Because possession of a single ALDH2*2 allele is sufficient to produce substantially diminished enzyme activity (Crabb, et al., 1989), for analyses including ALDH2 genotype, individuals both homozygous and heterozygous for the ALDH2*2 allele were grouped together, and contrasted with individuals homozygous for the ALDH2*1 allele. Age was centered for analysis by subtracting the minimum observed age (10.73 years) from each participant’s age. Count data (not including age), considered both as predictors and outcomes, were log-transformed for analysis. Individuals who had never had a drink at the time of their latest assessment (n = 56) were excluded from analyses. Status as a lifetime never-drinker did not differ by possession of the ALDH2*2 allele at the latest assessment for which data was available for each individual (X2(1) = .48, p = .49) nor at IN (X2(1) = .06, p = .81), FU1 (X2(1) < .01, p = .96), or FU2 (X2(1) = .14, p = .70). In assessing the main effects of ALDH2 genotype, as well as effects of moderation by parental alcohol use and misuse, and peer deviance, all 300 genotyped
