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Clarifying the sources of variation among autism symptom domains is important to the identification of homogenous subgroups for molecular genetic studies. This study explored the genetic and environmental bases of nonverbal communication and social interaction, two symptom domains that have also been related to treatment response, in 1294 child and adolescent twins and siblings with pervasive developmental disorders (PDDs) from the Autism Genetic Resource Exchange under the age of 18. Twin/sibling resemblance was assessed through correlations and behavior genetic modeling of Autism Diagnostic Interview (ADI) nonverbal communication and social scores. Variation in these phenotypes was explained by additive genetic, dominant genetic, and unique environmental factors with no evidence for shared environmental factors. Broad heritability estimates were higher for nonverbal communication (45%) than social interaction (28%). Nonverbal communication and social scores were partially accounted for by the same underlying genetic and environmental factors. Gender differences were not supported. These results add to information on familial resemblance of these symptom domains based on correlational methods, and this study is one of the first to apply behavioral genetic modeling to a PDD population. The results have implications for molecular genetics as well as treatment.

Background: The distribution of fat and adipose tissue is an important predictor of disease risk. Variation in fat distribution during adolescence is correlated with fat distribution in adulthood., Objective: The objective was to gain insight into the relative contribution of genes and environment to the stability of subcutaneous fat distribution from early adolescence into young adulthood., Design: Ratio of trunk to extremity skinfold thickness (TER) data from the Leuven Longitudinal Twin Study (n = 105 Belgian twin pairs followed from 10 to 18 y of age) was entered into a longitudinal path analysis., Results: The best-fitting model included additive genetic sources of variance and nonshared environment. Heritabilities ranged between 84.3% (95% CI: 63.9-92.3%) and 88.6% (95% CI: 76.5-94.1%) in boys and between 78.4% (95% CI: 59.3-88.3%) and 88.3% (95% CI: 77.0-93.8%) in girls. The majority of the phenotypic tracking (boys: 0.40-0.78; girls: 0.38-0.72) could be attributed to the moderate-to-high genetic correlations (rG) (between 0.27-0.84 and 0.38-0.80 for the various age intervals in boys and girls, respectively). This rG could be attributed to both genetic sources of variance, which are the same throughout adolescence, as well as genetic sources of variance that are "switched-on" at a certain age, the effect of which is then transmitted to subsequent observations. Environmental correlations (rE) in boys ranged between 0.51 and 0.70 but contributed relatively little to phenotypic tracking because the amount of variance explained by the environment was low (11.4-15.7%). In girls rE was low to moderate at best (0.09-0.48)., Conclusion: Phenotypic tracking in subcutaneous fat distribution during adolescence is predominantly explained by additive genetic sources of variance.

Considerable evidence from twin and adoption studies indicates that both genetic and shared environmental factors play a substantial role in the liability to antisocial behavior. Although twin and adoption designs can resolve genetic and environmental influences, they do not provide information about assortative mating, parent-offspring transmission, or the contribution of these factors to trait variation. We examined the role of genetic and environmental factors for conduct disorder (CD) using a twin-parent design. This design allows the simultaneous estimation of additive genetic, shared and individual-specific environmental effects, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A retrospective measure of CD was obtained from twins and their parents or guardians in the Virginia Twin Study of Adolescent Behavior Development and its Young Adult Follow up sample. Both genetic and environmental factors play a significant role in the liability to CD. Major influences on individual differences appeared to be additive genetic (38%-40%) and unique environmental (39%-42%) effects, with smaller contributions from the shared environment (18%-23%), assortative mating (-2%), cultural transmission (approximately 2%) and resulting genotype-environment covariance. This study showed significant heritability, which is slightly increased by assortative mating, and significant effects of primarily nonparental shared environment on CD.