AIMS:

Health risk behaviors related to substance (ab)use and externalizing problem behavior threaten the healthy development of children and adolescents. Specifically, early onset substance use and conduct problems are key predictors of later addiction and clinical-level antisocial personality disorder. These are greatly debilitating conditions for any individual, but also the societal costs associated with these conditions are enormous. Harsh or inconsequent discipline, lack of warmth and sensitivity, abuse by parents, and parents' dependence on substance use are among the strongest predictors of substance (ab)use and conduct problems in childhood and adolescence.

Previous research over the past decade has indicated that family risks may have a particularly detrimental effect in children carrying specific genotypes, that regulate the activity within dopaminergic, serotonergic, GABAergic, and cholinergic pathways. In our proposal, we aim to identify gene-environment interactions that predict health risk behaviors in childhood and adolescence - focusing on genetic risk on the one hand, and on specific family and parenting risks on the other hand. Although the field of GxE research holds great promise, until now it has proven difficult to replicate GxE findings. This has two main causes: first of all, a lack of statistical power in most correlational studies focusing on GxE (e.g., Duncan & Keller, 2011) and secondly, a lacking specification of possible explanatory mechanisms underlying GxE (Dodge, 2010; Weeland, Overbeek, Orobio de Castro, & Matthys, 2014).

Thus, our overall aim is to 1) conduct cross-validated tests of gene-environment interactions related to the development of common addictive behaviors (smoking, alcohol, marijuana) and conduct problems or antisocial behavior in childhood and adolescence, and 2) to test possible mechanisms underlying this gene-environment interplay. With regard to this latter aim, we aim to examine specficially whether children's temperamental traits, such as for instance (but not limited to) levels of (dis)inhibiton and reward and punishment sensitivity, can be identified as explanatory factors underlying the gene-environment interactions that lead up to the development of health risk behaviors.