| Popis: |
Attention deficit hyperactivity disorder (ADHD) is a heritable disorder, which has detrimental effects on childhood development and is associated with maladaptive functioning in adulthood. Despite this, we are far from an understanding of the etiology and possible trajectories of ADHD, possibly due to investigations focusing on the contribution of single genes. In fact, single genes are likely not influential enough to alter behavior, but the additive effect of many genes may predispose an individual toward certain behaviors. Further, environmental input can activate or suppress genetic expression, thereby leading to vast individual differences in both normative behavior and psychopathological illness, including ADHD. This study investigated the effect of cumulative genetic sensitivity across three dopaminergic polymorphisms (DRD2 A1, DRD4 7R, and DAT1 10R) on ADHD symptomatology in very young children. In addition, we were interested in the G x E associations with ADHD symptomatology. Findings provide novel evidence regarding the effects of dopamine polymorphisms on inattention, and thus ADHD, symptomatology in very young children. Specifically, the findings suggest that the cumulative effect of genetic sensitivity across several dopamine polymorphisms predicts severity of symptomatology, particularly in males. In addition, a robust G x E interaction emerged, whereby a specific genetic predisposition moderated the effect of family context on behavior. This finding, lending support to the BSC model and the differential susceptibility hypothesis, suggests that genetic sensitivity can moderate environmental influence, for better and for worse. |
