This update on the Southern Illinois Twins and Siblings Study (SITSS) documents some of the follow-up studies that have been conducted and results that have been obtained from this sample. At the current time, 283 twin pairs, 8 triplet families, 98 non-twin sibling pairs, and 287 singletons have been enrolled in SITSS. Twins and triplets are tested as young as 1 year of age and then every year on their birthday through age 5 years. A variety of follow-up studies have been conducted for SITSS children through age 20. Results thus far have demonstrated significant genetic influences on social behaviors such as aggression, victimization, and attention toward facial expressions. Interesting interactions have been documented between the dopamine receptor D4 gene (DRD4) and the social environment (parental sensitivity or peer aggression) as they predict children's aggressive behaviors. In addition, increased difficulty with social interactions has been noted for twins versus singletons. Thus, this multi-trait, multi-method behavior genetic data set contributes to our understanding of the etiology of social behaviors in preschoolers and to predictors of similar behaviors through adolescence.

Background Prior work has suggested that genetic influences on Major Depressive Disorder (MDD) may be activated by the experience of negative life events. However, it is unclear whether these results persist when controlling for the possibility of confounding active gene-environment correlations (rGE). Methods We examined a sample of 1,230 adopted and biological siblings between the ages of 10 to 20 years from the Sibling Interaction and Behavior Study (SIBS). MDD was measured via a lifetime DSM-IV symptom count. Number of deaths experienced served as our environmental risk experience. Because this variable is largely independent of the individual's choices/behaviors, we were able to examine GxE while circumventing possible rGE confounds. Results Biometric analyses revealed pronounced linear increases in the magnitude of genetic influences on symptoms of MDD with the number of deaths experienced, such that genetic influences were estimated to be near-zero for those who had experienced no deaths but were quite large in those who had experienced two or more deaths (i.e., accounting for roughly two-thirds of the phenotypic variance). By contrast, shared and non-shared environmental influences on symptoms of MDD were not meaningfully moderated by number of deaths experienced. Conclusions Such results constructively replicate prior findings of genetic moderation of depressive symptoms by negative life events, thereby suggesting that this effect is not a function of active rGE confounds. Our findings are thus consistent with the notion that exposure to specific negative life events may serve to activate genetic risk for depression during adolescence.

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