The standardized estimate for the genetic parameter from SR to CON (path a12) was low and non-significant [0.002 (−0.01 to 0.02)], and constraining it to zero did not significantly worsen model fit. Further, after accounting for SR, the proportion of environmental covariance explained by environmental influences on CON [(e23 × e24)/(e13 × e14 + e23 × e24 + e33 × e34)] was negligible [0.01 (−0.03 to 0.05)], and paths e23 and e24 could be constrained to zero without a significant decrement in fit (see online Supplementary material). Therefore, CON explained the covariation between MDD and AUD solely via genetic mechanisms: a moderate proportion of the genetic covariance was explained by genetic influences on CON (0.32; see Table 4). In this model, genetic influences both specific to and shared between CON and SR accounted for 66% of the genetic covariation [A = 0.66 (0.38–0.94)], and unique environmental influences explained 20% of the unique environmental covariation [E = 0.20 (0.03–0.38)].
