Very early in the discovery of the low LR phenotype Schuckit and colleagues found that the less intense response to alcohol was not just subjective but also extended to hormonal responses. They initially found that sons of alcoholics demonstrated lower cortisol levels after drinking (Schuckit et al. 1987a). In that same year they also reported lower prolactin levels following alcohol challenge in this same group of individuals (Schuckit et al. 1987b) and finally, they reported lower ACTH levels in sons of alcoholics following high doses of alcohol (Schuckit et al. 1988). These findings were partially replicated in a sample of sons of alcoholics selected from the Consortium on the Genetics of Alcoholism (COGA) study where lower level of intensity of response to alcohol as measured by changes in cortisol were found (Schuckit et al. 1996). Although hormone studies have the advantage of using objective measures that may be closer to the mechanisms underlying LR than subjective measures, there have been relatively few other human studies that have used hormone responses to index LR. In one study, Asians with ALDH2*2 alleles,
