allowed an ADE structure for INATT and HYP/IMP and an ACE structure for CDP and AlcProb and hypothesized one latent genetic factor (G) that influenced all four externalizing outcomes. The latent genetic factor was influenced by additive (A) and non-additive (D) genetic factors. In order for the model to be identified, we constrained the additive path, a, to 1, which forced the non-additive loading, d, to be a scalar proportion of the additive genetic effect on the latent G factor. One common latent nonshared environmental (E) factor was also allowed to influence all four outcomes. We also hypothesized one common shared environmental factor (C1) between CDP and AlcProb, with additional specific/independent shared environmental effects (C2) on AlcProb. The residuals for each outcome were partitioned into specific additive (A), specific non-additive (D; for ADHD subtypes only), specific shared environmental (C; for CDP and AlcProb only), and specific nonshared environmental (E) components. Estimates of the proportion of the total variance that could be explained by additive genetic (a2), dominance (d2), shared (c2) and non-shared environmental factors (e2) were without covariate adjustment. This model also allowed for different mean values for each of the zygosity groups. 95% likelihood-based confidence intervals were also computed
