Lifetime course of eating disorders: design
and validity testing of a new strategy to define
the eating disorders phenotype
M. Anderluh1,2*, K. Tchanturia1, S. Rabe-Hesketh1, D. Collier1and J. Treasure1
1Eating Disorders Unit, Institute of Psychiatry, King’s College London, London, UK
2University Children’s Hospital, University Medical Centre, Ljubljana, Slovenia
Background. Aetiological studies of eating disorders would benefit from a solution to the problem of instability of
eating disorder symptoms. We present an approach to defining an eating disorders phenotype based on the retro-
spective assessment of lifetime eating disorders symptoms to define a lifetime pattern of illness. We further validate
this approach by testing the most common lifetime categories for differences in the prevalence of specific childhood
Method. Ninety-seven females participated in this study, 35 with a current diagnosis of restricting anorexia nervosa,
32 with binge/purging subtype of anorexia nervosa and 30 with bulimia nervosa. Subjects were interviewed by a
newly developed EATATE Lifetime Diagnostic Interview for a retrospective assessment of the lifetime course of eating
disorders symptoms and childhood traits reflecting obsessive–compulsive personality.
Results. The data illustrate the extensive instability of the eating disorders diagnosis. Four most common lifetime
diagnostic categories were identified that significantly differ in the prevalence of childhood traits. Perfectionism and
rigidity were more common in groups with a longer duration of underweight status, longer episodes of severe food
restriction, excessive exercising, and shorter duration of binge eating.
Conclusions. The assessment of lifetime symptoms may produce a more accurate definition of the eating disorders
phenotype. Obsessive–compulsive traits in childhood may moderate the course producing longer periods of under-
weight status. These findings may have important implications for nosology, treatment and future aetiological studies
of eating disorders.
Received 8 March 2007; Revised 4 February 2008; Accepted 29 February 2008; First published online 1 April 2008
Key words: Eating disorders, lifetime course, lifetime diagnostic categories.
Anorexia nervosa and bulimia nervosa are complex
disorders in which both genes and environment in-
teract in a developmental and sociocultural context.
However, aetiological studies have been hampered
because of the unstable clinical phenotypes (Fairburn
& Harrison, 2003; Collier & Treasure, 2004). Flux be-
tween the various eating disorders diagnosis is com-
mon and was first observed in several follow-up
treatment studies (Collings & King, 1994; Eckert et al.
1995; Fairburn et al. 1995; Bulik et al. 1997; Strober et al.
1997; Herzog et al. 1999; Eddy et al. 2002); as many as
50% of individuals with anorexia nervosa go on to
develop bulimia nervosa, and among individuals
with bulimia nervosa, nearly 30% report a history of
anorexia nervosa (Keel & Mitchell, 1997). Milos et al.
(2005) found in a prospective study that less than
one-third of cases retained the same eating disorders
diagnosis over a 30-month observation period. This
creates difficulties for aetiological research in areas
examining unchanging variables such as genetic
polymorphisms or antecedent risk factors, as any
association based on acute diagnosis will change over
One solution to overcoming the problem of unstable
clinical phenotypes is to determine an extended clini-
cal phenotype by considering symptoms and traits
over the life course (Collier & Treasure, 2004). Child-
hood obsessive–compulsive personality traits are
heritable (Eley et al. 2003; P. Liao et al. unpublished
observations), and are associated with anorexia ner-
vosa (Anderluh et al. 2003). Childhood risk factors may
be particularly valuable because they occur during
development, and may therefore be closer to the
psychosocial and biological processes that underlie
* Address for correspondence: M. Anderluh, M.D., Child
Psychiatry Unit, University Children’s Hospital, University Medical
Centre, Vrazov trg 1, 1525 Ljubljana, Slovenia.
Psychological Medicine (2009), 39, 105–114.
f 2008 Cambridge University Press
Printed in the United Kingdom
the development of eating disorders (P.-C. Liao et al.,
unpublished observations). These traits fulfil many of
the criteria of an endophenotype (or an intermediate
phenotype) (Gottesman & Gould, 2003) in that they
are associated with the disease, are present in first-
degree relatives of patients (Lilenfeld et al. 1998) and
are stable traits that are present before illness onset
and remain after recovery (Srinivasagam et al. 1995;
Fairburn et al. 1999; Holtkamp et al. 2005). In addition,
they appear to be clinically important as there is evi-
dence that obsessive–compulsive personality traits
are associated with poor outcome (Crane et al. 2007).
We were therefore interested in whether they had
an impact on the lifetime course of eating disorder
The aim of this study was to retrospectively exam-
ine the life course of eating disorders in adult females
with anorexia and bulimia nervosa to determine the
most common lifetime diagnostic categories. We also
examined the prevalence of childhood obsessive–
compulsive traits across the lifetime categories and
their impact on the lifetime course. To minimize biases
related to retrospective reporting and to enhance the
reporting accuracy, we developed an instrument
with life events as anchor points along the lifeline, an
adaptation of the Longitudinal Interval Follow-up
Evaluation (LIFE; Keller et al. 1987; Herzog et al. 1999;
Kordy, 2005), to assess the lifetime course of eating
The sample included 97 patients with eating disorders
accepted for treatment in in-patient and out-patient
programmes of the Eating Disorders Unit of the
Maudsley Hospital, London, a secondary and tertiary
referral centre, and presents an extended sample of
a previous study (Anderluh et al. 2003). It included
35 females with a current ICD-10 (WHO, 1992) diag-
nosis of anorexia nervosa, restricting subtype, 32
females with anorexia nervosa, binge/purging sub-
type, and 30 female participants with a current ICD-10
diagnosis of bulimia nervosa. To avoid possible re-
porting biases related to acute physical state, patients
who fulfilled the diagnostic criteria and were willing
to participate were entered in the study 3–4 weeks
after the beginning of treatment. Those with a history
of psychotic disorder according to the ICD-10 criteria
were excluded. All participants were native English
speakers. The study was approved by the South
London and Maudsley National Health Service Trust
research ethics committee. Written informed consent
Specialists in the Eating Disorders Unit made the
initial screening diagnosis of eating disorders using
the ICD-10 criteria (WHO, 1992). Participants were
then interviewed by a trained researcher (one of six
postgraduate psychologists and psychiatrists) using
a semi-structured EATATE interview. On the date of
the interview, data on demographic characteristics
were collected and the subject’s weight and height
The EATATE Lifetime Diagnostic Interview
The EATATE interview was developed for the
European Healthy Eating Project (QLK-1999-916),
which examined genetic and environmental risk fac-
tors for eating disorders and obesity. (The instrument
is available upon request from M.A.) Its first part,
which is presented here, is a semi-structured diag-
nostic interview, adapted from the LIFE (Keller et al.
1987; Herzog et al. 1999; Kordy, 2005), to allow the
assessment of lifetime course of the disorders. It uses
items from the Eating Disorders Examination (EDE)
interview (Cooper et al. 1989) to produce an ICD-10
eating disorder diagnosis. It assesses body weight
and height during the whole course of the illness,
duration of periods when each of the symptoms of
eating disorders are present, and their severity: behav-
ioural (dieting, fasting, excessive exercising, binge
eating, vomiting, using laxatives, slimming pills and
other compensatory behaviours) as well as psycho-
pathological symptoms (inappropriate weight con-
cern, fear of food, eating and food preoccupation)
and menstrual status. The course of each symptom is
plotted on a lifeline, a time-line that spreads from the
point when first symptoms developed to the inclusion
in the study. As in ICD-10 we used 3 months’ dur-
ational criteria and their severity to determine the
symptoms present (described in more detail in the
online Appendix). To enhance the accuracy of retro-
spective reporting, anchor points are used along
the lifeline; these are significant life events such as
treatment status, birthdays, etc. We distinguished a
priori four subtypes of anorexia nervosa: restricting
subtype (no binging or purging present), purging
(vomiting or other purging behaviour present about
once in 2 weeks or more over a period of 3 months),
binge/purging (binging and purging behaviour pres-
ent once in 2 weeks or more over a minimum of
3 months) and binging subtype (binging present with
the same frequency as above, but no purging). As
suggested previously (Hay et al. 1996), two subtypes of
bulimia nervosa (purging and non-purging subtypes)
106 M. Anderluh et al.
were identified. The diagnoses of binge-eating dis-
order and eating disorder not otherwise specified
(EDNOS) were determined according to DSM-IV diag-
nostic criteria and research evidence (Cooper et al.
2003). The determination of subsequent subtype diag-
noses along the lifeline enabled us than to identify
lifetime diagnostic categories. The interview also
screened for lifetime obsessive–compulsive disorder
(OCD) using the ICD-10 diagnostic criteria (excluding
food and body-related obsessions) and for impulsive
behaviours (abuse of alcohol or illegal drugs, self-
harm, overdose, reckless spending, disinhibited or
reckless sexual activities, shoplifting or stealing,
interpersonal violence, violence to property, gambling
or fire setting). The interview takes on average about
45 minutes, although the length of the interview
depends grossly on the duration of the subject’s ill-
ness and symptoms stability. The interview showed
good inter-interviewer reliability for the assessment
of weight and behavioural symptoms (k coefficients
0.74–0.94), lower reliability for lifetime assessment of
psychopathological variables and good validity (data
available in the online Appendix).
The second part of the EATATE interview measures
obsessive–compulsive traits in childhood (described
in detail in Anderluh et al. 2003), including per-
fectionism, drive for order and symmetry, two traits
reflecting rigidity (inflexibility and being bound by
rules), and excessive doubt and cautiousness. The
instrument uses behavioural examples to assess the
traits and has high inter-rater reliability and validity
(Anderluh et al. 2003). It also assesses ICD-10 diag-
nostic criteria of OCD and obsessive–compulsive per-
sonality disorder (OCPD) in adulthood.
The clinical and demographic data were compared
across the three groups defined by current diagnosis
by using x2tests and a one-way analysis of variance.
The Tukey test was used for post hoc comparisons of
group differences. The chronological course of eating
disorder subtypes for each individual case was pre-
sented graphically; cases were grouped according to
their first eating disorder diagnosis.
To examine the relationship between childhood
obsessive–compulsive personality traits, as assessed
using previously defined criteria (Anderluh et al.
2003), and lifetime course of eating disorder symp-
toms, a x2test was used. To compare as diagnostically
homogeneous groups as possible, we selected from the
total sample the most common lifetime diagnostic
categories: (1) a group with lifetime restrictive anor-
exia nervosa, (2) a group with lifetime binge/purging
anorexia nervosa or with binge/purging anorexia
nervosa preceded by an episode of restrictive anor-
exia, (3) a group of cases with bulimia nervosa with
a previous episode of anorexia nervosa, and (4) a
group of lifetime bulimia nervosa cases. About three-
quarters of the total sample belong to one of those
categories (n=76). The lifetime categories reflect steps
on a continuum from restricting to bulimic subtypes of
eating disorders and obesity (Treasure & Collier,
We also compared the duration of eating disorder
symptoms in people with and without childhood ob-
sessive–compulsive traits. Because the distribution of
those variables was not normal, a non-parametric
Mann–Whitney test was used in the analysis. Al-
though every effort was made to obtain complete data
for all subjects, some data on childhood traits were
missing for 17% of subjects. Subjects with fully com-
pleted assessment of childhood traits did not differ
significantly from those with incomplete data on any
of the clinical parameters. All analyses were carried
out by using SPSS-PC release 11.0 (SPSS Inc., Chicago,
IL, USA) and all statistical tests used a 5% level of
Table 1 summarizes the demographic and clinical
characteristics across the groups defined by current
diagnosis: (1) restricting anorexia nervosa, (2) binge/
purging anorexia (binging and/or purging behaviour
present at least once in 2 weeks over a period of
3 months) and (3) bulimia nervosa. The groups did
not differ in current age, age at onset or duration of
illness (mean duration 10.67 years, S.D.=8.11). As ex-
pected, body mass index (BMI) at assessment differed
significantly across the groups (F=30.29, df=2.95,
p<0.001); both anorexia nervosa groups had a sig-
nificantly lower BMI (F=36.49, df=2.95, p<0.001).
There were no significant differences across the
groups on the mean of the highest adult BMI.
The three groups differed significantly in the mean
lifetime duration of binging, vomiting, laxative and
diuretic abuse and dieting, but not in the mean lifetime
duration of fasting or excessive exercising (data
presented in Table 1). No significant differences were
observed in mean lifetime duration of eating and food
preoccupation, fear of food or inappropriate weight
and shape concern (data not shown). However, the
confidence of this finding was low as the reliability of
the assessment of these items was low. There were
no significant differences between the groups in the
frequency of current or lifetime OCD or in the fre-
quency of current OCPD co-morbidity. The anorexia
Lifetime course of eating disorders107
Table 1. Description of the clinical characteristics of the sample included in the study grouped according to the current eating
Current age (years)a
Body mass index (kg/m2)
28.410.5 27.17.1 26.1 9.20.532.95
Age at onset of eating
Illness duration (years)
Duration of specific
17.15.3 16.64.916.42.9 0.23 2.94
11.38.7 10.57.19.7 8.80.322.94
Number of impulsive
Number of childhood traits
reflecting OCP presentg
1.7 188.8.131.52.92.714.95 2.81
184.108.40.206 1.71.6 1.4 6.522.92 0.002
n (%)n (%)n (%)x2
OCPD (no. of cases)
OCD (no. of cases)
OCP, Obsessive–compulsive personality; OCPD, obsessive–compulsive personality disorder; OCD, obsessive–compulsive
disorder; S.D., standard deviation; df, degrees of freedom; N.S., not significant.
aAge range=15–52 years for subjects with anorexia nervosa restricting type, 18–52 years for subjects with anorexia nervosa
binge/purging type, and 15–62 years for subjects with bulimia nervosa.
bSignificant differences between subjects with anorexia nervosa (both types) and bulimia nervosa (p<0.001, Tukey).
cSignificant differences between all three groups, between anorexia nervosa restricting type and anorexia nervosa binge/
purging type (p=0.03, Tukey), between anorexia nervosa, restricting type and bulimia nervosa (p<0.001, Tukey), and between
binge/purging type of anorexia nervosa and bulimia nervosa (p=0.04, Tukey).
dSignificant differences between subjects with anorexia nervosa restricting type and subjects with anorexia nervosa binge/
purging type and bulimia nervosa (p<0.001, Tukey).
eSignificant differences between subjects with anorexia nervosa restricting type and bulimic type (p<0.01, Tukey) and
between subjects with anorexia nervosa restricting type and bulimia nervosa (p<0.001, Tukey).
fNumber of impulsive behaviours during her lifetime that is also plotted on the lifetime scale (abuse of alcohol, illegal drugs,
self-harm, overdose, reckless expenditure, disinhibited or reckless sexual activities that could be described as disinhibited or
reckless, shoplifting or theft, interpersonal violence, provoking fights or arguments breaking objects, gambling or fire setting).
Significant differences between restricting type of anorexia nervosa and bulimia nervosa (p<0.001, Tukey) and binge/purging
type of anorexia nervosa and bulimia nervosa (p<0.01, Tukey).
gNumber of childhood traits reflecting OCP type present, including childhood perfectionism, drive for order and symmetry,
rule bound, inflexibility and excessive doubt or cautiousness. Significant differences between the two groups with anorexia
nervosa and the group with bulimia nervosa (p<0.01, Tukey).
108M. Anderluh et al.
nervosa groups had a higher prevalence of childhood
obsessive–compulsive personality traits than the bu-
limia nervosa group (x2=6.52, df=2.92, p=0.002).
Lifetime eating disorder diagnosis
Detailed information on the time course of each indi-
vidual eating disorder symptom was obtained. In 40%
(n=38) of subjects who participated in the study,
at least one diagnostic crossover was observed be-
tween different eating disorder subtypes during their
illness. Thirty-seven per cent of those (n=14/38)
satisfied criteria for three or more diagnostic sub-
types during their lifetime. The study sample included
cases with widely varied illness duration; 12% of
the cases had illness duration equal to or less than
the observed mean duration in which diagnostic
crossovers occurred in the subsequent subtypes. This
suggests that the real crossover rates are likely to be
even higher than that reported in the study. The life-
time data are illustrated in Figs 1–3.
Restricting anorexia nervosa
At the onset, over half of the participants in the study
(n=55) fulfilled the diagnostic criteria for the restrict-
ing subtype of anorexia nervosa (Fig. 1). Of those 55,
38% (n=21/55) developed regular binging and/or
purging (defined as at least once in 2 weeks for 3 con-
secutive months) during the course of the illness. All
diagnostic crossovers occurred within 7 years of onset.
The median duration of restricting anorexia nervosa
20 15 1050
Fig. 1. Retrospective lifetime eating disorders course in cases
with restricting anorexia nervosa at onset (n=55). The solid
vertical line shows the median duration of restrictive subtype
before diagnostic crossover (3 years), the broken line shows
the suggested durational criteria of 7 years to determine pure
restricting anorexia nervosa. The numbers on the right
present the total duration of the illness. EDNOS, Eating
disorder not otherwise specified; BED, binge-eating disorder;
PAN, purging anorexia nervosa; BAN, binge anorexia
nervosa; BPAN, binge/purging anorexia nervosa; PBN,
purging bulimia nervosa; NPBN, non-purging bulimia
nervosa; RAN, restrictive anorexia nervosa.
20 15 1050
Fig. 2. Retrospectively assessed lifetime course of eating
disorder in cases with binge/purging types of anorexia
nervosa at onset (n=25). The vertical line shows the median
duration before diagnostic crossover (1 year). RAN,
Restrictive anorexia nervosa; PAN, purging anorexia
nervosa; BAN, binge anorexia nervosa; BPAN, binge/
purging anorexia nervosa; PBN, purging bulimia nervosa.
Fig. 3. Retrospective assessment of lifetime course of eating
disorders in cases with bulimia nervosa at illness onset
(n=18). The vertical line shows the median duration of
bulimia nervosa before diagnostic crossover (3 years).
EDNOS, Eating disorder not otherwise specified; BPAN,
binge/purging anorexia nervosa; PBN, purging bulimia
nervosa; NPBN, non-purging bulimia nervosa.
Lifetime course of eating disorders109
in these cases was 3 years. In 62% (n=12/21) of cases
crossover occurred after 3 or more years of duration of
restricting anorexia nervosa. About one-third of those
cases developed bulimia nervosa and two-thirds de-
veloped binge/purging subtypes of anorexia nervosa
Binge/purging anorexia nervosa
A quarter of the subjects (n=24) had an onset diag-
nosis of binge/purging subtypes of anorexia nervosa
(Fig. 2). Purging anorexia nervosa was the most com-
mon of the three subtypes (n=18), with 6/24 subjects
fulfilling diagnostic criteria for binge/purging anor-
exia nervosa. There were no cases with binging
anorexia at the beginning of the illness. Diagnostic
crossover occurred in half of the cases. The median
time at which a change in the diagnostic subtype
occurred was 1.0 year (Fig. 2). Nearly one-third of
cases (7/24) developed bulimia nervosa (more com-
monly binge/purging anorexia nervosa than purging
anorexia nervosa). The second most common cross-
over was to a different subtype of binge/purging
anorexia nervosa (two subjects with the purging
subtype developing an episode of binge/purging an-
orexia nervosa and one with binge/purging anorexia
developed binging anorexia nervosa). Only four cases
(18%) progressed to restricting anorexia nervosa (one
later progressed to bulimia nervosa and the other to
purging anorexia nervosa). This group had the short-
est duration of illness before inclusion in the study
(with median time of 7.3 years), with two exceptions
who have had bulimia nervosa for over 30 years.
The third group, 18.5% (n=18/97) of the whole
sample, fulfilled diagnostic criteria of bulimia nervosa
at the beginning of their illness (Fig. 3). Less than one-
fifth of cases (17%) changed diagnosis. The median
time of change in diagnosis was 3 years. One of them
progressed to EDNOS and in three cases binge/
purging anorexia nervosa developed, in one as a
transient episode during normal weight bulimia ner-
vosa. Only three (16.7%) cases fulfilled criteria of non-
purging subtype at any time during the illness.
Childhood obsessive–compulsive personality traits
across the lifetime diagnostic categories
Frequencies of the assessed childhood personality
traits were compared across the lifetime diagnostic
categories: (1) a group with lifetime restricting anor-
exia nervosa (n=21) (to exclude subjects at risk of
crossover, only cases with an illness duration >7 years
were included), (2) bulimic subtypes of anorexia
nervosa (n=25) (with or without a previous episode of
restricting anorexia nervosa), (3) bulimia nervosa with
a previous episode of anorexia nervosa (n=15), and
(4) lifetime only bulimia nervosa (n=15). Although
the additional durational inclusion criteria led to age
differences in category 1 (current age, but not age of
onset, was higher in this category), this enabled us to
include a pure restrictive anorexia nervosa group
in the analysis. The groups differed significantly in the
prevalence of three of the five childhood traits (see
Table 2), but not in the prevalence of adult OCPD.
Table 2. Frequencies of the childhood traits reflecting obsessive–compulsive personality and the frequency of obsessive–compulsive
personality disorder (OCPD) in adulthood across the four lifetime diagnostic groups (n=76)
of RAN or
BN with an
episode of AN
Order and symmetry
Excessive doubts and
15/21 71.416/25 64.0 7/1546.76/1540.04.706
RAN, Restricting anorexia nervosa; BPAN, binge/purging anorexia nervosa; BN, bulimia nervosa; AN, anorexia nervosa;
df, degrees of freedom; N.S., not significant.
aThe number of the subjects is reported individually for each analysis because of some missing data.
110 M. Anderluh et al.
The greatest variability across the lifetime cat-
egories was in the two traits that represent childhood
rigidity (inflexibility and rule bound) and childhood
perfectionism. Childhood inflexibility was present
in 80% of the participants in group 1, in 52% of the
participants in group 2, 27% in group 3 and 20% in
group 4. Being bound by rules was similarly more
common in groups 1 and 2, especially in group 2
(87%), compared to the group with lifetime bulimia
were also observed in the frequency of perfectionism
in childhood. Again, it was most common in group 2
(76%), followed by groups 1 (48%) and 3 (40%), and
was least common in the lifetime bulimia nervosa
Childhood obsessive–compulsive personality traits
associated with lifetime symptoms
The examination of the influence of childhood traits
on the duration of specific eating disorder behaviours
using the whole study sample revealed that partici-
pants who reported inflexibility in childhood tended
to have significantly longer duration of dieting (p<
0.005), fasting (p<0.01) and lifetime duration of
anorexia nervosa (p<0.005) and shorter duration of
periods of regular binge eating (p<0.001) than subjects
without this trait (Table 3). Subjects who reported
being bound by rules in childhood tended to experi-
ence significantly longer lifetime periods of excessive
exercising (p<0.005) than those without. The duration
of underweight status tended to be longer if either
of the rigidity traits was reported and was longest
in those subjects with both rigidity traits present (p=
0.001). Similar, although less significant, were relation-
ships between the presence of perfectionism and drive
for order and symmetry in childhood and lifetime
duration of underweight status (p=0.03 and p=0.05).
Excessive cautiousness was found to be significantly
related to duration of excessive exercising (p<0.02)
and fasting (p<0.05). Excessive doubt was not sig-
nificantly associated with the duration of any of the
eating disorder behaviours.
This study confirms and illustrates the temporal in-
stability of eating disorder subtype diagnosis through
retrospective assessment of lifetime symptoms. Based
on the lifetime data, four of the most common lifetime
diagnostic courses were distinguished: lifetime anor-
exia nervosa, binge/purge anorexia nervosa with or
without an antecedent episode of restrictive anorexia
nervosa, bulimia nervosa after an episode of anorexia
nervosa, and lifetime bulimia nervosa. These lifetime
categories differed in the prevalence of childhood
obsessive–compulsive traits, suggesting that lifetime
categories might offer a valid approach to defining
more homogeneous eating disorder phenotypes.
Table 3. Differences in the duration (years) of eating disorder symptoms between subjects with childhood obsessive–compulsive
type personality traits and those without these traits in childhood in the whole sample (df=92)
Mean (S.D.)p* Mean (S.D.)p* Mean (S.D.)p* Mean (S.D.)p* Mean (S.D.)p*
Laxative abuse Yes
Excessive exercising Yes
5.3 (5.8) 0.003
df, Degrees of freedom; S.D., standard deviation; N.S., not significant.
* The non-parametric Mann–Whitney test was used to test the differences between the groups.
Lifetime course of eating disorders 111
Subjects with childhood traits of perfectionism and
rigidity experienced longer periods of underweight
status and longer periods of severe food restriction
and excessive exercising, as well as shorter periods of
binge eating. This suggests that obsessive–compulsive
traits might influence the shape of the eating disorder
course and present a way of determining a more
homogeneous eating disorders phenotype.
This approach, using a retrospective assessment of
lifetime eating disorders and childhood traits, pre-
sents, to our knowledge, a unique approach in eating
disorders phenotype studies. The EATATE diagnostic
instrument is, to our knowledge, the first to retro-
spectively measure the course of traits and symptoms
over a lifetime. Compared to the currently used in-
struments for retrospective assessment of eating dis-
orders history (e.g. SIAB-EX; Fichter & Quadlieg,
2001), which assess the worst ever symptoms only,
with no time-line perspective, the EATATE offers a
more comprehensive view on the past course of the
symptoms and the disorder.
The assessment of lifetime symptoms enabled us
to confirm and extend the findings from previous
studies. Crossover rates from anorexia nervosa to
bulimia nervosa were found to be similar to those in
the prospective studies (Eckert et al. 1995; Strober et al.
1997; Herzog et al. 1999; Eddy et al. 2002). Crossover
rates were comparable in women who had either
restricting or binge/purging subtype of anorexia
nervosa at the illness onset. However, time elapsed
before change was longer in the restricting group.
Examination of the time course of the diagnostic cross-
overs showed that, in 60% of subjects where diag-
nostic crossover from restrictive anorexia nervosa
occurred, it was after 3 years of illness, the period that
has been used before to determine pure restricting
subtype (Bergen et al. 2003). Once binging behaviour
began, it was rare for restricting anorexia nervosa to
re-emerge. Linkage studies of restricting anorexia
nervosa on multiply affected families demonstrated a
specific locus on chromosome 1 (Grice et al. 2002) that
was not evident for a broader definition of anorexia,
indicating that restricting illness may present the
most homogeneous phenotype among eating dis-
orders. Based on our results, extension of durational
criteria to 7 years would substantially improve the
homogeneity of restricting anorexia nervosa samples
and the power of genetic studies (a decrease of mis-
classified cases from 60% to 18% and 5% was ob-
served after extension of durational criteria from 3 to
5 and 7 years respectively). However, that would limit
the number of cases available for study.
The crossover rate in women with bulimia nervosa
at the illness onset was just over one-third that
for women with anorexia nervosa. Crossover from
bulimia to anorexia nervosa has been found to be rare
(0–7%) in the majority of follow-up studies (Collings
& King, 1994; Fairburn et al. 1995; Keel & Mitchell,
1997; Keel et al. 2000). However, more recently, a
higher crossover rate of 27% was reported in a large
study of affected relative pairs (Tozzi et al. 2004). The
crossover rate of 17% found in our study is consistent
with this as it fits within the interval of crossover rates
suggested in the previous studies.
The four common lifetime groups differed signifi-
cantly in three of the five childhood traits assessed,
suggesting that those traits might be linked to devel-
opment and maintenance of some of the eating dis-
order symptoms. By contrast, lifetime categories
did not differ in the prevalence of adult OCPD. This
confirms the discriminatory validity of the lifetime
grouping approach and suggests that taking into
account lifetime symptoms and traits offers compre-
hensive and more stable clinical phenotypes for future
This paper is an extension of our previous study
on temperamental traits in eating disorders. We pre-
viously reporteda strong
obsessive–compulsive personality type traits in child-
hood and the likelihood of developing an eating
disorder later in life. Our findings suggest that pre-
morbid personality traits may shape the lifetime
course of the disorders. Traits such as being bound
by rules, inflexibility and striving for perfection can
facilitate persistent dietary restriction and the control
of appetite. Subjects with those traits experienced
significantly longer periods of strict dieting, fasting
and excessive exercising during their illness and less
binge eating when compared to patients without those
traits. Participants with both rigidity traits tended to
experience significantly longer periods of under-
weight status than those without them (p=0.001).
Childhood obsessive–compulsive personality type
traits might thus present not only the risk for eating
disorder, as described previously (Anderluh et al.
2003), but also the maintenance factor of its restrictive
symptoms. In a systematic review of treatment trails
we have found that these traits moderate outcome
(Crane et al. 2007) and may be linked to set shifting
(Tchanturia et al. 2004) and weak central coherence
information processing styles that might also be part
of the endophenotype (Lopez et al. 2008).
The absence of any links between observed
childhood obsessive–compulsive traits and purging
suggests that other factors are involved in the main-
tenance of bulimic behaviours. Impulsivity might be
one of them. The continuum of eating disorder symp-
toms that spreads from restricting to bulimic symp-
toms may correspond to the continuum of personality
traits spreading from compulsive to impulsive type
112M. Anderluh et al.
traits. Eating disorders are clinically heterogeneous
disorders, with an array of symptoms and traits that
are present to different degrees in different individuals
at a particular time, such as binge eating, restricting
rigidity, perfectionism and impulsivity. A central
question is whether this results from aetiological
heterogeneity (Kendler et al. 2000), which could occur
through the differential effects of genes or environ-
ment or their interaction. Thus, a particular suscep-
tibility gene or type of environmental event could
predispose to a certain type or cluster of symptoms,
such as perfectionism or impulsivity. Perfectionism
(Tozzi et al. 2004) and impulsivity (Rietveld et al. 2004)
are both partly heritable and show a genetic influence.
It is thus likely that specific genes predispose to
specific eating disorder-related traits.
The study had several limitations. First, the retro-
spective assessment was subject to inaccuracies of
memory. Anchor points were used as cues in the
interview to ameliorate this. Data from additional
informants, although difficult to obtain, given the
subjects’ age and duration of their illness, could also
be helpful to override this. Second, the participants
were recruited from a secondary and tertiary treat-
ment centre that has biased the sample towards more
severe cases with longer illness duration. However,
observation of cases with long illness duration enabled
us to describe the longitudinal course of the illness.
Third, the instrument only measured childhood
OCPD traits, which may be more closely linked to the
restricting symptoms in eating disorders (Devlin et al.
2002). A broader spectrum of personality traits should
be assessed to investigate the links between the traits
and bulimic behaviour. Fourth, studies with a larger
sample size would be needed to confirm our findings.
Our study presents a new approach to determine
the eating disorder phenotype. Lifetime diagnostics
may have implications for therapy by focusing on
the lifetime instead of the current symptoms, as well
as for nosology in eating disorders. The observed
relationship of childhood obsessive–compulsive traits
and lifetime symptoms offers a comprehensive pheno-
type assessment for future aetiological studies.
This study was supported by grant QLK-1999-916
from the European Commission Framework V pro-
gramme. We thank Rudolf Uher and Andrej Blejec
for comments on the manuscript and the referee for
Supplementary material accompanies this paper on
the Journal’s website (http://journals.cambridge.org).
Declaration of Interest
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