Objectives: This study investigated for the first time the extent to which autistic-like traits in the general population are explained by genetic and environmental influences in 12-year-olds. The second set of analyses explored the etiological overlap between specific autistic traits (social impairments, communication impairments, and RRBIs) in extreme scoring individuals at age 12.
Methods: Parents of 5,900 12-year-old twin pairs completed the Childhood Asperger Syndrome Test (CAST), a population-based screening tool for autism spectrum disorders. Structural equation model fitting was conducted in the full sample to examine the extent to which genes and environment influence variation in autistic traits at age 12. DeFries-Fulker (DF) regression analysis was employed to examine the heritability of the total scale and subscales at the impaired extremes. A bivariate extension of DF analysis was used to analyze the degree of shared genetic etiology between specific autistic traits.
Results: In the full sample analysis, high heritability for autistic traits was found: 76% for males (95% CI 0.69-0.79) and 52% (95% CI 0.43-0.61) for females. The influence of the shared environment was significantly greater in females (26%, 95% CI 0.18-0.34) than in males (2%, 95% CI 0.005-0.09). In the extremes analyses, high heritability was found for the total scale and the individual subscales (0.67-0.80). Estimates of bivariate heritability (shared genetic influences between specific autistic traits) were modest overall, ranging from 0.31-0.53 for males and 0.10-0.28 for females.
Conclusions: Parent-rated autistic-like traits showed high heritability and modest shared environmental effects at age 12. Specific autistic-like traits -- social impairments, communication impairments, and RRBIs -- had partly non-overlapping genetic influences, which concurs with previous studies of younger children. These data support the notion that the autistic triad is largely fractionable and there may be symptom-specific causal influences underlying autistic traits. These findings also concur with recent molecular genetic findings that have related specific genes to specific aspects of the autism phenotype, and support further research into symptom-specific causal pathways relevant to ASD.