which pathways for the AA and EA participants were set to be equal, also included A, C, and E variance components for both phenotypes. Additional tests conducted with each of the three best-fitting models to assess significance of the cross-phenotype additive genetic (a21), shared environmental (c21), and unique environmental pathways (e21) (i.e., covariances) indicated significance of a21 in all three models, c21 in the EA model, and e21 in the EA and full sample models. The resulting final models are shown with unstandardized path coefficients in Figures 1, 2, and 3. The standardized variance component estimates and correlations are reported with 95% confidence intervals in Table 2. For both the AA and EA subsamples, age at first drink was attributable to shared environmental as well as additive genetic and unique environmental sources of variance. Very similar estimates of C were observed in the AA and EA models (C=0.25 for AA, 0.27 for EA), but A estimates were considerably higher in the EA than AA model (0.44 vs. 0.26). The AA and EA models also diverged on problem alcohol use. No evidence of a shared environmental effect was observed in the AA model, whereas 33% of the variance in problem use
