A significant genetic influence on target P3 generation was found, but no significant associations of target P3 with alcohol use were observed. In contrast, variation in novel P3 latency was attributed to gene–environment interactions. P3 latency correlated positively with the Mm-MAST, and the effects of the Mm-MAST on P3 latency were significantly modified by genetic influences (Table 5). Similarly, the variation in parietal amplitude of novel P3 was attributable to gene–environment interaction. The effect of alcohol abuse, as measured with RAPI at age 18, on parietal amplitude of novel P3 was modified significantly by genetic influences. At the same time, P3 amplitude correlated negatively with RAPI (Table 6).
