Figure 2 illustrates the well-known association between P3AR and alcoholism risk in a plot that presents the grand mean waveforms separately for adolescents in the top and bottom deciles of AAU. The A (genetic), C (shared environmental), and E (non-shared environmental) estimates for AAU were 0.39 (95% confidence interval [CI]: 0.22, 0.58), 0.35 (95% CI: 0.17, 0.53), and 0.26 (95% CI: 0.22, 0.30), respectively, all of which were statistically significant. The A and E estimates for P300 amplitude were 0.63 (95% CI: 0.44, 0.75) and 0.36 (95% CI: 0.31, 0.42), respectively, and both were statistically significant. The C estimate, 0.01 (95% CI: 0.00, 0.18), was not significantly different from 0 and remained 0.01 throughout the moderation analysis. These values are consistent with those reported previously (van Beijsterveldt & van Baal, 2002). Approximately 3% of the variance in P300 amplitude was due to genetic covariance with AAU, whereas only 1% of the variance in P300 amplitude was due to shared environmental covariance. The genetic correlation was -0.23 (rA; 95% CI: -0.54, 0.00) and the nonshared environmental correlation was -0.06 (rE; 95% CI: -0.17, 0.00).
