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

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1 Psychological Medicine (2011), 41, f Cambridge University Press 2011 doi: /s x Is childhood OCD a risk factor for eating disorders later in life? A longitudinal study ORIGINAL ARTICLE 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 * Address for correspondence : Dr N. Micali, Brain and Behaviour Sciences Unit, UCL Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK. ( nadia.micali@kcl.ac.uk) & 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 retrospectively 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 convenience 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

2 2508 N. Micali et al. absence of an ED in adolescence. Unfortunately, although the study included 1709 subjects the prevalence 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 relationship 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 population, we followed up a cohort of adolescents/young adults with OCD onset during childhood or adolescence. 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 contacted 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 experienced 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 symptoms (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 wellvalidated interview (face-to-face or web-based) for parents and young people, used across the world, that generates IDC-10 and DSM-IV diagnoses algorithmically, 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 diagnosing ED in young people aged years compared with other instruments considered gold-standard (House et al. 2008). For parents who had difficulties using the webbased DAWBA, a trained researcher facilitated completion 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 analysis of variance) and non-parametric tests as appropriate, 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 bivariate 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 p value <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

3 OCD and onset of ED 2509 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 partial 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 compulsions, only two participants had these at baseline (6.2%) in the absence of any baseline ED psychopathology. In relation to age, there was no difference between 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 , p<0.05). A family history of ED was more common in participants 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 , 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 , p<0.05) and marginally on the C-YBOCS obsessions subscale (OR 1.1, 95% CI , p=0.05) compared with participants who did not develop an AD. There was a trend for gender differences (OR 2.1, 95% CI , 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 , 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,

4 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 No No No No EDNOS 3 F 17 OCD No No No Yes AN 4 F 14 OCD Restricting food intake during the day No No Yes AN Specific eating disorder and eating a large meal in the evening 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 No No EDNOS-AN avoid needing to use the toilet ; Contamination fears : checking food and avoiding eating near bins 8 F 15 OCD AN No No No EDNOS-AN AN 9 M 11 OCD No No No No EDNOS Tourette s syndrome ODD IDDM 10 F 11 OCD 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 Binge-eating when unhappy No No No EDNOS 15 M 17 OCD No Food has to be perfect : the right Yes No BED taste and temperature Eating limited range of foods 16 F 10 OCD 99.5 No No No No EDNOS-AN 17 M 11 OCD No No No No Subthreshold 2510 N. Micali et al. 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.

5 OCD and onset of ED 2511 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* ( ) Child variables at baseline Age of onset of OCD, Mean (S.D.) 8.7 (2.6) 9.9 (2.9) 0.9 ( ) Duration of illness, Mean (S.D.) 4 (3.8) 3.6 (2.7) 1.0 ( ) C-YBOCS total baseline 23.2 (5.4) 20.9 (8.1) 1.0 ( ) CYBOCS Obsessions 11.1 (3.5) 9.6 (4.9) 1.1 ( ) C-YBOCS Compulsions 12.1 (2.5) 11.2 (4.1) 1.1 ( ) C-YBOCS ritualized eating 5 (33.5%) 24/93 (25.8 %) 1.4 ( ) Other co-morbid Axis I disorders, n ( %) 8 (50 %) 48 (43.6%) 1.2 ( ) 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 ( ) (68.8%) 53 (48.2%) Ref. >20 4 (25 %) 41 (37.3%) 0.5 ( ) Missing 0 5 (4.5%) 1.9** ( ) Persistent OCD, n (%) 11 (68.7%) 41 (37.3%) 5.9* ( ) 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# ( ) Family history of OCD, n (%) 1 (6.2%) 15 (94 %) 0.9 ( ) 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. 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 development of ED. A diagnosis of ED at baseline was associated with an almost doubled risk for persistent OCD. The relationship between childhood onset OCD and later ED has been suggested previously in the literature. 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 population 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 particular 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

6 2512 N. Micali et al. 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 disordered 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 prevention or early intervention for ED. Despite small numbers, there was a slight increase in the percentage of a family history of ED in participants who had an ED at follow-up. The exact relationship 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 intervention. We attempted to address the specificity of predictors 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 particular 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; therefore, 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 overestimation. 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 evidence that, in the context of a child/adolescent presenting 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 providing 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. 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