Although genotype frequencies did not differ significantly by sex, supplementary analyses examined whether differences in peak BrAC could be attributed to the somewhat higher proportion of females in the AA group. Descriptive results showed similar genotype differences in BrAC in both sex groups, with the magnitude of genotype differences being somewhat greater for females (GA/GG: M=91.67mg%, SD=12.74, AA: M=68.20mg%, SD=25.57) than males (GA/GG: M=96.29mg%, SD=18.71, AA: M=81.69mg%, SD=24.06). Although limited by a small sample size, this pattern indicates that significant OPRM1 effects could not be attributed to a relatively higher proportion of females in the AA group. For further confirmation, a two-step linear regression model examined sex and OPRM1 as predictors of peak BrAC, estimating incremental variance in BrAC as a function of genotype. Sex accounted for an estimated 6% of variance in peak BrAC at Step 1 (β = −.30, t = −1.88, adjusted r2 = .06, stepwise F (1,36) = 3.52, p = .07). With the addition of OPRM1 (Step 2) the model accounted for 14% of the variance in peak BrAC (adjusted r2 = .14, stepwise F
