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Relationship Between Eating Disorder Symptoms and Autistic/OCD Traits in Non-Clinical Sample

This investigation aims to explore the relationship between eating disorder symptomatology and its association with typical autistic and OCD traits in a non-clinical sample. The study will examine the association between ED, ASD, and OCD measures, as well as investigate specific traits linking ASD and ED.

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Relationship Between Eating Disorder Symptoms and Autistic/OCD Traits in Non-Clinical Sample

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  1. An investigation into the relationship between eating disorder symptomatology and its association with typical autistic and OCD traits in a non-clinical sample Camilla Parkinson & Dr. William Mandy

  2. Background Literature • Autism Spectrum Disorder (ASD) is defined by a triad of deficits • Communication skills, Social skills, stereotyped and repetitive behaviour patterns • ED’s are defined into three subgroups for diagnosis • Anorexia Nervosa (AN), Bulimia Nervosa (BN), Eating Disorder Not Otherwise Specified (EDNOS) • Recent research has shown a potential association between ED’s and ASD (Coombs et al, 2011; Gillberg & Rastam, 1992; Hambrook et al, 2008; Pooni et al, 2012; Zucker et al, 2007) • Gillberg & Rastam (1992) found a significant minority (20%) of their 51 AN participants had comorbid diagnoses of Autism • Hambrook et al (2008) observed significantly higher scores for ASD measures in their AN sample • Zucker et al (2007) found ASD was over represented in AN samples • Tchanturia et al (2005,2007) observed set shifting impairments in their ED samples, a characteristic well associated with ASD (Hill, 2004) • Theory of Mind deficits have been observed for ED’s (Tchanturia et al, 2004) and ASD (Baron-Cohen, 2001) • These findings indicate ASD or elevated Autistic traits may be potential risk factors in Eating Disorder development

  3. These findings aren’t without their problems however: • The prevalence of OCD in ED’s is greater than that of ASD (Hsu et al, 1993; Gillberg & Rastam, 1992; Halmi et al, 1991) • The literature on the association between OCD and ED is extensive and well established • OCD and ASD share many similar characteristics (Gillberg & Billstedt, 2000) • Previous studies, by not controlling for OCD levels in their samples may have been assuming they were measuring ASD in ED patients, but in fact participants were merely scoring high for subscales measuring similar symptoms to OCD • This could be the case for Coombs et al (2011) and Hambrook et al (2008) – both only observed sig associations for ‘non-social’ subscales (e.g. Attention switch, attention to detail), characteristics equally associated with OCD

  4. Coombs, E., Brosnan, M., Bryant-Waugh, R., Skevington, S.M. (2011) • To date only one study has explored the similarity in ASD and ED symptomatology in a sample of subclinical children. • Their sample was aged 11-14 years and researchers used the EAT-26 (Garner et al, 1982) and the AQ (Baron-Cohen et al, 2001) questionnaires to explore symptomatology similarity. • There was additional focus on digit ratio as an indication of prenatal testosterone levels (pT) as an additional predictor of EAT scores Results • Researchers only found the AQ as a significant predictor of EAT-26 scores when controlling for the effects of gender • Without controlling for gender the AQ total did not sig predict eating abnormality • The AQ subscales ‘attention to detail’ and ‘communication’ significantly predicted EAT-26 scores. • The pT variable did not significantly correlate with either the EAT-26 or the AQ

  5. This study will closely replicate that of Coombs et al (2011) • Using both the EAT-26 and the AQ to measure abnormal eating and ASD symptom levels • The non-significant pT variable will not be further explored by this project. • Instead an OCD scale will be included as an additional variable: • No studies have explored the relationship between ASD and ED whilst controlling for OCD levels • Would any effects between ASD measures and ED scores persist with the OCD scale included in the model? • Which would better predict abnormal eating scores, the ASD scale or the OCD measure?

  6. A ‘Theory of Mind’ test will also be included as an additional direct measure of social cognition • Results for this measure should lend support to social and communication subscales of our ASD measure • Tchanturia et al (2004) found that AN patients scored sig lower on TOM tasks, indicating TOM deficits • Oldershaw et al (2010) found the effect reported by Tchanturia (2004) did not persist in a sample of recovered AN patients • They concluded the starved state was causing deficits to social cognition • We predicted our subclinical sample to display varying extremes of abnormal eating behaviour • It was our aim to explore whether TOM deficits occur in samples displaying low severity ED

  7. Project Aims • Our main aim is to test if the association between ASD and ED is present in a subclinical adolescent sample • We wish to ascertain if any effects between ASD and ED measure persists while controlling for levels of OCD • We will investigate associations between subscales of ED, ASD and OCD measures • In order to ascertain what traits of ASD specifically are associating with ED • What types of eating behaviour are related to ASD • Whether it is obsessional or compulsive behaviour that is linked to low severity abnormal eating behaviour

  8. Hypotheses • Individually, both the ASDand the OCD scores should significantly correlate with ED scores. These relationships should strengthen when controlling for gender. • ‘Attention to Detail’ and ‘Communication’ ASD subscales should directly predict ED scores. • The OCD variable will be included in the analysis of the ASD variables as predictors of ED behaviour to control for its effects. • When controlling for OCD we predict that the relationship between the ASD variables and the ED scores will be in some way effected. If past research is anything to go by, we should assume it may potentially reduce any significant relationships. There is a lack of directly comparable research however, making a strong hypothesis difficult to form.

  9. We also aimed to explore the following additional hypotheses: • The following gender differences should be observed; males should score significantly more than females for both ASD scores and average weight values, females should score significantly more than males for total ED and TOM scores. • The TOM scores should inversely correlate with ASD scores. • The TOM scores should also significantly correlate with our ED measure.

  10. Methodology Participants • Subclinical adolescents (n=124) from an independent school • Aged between 15-17 years (mean= 16.77, SD=.44) • Self-selected sampling, response rate was 62% • Gender was equally distributed (m=60, f=64) • Height and Weight information was collected to calculate average BMI information for males (21.40) and females (20.98) Design • Within-participants design was selected • Non-clinical sample was chosen to explore subclinical levels of abnormal eating

  11. Method Continued… Measures: • As in the Coombs et al (2011) study the following measures were selected: • AQ (Baron-Cohen et al, 2001) = 50 item questionnaire, four point likert scale, test-retest and inter-rater reliability of this measure is excellent, and the internal consistency of the 5 subscales varies from moderate to high (e.g. ‘social skills’ Cronbach  = .77) • EAT-26 (Garner et al, 1982) = 26 item questionnaire with 3 subscales, six point likert scale, test-retest reliability is good and internal consistency for the scale is excellent (Cronbach = .90) • The following additional scales were also included: • ChOCI-R (Uher et al, 2007) = 25 item scale, three point likert scale, only questionnaire sections used, qualitative severity rating excluded, the scale has good internal consistency, with a Cronbach  of .72 for the sections used • The ‘Reading the Mind in the Eyes’ test (Baron-Cohen et al, 1997) = Child version was selected

  12. Procedure • The study took place in a classroom setting, during class time. • Students were provided with information sheets and consent forms (for those +16). • The 3 self report questionnaires were completed independently (no discussion was permitted). • The ‘Mind & Eyes’ test was displayed to the class as a whole via Powerpoint. • Participants were fully debriefed before leaving.

  13. Results Assumptions of normal distribution of data/errors • Both the EAT-26 and ChOCI-R scales were not normally distributed, both had significant positive skew and issues with significant kurtosis. Graph 1: Histograms depicting the significant (p<.001) skew and kurtosis issues in the distributions of the EAT-26 and ChOCI-R variables.

  14. A multiple regression highlighted a relatively large number of unusually large values in the residuals • The mahalanobis distance value (18.28) was large enough to assume influential cases were biasing the analysis • It was deemed necessary to transform the two variables • EAT-26 was given a Logarithm(i+ 1) transformation • ChOCI-R was transformed using a reciprocal transformation Graph 2: Histograms of the distribution of the log transformed EAT-26 and reciprocally transformed ChOCI-R variables

  15. These transformations fixed the significant skew and kurtosis issues (see graph 2) , reduced the mahalanobis distance value (14.5) and the number of large residual values (see graph 3). • The transformed variables were used throughout all further analyses. Graph 3: Histograms of the distribution of the standardized residuals of the EAT-26 variable before and after its Logarithm transformation.

  16. Subscales of the EAT-26, AQ and ChOCI-R were also to be included in both our main and an exploratory analysis. • These subscales also violated the assumption of normal distribution: • EAT-26: A Square Root transformation reduced the impact of the bias but did not fully correct the issues with normal distribution • AQ: ‘Attention Switch’ & ‘Local Detail’ were the only AQ subscales to be included in detailed analyses. Neither violated any of the assumptions and therefore no transformation was required for this scale. • ChOCI-R: Reciprocal transformations corrected all violations of normality for subscales ‘Obsessions’ & ‘Compulsions’

  17. ANOVA • An ANOVA was run on all variables to ascertain whether there were any sig. gender differences • Results: • A sig. gender difference was observed for the AQ scale (F(123) = 3.973, p<.05), and the AQ subscale ‘imagination’ (F(123)=5.02, p<.05). • Sig gender differences were also observed between ‘ideal’ (F(120) = 118.60, p<.001) and ‘actual’ (F(120) = 39.83, p<.001) weight scores. • Contrary to our hypothesis, there was no sig. gender difference for the EAT-26(Log) variable (F(123) = .538, p >.05), although the ‘Dieting’ subscale did approach significance (sig. =.061) Correlations • A correlational analysis was conducted including all variables • The results of this analysis can be seen on the Table 1 on the following slide.

  18. *p < .05, **p < .01

  19. Multiple Regression 1 • A multiple regression explored any variables of interest highlighted by the correlation analysis • This resulted in 2 sig models being produced: • Model 1: • ‘Local Detail’ (LD) and ‘Attention Switch’ (AS) combined significantly predicted the EAT-26 scores (F(123) =2.895, p<.05) • Model 1 explained 6.7% of the variance. • Neither subscale reached significance alone (‘LD’: ß=.025, t=1.528, p>.05; ‘AS’: ß=.032, t=1.962, p>.05), but combined explained enough variance for the model to reach significance. ’Gender’ was controlled for and did not sig predict EAT-26 scores (ß=.040, t=-1.111, p>.05). • Model 2: • ChOCI-R was additionally included in the 2nd model via forced entry. • Model 2 also sig predicted EAT-26 scores (F(123)=4.059, p<.05) • This model explained 12% of the variance with the inclusion of the OCD scale. • ChOCI-R sig predicted EAT-26 (ß=-16.072, t=-2.666, p<.01) and reduced the other predictor variables significance scores further (‘LD’: sig=.398; ‘AS’: sig=.674; ‘Gender’: sig=.562).

  20. Multiple Regression 2 • To better understand why the significance values of the AQ subscales reduced so noticeably upon the inclusion of the ChOCI-R variable we ran a second multiple regression: • Instead of introducing the ChOCI-R variable into the second step of the regression, its subscales ‘Obsessions’ and ‘Compulsions’ were entered in its place. • Results: • The first model produced unchanged ß, t and significance values • The second model was significant (F(123) = 3.561, p<.005) • ‘Obsessions’ significantly predicted EAT-26(Log) scores (ß =-6.728, t=-2.733, p<.05) • Again, no other variables were significant, including ‘Compulsions’ (ß=-.133, t=-.043, p>.05) • Significance values of ‘Attention Switch’ and ‘Local Detail’ reduced in the same way as before

  21. Exploratory Analysis of EAT-26 subscales • We explored how ASD/OCD variables associated with specific types of abnormal eating behaviour. • To do so we removed EAT-26(Log) as the dependent variable, and ran the previous ‘Multiple regression analysis 1’ three times with ‘Oral Control’, ‘Dieting’ and ‘Bulimia’ subscales as the dependent variable. • Results: • ‘Oral Control’: Neither of the 2 models were statistically significant • ‘Dieting’: • Model 1: Both ‘Attention Switch’ and ‘Gender’ approached significance. Indicating as one might predict that Gender came close to predicting abnormal eating behaviour, girls exhibiting more dieting behaviour than boys. • Model 2: ChOCI-R behaved similarly to previous analyses, it sig predicted ‘Dieting’ scores and reduced significance values for AQ variables and ‘Gender’ • ‘Bulimia’: • Model 1 was non-significant, none of the predictors individually reaching significance, although attention switch approached it (ß=.066, t=1.907, sig=.059) • Model 2 was significant upon the inclusion of the ChOCI-R which predicted ‘Bulimia’ eating behaviour.

  22. Discussion • One of our predictions was only partially supported: • The AQ did not sig predict EAT-26 scores • However, the ChOCI-R did, and all 3 of its subscores. Neither of these relationships became stronger when controlling for ‘Gender’ • Only ‘Local Detail’ and ‘Attention Switch’ had sig relationships with ED scores, this partially supports findings of Coombs et al (2011) and Hambrook et al (2008). • Social and Communicative subscales had no significant correlation or predictive relationship with ED scores, this contradicts Zucker et al (2007) who made bold statements about impaired social function and social cognition deficits in AN patients which they state reflect ASD impairments. • This deficit in association between social and communicative subscales and abnormal eating also poses threats to claims made by Gillberg, Rastam and colleagues (1992) about shared traits between those with ED and ASD, and their reported levels of comorbidity.

  23. A potential mediation relationship (see Diagram 1) was observed in the data • ‘Local Detail’ and ‘Attention Switch’ explained enough combined variance to produce a significant model (when controlling for ‘Gender’), and predict the EAT-26 scores • However, when the OCD measure or its subscale ‘Obsessions’ were included in the model, not only did they also significantly predict the EAT-26 scores, but in doing so reduced the combined effect of the ‘non-social’ AQ subscales to non-significance.

  24. Mediation Relationship between AQ subscales and ChOCI-R ChOCI-R** (Obsessions)** ‘Local Detail’* & “Attention Switch’* EAT-26(Log) *p < .05, ** p < .01 Diagram 1: The variable ChOCI-R and its subscale ‘Obsessions’ were found to potentially mediate the significant relationship between the combined AQ subscale predictors ‘Local Detail’ and ‘Attention Switch’ with the EAT-26 scores

  25. Limitations • Sample • Homogenous in ethnicity and age range, potentially variables worth exploring • Self-selecting sample – could impact data, those anxious about subject material may have not taken part (excluding potentially interesting data from analysis) • Sample was not quite large enough (demonstrated by small effect sizes). This could also have resulted in smaller effects, worthy of exploration, being missed. • Self report – Social desirability bias, demand characteristics • Cross-sectional • Causality cannot be inferred by cross-sectional research • It would be worthwhile exploring whether these effects persist into adulthood (especially with the inclusion of greater severity ED participants) • A longitudinal replication of this study could provide potentially interesting results • The inclusion of clinical comparison groups adding new depth to the project

  26. References Baron-Cohen, S., Wheelwright, S., Joliffe, T. (1997). Is there a “language of the eyes”? Evidence from normal adults, and adults with Autism or Asperger Syndrome. Visual Cognition, 4(3): p. 311-331. Baron-Cohen, S. (2001). Theory of mind in normal development and Autism. Prisme, 34:p.174-183. Baron-Cohen, S., Wheelwright, S., Skinner, R., Martin, J., Clubley, E. (2001). The Autism-Spectrum Quotient (AQ): evidence from Asperger Syndrome/high-functioning autism, males and females, scientists and mathematicians. Journal of Autism and Developmental Disorders, 31: p. 5-17. Coombs, E., Brosnan, M., Bryant-Waugh, R., Skevington, S.M. (2011). An investigation into the relationship between eating disorder psychopathology and autistic symptomatology in a non-clinical sample. British Journal of Clinical Psychology; 50: p. 326-338. Garner, D.M., Olmsted, M.P., Bohr, Y., Garfinkel, P.E. (1982). The Eating Attitudes Test: Psychometric features and clinical correlates. Psychological Medicine, 12: p.871-878. Gillberg, C. & Billstedt, E. (2000). Autism and Asperger syndrome: Coexistence with other clinical disorders. Acta Psychiatrica Scandinavica, 102: p.321-330. Gillberg, C.; Råstam, M. (1992). Do some cases of anorexia nervosa reflect underlying autistic-like conditions? Behavioural Neurology, 5(1): p.27-32. Hambrook, D., Tchanturia, K., Schmidt, U., Russell, T., Treasure, J. (2008). Empathy, systemizing, and autistic traits in anorexia nervosa: A pilot study. British Journal of Clinical Psychology, 47: p.355-359.

  27. Hill, E. (2004). Executive dysfunction in autism. Trends in Cognitive Sciences, 8(1): p.26-32. Pooni, J., Ninteman, A., Bryant-Waugh, R., Nicholls, D., Mandy, W. (2012). Investigating Autism Spectrum Disorder and Autistic Traits in Early Onset Eating Disorder. International Journal of Eating Disorders, 45(4): p. 583-591. Rahman, L., Richardson, H.B., Ripley, H.S. (1939). Anorexia Nervosa with psychiatric observations. Psychosomatic Medicine, 1: p.335-365. Rastam, M. (1992). Anorexia Nervosa in 51 Swedish Adolescents: Premorbid problems and comorbidity. Journal of the American Academy of Child & Adolescent Psychiatry, 31(5): p.819-829. Rothenburg, A. (1988). Differential Diagnosis of Anorexia Nervosa and Depressive Illness: A Review of 11 Studies. Comprehensive Psychiatry, 29(4): p.427-432. Tchanturia, K., Happe ́, F., Godley, J.,Treasure, J., Bara-Carril, N., Schmidt, U. (2004). ‘Theory of Mind’ in Anorexia Nervosa. European Eating Disorders Review, 12: p.361-366. Uher, R., Heyman, I., Turner, C.M., Shafran, R. (2008). Self-, parent-report and interview measures of obsessive–compulsive disorder in children and adolescents. Journal of Anxiety Disorders, 22: p.979-990. Zucker, N.L., Losh, M., Bulik, C.M, LaBar, K.S., Piven, J., Pelphrey, K.A. (2007). Anorexia Nervosa and Autism Spectrum Disorders: Guided Investigation of Social Cognitive Endophenotypes. Psychological Bulletin, 133(6): p.976-1006.

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