Scand J Med Sci Sports 2008: 18: 108–118
Printed in Singapore . All rights reserved
DOI: 10.1111/j.1600-0838.2007.00657.x
Prevalence of eating disorders and the predictive power of risk
models in female elite athletes: a controlled study
M. K. Torstveit1, J. H. Rosenvinge2, J. Sundgot-Borgen1,3
1
The Sports Medicine Department, The Norwegian School of Sport Sciences, Oslo, Norway, 2Department of Psychology, University
of Tromso, Tromso, Norway, 3The Norwegian Olympic Training Centre, Oslo, Norway
Corresponding author: Monica Klungland Torstveit, The Norwegian School of Sport Sciences, PO Box 4014, Ullevaal stadion,
0806 Oslo, Norway. Tel: 1Int 47 23 26 23 56, Fax: 1Int 47 22 23 42 20, E-mail: monica.torstveit@nih.no
Accepted for publication 14 February 2007
The purposes of this study were to examine the percentage
of female elite athletes and controls with disordered eating
(DE) behavior and clinical eating disorders (EDs), to
investigate what characterize the athletes with EDs, and
to evaluate whether a proposed method of screening for EDs
in elite athletes does not falsely classify sport-specific
behaviors as indicators of EDs. All athletes representing
the national teams at the junior or senior level, aged 13–39
years (n 5 938), and age-group matched, randomly selected
population-based controls (n 5 900) were invited to partici-
pate. From the screening data, a random sample of athletes
Disordered eating (DE) refers to a spectrum of
attitudes and behaviors like a preoccupation with
body weight and shape, food restriction, and dieting
as well as bingeing, vomiting, and the abuse of
diuretics, laxatives and diet pills. The purpose of
DE is to accomplish a lean body weight to compen-
sate for pervasive body dissatisfaction. In many
cases, people with DE also have a body image
problem, i.e. an inability to acknowledge their
change in body weight (American Psychiatric Asso-
ciation, 1994). They often continuously feel ‘‘fat’’
and the DE behaviors may become more intensified
to a degree that the individual eventually satisfy us
the criteria of a clinically significant eating disorder
(ED) (Sundgot-Borgen, 1994). This may amount to
either anorexia nervosa (AN) or bulimia nervosa
(BN) or an Eating Disorder Not Otherwise Specified
(EDNOS) (Sundgot-Borgen, 1993; Johnson, 1994;
Shisslak et al., 1995). Conventionally, EDNOS is
considered to be present when one or more criteria
for AN or BN are not present or lack the required
duration or frequency (American Psychiatric Asso-
ciation, 1994).
Conceptually and clinically, EDs may be described
as a continuum ranging from milder forms (i.e. DE)
to subclinical EDs and finally serious AN or BN
(Johnson, 1994; Shisslak et al., 1995). Given such a
108
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Journal compilation & 2007 Blackwell Munksgaard
(n 5 186) and controls (n 5 145) were subjects for a clinical
interview. More athletes in leanness sports (46.7%) had
clinical EDs than athletes in non-leanness sports (19.8%)
and controls (21.4%) (Po0.001). Variables predicting
clinical EDs, and thus candidates for valid screening proce-
dures, were menstrual dysfunction in leanness athletes, self-
reported EDs in non-leanness athletes, and self-reported
use of pathogenic weight control methods in controls.
Hence, statistically based risk factors are not universally
valid, but specifically related to athletes and non-athletes,
respectively.
spectrum as a clinical and conceptual understanding,
DE features may represent obvious and parsimonious
candidates in the search for risk factors predicting
EDs. Indeed, a recent controlled study (Fairburn et
al., 2005) identified a range of DE behaviors that
predicted future EDs, like eating in secret, laxative
abuse and a fear of losing control over eating.
At least with respect to elite athletes, the preva-
lence of subclinical DE, EDNOS and clinical EDs
has been poorly established. Another area that needs
more knowledge is the testing of the risk status of DE
relative to EDNOS, AN and BN among athletes.
Obviously, determining the prevalence of EDs is
important to estimate the magnitude of the problem
in general as well as specialized populations. A meta-
analysis (Smolak et al., 2000) did not find clear
evidence for an increased risk of EDs among athletes.
On the other hand, sample size and heterogeneity, as
well as other major methodological flaws, limit this
conclusion, and the conclusion has been refuted in
single studies with better methodology (e.g. Sundgot-
Borgen, 1993; Byrne & McLean, 2001; Byrne &
McLean, 2002; Sundgot-Borgen & Torstveit, 2004).
Nevertheless, there is a need for further empirical
testing with improved designs that may also address
sport-specific classification problems. Indeed, many
sports, and leanness sports in particular, may have

‘‘unwritten’’ demands for sport performance (such as
if you are a long-distance runner you should look like
an anorectic) that somewhat trigger DE behaviors
(Sundgot-Borgen, 1993). Moreover, features that
may well be interpreted as indicators of DE in the
general population may appear as ‘‘normal,’’ appro-
priate or functional behaviors among elite athletes
who want to excel in their sports. This may increase
the risk of false-positive prevalence figures. On the
other hand, these athletes may avoid reporting DE,
assuming that if they do, this will lead to problems
qualifying for the team, or that they will be left out
from the team. In such cases, an increased risk for
false-negative subjects may be the result (Sundgot-
Borgen, 1993, 1994). Also, an empirical test of risk
factor models may be more convenient using athlete
samples where the prevalence of EDs may be higher
than in a general adolescent population.
Screening for female elite athletes at risk for EDs is
important for early detection and treatment efficacy.
However, the screening tool should have adequate
positive predictive power, and relate to diagnostic
criteria for EDs in a valid and explicit manner. Very
few studies have examined the percentage of female
elite athletes and controls at risk for EDs, and then
evaluated how many of these actually met the criteria
for clinical EDs (Sundgot-Borgen, 1993; Byrne &
McLean, 2002; Black et al., 2003; Sundgot-Borgen &
Torstveit, 2004). Moreover, to our knowledge, no
study has compared the validity of various risk
models in both athletes and controls. Although
several screening tools are available (e.g. Garner
et al., 1984; Beglin & Fairburn, 1992; Rosenvinge
et al., 2001; Bauer et al., 2005; Siervo et al., 2005)
they are not particularly address athletes. Hence, one
may stand the risk of falsely classifying sport-specific
adaptive or functional behaviors as indicators or risk
factors of DE or EDs, i.e. athletes are often extre-
mely motivated to reduce weight or body fat and
some may be abusing unhealthy weight loss methods
to make required weight demands. These athletes
could get a high DT score and report the use of these
methods without thinking about this behavior as an
accepted method for enhancing performance (Sund-
got-Borgen, 1994). This could delay the identification
of the DE behaviors and the treatment process for
these athletes.
The same sensitivity–specificity problem may exist
with respect to risk factors. In the literature, several
risk factors have been identified in case–control
studies (Fairburn et al., 1997, 1998, 1999) and pro-
spective (Fairburn et al., 2005) studies, but these risk
factors may not be relevant for athletes as athletes
have not been included in such studies. However, the
concept of ‘‘the female athlete triad’’ (the triad)
(Yeager et al., 1993) offers a framework for a
potential sport-specific risk factor model. Here, it is
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Eating disorders in athletes and controls
suggested that in physically active females an inter-
related pathogenesis exists between (1) DE/EDs, (2)
menstrual dysfunction, and (3) osteoporosis/low
bone mineral density. Moreover, it has been sug-
gested that females who present with one of the
components of the female athlete triad should be
screened for the other components (Otis et al., 1997;
IOC, 2005). No studies have, however, tested the
predictive validity of these female athlete triad com-
ponents related to EDs, or compared a triad-based
risk model with the validity of models including only
risk criteria for EDs. Moreover, no data exist on
possible differences between athletes competing in
leanness sports vs non-leanness sports with respect to
the predictive validity of the triad components. In
addition, controlled studies aiming to investigate the
percentage of elite athletes and non-athletes defined
in the different categories of the DE spectrum are
lacking. Finally, if a triad-based risk model may be
empirically established for elite athletes, it is not
known whether this also applies to non-athletes.
A validation of different sets of risk criteria in female
elite athletes and controls is therefore highly needed.
Thus, the aims of the present study were (1) to
investigate the point prevalence of DE behavior and
the clinical EDs (i.e. EDNOS, AN, and BN) in female
elite athletes and controls from the general popula-
tion, (2) to investigate what characterizes female elite
athletes with clinical EDs and (3) to test the predictive
validity of the triad components relative to EDs
among female elite athletes and controls.
Materials and methods
Recruitment
The total population of female elite athletes in Norway, aged
13–39 years (n 5 938), and non-athletic subjects in the same age-
group (n 5 900) were invited to participate. Permission to
conduct the study was provided by the Norwegian Olympic
Committee and the Norwegian Confederation of Sports, the
Data Inspectorate and the Regional Committee for Medical
Research Ethics. The secretary general of each sport federation,
and the head of the healthcare team for each of the national
teams received detailed written information about the aims and
procedures of the study. In addition, all secretary generals were
asked to return a list containing names, ages and addresses of all
eligible athletes in their federation competing for national teams.
All participants received an information letter and had to
complete a written consent form in order to participate. Parents
of responders younger than 18 years of age had the opportunity
to refuse participation on behalf of their child, while written
parental consent was required for responders younger than 16.
Participants
A total of 669 elite athletes participated in part I of the study.
An elite athlete was defined as one who qualified for the
national team at the junior or senior level, or who was a
member of a recruiting squad for that team. The athletes
competed in 66 different sports/events representing technical,
endurance, esthetic, weight class, ball game, power and anti-
109
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Torstveit et al.

SELECTION FOR PART I

ATHLETES CONTROLS
(n=938) (n=900)

Non-receivers Non-receivers
(N=31)* (N=23)**

Excluded Excluded
(n=149)† (n=12)††

Fig. 1. Flow chart showing selec-

Available for Available for
tion of athletes and controls sam-
participation participation
ples based on (part I)
(n=758) (n=865)
questionnaire mailing, exclusion
process and questionnaire re-
Non- Non- sponse, and selection for part II.
responders responders *Owing to the fact that they were
(n=89) (n=258) representing teams in other coun-
tries or were travelling. **Owing
Responders Responders to problems finding their ad-
(n=669) (n=607) dresses. wSeventy-six athletes had
88.3% 70.2% ended their career, 35 did not
compete at the national level, 15
were injured, eight were pregnant
SELECTION FOR PART II and did not plan to continue their
athletic career after the delivery,
five were older than 39 years of
age, nine did not complete the
questionnaire satisfactorily and
Random selection of Random selection of
athletes‡ controls‡
one athlete competed in two dif-
(n=300) (n=300) ferent sport groups. wwNine did not
understand the Norwegian lan-
guage and three were severely ill
and were unable to fill in the
Participants Participants
questionnaire. zStratified by age-
(n=186) (n=145)
62.0% 48.3%
group and the ‘‘risk-profile’’ for
the female athlete triad.

gravitation sports. An overview of these sports has been
published elsewhere (Torstveit & Sundgot-Borgen, 2005).
The athletes had to be 13–39 years old. Exclusion criteria in
part I of the study are given in Fig. 1.
A bureau of statistics composed a comparison group
consisting of a randomly selected sample of females
(n 5 900) from the total population of citizens in Norway
aged 13–39 years representative of the total population in
terms of age and geographical distribution. 607 controls
participated in part I of the study. Exclusion criteria are given
in Fig. 1. Amount of physical activity among the controls was
defined as the total hours of physical activity per week
including physical education lessons, recreational sports and
active daily living like walking. None of the females competed
in sports for a national team.
Methods and assessment procedures
Part I: screening
Questions regarding menstrual, body weight, training, injury,
and dietary history, oral contraceptive use and pregnancy,
physical activity patterns, nutritional habits, use of pathogenic
weight control methods (PWCM), and self-reported EDs were
composed in this study. In addition, the Body Dissatisfaction
(BD) and Drive for Thinness (DT) subscales from the EDI
(Garner et al., 1984) were used. Questions and subscales were
sent to each of the 938 eligible athletes and 900 eligible
controls. The response rate of the athletes and controls was
88.3% and 70.2%, respectively (Fig. 1).
Selection for part II
Based on data from part I, a random selection of athletes
(n 5 300) and controls (n 5 300) were invited to participate in a
clinical interview (part II of the study). This sample was
stratified based on age group (13–19, 20–29 and 30–39 years)
and the ‘‘risk-profile’’ for the female athlete triad. The risk
criteria used in this selection process were a BMI o18.5 kg/m2,
use of PWCM EDI-DT
15, EDI-BD
14, self-reported
ED, self-reported menstrual dysfunction, or self-reported
stress fracture (Torstveit & Sundgot-Borgen, 2005). Alto-
gether, 186 athletes (62%) and 145 controls (48%) partici-
pated (Fig. 1).
Part II: Clinical interview and body composition measurements
A PhD especially trained in EDs conducted all the interviews,
and each interview lasted from 45 to 60 min. The same person

110

conducted all the interviews, but a random selection of
subjects (n 5 15) was also interviewed by another expert
(psychiatrist). In the latter subgroup, all the diagnoses based
on the primary expert were confirmed by the secondary expert.
The Eating Disorder Examination (EDE) (Cooper et al., 1989)
was used as an interview guide to determine the presence of
AN BN or EDNOS according to the DSM-IV criteria (Amer-
ican Psychiatric Association, 1994). For statistical purposes
due to small size diagnostic groups, subjects with EDNOS,
AN, or BN, were pooled and categorized as having ‘‘clinical
EDs.’’
Body composition including percentage body fat and fat-
free mass was measured with dual-energy X-ray absorptiome-
try (DXA) (Prodigy, Lunar, software version 5.6). All scan-
ning and analyses were conducted by the same operator and
all measurement results were double checked for possible
mistakes in the analysis. During the study period, no machine
drift was observed. A quality assurance test by using a
calibration block was conducted each morning. Additionally,
a weekly quality assurance test measuring the aluminum spine
phantom to monitor the stability of the scanner over time was
performed. The CV for body composition measurements was
1.0% for fat percentage, 0.4% for fat-free mass, and 0.3% for
total body mass.
Indicators of DE
Indicators of DE behaviors were (a) ‘‘self-reported EDs’’ i.e. a
subjective experience of past or current EDs, (b) underweight
BMI o18.5 kg/m2 (World Health Organization, 2000), (c)
high scores on two subscales from the EDI i.e. EDI-DT
(
15), and EDI-BD (
14) and (d) the use of PWCM (diet
pills, hunger-repressive pills, laxatives, diuretics, or vomiting).
The EDI has been found to be suitable for use as a screening
instrument for EDs in a non-clinical setting (Garner et al.,
1984), and the two subscales EDI-DT and EDI-BD have been
shown to be the only measures that predicted the development
of EDs (Garner et al., 1987). Furthermore, high EDI-DT and
EDI-BD scores have also been used as selection criteria when
investigating the prevalence of EDs in elite athletes (Sundgot-
Borgen, 1993). Therefore, participants in this study were
classified as at risk for developing EDs, and thus the triad, if
their scores on the EDI-DT or EDI-BD subscales were at or
above the mean score for known anorectics (Garner et al.,
1984). Low energy availability was not included as this would
be difficult for the responders to report. Also, clinical experi-
ence implies that a majority of athletes with low energy
availability are not aware of the situation.
Definitions of risk models
The simplest model included only the variable ‘‘self-reported
EDs’’ (model 1). Model 2 included all the four indicators of
DE behaviors (a–d). Model 3 included all the variables in
model 2 plus menstrual dysfunction and the reporting of stress
fractures. Menstrual dysfunction was considered to be present
if any of the following symptoms were reported on the
questionnaire: lifetime or current primary or secondary ame-
norrhea, or current oligomenorrhea or a menstrual cycle less
than 22 days, which may reflect a short luteal phase and luteal
inadequacy that may be the first stage in the development of
amenorrhea (DeSouza et al., 1998). In this study, primary
amenorrhea was defined as the absence of menarche by the age
of 16 and secondary amenorrhea was defined as the absence of
three or more consecutive menstrual cycles after menarche and
outside pregnancy. Furthermore, oligomenorrhea was defined
as menstrual cycles of 35 days or more. Subjects younger than
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Eating disorders in athletes and controls
16 years of age were excluded from the analyses related to
menstrual dysfunction.
Statistical analysis
All analyses were performed using SPSS software, version 11.0
(SPSS, Evanstron, illinois, USA). Results are expressed as
mean value and standard deviation (SD) or 95% confidence
intervals (CI). For parts of the analysis, the athletes were
divided into those who competed in leanness and non-leanness
sports, respectively. Leanness sports were defined as sports in
which leanness and/or a specific body weight were considered
important for performance (e.g. endurance, esthetic, weight-
class, and anti-gravitation sports). Non-leanness sports com-
prised sports where leanness was considered less important for
performance (e.g. technical, ball game and power sports). All
group comparisons were carried out using two-sample Stu-
dent’s t-tests for continuous data and chi-square tests for
categorical data. Differences were considered to be statistically
significant for P-values o5%. Binary logistic regression
analysis was used to adjust for differences in age and BMI
between groups, and to test the predictive power [i.e. odds
ratio, (OR)] of DE variables arranged as three risk models for
a clinical diagnosis of EDs.
The EDI subscales were tested for reliability using Cron-
bach’s a values, being 0.90 and 0.89 for EDI-DT for athletes
and controls, respectively, and 0.90 for EDI-BD for both
athletes and controls.
Results
Subject characteristics
The athletes participating in the clinical part were
younger, and had lower age-adjusted BMI values
and percent body fat compared with the controls
(Po0.001). Furthermore, athletes competing in lean-
ness sports were younger, and had lower age-ad-
justed BMI values and percent body fat compared
with athletes competing in non-leanness sports
(Po0.001) (Table 1). The athletes trained on average
13.9 (SD 5.6) hours per week. The comparison group
reported to be physically active 5.3 (SD 5.3) hours
per week.
Prevalence of DE, EDNOS, AN and BN
Adjusting for age, no differences were found between
athletes and controls with respect to any of the
criteria for DE or clinical EDs (Table 2). Fewer
athletes competing in leanness sports than athletes
competing in non-leanness sports and controls had a
high score on the EDI-BD subscale (Po0.05), but
more were diagnosed with clinical EDs, also after
adjusting for age and BMI (Po0.001) (Table 2). A
total of 46.2% of the athletes and 51.7% of the
controls reported one or more of the five indicators
of DE. The same was seen for 48.9% of the leanness
athletes and 43.8% of the non-leanness athletes.
A total of 23.7% and 18.6% of the athletes and
controls, respectively, reported DE behaviors, and
were also diagnosed with clinical EDs (true posi-
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Torstveit et al.
Table 1. Anthropometric data from part II of the study for athletes competing in leanness sports (n 5 90), non-leanness sports (n 5 96), athletes total
(n 5 186), and for the comparison group (n 5 145)

M (SD)

Leanness Non-leanness Athletes total Controls

(n 5 90) (n 5 96) (n 5 186) (n 5 145)

Age (years) 20.8 (6.3)a,b 23.5 (5.0)c 22.2 (5.8)b 29.6 (7.9)
Weight (kg) 57.3 (7.4)a,b 65.6 (7.8) 61.5 (8.7)b 66.4 (12.3)
Height (cm) 166.2 (6.5)a 170.0 (6.7)c 168.1 (6.9)d 166.2 (6.3)
BMI (kg/m2) 20.7 (2.1)a,b 22.7 (2.2)d 21.7 (2.4)b 24.0 (4.2)
Body fat (%)* 21.0 (6.7)a,b 27.3 (6.3) 24.2 (7.2)b 35.5 (7.1)

*Body fat was measured with dual energy x-ray absorptiometry (DXA).
a
Po0.001 compared with non-leanness.
b
Po0.001 compared with controls.
c
Po0.05 compared with controls.
d
Po0.01 compared with controls.
BMI, body mass index.

Table 2. Prevalence of indicators of disordered eating (low body mass index (BMI), high EDI-DT and EDI-BD score, use of pathogenic weight control
methods (PWCM), and self-reported eating disorders) as well as clinical eating disorders (EDs) in athletes (n 5 186) and controls (n 5 145), and in
athletes representing leanness (n 5 90) and non-leanness sports (n 5 96) adjusted for age differences between the groups. These data are from part II of
the study.

BMIo 18.5 EDI-DT
15 EDI-BD
14 PWCM Self-reported EDs EDNOS AN BN Total clinical EDs*

Athletes 9.7% 8.5% 17.0% 27.7% 27.3% 19.9% 4.8% 8.1% 32.8%
Controls 2.8% 6.6% 23.0% 34.5% 21.4% 17.2% – 4.2% 21.4%
P-value NSa NS NS NS NS NS NSa NS NSb
LS 15.6%e 11.0% 11.0%c 23.8% 30.1% 26.7% 8.9% 11.1% 46.7%d
NLS 4.2% 6.3% 22.1% 31.5% 24.7% 13.5% 1.1% 5.2% 19.8%
P-value NSa NS Po0.05 NS NS Po0.05 Po0.05 NS Po0.001

*Clinical EDs is the total point prevalence of EDNOS, AN, and BN.
a
Significant at Po0.01 if not adjusted for age.
b
Significant at Po0.05 if not adjusted for age.
c
Po0.05 compared with controls.
d
Po0.001 compared with controls.
e
Po0.001 compared with controls, but non-significant when adjusted for age.
LS, leanness sports; NLS, non-leanness sports; EDNOS, eating disorder not otherwise specified; AN, anorexia nervosa; BN, bulimia nervosa; BMI, body
mass index; BD, body dissatisfaction; DT, drive for thinness.

tives), while 9.1% and 2.8% of the athletes and
controls, respectively, were diagnosed with an ED
without having reported DE behavior (false nega-
tives) (Po0.05). Twenty-two percent of the athletes
and 33.1% of the controls reported DE behaviors,
but were not diagnosed with an ED (false positives)
(Po0.05). More athletes competing in leanness
sports were classified as true positives (32.2%) and
false negatives (14.4%) compared with athletes com-
peting in non-leanness sports (15.6% and 4.2%,
respectively) (Po0.05). No differences between lean-
ness and non-leanness athletes were found in the
percentage of false positives (16.7% vs 27.1%, re-
spectively).
As part of the analysis, the prevalence of clinical
EDs found among those participating in the clinical
part of the study was standardized according to the
distribution of risk and not at-risk subjects for the
triad included in part I of the study [the total
population of elite athletes (n 5 669) and controls
(n 5 607)]. By doing this, it was estimated that 28.1%
and 20.8% of the total population of athletes and
controls, respectively, had clinical EDs.
Eight of the nine athletes diagnosed with AN, 10 of
the 15 athletes diagnosed with BN and 24 of the 37
athletes diagnosed with EDNOS competed in lean-
ness sports. Further characteristics of the athletes
with EDs are given in Table 3.
Predictive power of risk models and risk variables for
clinical EDs
Model 1 (self-reported EDs) raised the probability of
a clinical ED diagnosis among the athletes (Table 4),

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Eating disorders in athletes and controls
Table 3. Characteristics (M1SD) of female elite athletes diagnosed with clinical eating disorders (EDs). These data are from part II of the study.

Age Age at sport Age at Age at first Training DT BD BMI Body

(years) specialization menarche diet attempt volume (kg/m2) fat
(years)* (years) (years)w (h/week) (%)z

AN (n 5 9) 21.9 (8.9) 13.9 (4.4) 13.4 (1.1) 16.3 (3.4) 13.3 (4.2) 8.3 (7.3)b 8.1 (6.9) 18.9 (1.5)a,d,e 12.8 (4.0)a,c,e
BN(n 5 15) 19.7 (3.9) 12.0 (4.2) 14.1 (1.2) 17.5 (4.2) 14.7 (4.6) 11.1 (8.5)f,g 12.0 (10.4)b 21.7 (2.5) 25.6 (6.8)
EDNOS(n 5 37) 21.3 (5.7) 13.1 (5.8) 13.3 (1.3) 16.1 (2.3) 14.4 (6.2) 5.2 (6.3)g 8.2 (7.3) 21.7 (2.3) 24.4 (7.3)
Healthy (n 5 125) 22.7 (5.7) 14.0 (4.8) 13.5 (1.4) 16.3 (3.5) 13.7 (5.7) 2.1 (3.7) 5.1 (5.9)f 21.9 (2.4) 24.9 (6.7)

*When the athletes started to specialize the training in their specific competitive sport.
w
Only for those who reported that they had tried to diet.
z
Measured with dual energy x-ray absorptiometry (DXA).
a
Po0.001 compared with healthy.
b
Po0.05 compared with healthy.
c
Po0.001 compared with BN.
d
Po0.05 compared with BN.
e
Po0.001 compared with EDNOS.
f
Po0.05 compared with EDNOS.
g
Po0.01 compared with healthy.
AN, anorexia nervosa; BN, bulimia nervosa; EDNOS, eating disorders not otherwise specified; DT, Drive for Thinness; BD, Body Dissatisfaction; BMI, body
mass index.

Table 4. Probability [odds ratio (OR) and 95% confidence intervals (CI)] for a clinical ED diagnose according to three predefined risk models. These data
are from part II of the study.

OR (CI) Cox and Snell R2

Model 1* Model 2w Model 3z

All subjects (n 5 331) 3.24 (1.66–6.30)a – 13.00 (2.88–58.64)a 0.194

Athletes (n 5 186) 3.71 (1.44–9.55)b – 8.62 (1.82-40.91)b 0.191
Controls (n 5 145) – – –
Leanness athletes (n 5 90) – – 8.00 (1.48–43.40)c 0.159
Non-leanness athletes (n 5 96) 9.60 (1.77–52.17)b – – 0.207

*Model 1: self-reported EDs.

w
Model 2: self-reported EDs, body mass indexo18.5 kg/m2, one or more PWCM, and scores
15 and 14 on the DT and BD scales, respectively.
z
Model 3: All the variables in model 2 with the addition of menstrual dysfunction and the reporting of stress fractures.
a
Po0.001.
b
Po0.01.
c
Po0.05 (Wald statistics).
PWCM, pathogenic weight control methods; EDs, eating disorders; BD, body dissatisfaction; DT, drive for thinness.

but this was related to being active in non-leanness
sports only (Table 5). Adjusted for the other models,
model 2 was a poor predictor of clinical EDs. Only
one variable from this model (i.e. self-reported use of
PWCM) uniquely contributed to the probability, but
only for the non-athletic comparison group. In fact,
none of the models predicted an ED diagnosis for the
comparison subjects. Menstrual dysfunction signifi-
cantly contributed to the predictive status of model 3.
However, the effect was specific to athletes compet-
ing in leanness sports. Thus, support to models 1 and
3 in predicting EDs was sport-specific related. More-
over, while model 1 predicted EDs in non-leanness
sports, model 3, which comprised the female athlete
triad components, predicted EDs particularly for
leanness sport athletes.
Dropout analysis
Of those 300 athletes and 300 in the non-athletic
comparison group who were invited to participate in
the clinical part of the study, 114 athletes and 155
controls did not meet for the clinical interview. In the
comparison group, no statistically significant differ-
ences were found between participants and dropouts
in terms of age, body weight, BMI, physical activity
level, previous pregnancy, smoking habits, menstrual
dysfunction, prevalence of stress fractures, oral con-

113
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Torstveit et al.
Table 5. Probability [odds ratio (OR) and 95% confidence intervals (CI)] for a clinical ED diagnose entering the singular risk variables used to compose
the three risk models. These data are from part II of the study.

Self-reported EDs BMI o18.5 kg/m2 EDI-DT
15 EDI-BD
14 PWCM MD Stress Cox and
fractures Snell R2

Model 1 X
Model 2 X X X X X
Model 3 X X X X X X X
Total 2.76b – – – 2.23b 2.16b – 0.159
(n 5 331) (1.39–5.48) (1.16–4.31) (1.20–3.90)
Athletes 3.61c – – – – 2.50c – 0.168
(n 5 186) (1.53–8.52) (1.18–5.29)
Controls – – – – 5.50c 0.158
(n 5 145) (2.06–14.68)
Lean athletes – – – – – 7.35a – 0.305
(n 5 90) (2.25–23.98)
a
Non-lean athletes 12.44 – – – – – – 0.185
(n 5 96) (3.45–44.92)
a
Po0.001.
b
Po0.01.
c
Po0.05 (Wald statistics).
PWCM, pathogenic weight control methods; MD, menstrual dysfunction; BMI, body mass index; BD, body dissatisfaction; DT, drive for thinness.

traceptive use or self-reported EDs. Possibly due to
long distances, more dropouts than participants
came from parts of the country distant to the site
where the interviews were conducted.
Among the athletes, no differences were found
between the participants and the dropouts in terms
of age, age of sport specialization, training volume,
height, smoking habits, prevalence of stress fractures,
national or international ranking performance or
oral contraceptive use. However, athletes who parti-
cipated in the clinical interview had a significantly
lower body weight (60.3  8.8 kg) and BMI
(21.1  2.4 kg/m2) compared with the dropouts
(63.7  9.3 kg and 22.1  2.2 kg/m2, respectively)
(Po0.01). Moreover, a significantly higher percen-
tage of the participants than the dropouts reported
menstrual dysfunction (43.2% vs 24.6%, respec-
tively) (Po0.001) and self-reported EDs (26.9% vs
13.2%, respectively) (Po0.01). In addition, a signifi-
cantly lower percentage of participants compared
with dropouts reported previous pregnancy (7.1%
vs 15.0%, respectively) (Po0.05).
Discussion
Prevalence of DE, EDNOS, AN and BN
The first aim of this study was to investigate the point
prevalence of DE and clinical EDs. Many previous
studies (Smolak et al., 2000; Byrne & McLean, 2001;
Sundgot-Borgen & Torstveit, 2004) have consistently
showed a higher prevalence among athletes com-
pared with controls. However, as EDs are over-
represented in younger adolescents (van Hoeken
et al., 2003), cohort effects may confound such
findings. The fact that the athletes in the present
study were younger than the controls may thus partly
explain the unadjusted higher prevalence of EDs in
the athletic group. However, when age was con-
trolled for, no statistically significant difference was
found between athletes and controls. This is also
reported in previous studies (Sundgot-Borgen, 1993;
Beals & Manore, 1994, 2002; Fogelholm & Hiillos-
korpi, 1999; Byrne & McLean, 2001, 2002; Black
et al., 2003; Sundgot-Borgen & Torstveit, 2004).
In agreement with recent research on DE/EDs
among elite athletes (Byrne & McLean, 2002; Black
et al., 2003; Sundgot-Borgen & Torstveit, 2004), we
found a higher percentage of athletes competing in
leanness sports who had clinical EDs compared with
both athletes competing in non-leanness sports and
controls. Other studies have found that athletes
competing in leanness sports are dissatisfied with
their bodies (Byrne & McLean, 2002). However,
our findings (Table 3) suggest that body dissatisfac-
tion may not be essential as fewer athletes competing
in leanness sports than non-leanness sports are dis-
satisfied with their bodies. Other studies (Sundgot-
Borgen, 1994; Beals & Manore, 2000; McNulty et al.,
2001) have found that other factors, such as the
demands of their specific sport, may drive leanness
athletes toward dieting and use of PWCM. This
could also be the case for our leanness athletes.
One may also argue that actual leanness directly
influences body satisfaction as the leanness athletes
in our study, who are in fact leaner, are more satisfied
with their bodies, while the non-leanness athletes,
who have a higher percentage of body fat, have
higher EDI-BD scores. This could also partly explain

114

the finding that approximately 32% of the non-
leanness athletes reported the use of PWCM com-
pared with 24% of the leanness athletes.
It is noteworthy that the prevalence of BN among
the non-athletic participants randomly selected from
the general population was about two times higher
than the prevalence reported in the mainstream of
previous general population studies (Rosenvinge
et al., 1999; Favaro et al., 2003; Hoek & van Hoeken,
2003; Van Hoeken et al., 2003). Several explanations
may be relevant, like differences in case definition
methods, age cohort effects or possibly that in the
pursuit of losing weight, an increasing number of
females are willing to try extreme weight control
methods, such as purging, instead of a strict restric-
tive energy intake, leading to loss of control and
possibly development of BN. Another possibility
could be selection effects in our study, but this is
contradicted by the dropout analysis showing no
differences between the participants and the dropouts
in terms of factors associated with EDs.
It should also be noted that the prevalence of
clinical EDs as a total (EDNOS, AN, and BN) was
somewhat higher in both athletes and controls than
that found in comparable studies (Byrne & McLean,
2002; Sundgot-Borgen & Torstveit, 2004). For this
finding, at least four explanations may be offered.
First, in the screening part of the study, a high
number of risk variables was included, leading to a
higher probability of detecting more females at risk
for EDs and thus reducing the number of false-
negative subjects. Second, due to the increased focus
DE/EDs in society in general and among athletes in
particular, it is probably less stigmatizing to report
eating problems today. Third, there could be a true
increased prevalence of EDs due to more focus on
body composition and health in general, and, parti-
cularly with athletes, optimal body composition for
sports performance. Finally, the inclusion of the
EDNOS category as part of the DSM-IV criteria
for EDs may result in more subjects being classified
as true positive cases. As previous studies focused
only on AN, BN and different subclinical EDs
(Burckes-Miller & Black, 1988; Sundgot-Borgen,
1993; Shisslak et al., 1995; Johnson et al., 1999),
one may then expect higher prevalence figures in the
present study.
Including EDNOS in addition to AN and BN in
the definition of clinical EDs does not necessarily
accurately address the dietary problems of the ma-
jority of female athletes as indicated by the high
percentage of athletes and controls suffering from
various severities of DE. Also, the prevalence of
athletes with DE would probably have been higher
if we had asked athletes about low energy availabil-
ity. The reason why this was not done has been
explained previously. Low energy availability is diffi-
16000838, 2008, 1, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1600-0838.2007.00657.x by University Of Sydney, Wiley Online Library on [13/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Eating disorders in athletes and controls
cult to measure, but we have found that athletes for
shorter or longer periods are low in energy avail-
ability. In some cases, this is on purpose but for some
athletes this is due to lack of knowledge related to the
energy needs in their sports. Within sports medicine,
low energy availability has been considered as an
indicator for DE (IOC, 2005). Shisslak et al. (1995)
have assumed that DE occurs on a spectrum, indi-
cating a progression in some individuals from less to
more severe disturbances in eating behavior. We
found that all the different DE behaviors, ranging
from prolonged and/or excessive dieting (associated
with a high EDI-DT score and/or low BMI) dissa-
tisfaction with own body (associated to high EDI-
BD score), use of PWCM, and finally clinical EDs,
were prevalent in both the athletes and the compar-
ison group. However, due to the cross-sectional de-
sign of this study, we cannot conclude that these DE
behaviors occur on a spectrum progressing in sever-
ity over time. Nevertheless, a total of 24% of the
athletes and 19% of the controls, who reported DE
behavior, were also diagnosed with an ED. This
indicates that a significant number of females meet-
ing the DSM-IV criteria for AN, BN, or EDNOS
also meet the criteria for DE at some stage along the
spectrum. On the other hand, 9% and 3% of the
athletes and controls, respectively, were diagnosed
with EDs without having reported DE behaviors.
This proportion of false negatives may be due to
underreporting of DE behavior and emphasizes the
need for conducting clinical interviews to diagnose
EDs, in addition to screening by means of question-
naires. Clinical interview seems especially important
for leanness sport athletes, as over 14% were classi-
fied as false-negative subjects in our study.
It has been suggested that limiting the definition of
the DE component of the female athlete triad to
clinical EDs may be too restrictive as this could
potentially exclude a significant number of athletes
and controls who express one or more DE behaviors
and who are therefore at increased risk for develop-
ing EDs and possibly skeletal demineralization (Otis
et al., 1997), and thus need professional help. In our
study, a significant number of females were diag-
nosed with EDs; however, almost one fourth of the
athletes and more than one third of the controls
reported DE behavior without being diagnosed with
clinical EDs. These females are at increased risk for
developing serious EDs like AN and BN (Sundgot-
Borgen, 1993, 1994) and this emphasizes the impor-
tance of investigating the whole DE spectrum, rather
than focusing only on the endpoint: clinical EDs.
Characteristics of the athletes with EDs
As expected when investigating the athletes diag-
nosed with the different types of EDs in more detail,
115

Torstveit et al.
athletes diagnosed with AN had a very low mean
body fat percentage (12.8%). On the other hand,
their mean BMI value was 18.9 kg/m2, and thus in
the lowest range of the WHO’s normal body weight
range (WHO, 2000). A higher percentage of fat free
mass may account for this finding, and indicate that
BMI may be inadequate to identify athletes with AN.
Our results showed that in the athletes diagnosed
with AN, 83.0% of the total body mass was fat-free
mass, and this was a higher percentage as compared
with the athletes without ED (67.2%), those diag-
nosed with BN (68.6%) and EDNOS (67.6%)
(Po0.001).
Athletes diagnosed with BN in our study were
characterized with quite high mean EDI-DT and
EDI-BD scores, and a mean body fat percentage of
25.6. These athletes may therefore be dissatisfied with
their bodies, they strive for thinness and their body
types are different as compared with the anorexic
athletes due to a higher percentage of body fat.
However, one should notice that the mean BMI
values in all the groups indicate a normal body
weight according to the WHO (WHO, 2000), again
suggesting caution in using BMI as a criterion to
identify athletes with EDs. Despite extreme focus on
thinness and a specific body weight often seen in
patients with BN and EDNOS (American Psychiatric
Association, 1994), there were no statistical differ-
ences between the athletes in our study diagnosed
with these two disorders and the athletes without
EDs in terms of characteristics like BMI, body fat
percentage, age of menarche and training volume. A
higher percentage of athletes representing leanness
sports as compared with the percentage of athletes
competing in non-leanness sports met the criteria for
BN. This might be explained by the fact that DE
(including restrictive eating) is more common among
those competing in leanness sports, and a previous
study (Sundgot-Borgen, 1994) has shown that ath-
letes with restrictive eating and or DE, if not treated,
develop more bulimic eating behavior and/or BN
after a shorter or longer period with restrictive
eating.
Predictive power of risk criteria for EDs
It has been suggested that the use of questionnaires in
diagnosing subjects with EDs is not satisfactory, and
that an additional clinical interview is necessary to
optimize case identification (Sundgot-Borgen, 1993;
Byrne & McLean, 2001; van Hoeken et al., 2003).
Even if a two-stage screening approach is the most
widely accepted procedure for case identification,
methodological problems such as poor sensitivity/
specificity of the screening instrument and small
sample sizes may still cause problems (van Hoeken
et al., 2003). When investigating the OR of the three
116
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risk models introduced in the present reasonably
large sample, the variables comprising the female
athlete triad (model 3) raised the probability of a
clinical ED diagnosis among the subjects in total, as
well as in the total athletic group. This finding was
further supported when examining the contribution
of individual variables, such as menstrual dysfunc-
tion, when adjusted for the other variables, signifi-
cantly contributed to the predictive power in the
same groups. However, when dividing the athletes
into those competing in sports focussing on thinness
and/or a low body weight and those competing in
sports focusing less on these factors, menstrual
dysfunction was an important factor for prediction
of EDs only in the leanness athletes, while model 1
(self-reported EDs) raised the probability of a clinical
ED in the non-leanness athletes. The finding that
menstrual dysfunction predicted clinical EDs may
boarder on being pseudoempirical in nature, but this
argument is weakened by the fact that amenorrhea is
not a DSM-IV-criterion for BN and EDNOS, which
were the largest clinical groups in our material. It
has, however, been claimed that when screening for
one of the female athlete triad components, one
should also screen for the other two (Otis et al.,
1997). We know that many athletes underreport DE
behavior like the use of PWCM or self-reported EDs
(Sundgot-Borgen, 1993), and asking only about these
behaviors may result in an increased number of false-
negative subjects. In contrast, questions about men-
strual dysfunction may seem less threatening for
some athletes, and may be easier to answer honestly.
Furthermore, as preoccupation with food, dieting
and use of PWCM may seem like a natural part of
competing in their sport, athletes may not consider
such DE behaviors or EDs to be a problem. This is
especially likely among athletes competing in lean-
ness sports.
Self-reported EDs (model 1) seem to be useful as a
screening variable in athletes, but only in athletes
competing in non-leanness sports. This may partly be
due to the fact that, possibly in contrast to leanness
athletes, non-leanness athletes do not see their eating
problem as a natural part of their sport, and thus
are more prone to self-report their own experience
of an ED.
An unexpected finding was the fact that model 2,
when adjusted for the other models, was a poor
predictor of clinical EDs in the athletes as well as
in the non-athletic comparison group. Only one
variable from this model (i.e. self-reported use of
PWCM) uniquely contributed to the probability, but
only among the controls. Hence, the OR was sub-
stantially increased, indicating that vomiting and
self-medication to improve dieting in fact predicted
a clinical ED in this non-athletic group. This finding
is in accordance with a recent longitudinal general

population study (Fairburn et al., 2005) also report-
ing similar specific behaviours as increasing the risk
for a future clinical ED.
In fact, none of the models predicted an ED
diagnosis in the comparison group. This may indi-
cate that risk factors or risk models may be better
conceptualized as sample-specific rather than univer-
sal in nature. Also, a somewhat low total explanatory
status of EDs using the proposed screening variables
(Tables 4 and 5) underlines the need for further
research regarding the validity of screening models.
Limitations and generalization of the results
Despite the known possible limitations of cross–
sectional studies (i.e. self-selection, inadequate sam-
pling methods and a volunteer effect), the prevalence
results from this study seem generalizable to female
elite athlete populations and to non-athletic preme-
nopausal women in general. Results with respect to
the relationship between DE indicators and clinical
EDs should, however, be interpreted with caution, as
a cross-sectional design allows for a statistical prob-
ability analysis only. A genuine risk analysis will
need a long-term prospective design.
16000838, 2008, 1, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/j.1600-0838.2007.00657.x by University Of Sydney, Wiley Online Library on [13/08/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Eating disorders in athletes and controls
leanness sports compared with both athletes compet-
ing in non-leanness sports and controls. Therefore,
we need to emphasize what kind of athletes we
address when we talk about a higher prevalence of
EDs in the sports environment.
Using a risk criteria model including questions
about menstrual dysfunction may be valuable in
detecting EDs in leanness sport athletes, while using
only self-reported EDs as a selection criterion may
predict clinical EDs in non-leanness athletes. The
same screening models used for athletes may not
apply for controls, where more focus should possibly
be on DE behaviors like use of PWCM. Until a valid
screening model is developed, an additional clinical
interview is necessary to distinguish true EDs from
subclinical symptoms included in the spectrum of DE
in young female athletes and controls. In a further
development of a valid screening model, future
research would need to use a long-time prospective
epidemiological cohort study design.
Key words: anorexia nervosa, bulimia nervosa, ED-
NOS, the female athlete triad.

Perspectives
A high percentage of both athletes and controls met
the criteria for DE and clinical EDs, with no differ-
ences between the groups. However, in accordance
with previous studies (Byrne & McLean, 2002;
Sundgot-Borgen & Torstveit, 2004), a higher preva-
lence of EDs was found among athletes competing in
Acknowledgements
This study was supported by research grants from The
Norwegian Olympic Committee and Confederation of Sport,
and The Norwegian Foundation for Health and Rehabilita-
tion. We acknowledge professor Ingar Holme for statistical
advice, Jennifer Arnesen for English revision of the manu-
script and Elin Kolle and Katrine M. Owe for help with the
collection of data.

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