When analyzing data from all twins, MZ correlations were greater than the DZ correlations, and DZ correlations were greater than half the MZ correlations, suggesting the role of genetic and shared environmental influences respectively (Adolescent cannabis: rMZ=0.78, rDZ=0.54; rVUS: rMZ=0.41, rDZ=0.26). Results from the final bivariate genetic model are presented in Figure 1 (parameter estimates for the full model are in Table S5). Shared environmental (Δχ2(2df)=1.98), or additive genetic (Δχ2(2df)=2.32) influences, but not both (Δχ2(2df)=2.32) could be constrained to zero for rVUS – constraining shared environmental factors (estimated at 12%) to zero provided a modest improvement in fit. Correspondingly, variance in adolescent cannabis use was attributable to additive genetic (h2adol. cannabis: 54%), shared environmental (24%) and individual-specific environmental influences while variance in rVUS could be partitioned into additive genetic (h2rVUS: 42%) and individual-specific environmental sources. The covariance between adolescent cannabis use and rVUS was attributable to both genetic (rg=0.57) and, to a lesser extent, individual-specific (re=0.21) contributions.
