The current study has a number of strengths, which help validate the findings and add to the growing literature on epistatic interactions between these polymorphisms. First, to extend beyond prior studies, we selected a population of social drinkers and controlled for individual differences in recent drinking in our analyses. Prior studies have established that there are differences in alcohol response in the laboratory, which are dependent on prior drinking behavior in the community. Heavy drinkers reported greater acute positive subjective effects and stimulation, and less sedative effects when compared to social drinkers administered controlled doses of alcohol (King et al., 2011). Social drinkers reported greater “high” than heavy drinkers after ingesting high ethanol doses (0.56–1 g/kg), and time since last drink altered responses to acute alcohol administration (Turkkan et al., 1988). Second, we restricted smoking in our inclusion/exclusion criteria to reduce the impact of nicotine use and dependence. Both the OPRM1 A118G SNP and DAT1 VTNR polymorphism have been associated with nicotine initiation, use and dependence (Verhagen et al., 2012). Smoking also has been shown to alter availability of both
