It is fair to suggest that the natural covariation between P3AR and AAU has hindered explicating the role of AAU in producing P3AR. Adolescents who consume the greatest amounts of alcohol are expected to manifest P3AR, whether P3AR is caused by AAU or is an expression of a genetic risk for AAU. Thus, both the P3AR endophenotype hypothesis and the alcohol exposure hypothesis explain why P300 amplitude is associated with AAU in adolescents with alcohol use histories. However, the two hypotheses diverge as to the expected genetic and environmental (G-E) contributions underlying P300 amplitude at different points along the alcohol exposure continuum. The endophenotype hypothesis, for instance, predicts that P300 amplitude relates to risk for AAU independent of whether the risk for alcohol misuse is manifested or not. In this case, the G-E interplay underlying P300 amplitude would be similar for all individuals regardless of varying AAU histories. With the alcohol exposure hypothesis, an individual’s genetic contribution to P300 amplitude would be moderated by alcohol exposure. For instance, an individual whose genes confer a tendency to have large amplitude P300
