Abstract
P3 amplitude reduction (P3AR) is associated with adolescent alcohol use (AAU) and highly heritable, suggesting that P3AR may index a genetic predisposition (e.g., an endophenotype) for AAU. However, because P3AR and AAU covary naturally in the population, these observations are also consistent with P3AR reflecting neurotoxic effects of AAU on the developing adolescent brain. In this report, we describe the use of recent advancements in biometric modeling to examine changes in the genetic and environmental contributions to variability in P3 amplitude related to cumulative AAU by late adolescence in a large community-based twin sample. We found that the genetic and environmental contributions to variability in P3 amplitude were unaffected by AAU. This suggests that P3AR indexes risk for alcoholism independent of any deleterious effect of AAU on adolescent brain development.