Our data suggest that the H2 haplotype is protective against CSA-associated risk for higher lifetime alcohol consumption and alcohol dependence. The extent of these protective effects suggests that one or more of the genes within the H2 haplotype are playing an important role in stress-associated risk for alcohol consumption and dependence. Although the evidence (Le et al. 2000; Hansson et al. 2006; Sommer et al. 2008; Heilig & Koob, 2007; Pastor et al. 2008) from animal research is quite strong, it is premature to conclude that these protective effects are due to a CRHR1 polymorphism. Additional research is needed to determine definitively the gene or genes responsible for these protective effects. Gene expression studies have provided strong evidence in favor of MAPT (Caffrey et al. 2006; Caffrey et al. 2008) versus CRHR1 (Campdelacreu et al. 2006) involvement in PSP risk, although other research (Cruchaga et al. 2009) suggests that multiple genes may be involved. However, since our finding involves a G × E interaction rather than a main effect, it will be considerably more difficult to conduct this type of
