Despite this being the largest genetic study of initial alcohol sensitivity to date, it is possible that the retrospective SRE assessment in approximately half of the total sample compromised our statistical power to detect influential loci. Individuals in both samples for whom multiple waves of data were available generally reported increasing SRE scores in later assessments despite the reporting period being constant (i.e., the first five or so times they drank alcohol); this raises the possibility that current drinking experiences influence reporting of past sensitivity. This may have contributed to the discrepancy in h2SNP estimates across the ALSPAC and S4S samples. The moderate estimate in ALSPAC encourages us that genetic factors are, indeed, influential, though power analyses indicated <10% power to detect a h2SNP of 0.30 in the smallest S4S subgroup, AMR. The EUR samples were more adequately powered: In ALSPAC, we estimated 64% power to detect h2SNP of 0.20 and 99% power to detect h2SNP of 0.36 (the actual estimate), and 61% power to detect h2SNP of 0.30 the S4S EUR ancestry group. Despite the lack of genome-wide significant variants, the current report represents an important initial effort to improve our understanding of the biological underpinnings of alcohol sensitivity.
