Genes contribute to between 40% and 60% of the risk for alcohol use disorders (AUDs), operating in large part through several different intermediate characteristics, or phenotypes, including a low level of response (LR) to alcohol [1, 2]. Regarding LR, it is hypothesized that a low response per drink produces a need for more drinks to get desired effects, which then contributes to higher levels of consumption. This, in turn, may enhance the risk for alcohol-related problems, including alcohol abuse and dependence [2, 3]. A low LR to alcohol has been documented to relate to heavier drinking in animal models and humans as early as age 12 [4–6]. LR is genetically-influenced with estimated heritabilities of 40%-to-60% [7, 8], and a low LR predicts later heavy drinking and alcohol problems in adults and adolescents [7, 9–11].
