Although polygenic scores reflect the state of the science when considering measured genetic risk for complex behavioral outcomes like alcohol use (Bogdan et al., 2018; Salvatore et al., 2014), we also recognize that, at present, they account for just a fraction of the variation. In order to examine whether our observed polygenic gene-by-environment effects were spurious, we ran two sets of sensitivity analyses. First, we ran a parallel set of analyses using parental history of alcohol dependence as our index of one’s genetic predisposition. Consistent with our polygenic analyses, we found that, among married individuals at age 21, a parental history of alcohol dependence was associated with higher heavy episodic drinking compared to those without this parental history. However, the pattern of effects at age 25 differed across the polygenic risk score and parental history analyses. Specifically, there were no differences in heavy episodic drinking among married individuals as a function of parental history of alcohol dependence, but there were differences as a function of polygenic risk scores. Thus, although the polygenic risk and parental history models are consistent in
