the lack of an interaction between genotype and medication might be considered less meaningful. On the other hand, it is also possible that the OPRM1 gene by naltrexone interaction might not be as salient in this younger, less severe, and lower drinking population, compared to more severely affected treatment seekers. For instance, one might speculate that during the onset of alcohol dependence, reward salience might be more important than “compulsive” drinking. This could hypothetically mean that dopamine gene effects might be more salient in early-stage dependence, and only in later stages of dependence would opioid gene effects, and their interaction with naltrexone, become more salient and important. In general, this study population was less severe in amount of alcohol consumption and dependence symptoms, and their OCDS scores were much lower than in clinical trials where the asp40 SNP was associated with naltrexone response (e.g. Anton et. al. 2008). This might suggest that “habit” or “compulsive drinking” might be more influenced by the opioid system and moderated by naltrexone, especially in those where naltrexone might be more pharmacologically powerful (OPRM1 asp40 carriers).
