Our results provided no evidence that AAU moderated the G-E interplay underlying P300 amplitude. In particular, no effective change in genetic variance across the range of AAU was estimated even when the model allowed for moderating effects of AAU to be present. The robustness of the G-E interplay underlying P300 amplitude supports P3AR as an endophenotype for alcoholism risk, rather than a biological marker sensitive to the effects of AAU. While it is impossible to conclude that AAU is benign in regards to P300 amplitude, these results suggest that AAU is not systematically reducing P300 amplitude enough to compromise the clinical utility of P300 amplitude as an alcoholism endophenotype in this unselected community sample of adolescents.
