life events triggers a genetic susceptibility to depression. Conversely, “protective” environments, such as marriage-like relationships and low stress levels, can buffer against or reduce the impact of genetic predispositions to depressive problems. Many different processes are likely involved in the gene-environment interactions observed for substance use and antisocial behavior. For example, family environment and peer substance use/delinquency likely constitute a spectrum of risk or protection, and family/friend environments that are at the “poor” extreme may trigger genetic predispositions toward substance use and antisocial behavior, whereas positive family and friend relationships may compensate for genetic predispositions toward substance use and antisocial behavior. Social control also appears to be a particularly relevant process in substance use, as it is likely that being in a marriage-like relationship and/or being raised with a religious upbringing exert social norms that constrain behavior and thereby reduce genetic predispositions toward substance use. Further, the availability of the substance also serves as a level of control over the ability to express genetic predispositions, and accordingly, the degree to which genetic influences will be apparent on an outcome at the population level. In a compelling illustration of this effect, Boardman and colleagues used twin data from the National Survey
