decrease in fit is driven by the female portion of the sample, particularly the sex-specific genetic contributions to female phenotypic variance. Because the E term encompasses measurement error, in order to allow for the possibility of AUD-specific error we did not test whether the AUD-specific E path could be set to 0, though path estimates for AUD-specific E were quite low. Model 2, allowing for AUD-specific genetic influences, was selected as the best-fitting model. Final estimates of heritability and genetic and environmental correlations are presented in Table 5. We applied the same modeling approach to alternative phenotypic definitions of the diagnoses (e.g., modeling a DSM-IV dependence-only phenotype and modified AUD; coding AUD as 0, 1, 2 to capture the levels of severity that were initially proposed) and, while the overall fit of the model was worse than those reported here, the results did not change (available upon request).
