Recent developments in biometric modeling make possible the examination of how environmental exposure moderates G-E contributions to a phenotype of interest (Johnson, 2007; Purcell, 2002). To illustrate how these methods can be used to address our alternative hypotheses, we can model the contribution of A, C, and E to variability in P3 amplitude as a function of the degree of exposure to alcohol. Figure 1a visually depicts the G-E interplay underlying P300 amplitude in the population corresponding to the endophenotype hypothesis. Based on the results of the van Beijsterveldt and van Baal (2002) meta-analysis, the proportion of variance (Y axis) in P300 amplitude estimated to be due to genes (60%; A) and non-shared environment (40%; E) remains the same for all adolescents no matter how much alcohol they have consumed (as indicated on the X axis).
