Alcohol use disorder (AUD) has a strong genetic component with heritability estimates of about 50% (Oroszi and Goldman, 2004). AUD is polygenetic, with many genes likely contributing to AUD risk in different individuals, in different ways, and in interaction with the environment (Buhler et al., 2015). One strategy for increasing our understanding of genetic risk factors involved in AUD is the use of intermediate phenotypes for specific traits associated with the disorder. Intermediate phenotypes are those that: 1) are associated with risk for the disorder, 2) are associated with causes rather than effects of the disorder, 3) vary continuously in the general population, and 4) are detectable in unaffected family members of individuals with the disorder associated with that phenotype (Bearden and Freimer, 2006). The strength of studying intermediate phenotypes is that they may be less polygenic, and closer in proximity to genetic effects; this should increase statistical power to find gene associations with individual traits associated with AUD. Level of alcohol response meets basic criteria for an intermediate phenotype, and, as a result, alcohol administration under controlled human laboratory conditions is a useful tool to explore this genetic contribution to AUD risk (Salvatore et al., 2015).
