Additionally, emerging evidence from inferred genotype and molecular genetic studies indicate that with a few exceptions (e.g., genes influencing alcohol metabolism), environmental moderation of genetic risk among adolescents may occur via impact on broadly defined risk rather than genetic influences specific to drinking behaviors. For example, neighborhood factors were found to moderate genetic and environmental risk for behavior problems among 14-year-olds in a manner paralleling the GxE reported for alcohol consumption among young adults (Dick et al., 2009a). Likewise, similar patterns of GxE were found across alcohol-related phenotypes and rule-breaking/externalizing behaviors (e.g., Dick et al., 2009b; Legrand et al., 2008) and other substance use disorders (e.g., Covault et al., 2007; Harden et al., 2008) among adolescent samples. Finally, a recent report suggested more pronounced alcohol-related GxE associated with genetic risk for non-specific externalizing disorders than genetic risk specific to AUDs in early and mid-adolescence (Kendler et al., in press). These results are consistent with the notion that AUDs develop as the result of a genetically influenced, externalizing pathway (Krueger et al., 2002; McGue, Iacono, Legrand, Malone, & Elkins, 2001), and
