776 1.89 1.49 2.39 <.0001
Negative affect 1.27 0.89 1.80 .5337 1.79 1.48 2.15 <.0001
Overeating 1.12 0.79 1.58 .6537 2.08 1.74 2.48 <.0001
Fasting 0.90 0.57 1.42 .2837 1.23 1.06 1.43 .0074
Excessive exercise 1.15 0.89 1.49 .2835 1.13 0.95 1.35 .1749
Functional impairment 1.71 1.18 2.49 .0047 1.42 1.12 1.80 .0034
Mental health care 0.84 0.54 1.31 .4448 1.49 1.22 1.82 <.0001
Body Mass Index 0.05 0.02 0.13 <.0001 1.08 0.86 1.34 .5157
Binge Eating Disorder Purging Disorder
Thinness expectancy 1.36 1.03 1.78 .0280 2.01 1.45 2.77 <.0001
Denial costs 1.20 0.94 1.54 .1432 1.66 1.28 2.17 .0002
Body dissatisfaction 2.02 1.57 2.60 <.0001 2.29 1.73 3.02 <.0001

Dieting 1.58 1.25 1.99 .0001 2.74 2.08 3.61 <.0001
Negative affect 1.65 1.37 1.99 <.0001 1.70 1.40 2.07 <.0001
Overeating 2.84 2.08 3.88 <.0001 1.64 1.36 1.98 <.0001
Fasting 1.08 0.90 1.30 .4008 1.28 1.11 1.47 .0006
Functional impairment 1.56 1.26 1.94 <.0001 1.52 1.20 1.93 .0006
Mental health care 1.37 1.12 1.68 .0018 1.31 1.05 1.62 .0153
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95% CI 95% CI
Stice et al.
Body Mass Index 1.12 0.91 1.39 .2830 1.09 0.86 1.37 .4710
Notes. Bolded entries significant at p<.05. CI = confidence interval, HR = hazard ratio, LB = lower bound, UB = upper bound.

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Table 7
Results from Univariate Cox Regression Models Predicting Future Onset of Threshold Eating Disorder.

Stice et al.
95% CI 95% CI
Thin ideal internalization 1.47 0.66 3.28 .3512 1.81 1.31 2.51 .0003
Denial of thin-ideal costs 1.31 0.60 2.86 .5011 1.60 1.20 2.14 .0016
Body dissatisfaction 1.57 0.70 3.50 .2716 2.10 1.53 2.88 <.0001
Dieting 2.14 0.98 4.68 .0560 1.66 1.24 2.23 .0006
Negative affect 2.06 1.15 3.68 .0144 1.85 1.47 2.32 <.0001
Overeating 1.50 0.83 2.69 .1765 2.34 1.88 2.93 <.0001
Fasting 0.92 0.40 2.13 .8512 1.35 1.17 1.57 <.0001
Body Mass Index 0.16 0.03 0.75 .0201 0.96 0.71 1.29 .7651
Binge Eating Disorder Purging Disorder
Thin ideal internalization 1.52 1.13 2.06 .0062 1.92 1.36 2.71 .0002
Denial of thin-ideal costs 1.47 1.11 1.94 .0068 1.66 1.18 2.34 .0038

Dieting 1.51 1.14 2.00 .0038 2.35 1.68 3.29 <.0001
Negative affect 1.80 1.44 2.25 <.0001 1.72 1.34 2.21 <.0001
Overeating 3.38 2.25 5.10 <.0001 1.54 1.21 1.96 .0004
Fasting 1.16 0.95 1.41 .1390 1.20 0.98 1.46 .0788
Functional impairment 1.92 1.48 2.47 <.0001 1.45 1.08 1.95 .0140
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95% CI 95% CI
Stice et al.
Body Mass Index 1.17 0.92 1.50 .1937 1.10 0.83 1.46 .5163

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Table 8
Results from Univariate Cox Regression Models Predicting Onset of Core Eating Disorder Symptoms that Crosscut Eating Disorder Diagnoses.
Recurrent Compensatory
Stice et al.
Recurrent Binge Eating Behaviors
95% CI 95% CI
Denial costs 1.19 1.01 1.41 .0410 1.24 1.00 1.54 .0514
Body dissatisfaction 1.39 1.19 1.62 <.0001 1.39 1.14 1.70 .0010
Dieting 1.49 1.28 1.72 <.0001 2.08 1.71 2.54 <.0001
Negative affect 1.50 1.32 1.71 <.0001 1.41 1.25 1.58 <.0001
Overeating 1.70 1.47 1.98 <.0001 1.65 1.39 1.97 <.0001
Fasting 1.12 1.00 1.27 .0548 10.2 0.16 674.7 .2769
Body Mass Index 0.99 0.85 1.15 .8742 1.02 0.91 1.15 .7068
Overvaluation of
Weight/Shape Fear of Gaining Weight
Thinness expectancy 1.22 1.06 1.40 .0067 1.58 1.31 1.92 <.0001
Denial costs 1.25 0.99 1.59 .0649 1.43 1.17 1.74 .0005

Dieting 1.26 1.11 1.44 .0003 2.03 1.72 2.39 <.0001
Negative affect 1.31 1.15 1.48 <.0001 1.82 1.60 2.08 <.0001
Overeating 1.56 1.28 1.92 <.0001 1.64 1.45 1.87 <.0001
Fasting 1.26 1.11 1.42 .0003 1.41 1.28 1.56 <.0001
Excessive exercise 1.38 1.24 1.53 <.0001 1.25 1.11 1.40 .0002
Functional impairment 1.26 1.12 1.43 .0002 1.72 1.48 2.00 <.0001
Page 29
Recurrent Compensatory
Recurrent Binge Eating Behaviors
95% CI 95% CI
Stice et al.
Mental health care 1.12 0.99 1.26 .0717 1.34 1.16 1.54 <.0001
Body Mass Index 1.03 0.92 1.15 .5737 1.06 0.92 1.23 .4030

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Risk Factors that Predict Future Onset of Each DSM-5 Eating

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

We estimated models that predicted onset of subthrehold or threshold eating disorders, as

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

low body weight.

Design of Randomized Prevention Trials

Eating pathology—The semi-structured Eating Disorder Diagnostic Interview (EDDI;

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

sensitivity to intervention effects, and participants with versus without EDDI-diagnosed

Thin ideal internalization—The Ideal-Body Stereotype Scale–Revised assessed thin-

Positive thinness expectancies—The Thinness Expectancy scale (Hohlstein et al.,

Body dissatisfaction—The Body Dissatisfaction Scale (Stice et al., 2001) assessed

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

Functional impairment—Impairment in the family, peer group, romantic, and school

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

Rates of diagnostic progression, which is defined as a subthreshold level disorder that

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

Univariate Predictors of Specific Eating Disorders

care predicted future onset of sBED/BED. Greater thin-ideal internalization, thinness

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

Multivariate Predictors of Specific Eating Disorders

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

these eating disorders classes.

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

prevention programs to focus on individuals with prodromal eating disorder symptoms.

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

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Potential Risk Factor AN BN BED PD

Denial of costs of pursuing thin ideal G G G G

Body dissatisfaction AG CFG E G F FG

Weight control behaviors G G G G

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

Low interoceptive awareness C

Potential Risk Factor AN BN BED PD

Mental health care G G G G

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

Diagnostic Criteria for DSM-5 Eating Disorders

Weight and shape were 1 of the main aspects of self-evaluation

J Abnorm Psychol. Author manuscript; available in PMC 2018 January 01.

the Present High-Risk Sample.

Community Sample High Risk Sample

Race and Ethnicity [n, %]