Is childhood OCD a risk factor for eating disorders
later in life? A longitudinal study
N. Micali*, K. Hilton, E. Natatani, I. Heyman, C. Turner and D. Mataix-Cols
King’s College London, Department of Child and Adolescent Psychiatry, Institute of Psychiatry, London, UK
Background. It has been suggested that childhood obsessive-compulsive disorder (OCD) may be a risk factor for the
development of an eating disorder (ED) later in life, but prospective studies are lacking. We aimed to determine the
prevalence of ED at follow-up and clinical predictors in a longitudinal clinical sample of adolescents/young adults
diagnosed with OCD in childhood.
Method. All contactable (n=231) young people with OCD assessed over 9 years at a national and specialist
paediatric OCD clinic were included in this study. At follow-up, 126 (57%) young people and parents completed the
ED section of the Developmental and Well-being Assessment. Predictors for ED were investigated using logistic
Results. In total, 16 participants (12.7%) had a diagnosis of ED at follow-up. Having an ED was associated with
female gender and persistent OCD at follow-up. There was a trend for family history of ED being predictive of ED
diagnosis. Five (30 %) of those who developed an ED at follow-up had ED symptoms or food-related obsessions/
compulsions at baseline. A diﬀerence in predictors for an ED versus other anxiety disorders at follow-up was
Conclusions. This study provides initial evidence that baseline clinical predictors such as female gender and family
history of ED might be speciﬁc to the later development of ED in the context of childhood OCD. Clinicians should be
alert to ED subthreshold symptoms in young girls presenting with OCD. Future longitudinal studies are needed to
clarify the relationship between childhood OCD and later ED.
Received 25 November 2010 ; Revised 14 April 2011 ; Accepted 20 April 2011 ; First published online 7 June 2011
Key words : Development, eating disorders, follow-up, OCD.
The overlap between obsessive-compulsive disorder
(OCD) and eating disorders (ED) is well studied.
Epidemiological studies have conﬁrmed a positive
association, with an estimated lifetime prevalence of
ED in subjects with OCD of between 11 and 42%
(Rubenstein et al. 1992; Rasmussen & Eisen, 1994;
Sallet et al. 2010). In contrast, the lifetime prevalence of
ED in adults is about 0.6 % for anorexia nervosa (AN),
1% for bulimia nervosa (BN) and 3% for binge eating
disorder (BED) (Jacobi et al. 2004; Hudson et al. 2007).
OCD occurs at rates of 1–4% in community surveys,
whereas estimates of the prevalence of lifetime OCD in
subjects with ED are of the order of 10–40 % for AN
and between 0% and 40% for BN (for reviews, see
Godart et al. 2002; Swinbourne & Touyz, 2007; Altman
& Shankman, 2009). Genetic, neuropsychological and
personality links have been suggested as underlying
these associations (Serpell et al. 2002; Anderluh et al.
2003; Halmi et al. 2005; Silberg & Bulik, 2005).
Recent research has postulated a possible causal
relationship between childhood OCD and ED onset.
Research on clinical samples of individuals with ED
has retrospectively identiﬁed the presence of OCD
before the onset of the ED. The prevalence of retro-
spectively reported OCD with onset prior to the ED
varies between studies, ranging from 33% to 86% of
cases (Speranza et al. 2001; Godart et al. 2002; Kaye
et al. 2004). This wide range is likely to be due to the
fact that most studies relied on clinical and/or con-
venience samples, often small samples, and therefore
probably accounted for by selection bias. Recall bias
might also partly explain the high percentages.
A recent longitudinal study by Buckner et al. (2010)
investigated the relationship between OCD and ED
onset in a sample of adolescents recruited for a study
on adolescent depression. Results revealed that OCD
in adolescence predicted AN in adulthood, in the
* Address for correspondence: Dr N. Micali, Brain and Behaviour
Sciences Unit, UCL Institute of Child Health, 30 Guilford Street,
London WC1N 1EH, UK.
(Email : firstname.lastname@example.org)
Psychological Medicine (2011), 41, 2507–2513. fCambridge University Press 2011
absence of an ED in adolescence. Unfortunately,
although the study included 1709 subjects the preva-
lence of both OCD at baseline and AN at follow-up
was very low in this study (0.5% for each disorder),
with a large odds ratio (OR) and very wide 95 %
conﬁdence intervals (CI). This study did not show a
relationship between OCD at baseline and BN.
The aim of the current study was to build on the
existing literature and investigate the temporal re-
lationship between childhood OCD and later ED from
a longitudinal perspective. In order to overcome some
of the problems encountered by previous studies, such
as recall bias or sample size limitations due to the low
prevalence of both OCD and ED in the general popu-
lation, we followed up a cohort of adolescents/young
adults with OCD onset during childhood or ado-
lescence. We aimed: (1) to determine the prevalence of
ED at follow-up; (2) to investigate possible risk factors
for ED at follow-up in this selective sample.
All young people seen at the National & Specialist
OCD Clinic for Young People at the Maudsley
Hospital, London, UK, between July 1996 and June
2005, who received a diagnosis of OCD at assessment,
were included in the study. This clinic provides
specialist assessment and treatment for young people
with OCD from across the UK (for details, see Micali
et al. 2010). The sample consisted of 276 young people.
After ethical approval was obtained from the South
London and Maudsley (LRECs no. 04/Q0705/7) and
Institute of Psychiatry (no. 117/04) research ethics
committees, the families of all participants were con-
tacted by letter, followed by a telephone call, and
invited to participate. Of the 276 families, 45 (16 %)
were not contactable, despite using multiple tracing
methods. A total of 231 were therefore eligible,
contacted and invited to participate. Of these, 89
(38.5%) declined participation. The methodology for
this follow-up study is detailed in Micali et al. (2010).
Initial clinical assessment was carried out by experi-
enced clinicians specializing in the diagnosis and
management of OCD and DSM-IV criteria were
used to make psychiatric diagnoses. The Children’s
Yale–Brown Obsessive Compulsive Scale (C-YBOCS;
Goodman et al. 1989) was used to measure impact and
severity of the disorder. The Strengths and Diﬃculties
Questionnaire was administered as a general measure
of childhood emotional and behavioural symp-
toms (Goodman et al. 2003). Demographic and other
relevant clinical data were obtained during clinical
assessment and ongoing treatment in the clinic. These
data were collected as part of routine clinical practice
and ongoing clinical audit. All patient records were of
a high standard.
The main outcome variable was presence of ED.
Participants and their parents were asked to complete
the computerized version of the Developmental and
Well-Being Assessment (DAWBA; Goodman et al.
2000) to establish the presence/absence of DSM-IV
ED diagnoses at follow-up. The DAWBA is a well-
validated interview (face-to-face or web-based) for
parents and young people, used across the world,
that generates IDC-10 and DSM-IV diagnoses algor-
ithmically, which are then cross-validated by trained
clinicians after review of the responses. The DAWBA
has been used for young adults as well as adolescents
(Meltzer et al. 2005). We have previously shown that
the ED section of the DAWBA was better at diagnos-
ing ED in young people aged 13–18 years compared
with other instruments considered ‘gold-standard’
(House et al. 2008).
For parents who had diﬃculties using the web-
based DAWBA, a trained researcher facilitated com-
pletion of the assessment over the telephone. All
participants who had fully completed the DAWBA
(either parent or young person version or both)
were included. Anonymized computer ratings were
reviewed by a clinical trained rater (N.M.) to generate
ﬁnal DSM-IV diagnoses.
Group comparisons used parametric (one-way analy-
sis of variance) and non-parametric tests as appro-
priate, after testing for normality. Bivariate linear
regression models tested for predictors of continuous
outcomes. Binary logistic regression models examined
predictors of binary outcomes. Potential covariates
likely to inﬂuence outcomes were ﬁrst tested in bi-
variate models and included in multivariate models
when signiﬁcant. All analyses were performed using
SPSS (version 15) for Windows (SPSS Inc., USA) and
Stata (version 9 for Windows ; StataCorp, USA). All
statistical tests presented are two-tailed. Statistical
signiﬁcance was deﬁned as a pvalue <0.05.
In total, 142 (61.5%) of the young people who were
eligible participated in the follow-up study and 126
(88.7%) DAWBAs were completed. Of these, 17 had
2508 N. Micali et al.
been completed by young people only, 68 by parents
only and 41 by both young people and their parents.
Sociodemographic characteristics and length of
The mean length of follow-up was 5.1 (S.D.=2.7, range
1–11) years. Mean age at follow-up was 18.6 (S.D.=3.5,
range 11–28) years. As detailed in Micali et al. (2010),
the majority of young people who participated in the
follow-up were boys (n=88, 62 %). The mean duration
of OCD at ﬁrst assessment in the clinic was 3.7 (S.D.=
2.8) years and the mean C-YBOCS score at baseline
was 21.6 (S.D.=8.1), indicating moderately severe OCD.
Prevalence of ED at baseline
Two participants had a diagnosis of ED at baseline
(1.4%); one AN and one eating disorder not otherwise
ED at follow-up
Altogether, 16 participants (12.7 %) had a diagnosis of
ED at follow-up [13 females (81%) and three males
(19%)]. Two had a diagnosis of AN (1.6%), one of BN
(0.8%), ﬁve of EDNOS-AN (3.5%), seven of EDNOS
(4.9%) and one of BED (0.8%). One participant had
symptoms of ED that did not amount to a full or par-
tial diagnosis (See Table 1).
Altogether, 13 of the 16 participants (81%) who had
an ED at follow-up were female. Of note, one of the
participants who had an ED at baseline did not have
an ED at follow-up.
OCD and ED symptoms at baseline
We were particularly interested in determining
whether participants who had a diagnosis of ED at
follow-up had any ED-related symptoms at baseline.
As highlighted in Table 1, three (18.7 %) of the 16 who
had an ED at follow-up had some ED symptoms at
Moreover, two (6.2%) developed ED in the year
following the OCD assessment, i.e. during treatment
In relation to food-related obsessions and compul-
sions, only two participants had these at baseline
(6.2%) in the absence of any baseline ED psychopath-
ology. In relation to age, there was no diﬀerence be-
tween groups in terms of age at baseline, duration of
follow-up and age of onset of OCD.
Predictors for a diagnosis of ED at follow-up
Age at follow-up did not diﬀer amongst participants
who developed an ED and those who did not (see
We were particularly interested in identifying
possible predictors amongst baseline and demographic
characteristics that might predict an ED diagnosis at
follow-up. The strongest predictor of ED at follow-up
was female gender (OR 9.2, 95 % CI 2.5–34.7, p<0.05).
A family history of ED was more common in partici-
pants who had an ED at follow-up compared with
those who did not (12.5% v. 3.6%); there was a trend
towards statistical signiﬁcance. Age of onset of OCD,
duration of OCD, C-YBOCS total score and subscores
at baseline did not predict ED diagnosis at follow-up
and nor did the ritualized eating item of the C-YBOCS
at baseline. We also investigated whether speciﬁc
obsessions (symmetry, aggressive and hoarding/
saving obsessions) and compulsions (symmetry and
aggressive) predicted the onset of an ED (data not
shown). Persistent OCD (i.e. having a diagnosis of
OCD at follow-up, as detailed in Micali et al. 2010) was
associated with a diagnosis of ED at follow-up (OR 1.9,
95% CI 1.1–3.4, p<0.05) (see Table 2).
Speciﬁcity of predictors for ED at follow-up
In order to explore whether factors identiﬁed as
predictors of ED at follow-up were speciﬁc for ED,
we also compared participants who developed any
anxiety disorder (AD) other than OCD at follow-up
(n=49) with participants who did not develop any AD
other than OCD at follow-up (n=77). Young adults
who developed an AD at follow-up had statistically
signiﬁcant scores on the baseline total CYBOCS scale
(OR 1.1, 95% CI 1.01–1.2, p<0.05) and marginally on
the C-YBOCS obsessions subscale (OR 1.1, 95 % CI 1.0–
1.2, p=0.05) compared with participants who did not
develop an AD. There was a trend for gender diﬀer-
ences (OR 2.1, 95 % CI 1.0–4.4, p=0.05). Age of onset,
duration of OCD, ritualized eating on the baseline
C-YBOCS and family predictors were all comparable.
Persistent OCD was associated with the presence of an
AD at follow-up (OR 1.6, 95 % CI 1.1–2.3, p=0.01).
This study conﬁrms the existing studies on the
relationship between childhood onset OCD and the
development of ED and adds new evidence to these
(Kaye et al. 2004; Buckner et al. 2010; Sallet et al. 2010).
This is the ﬁrst study to show that amongst children
and adolescents with OCD (n=126), followed up after
about 5 years, 13 % (n=16) had a diagnosis of ED at
follow-up. Although one had an ED and three had
some ED symptoms at baseline, the majority had
developed an ED during the follow-up period for
the ﬁrst time since their initial presentation with
OCD. Very few had eating-related obsessions or
compulsions. Female gender was a strong predictor,
OCD and onset of ED 2509
Table 1. Characteristics of participants with an eating disorder (ED)diagnosis at follow-up
height ED symptoms
Food related obsessions
1 F 10 OCD 92.4 Some worries about weight No No No EDNOS-AN
Restricting food intake at times
2 F 14 OCD 127.5 No No No No EDNOS
3 F 17 OCD 104.6 No No No Yes AN
4 F 14 OCD 104.6 Restricting food intake during the day
and eating a large meal in the evening
No No Yes AN
Speciﬁc eating disorder
5 F 10 OCD 99.3 No No No Yes BN
6 F 10 OCD – No No No No EDNOS
7 F 12 OCD 98.0 No Restricting food intake to
avoid needing to use the toilet ;
No No EDNOS-AN
Contamination fears : checking
food and avoiding eating near bins
8 F 15 OCD – AN No No No EDNOS-AN
9 M 11 OCD 131.1 No No No No EDNOS
10 F 11 OCD 115.3 No No No No EDNOS-AN
11 M 14 OCD – No No No No EDNOS-AN
12 F 10 OCD – No No Yes No EDNOS
13 F 16 OCD – No No No No EDNOS
Mild learning disability
14 F 13 OCD 185.1 Binge-eating when unhappy No No No EDNOS
15 M 17 OCD – No Food has to be perfect : the right
taste and temperature
Yes No BED
Eating limited range of foods
16 F 10 OCD 99.5 No No No No EDNOS-AN
17 M 11 OCD 108.6 No No No No Subthreshold
F, Female ; M, male; OCD, obsessive-compulsive disorder; EDNOS, eating disorder not otherwise speciﬁed ; AN, anorexia nervosa ; BN, bulimia nervosa ; IDDM, insulin-dependent
diabetes mellitus ; BED, binge eating disorder.
2510 N. Micali et al.
consistent with the epidemiology of ED. It was found
that 12% of participants who developed an ED had a
family history of ED v. 3.6 % of participants who did
not develop an ED. Although numbers in each group
were small, this trend suggests that a family history of
ED might partly explain a higher risk for the devel-
opment of ED. A diagnosis of ED at baseline was as-
sociated with an almost doubled risk for persistent
The relationship between childhood onset OCD and
later ED has been suggested previously in the litera-
ture. Due to the biases in the existing literature
(i.e. investigating this relationship retrospectively or in
samples that had originally been collected for other
purposes) (Micali and Heyman, 2006), we speciﬁcally
designed this study to determine whether a temporal
relationship could be established between childhood
onset OCD and a later ED. More research is needed to
understand the mechanisms of this relationship. The
diﬃculty in researching this topic in general popu-
lation longitudinal studies lies in the large numbers
needed due to the relatively low prevalence of both
OCD and ED. Only one study to date has investigated
this in a prospective sample of adolescents (Buckner
et al. 2010), conﬁrming a temporal link between OCD
in adolescence and adult AN. Our study conﬁrms this
ﬁnding, with a slight preponderance at follow-up of
full and partial syndrome AN (eight participants)
compared with other ED. One subject had developed
BN and one BED, although the prevalence of both
disorders was not higher in this sample compared
with ﬁndings in the general population, it is of note
that participants also developed ED other than AN at
We were also interested in testing the hypothesis
that speciﬁc obsessions and/or compulsions (in par-
ticular eating-related obsessions/compulsions) might
explain the development of later ED by priming
children and adolescents to have a ritualized eating
pattern. Moreover, some authors have identiﬁed
an association between contamination obsessions and
cleaning rituals and ED (Hasler et al. 2005) ; whereas
others highlighted a high co-morbidity of aggressive
and symmetry obsessions/compulsions in ED (Halmi
et al. 2003). We did not ﬁnd any relationship between
speciﬁc obsessions/compulsions in childhood and
later ED. This might be explained by low numbers in
our study and the lack of power in rejecting the null
We further sought to identify possible predictors
that might allow early intervention and/or prevention
of ED. Gender certainly plays a prime role in the risk
for ED and female gender is a well-known and ﬁxed
risk factor for ED (Jacobi et al. 2004). However, it
Table 2. Predictors for eating disorders (ED)at follow-up : odds ratios (OR)and 95 %conﬁdence intervals (CI)
Predictors ED at follow-up (n=16) No ED at follow-up (n=116) OR (95% CI)
Gender (female), n(%) 13 (81 %) 48 (38%) 9.2* (2.5–34.7)
Child variables at baseline
Age of onset of OCD, Mean (S.D.) 8.7 (2.6) 9.9 (2.9) 0.9 (0.7–1.1)
Duration of illness, Mean (S.D.) 4 (3.8) 3.6 (2.7) 1.0 (0.9–1.2)
C-YBOCS total baseline 23.2 (5.4) 20.9 (8.1) 1.0 (1.0–1.1)
CYBOCS Obsessions 11.1 (3.5) 9.6 (4.9) 1.1 (0.9–1.2)
C-YBOCS Compulsions 12.1 (2.5) 11.2 (4.1) 1.1 (0.9–1.2)
C-YBOCS ritualized eating 5 (33.5 %) 24/93 (25.8 %) 1.4 (0.4–4.6)
Other co-morbid Axis I disorders, n( %) 8 (50 %) 48 (43.6 %) 1.2 (0.4–3.7)
ED at baseline 1 (6.2%) 1 (0.8%) –
Child variables at follow-up
<15 1 (6.3 %) 11 (10 %) 0.4 (0.1–3.7)
15–20 11 (68.8%) 53 (48.2%) Ref.
>20 4 (25 %) 41 (37.3%) 0.5 (0.1–1.6)
Missing 0 5 (4.5 %) 1.9** (1.1–3.4)
Persistent OCD, n( %) 11 (68.7 %) 41 (37.3%) 5.9* (1.8–19.6)
Any other anxiety disorder, n( %) 12 (75.0%) 37 (33.6%)
Family history of ED, n( %) 2 (12.5%) 4 (3.6 %) 3.8#(0.6–22.6)
Family history of OCD, n( %) 1 (6.2 %) 15 (94 %) 0.9 (0.1–7.6)
OCD, Obsessive-compulsive disorder ; C-YBOCS, Children’s Yale–Brown Obsessive Compulsive Scale.
*p<0.01, ** p<0.05, #p=0.1.
Results are risk ratios from multinomial logistic regression.
OCD and onset of ED 2511
remains to be understood whether gender is an
additional risk factor or whether it moderates the
relationship between OCD and later ED.
Of the 15 participants with an ED at follow-up who
did not have baseline ED, ﬁve (30 %) had either dis-
ordered eating (i.e. some behaviours characteristic of
ED) or food-related obsessions and compulsions.
This ﬁnding suggests that these symptoms might be
relevant in identifying a child/adolescent at increased
risk for ED and who is potentially a target for pre-
vention or early intervention for ED.
Despite small numbers, there was a slight increase
in the percentage of a family history of ED in partici-
pants who had an ED at follow-up. The exact re-
lationship between family ED history and childhood
onset OCD in increasing the risk for ED needs further
elucidation and is beyond the scope of this study.
However, family ED history might also be used to
identify young people who present with OCD who
might beneﬁt from targeted prevention/early inter-
We attempted to address the speciﬁcity of pre-
dictors for ED at follow-up in an exploratory fashion
by investigating diﬀerences between participants
who developed an AD at follow-up and those who did
not. Predictors for AD at follow-up seemed to diﬀer
compared with those identiﬁed for ED : in particular,
gender was a very marginal predictor for AD.
C-YBOCS score at baseline was a stronger predictor.
Family history of ED and gender showed a stronger
association with ED. These are known risk factors for
ED; therefore, it remains to be established whether
childhood OCD is a mediator of eﬀect or acts in an
additive fashion to other known risk factors. These
ﬁndings require conﬁrmation and extension in larger
This study has several strengths. First, it is the ﬁrst
study to follow up young adults with childhood onset
OCD in order to establish the temporal relationship
between the latter and ED. Second, it is the largest
follow-up to date of children and adolescents with
OCD, using a sample with diﬀerent levels of severity.
It is important to note relevant limitations, in par-
ticular the relatively small number of participants who
had an ED at follow-up, which might have aﬀected the
power to determine relevant associations. Although
attrition did not relate to sociodemographic variables
or illness (OCD) characteristics (see Micali et al. 2010),
we cannot exclude the possibility of selection bias.
A total of 10 participants were <15 years amongst
those who did not develop an ED at follow-up ; there-
fore, below the peak age of onset for ED. However,
this would lead to an underestimation of the risk for
developing an ED after OCD rather than an over-
In summary, our study conﬁrms previous reports
of childhood onset OCD increasing the risk for later
onset ED. Further elucidation of the mechanisms and
possible mediators is needed. The preliminary evi-
dence that, in the context of a child/adolescent pres-
enting to services with OCD, girls, those with a family
history of ED and children presenting with disordered
eating or food-related obsessions and compulsions
might be at particular risk for developing a later ED
is of relevance to clinicians in the ﬁeld. The role of
prevention/early intervention for this subcategory of
children might need evaluating.
We thank all participants and their families for taking
part in the study and Professor R. Goodman for pro-
viding advice. Thanks to Christine Tang and Hala Ali
for help in carrying out the study. This study was
funded by the R&D Fund, South London & Maudsley
NHS Foundation Trust. Dr Nadia Micali is supported
by an NIHR Clinician Scientist Award.
Declaration of Interest
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