Similar to previous studies examining interaction between childhood adversity and genes affecting neuronal processes putatively related to substance addiction (Caspi et al., 2003; Kaufman et al., 2007), we found that both ADH1B-rs1229984 (higher-risk genotype, i.e. lack of the protective allele) and childhood adversity together increase risk for problematic alcohol use beyond the influence of each risk factor individually. Specifically, ADH1B-rs1229984 has a significantly greater impact on problematic drinking among individuals who experienced childhood adversity than among those who did not. We propose this is due to the direct impact of ADH1B on alcohol metabolism and, consequently, consumption. Since the ADH1B-rs1229984 protective A allele leads to an enzyme with greater activity than the more common variant, individuals with the AA and AG genotypes may limit alcohol consumption because of subtle adverse effects that accompany the degradation of ethanol (Hurley & Edenberg, 2012). Therefore, ADH1B-rs1229984 appears to have a stronger effect on alcohol consumption, and consequently the progression to AUDs, among those with childhood adversity, a group in which alcohol consumption would likely be increased. We considered the effect of ADH1B-rs1229984 on
