For individual low-dose symptoms, the ADH1B-ALDH2 interaction was statistically significant at the .05 level for sleepy (step χ2 = 10.58, 4 df, p = .032). The second row of Table 2, however, shows that the pattern for sleepy for ADH1B in ALDH2*1/*1 is in the opposite direction from that predicted (and that seen in ALDH2*1/*2), with individuals with no ADH1B*2 alleles having the highest rate (26%) of endorsing sleepy and those with two ADH1B*2 alleles having the lowest rate (15%); this effect may be spurious, due in part to the small sample size of ADH1B*1/*1 in ALDH2*1/*1 (n = 39). No other interaction terms approached significance (p’s > .11) so only main effects were considered. With both ALDH2 and ADH1B genotypes entered, only ALDH2 genotype was significantly associated with individual alcohol related symptoms. Details on these analyses are not presented given ALDH2 associations have already been described above and are shown in Table 1. The percentages of participants who endorsed each of the six low-dose symptoms across ADH1B genotype when stratified by ALDH2 genotype, however, are shown in Table 2 to provide additional details; only one participant had ALDH2*2/*2 and ADH1B*1/*1 so this column is not included in the table.
