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Genetic and Environmental Components of the Relationship Between the ASD Triad and Mental Health Problems Measured by Strengths and Difficulties Questionnaire (SDQ)

Saturday, 4 May 2013: 09:00-13:00
Banquet Hall (Kursaal Centre)
B. Tick, F. Rijsdijk, F. McEwen and F. Happe, SGDP, IoP, King's College London, London, United Kingdom
Background: Autism Spectrum Disorders (ASD) has a higher prevalence rate than thought before: ~0.6% to 1% in children as well as adolescents (Baird et al., 2006). In addition, the presence of other psychiatric disorders in children with ASD is becoming increasingly recognised (Simonoff et al., 2008). It is, however, not clear why these disorders covary and researchers are trying to understand the nature and origin of the elevated rates of psychiatric diagnosis in ASD sufferers.

Objectives: The aim is to examine the genetic and environmental overlap between the distinct parts of the ASD triad (social interaction, communication and rigid and repetitive interests) and other psychiatric difficulties as measured by the Strengths and Difficulties Questionnaire (SDQ). SDQ measures emotional and conduct problems, hyperactivity/inattention, peer relationships and prosocial behaviour. The sample is an existing selected twin dataset sourced from Twins Early Development Study (TEDS).

Methods: The genetic and environmental overlap between ASD and SDQ will be tested using a bivariate threshold liability model consisting of MZ and DZ concordant/discordant ASD pairs as well as controls. To control for the fact that the sample is selected for ASD diagnosis, we fix the ASD parameters to population known values. Then, using the ratio of MZ:DZ cross-twin & cross-trait correlations of ASD and SDQ we estimate the genetic and environmental correlations to examine the aetiology of the comorbidity between these two traits. This method proved successful in the past for detecting comorbidity between schizophrenia and associated endophenotypes and is described in detail elsewhere (Rijsdijk et al., 2007).

Results: Preliminary results for the composite SDQ show a phenotypic correlation with ASD of .38. This covariance was largely due to overlapping genetic influences (71%) with the remaining 29% of the covariance due to non-shared environmental influences. Similarly, using the emotional subscale of SDQ, we report phenotypic correlation of .37, 67% of covariance is explained by genes and 30% by non-shared environments.

Conclusions: The current results indicate pleiotropic genetic effects influencing both the genetic liability to ASD and other psychiatric difficulties.

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