The activity of the hypothalamic–pituitary–adrenal (HPA) axis, an important mediator of the stress response (see Clarke et al. 2007 for a review) is of interest in relation to the effects of environmental stress on the level of alcohol consumption and the risk of AD. CRHR1, which encodes the corticotrophin releasing hormone receptor 1, has been evaluated as a candidate locus moderating the effects of stress on alcohol consumption. Treutlein et al. (2006) found that two haplotype tagging SNPs (rs242938, rs1876831) in CRHR1 were associated with binge drinking in two independent samples: the Mannheim adolescent sample and a sample of alcohol-dependent adults. Blomeyer et al. (2008) extended these findings by examining the interaction effects on drinking of these variants and life stress in adolescents from the Mannheim Study. They found that rs1876831 moderated the effect of negative life events on the maximum amount of alcohol consumed per occasion and lifetime rates of heavy drinking. They did not find a G × E interaction for rs242938. Dahl et al. examined five SNPs in CRHR1 in a sample of alcohol dependent and control
