Chunk #29 — Discussion — Contrast with Interpretation of Results from the only Prior Study of ADH1B and Childhood Adversity Effects on Alcohol-Related Phenotypes
were not exposed. Our results are only partially consistent with theirs. In addition to the fact that we observed an interaction only for AUD symptoms and Meyers et al. (2013b) found an interaction for both maxdrinks and AUD symptom phenotypes, the studies differ in the nature of the GxE interaction. Whereas we observed a protective effect of the rs1229984 A allele in EA men who had not been exposed to adverse events in childhood (OR=0.24, CI:0.15–0.36, p<0.001), but no protective effect in A-allele carriers who had been exposed (OR=0.57, CI:0.32–1.01, p=0.056), Meyers and colleagues found that the contribution of the rs1229984 genotype was greater in the childhood adversity-exposed than the unexposed group. The outliers in our study were the A-allele carriers who had not been exposed to childhood adversity. They endorsed an average of 3.6 AUD criteria, approximately 3 fewer than the exposed carriers (6.3), unexposed noncarriers (6.3), and exposed noncarriers (7.0). By contrast, the outliers in Meyers et al.’s study were the noncarriers exposed to adversity in childhood, who endorsed the largest number of AUD criteria. In other words, we found that childhood adversity attenuated the protective effects of the A allele, whereas Meyers et al. found that the
