combining alcohol administration with a longitudinal follow-up revealed that participants reporting more of the stimulant effects of alcohol and less of the sedative effects in the lab had a higher frequency of binge drinking, which was in turn a risk factor for the development of alcoholism at follow-up (King et al., 2011a). These recent findings have called for a paradigm shift in the interpretation of subjective response to alcohol and its etiological and clinical significance (King et al., 2011b). The present study builds upon this emerging literature to suggest that greater consilience in the OPRM1 findings may be reached by focusing on the genotype interactions with the stimulant and rewarding dimensions of alcohol’s effects.
