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Is childhood OCD a risk factor for eating disorders later in life? A longitudinal study

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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 regression. 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 identified. 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.
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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
regression.
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
identified.
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.
Introduction
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 : nadia.micali@kcl.ac.uk)
Psychological Medicine (2011), 41, 2507–2513. fCambridge University Press 2011
doi:10.1017/S003329171100078X
ORIGINAL ARTICLE
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.
Method
Participants
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).
Baseline data
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.
Follow-up data
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.
Data analyses
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.
Results
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
follow-up
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
specified (EDNOS).
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
baseline.
Moreover, two (6.2%) developed ED in the year
following the OCD assessment, i.e. during treatment
for OCD.
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
Table 2).
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).
Discussion
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
ID Gender
Baseline data
Age
(yr) Diagnosis
Weight
for
height ED symptoms
Food related obsessions
and compulsions
Family
history
of ED
Developed ED
whilst receiving
OCD treatment
Diagnosis
at follow-up
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
Epilepsy
Cerebral palsy
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
AN
9 M 11 OCD 131.1 No No No No EDNOS
Tourette’s syndrome
ODD
IDDM
10 F 11 OCD 115.3 No No No No EDNOS-AN
11 M 14 OCD No No No No EDNOS-AN
Tourette’s syndrome
12 F 10 OCD No No Yes No EDNOS
13 F 16 OCD No No No No EDNOS
Mild learning disability
Epilepsy
Hydrocephalus
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
OCD.
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
follow-up.
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
hypothesis.
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
Age
a
(years)
<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 variables
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.
a
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-
vention.
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
studies.
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-
estimation.
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.
Acknowledgements
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
None.
References
Altman SE, Shankman SA (2009). What is the association
between obsessive-compulsive disorder and eating
disorders ? Clinical Psychology Review 29, 638–646.
Anderluh MB, Tchanturia K, Rabe-Hesketh S, Treasure J
(2003). Childhood obsessive-compulsive personality traits
in adult women with eating disorders : defining a broader
eating disorder phenotype. American Journal of Psychiatry
160, 242–247.
Buckner JD, Silgado J, Lewinsohn PM (2010). Delineation of
differential temporal relations between specific eating and
anxiety disorders. Journal of Psychiatric Research 44, 781–787.
Godart NT, Flament MF, Perdereau F, Jeammet P (2002).
Comorbidity between eating disorders and anxiety
disorders : a review. International Journal of Eating Disorders
32, 253–270.
Goodman R, Ford T, Richards H, Gatward R, Meltzer H
(2000). The Development and Well-Being Assessment :
description and initial validation of an integrated
assessment of child and adolescent psychopathology.
Journal of Child Psychology and Psychiatry 41, 645–655.
Goodman R, Ford T, Simmons H, Gatward R, Meltzer H
(2003). Using the Strengths and Difficulties Questionnaire
(SDQ) to screen for child psychiatric disorders in a
community sample. International Review of Psychiatry 15,
166–172.
Goodman WK, Price LH, Rasmussen SA, Mazure C,
Delgado P, Heninger GR, Charney DS (1989). The
Yale–Brown Obsessive Compulsive Scale, II. Archives of
General Psychiatry 46, 1011–1016.
2512 N. Micali et al.
Halmi KA, Sunday SR, Klump KL, Strober M, Leckman JF,
Fichter M, Kaplan A, Woodside B, Treasure J, Berrettini
WH, Al Shabboat M, Bulik CM, Kaye WH (2003).
Obsessions and compulsions in anorexia nervosa subtypes.
International Journal of Eating Disorders 33, 308–319.
Halmi KA, Tozzi F, Thornton LM, Crow S, Fichter MM,
Kaplan AS, Keel P, Klump KL, Lilenfeld LR, Mitchell JE,
Plotnicov KH, Pollice C, Rotondo A, Strober M,
Woodside DB, Berrettini WH, Kaye WH, Bulik CM
(2005). The relation among perfectionism, obsessive-
compulsive personality disorder and obsessive-
compulsive disorder in individuals with eating disorders.
International Journal of Eating Disorders 38, 371–374.
Hasler G, Lasalle-Ricci VH, Ronquillo JG, Crawley SA,
Cochran LW, Kazuba D, Greenberg BD, Murphy DL
(2005). Obsessive-compulsive disorder symptom
dimensions show specific relationships to psychiatric
comorbidity. Psychiatry Research 135, 121–132.
House J, Eisler I, Simic M, Micali N (2008). Diagnosing
eating disorders in adolescents : a comparison of the
eating disorder examination and the development and
well-being assessment. International Journal of Eating
Disorders 41, 535–541.
Jacobi C, Hayward C, de Zwaan M, Kraemer HC, Agras WS
(2004). Coming to terms with risk factors for eating
disorders : application of risk terminology and suggestions
for a general taxonomy. Psychological Bulletin 130, 19–65.
Kaye WH, Bulik CM, Thornton L, Barbarich N, Masters K
(2004). Comorbidity of anxiety disorders with anorexia
and bulimia nervosa. American Journal of Psychiatry 161,
2215–2221.
Micali N, Heyman I (2006). Comorbidity of anxiety with
eating disorders and OCD. American Journal of Psychiatry
163, 326–327, author reply 327–329.
Micali N, Heyman I, Perez M, Hilton K, Nakatani E,
Turner C, Mataix-Cols D (2010). Long-term outcomes
of obsessive–compulsive disorder : follow-up of 142
children and adolescents. The British Journal of Psychiatry
197, 128–134.
Meltzer H, Gatward R, Corbin T, Goodman R, Ford T
(2005). Persistence, Onset, Risk Factors and Outcomes of
Childhood Mental Disorders. HMSO : London.
Hudson JI, Hiripi E, Pope Jr. HG, Kessler RC (2007).
The prevalence and correlates of eating disorders in the
National Comorbidity Survey Replication. Biological
Psychiatry 61, 348–358.
Rasmussen SA, Eisen JL (1994). The epidemiology and
differential diagnosis of obsessive compulsive disorder.
Journal of Clinical Psychiatry 55 Suppl., 5–10 ; discussion
11–14.
Rubenstein CS, Pigott TA, L’heureux F, Hill JL, Murphy DL
(1992). A preliminary investigation of the lifetime
prevalence of anorexia and bulimia nervosa in patients
with obsessive compulsive disorder. Journal of Clinical
Psychiatry 53, 309–314.
Sallet PC, de Alvarenga PG, Ferrao Y, de Mathis MA,
Torres AR, Marques A, Hounie AG, Fossaluza V,
do Rosario MC, Fontenelle LF, Petribu K,
Fleitlich-Bilyk B (2010). Eating disorders in patients
with obsessive-compulsive disorder : prevalence and
clinical correlates. International Journal of Eating Disorders
43, 315–325.
Serpell L, Livingstone A, Neiderman M, Lask B (2002).
Anorexia nervosa : obsessive-compulsive disorder,
obsessive-compulsive personality disorder, or neither ?
Clinical Psychology Review 22, 647–669.
Silberg JL, Bulik CM (2005). The developmental
association between eating disorders symptoms
and symptoms of depression and anxiety in juvenile
twin girls. Journal of Child Psychology and Psychiatry 46,
1317–1326.
Speranza M, Corcos M, Godart N, Loas G, Guilbaud O,
Jeammet P, Flament M (2001). Obsessive
compulsive disorders in eating disorders. Eating
Behaviour 2, 193–207.
Swinbourne JM, Touyz SW (2007). The co-morbidity of
eating disorders and anxiety disorders : a review.
European Eating Disorders Review 15, 253–274.
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... Prevalence rates of OCD in AN are considerably higher than rates in other ED diagnoses (Swinbourne et al., 2012;Mandelli et al., 2020), suggesting more similar mechanisms are at play in AN and OCD. OCD is considered a risk factor for AN (Bulik et al., 1997;Thornton and Russell, 1997;Buckner et al., 2010;Micali et al., 2011), and co-occurrence of these conditions is linked to poorer outcomes, such as an earlier age of ED onset, longer ED duration, and greater ED severity (Milos et al., 2002;Cumella et al., 2007). ...
Article
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Anorexia nervosa (AN) and obsessive–compulsive disorder (OCD) are commonly reported to co-occur and present with overlapping symptomatology. Executive functioning difficulties have been implicated in both mental health conditions. However, studies directly comparing these functions in AN and OCD are extremely limited. This review provides a synthesis of behavioral and neuroimaging research examining executive functioning in AN and OCD to bridge this gap in knowledge. We outline the similarities and differences in behavioral and neuroimaging findings between AN and OCD, focusing on set shifting, working memory, response inhibition, and response monitoring. This review aims to facilitate understanding of transdiagnostic correlates of executive functioning and highlights important considerations for future research. We also discuss the importance of examining both behavioral and neural markers when studying transdiagnostic correlates of executive functions.
... An improved understanding of the overlap among eating disorders, OCD, and intermediate phenotypes such as anxiety symptoms could aid in conceptualizing mechanisms and processes contributing to the clinical and genetic overlap among these disorders. Additionally, symptom dimensions may transmute over development, shifting from childhood obsessivecompulsive symptoms to adolescent eating disorders (Anderluh, Tchanturia, Rabe-Hesketh, & Treasure, 2003;Micali et al., 2011) and vice versa. Thus, shared and unique risk factors may contribute to the symptoms of OCD and eating disorders across development. ...
Article
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Background Clinical, epidemiological, and genetic findings support an overlap between eating disorders, obsessive-compulsive disorder (OCD), and anxiety symptoms. However, little research has examined the role of genetics in the expression of underlying phenotypes. We investigated whether the anorexia nervosa (AN), OCD, or AN/OCD transdiagnostic polygenic scores (PGS) predict eating disorder, OCD, and anxiety symptoms in a large developmental cohort in a sex-specific manner. Methods Using summary statistics from Psychiatric Genomics Consortium AN and OCD genome-wide association studies, we conducted an AN/OCD transdiagnostic genome-wide association meta-analysis. We then calculated AN, OCD, and AN/OCD PGS in participants from the Avon Longitudinal Study of Parents and Children to predict eating disorder, OCD, and anxiety symptoms, stratified by sex (combined N = 3212–5369 per phenotype). Results The PGS prediction of eating disorder, OCD, and anxiety phenotypes differed between sexes, although effect sizes were small. AN and AN/OCD PGS played a more prominent role in predicting eating disorder and anxiety risk than OCD PGS, especially in girls. AN/OCD PGS provided a small boost over AN PGS in the prediction of some anxiety symptoms. All three PGS predicted higher compulsive exercise across different developmental timepoints [ β = 0.03 ( s.e. = 0.01) for AN and AN/OCD PGS at age 14; β = 0.05 ( s.e. = 0.02) for OCD PGS at age 16] in girls. Conclusions Compulsive exercise may have a transdiagnostic genetic etiology, and AN genetic risk may play a role in the presence of anxiety symptoms. Converging with prior twin literature, our results also suggest that some of the contribution of genetic risk may be sex-specific.
... Notably, many of the studies that have tested the bidirectional relationship between OCD and EDs used designs that retrospectively examined the longitudinal sequence of when the disorders were diagnosed (e.g., Buckner et al., 2010;Micali et al., 2011;Thornton & Russell, 1997). However, this does not provide insight into which symptoms may have increased risk for the development of future symptoms. ...
Article
Background Despite the severity and high rate of co-occurrence between eating disorders (ED) and obsessive-compulsive disorder (OCD), less is known regarding the longitudinal sequencing of their comorbidity and whether and how their symptoms may influence one another over time. The current study sought to answer these questions by testing if a bidirectional, longitudinal relationship exists between ED symptoms and OCD obsessions and compulsions. Methods We examined the relationship between ED symptoms, obsessions and compulsions across five time points, each one week apart using auto-regressive cross-lagged panel modeling. The final sample consisted of 358 individuals from the community with moderate levels of ED and OCD symptoms, the majority of whom identified as White and male. Results Bivariate correlations revealed that ED symptoms, obsessions and compulsions were associated with one another across the five weeks. Two cross-lagged panel models indicated that ED symptoms predicted OCD symptoms at numerous time points and vice versa. However, we found this significant longitudinal associations across only certain weeks. Notably, the models found that only ED symptoms and OCD obsessions predicted one another across different time points across the five weeks; ED symptoms and OCD compulsions did not predict one another. Limitations. Due to the non-clinical nature of the sample, there is limited generalizability to clinical populations. Conclusions Our results provide preliminary evidence that there is a bidirectional, longitudinal relationship between ED symptoms and OCD symptoms among a community sample, particularly with respect to cognitive as opposed to behavioral symptoms.
... Given that childhood OC symptoms and traits have been implicated in later risk for AN (Anderluh, Tchanturia, Rabe-Hesketh, & Treasure, 2003;Micali et al., 2011) and recent work found OCD polygenic risk scores to predict ME in an epidemiological sample of adolescents , longitudinal associations between OC features and ME warrant further inquiry. ...
Article
Objective: Although maladaptive exercise (ME) is widely recognized as a clinical feature in transdiagnostic eating disorders, less is known about psychosocial factors that give rise to and perpetuate this behavior. This systematic review aimed to examine the empirical status of this association. Method: We reviewed 46 full text articles examining longitudinal associations between psychosocial variables and ME. Results: Eighteen studies met full inclusion criteria. Based on our qualitative synthesis, evidence suggests reasonably consistent associations between early concern with weight and shape, and negative affect on later development of ME. Discussion: Inconsistent and insufficient assessment of ME across a majority of studies underscores caution in interpretation of results, but guides important discussion for future clinical and research efforts.
... Similarly, the prevalence of OCD is higher in AN patients than in the population [5]. The prevalence of AN is also higher in OCD patients [6], which indicates significant co-morbidity between the two diseases. In accordance with the epidemiological associations, clinical studies revealed that AN and OCD have highly similar phenotypes, such as perfectionism, rigidity, persistency, obsessive thoughts [7], excessive [8], and ritual behaviors [9]. ...
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Anorexia nervosa (AN) and obsessive–compulsive disorder (OCD) exhibit a high co-morbidity rate, similar symptoms, and a shared genetic basis. However, an understanding of the specific underlying mechanisms of these commonalities is currently limited. Here, we collected Genome-Wide Association Analysis results for AN and OCD, and obtained genes hit by the top SNPs as the risk genes. We then carried out an integrative coexpression network analysis to explore the convergence and divergence of AN and OCD risk genes. At first, we observed that the AN risk genes were enriched in coexpression modules that involved extracellular matrix functions and highly are expressed in the postnatal brain, limbic system, and non-neuronal cell types, while the OCD risk genes were enriched in modules of synapse function, the prenatal brain, cortex layers, and neurons. Next, by comparing the expressions from the eating disorder and OCD postmortem patient brain tissues, we observed both disorders have similar prefrontal cortex expression alterations influencing the synapse transmission, suggesting that the two diseases could have similar functional pathways. We found that the AN and OCD risk genes had distinct functional and spatiotemporal enrichment patterns but carried similar expression alterations as a disease mechanism, which may be one of the key reasons they had similar but not identical clinical phenotypes.
... A 2004 study found that about two-thirds of 672 individuals with AN, BN, or both had one or more lifetime anxiety disorders [25]. Moreover, anxiety disorders, especially obsessive-compulsive disorder (OCD) in childhood, could be a risk factor for EDs later in life [26]. Although the etiology of anxiety has traditionally been focused on genetic factors, evidences indicate that the gut microbiota and its metabolites are closely linked to the host's central nervous system though a bidirectional communication. ...
Article
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Anxiety and eating disorders produce a physiological imbalance that triggers alterations in the abundance and composition of gut microbiota. Moreover, the gut–brain axis can be altered by several factors such as diet, lifestyle, infections, and antibiotic treatment. Diet alterations generate gut dysbiosis, which affects immune system responses, inflammation mechanisms, the intestinal permeability, as well as the production of short chain fatty acids and neurotransmitters by gut microbiota, which are essential to the correct function of neurological processes. Recent studies indicated that patients with generalized anxiety or eating disorders (anorexia nervosa, bulimia nervosa, and binge-eating disorders) show a specific profile of gut microbiota, and this imbalance can be partially restored after a single or multi-strain probiotic supplementation. Following the PRISMA methodology, the current review addresses the main microbial signatures observed in patients with generalized anxiety and/or eating disorders as well as the importance of probiotics as a preventive or a therapeutic tool in these pathologies.
... For instance, intense fear of weight gain with consequent food restriction is a defining feature of anorexia nervosa (AN) and is present in other ED diagnoses. Further, up to two-thirds of individuals with EDs report a lifetime AD (Bulik, Sullivan, Fear, & Joyce, 1997;Kaye, Bulik, Thornton, Barbarich, & Masters, 2004), and ADs and EDs demonstrate prospective relationships with one another (Buckner, Silgado, & Lewinsohn, 2010;Micali et al., 2011;Micali et al., 2015;Schaumberg et al., 2018). Studies with genetically-informed designs also confirm shared transmission of ED and anxiety risk (Keel, Klump, Miller, McGue, & Iacono, 2005;Silberg & Bulik, 2005). ...
Article
Eating disorders (EDs) and anxiety disorders (ADs) evidence shared risk and significant comorbidity. Recent advances in understanding of anxiety-based disorders may have direct application to research and treatment efforts for EDs. The current review presents an up-to-date, behavioral conceptualization of the overlap between anxiety-based disorders and EDs. We identify ways in which anxiety presents in EDs, consider differences between EDs and ADs relevant to treatment adaptions, discuss how exposure-based strategies may be adapted for use in ED treatment, and outline directions for future mechanistic, translational, and clinical ED research from this perspective. Important research directions include: simultaneous examination of the extent to which EDs are characterized by aberrant avoidance-, reward-, and/or habit-based neurobiological and behavioral processes; improvement in understanding of how nutritional status interacts with neurobiological characteristics of EDs; incorporation of a growing knowledge of biobehavioral signatures in ED treatment planning; development of more comprehensive exposure-based treatment approaches for EDs; testing whether certain exposure interventions for AD are appropriate for EDs; and improvement in clinician self-efficacy and ability to use exposure therapy for EDs.
... Roughly 70% of patients that receive CBT respond to the treatment, defined as a significant decrease of symptoms, and about half of patients remit, i.e., no longer fulfill diagnostic criteria for OCD 4 . Long-term follow-ups of CBT show that these beneficial outcomes are maintained up to three years after treatment 6,7 . However, CBT is not available to all patients, and to overcome existing treatment barriers of e.g., shortage of trained therapists, limited resources and geographical distances, internet-delivered CBT (ICBT) has been developed. ...
Article
Full-text available
Cognitive behavior therapy (CBT) is the recommended first-line intervention for children and adolescents with obsessive-compulsive disorder (OCD), but is not broadly accessible. Internet-delivered CBT (ICBT) with minimal therapist support is efficacious and cost-effective, at least in the short term. Whether the therapeutic gains of ICBT for OCD are sustained in the long run is unknown. In this study, 61 adolescents with OCD who participated in a randomized trial of ICBT were followed-up 3 and 12 months after treatment. The proportion of treatment responders and remitters remained stable from post-treatment to 3-month follow-up and increased significantly from 3-month to 12-month follow-up. This study suggests that the gains of ICBT for youth with OCD are not only maintained long-term, but that further improvements continue to occur during follow-up.
... BN is characterized by high rates of comorbidity and shared genetic liability with other disorders and symptoms (Munn-Chernoff et al., 2015;Munn-Chernoff & Baker, 2016;Yilmaz, Hardaway, & Bulik, 2015). BN is specifically associated with substance use (Kasset, Gershon, Maxwell, & Guroff, 1989;Kaye et al., 1996;Micali et al., 2015;Munn-Chernoff et al., 2013;Munn-Chernoff et al., 2015) and obsessive-compulsive disorders (Buckner, Silgado, & Lewinsohn, 2010;Godart, Flament, Perdereau, & Jeammet, 2002;Hofer et al., 2018;Kaye et al., 2004;Micali et al., 2011). While this comorbidity arises in part from latent liability, new research also indicates that specific symptoms may have differential roles in maintaining and advancing illness. ...
Article
While facets of both anxiety and impulsivity appear central to the development and maintenance of bulimia nervosa (BN), specific BN behaviors may be propagated by differing profiles of risk. The current study examined associations between dimensions of anxiety and impulsivity and BN symptoms (binge eating, vomiting, laxative misuse, driven exercise), both in terms of the presence of such behaviors and their frequency. Two hundred and four women (Mage = 25.7 years) who met DSM-IV criteria for full or subthreshold BN completed self-report measures of perfectionism (Frost Multidimensional Perfectionism Scale), anxiety (Spielberger Trait Anxiety Inventory), impulsivity (Barratt Impulsiveness Scale–11; Impulsive Behavior Scale), eating disordered behaviors (Eating Disorder Examination – Questionnaire), and associated psychiatric symptoms (Michigan Assessment Screening Test/Alcohol-Drug; Maudsley Obsessive-Compulsive Inventory). Factor analysis revealed multidimensional impulsive and anxiety-related traits (5 anxiety-related factors; 7 impulsivity-related factors). In zero-sensitive regression models, different facets of impulsivity evidenced association with the presence of binge eating (risk taking), laxative misuse (impulsive spending), and fasting (difficulty concentrating), along with the frequency of vomiting (long-term planning difficulties). In contrast, anxiety-related dimensions were only associated with driven exercise (high standards) and fasting (concern over mistakes, high standards, parental expectations). Overall, impulsive and anxiety-related factors and symptoms showed distinct associations with specific eating disorder behaviors, even among those with the same diagnosis.
Thesis
Dès la première description du Trouble du Spectre de l'Autisme, Kanner (1943) a souligné la présence momentanée de manifestations dépressives chez un des cas. Aujourd'hui, l'Episode Dépressif Caractérisé (EDC) est considéré comme étant un des troubles psychiatriques les plus fréquemment associés au TSA, ayant des répercussions à court, moyen et long termes sur l'enfant ayant un TSA et sa famille. Pourtant, aujourd'hui, il n'existe pas de consensus concernant la façon d'évaluer la symptomatologie dépressive chez les enfants et les adolescents ayant un TSA. Les objectifs de cette recherche sont de créer et de valider une échelle de repérage des signes de l'EDC, d'identifier les facteurs associés aux signes de l'EDC chez les enfants et les adolescents ayant un TSA et d'étudier les manifestations dépressives dans leur fonctionnement habituel. Quatre études ont été réalisées. La première a permis de créer l'échelle de repérage des signes de l'EDC spécifique aux enfants et aux adolescents ayant un TSA. Elle est composée de 3 parties : une évaluation des douleurs et des médicaments pris par l'enfant, le listing des changements environnementaux et l'évaluation de la symptomatologie dépressive ; en deux étapes : une description du fonctionnement habituel de l'enfant puis une mesure de l'ampleur des changements de comportements. La seconde étude visait à valider cette échelle (N=153). La fidélité inter-juges est très satisfaisante mais devra être évaluée sur un échantillon plus important (ρfiabilité=0,98 ; ρfiabilité=0,02). L'échelle a de bonnes validités apparente, de contenu et de critère et une excellente consistance interne (αéchelleEDC=0,91). Elle est composée de deux facteurs : un de changements comportementaux et l'autre de changements émotionnels et cognitifs. La troisième étude visait à identifier les facteurs associés à l'EDC chez les enfants et les adolescents ayant un TSA (N=58). Des facteurs individuels, notamment liés au parcours de soin concernant le diagnostic de TSA mais aussi la santé somatique ; familiaux, notamment le vécu parental et le désir d'avoir des amis sont liés à la symptomatologie dépressive. La quatrième étude avait pour objectif d'identifier des manifestations dépressives dans le fonctionnement habituel des enfants et des adolescents ayant un TSA (N=133). Plus d'un tiers de l'échantillon exprime de la tristesse quasiment tous les jours et plus d'un quart n'exprime quasiment jamais de joie. Plus de la moitié des enfants et des adolescents de l'échantillon ne prend aucun plaisir au quotidien. Un jeune sur cinq a des comportements auto-agressifs et 28% ont des comportements hétéro-agressifs tous les jours. La moitié de l'échantillon a des difficultés de sommeil et 58% en a d'appétit tous les jours. Enfin, trois quarts des jeunes expriment de la culpabilité ou de la dévalorisation tous les jours.
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Objective: The aim of this study is to explore current and lifetime prevalence of obsessive compulsive disorders (OCD) in eating disorder (ED) subgroups and subtypes defined by the DSM-IV and to study the chronology of appearance of these disorders taking into account the role played by denutrition. Method: Current and lifetime prevalence were investigated using the Mini International Neuropsychiatric Interview (MINI) and the Yale-Brown Obsessive Compulsive Scale in a sample of 89 DSM-IV ED patients (58 AN and 31 BN) and 89 matched controls. Results: Current and lifetime prevalence of OCD in ED was significantly higher than in general population (15.7% and 19% vs. 0% and 1.1%, P<.05). Anorexic patients presented a slightly higher current and lifetime comorbidity than bulimic patients (19% and 22.4% vs. 9.7% and 12.9%, n.s.). Purging anorexia was the diagnostic subtype, which presented the higher prevalences (29% and 43%), followed by restrictive anorexia (16%) and purging bulimia (13%). In the great majority of cases (65%), OCD diagnosis preceded ED diagnosis. Finally, OCD current prevalence and Y-BOCS scores of underweight patients were not significantly higher than normal-weight patients, suggesting that there were only limited links between denutrition and obsessionality.
Article
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Obsessive-compulsive disorder (OCD) often starts in childhood and adolescence and can be a chronic disorder with high persistence rates. There are few prospective long-term follow-up studies. To follow up young people with OCD to clarify persistence rates and relevant predictors, presence of other psychiatric disorders, functional impairment, service utilisation and perceived treatment needs. All young people with OCD assessed over 9 years at the National and Specialist Paediatric OCD clinic, Maudsley Hospital, London, were included. Sixty-one per cent (142 of 222) of all contactable young people and parents completed computerised diagnostic interviews and questionnaires. We found a persistence rate of OCD of 41%; 40% of participants had a psychiatric diagnosis other than OCD at follow-up. The main predictor for persistent OCD was duration of illness at assessment. High levels of baseline psychopathology predicted other psychiatric disorders at follow-up. Functional impairment and quality of life were mildly to moderately affected. Approximately 50% of participants were still receiving treatment and about 50% felt a need for further treatment. This study confirms that paediatric OCD can be a chronic condition that persists into adulthood. Early recognition and treatment might prevent chronicity. Important challenges for services are ensuring adequate treatment and a smooth transition from child to adult services.
Article
• The Yale-Brown Obsessive Compulsive Scale was designed to remedy the problems of existing rating scales by providing a specific measure of the severity of symptoms of obsessivecompulsive disorder that is not influenced by the type of obsessions or compulsions present. The scale is a clinician-rated, 10-item scale, each item rated from 0 (no symptoms) to 4 (extreme symptoms) (total range, 0 to 40), with separate subtotals for severity of obsessions and compulsions. In a study involving four raters and 40 patients with obsessive-compulsive disorder at various stages of treatment, interrater reliability for the total Yale-Brown Scale score and each of the 10 individual items was excellent, with a high degree of internal consistency among all item scores demonstrated with Cronbach's α coefficient. Based on pretreatment assessment of 42 patients with obsessive-compulsive disorder, each item was frequently endorsed and measured across a range of severity. These findings suggest that the Yale-Brown Scale is a reliable instrument for measuring the severity of illness in patients with obsessive-compulsive disorder with a range of severity and types of obsessive-compulsive symptoms.
Article
The objective is to evaluate the prevalence and associated clinical characteristics of eating disorders (ED) in patients with obsessive–compulsive disorder (OCD). This is a cross-sectional study comparing 815 patients with OCD. Participants were assessed with structured interviews and scales: SCID-I, Y-BOCS, Dimensional Y-BOCS, BABS, Beck Depression and Anxiety Inventories. Ninety-two patients (11.3%) presented the following EDs: binge-eating disorders [= 59 (7.2%)], bulimia nervosa [= 16 (2.0%)], or anorexia nervosa [= 17 (2.1%)]. Compared to OCD patients without ED (OCD-Non-ED), OCD-ED patients were more likely to be women with previous psychiatric treatment. Mean total scores in Y-BOCS, Dimensional Y-BOCS, and BABS were similar within groups. However, OCD-ED patients showed higher lifetime prevalence of comorbid conditions, higher anxiety and depression scores, and higher frequency of suicide attempts than did the OCD-Non-ED group. Primarily diagnosed OCD patients with comorbid ED may be associated with higher clinical severity. Future longitudinal studies should investigate dimensional correlations between OCD and ED. © 2009 by Wiley Periodicals, Inc. Int J Eat Disord 2010
Article
Studying children experiencing psychotic symptoms provides a unique opportunity to examine the vulnerability to psychosis within the context of development. Using neuroimaging techniques this study investigated cognitive control functions, brain volumetrics and white matter integrity in an at-risk cohort of children. Between-subjects assessment of brain function and structure among 11 school-going, non-treatment seeking children aged 11–13 who were at symptomatic risk for psychosis (AR) and 14 healthy control children aged 11–12 without subclinical psychotic symptoms (CON). MRI assessments included functional measures of response inhibition and error-related processes, whole brain voxel-based morphometry (VBM) of gray matter (GM) and diffusion tensor imaging (DTI) utilizing fractional anisotropy to probe white matter (WM) integrity. fMRI results showed reduced activity in the AR group within right frontal and bilateral temporal cortex for response inhibition and reduced activity within the anterior cingulate, insula and middle frontal gyrus for error-related processing (p < .05, corrected). VBM analysis revealed GM increases in the AR group within middle and superior temporal gyri, angular gyrus, orbitofrontal gyrus and GM decrease within the inferior temporal gyrus (p < .05, corrected). DTI analysis identified WM decreases in the AR group along the inferior fronto–occipital fasciculus, cingulum and inferior longitudinal fasciculus (p < .05, corrected). This multimodal investigation revealed aberrant prefrontal–temporal dysfunction in addition to cingulate and insular dysfunctions which provide potential early neurocognitive risk markers related to the susceptibility for developing psychosis and subsequently the neurodevelopmental trajectory leading to schizophrenia.
Article
This study examined the temporal sequencing of eating and anxiety disorders to delineate which anxiety disorders increase eating disorder risk and whether individuals with eating disorders are at greater risk for particular anxiety disorders. The sample was drawn from the Oregon Adolescent Depression Project. Temporal relations between specific eating and anxiety disorders were examined after controlling for relevant variables (e.g., mood disorders, other anxiety disorders) over 14 years. After excluding those with anorexia nervosa (AN) in adolescence (T1), OCD was the only T1 anxiety disorder to predict AN by age 30 (T4). No T1 anxiety disorder was associated with T4 bulimia nervosa (BN). Although T1 AN did not increase risk of any T4 anxiety disorder, T1 BN appeared to increase risk for social anxiety and panic disorders. Evidence that eating disorders may have differential relations to particular anxiety disorders could inform prevention and treatment efforts.
Article
Because eating disorders (EDs) and obsessive compulsive disorder (OCD) co-occur at high rates and can have functionally similar clinical presentations, it has been suggested that both constructs might be part of a common spectrum of disorders. Identifying the relationship between EDs and OCD may lead to the discovery of important shared core disease processes and/or mechanisms for maintenance. The objective of this paper is to understand the relationship between EDs and OCD by systematically reviewing epidemiological, longitudinal and family studies guided by five models of comorbidity posited by Klein and Riso (1993) and others. Though this literature is relatively small, the preponderance of evidence from these studies largely suggests that OCD/ED co-occur because of a shared etiological relationship. Limitations to extant literature, and suggestions for future research are discussed.
Article
Obsessive compulsive disorder (OCD) is currently classified as an anxiety disorder although it possesses many characteristics that distinguish it from other anxiety disorders. Clinically and neurobiologically, OCD appears to overlap somewhat with the eating disorders. To assess in a controlled fashion the lifetime prevalence of the eating disorders in patients with OCD, we administered portions of the Structured Clinical Interview for DSM-III-R, Patient Version (SCID-P), to 62 patients (31 men, 31 women) with a primary DSM-III-R diagnosis of OCD. Among the OCD patients, the lifetime prevalence of anorexia nervosa and/or bulimia nervosa was 12.9% (N = 8), and an additional 17.7% (N = 11) met subthreshold criteria for either anorexia or bulimia nervosa. Interestingly, unlike multiple epidemiologic studies that have reported a substantial female preponderance among patients diagnosed with anorexia or bulimia nervosa, there was no significant gender difference in the lifetime prevalence of eating disorders among the patients with OCD. Almost 13% (N = 4) of the men and 6.5% (N = 2) of the women with OCD met criteria for a lifetime diagnosis of anorexia nervosa and 3.2% (N = 1) of the men and 6.5% (N = 2) of the women with OCD met criteria at some time in their lives for bulimia nervosa. In addition, subthreshold criteria for anorexia nervosa or bulimia nervosa were met by an additional 12.9% (N = 4) of the men and 22.6% (N = 7) of the women. These data suggest that OCD patients, regardless of gender, have a substantial lifetime prevalence of anorexia and/or bulimia nervosa.
Article
The development design and reliability of the Yale-Brown Obsessive Compulsive Scale have been described elsewhere. We focused on the validity of the Yale-Brown Scale and its sensitivity to change. Convergent and discriminant validity were examined in baseline ratings from three cohorts of patients with obsessive-compulsive disorder (N = 81). The total Yale-Brown Scale score was significantly correlated with two of three independent measures of obsessive-compulsive disorder and weakly correlated with measures of depression and of anxiety in patients with obsessive-compulsive disorder with minimal secondary depressive symptoms. Results from a previously reported placebo-controlled trial of fluvoxamine in 42 patients with obsessive-compulsive disorder showed that the Yale-Brown Scale was sensitive to drug-induced changes and that reductions in Yale-Brown Scale scores specifically reflected improvement in obsessive-compulsive disorder symptoms. Together, these studies indicate that the 10-item Yale-Brown Scale is a reliable and valid instrument for assessing obsessive-compulsive disorder symptom severity and that it is suitable as an outcome measure in drug trials of obsessive-compulsive disorder.