Our primary aim was to characterize the overlap in genetic and environmental influences on initiation and disorder that were common across substances. Thus, we focused on estimating the common factor correlations. However, it should be noted that failing to correlate the residual ACE estimates might inflate the covariances between the common factors. In particular, failing to account for correlated measurement error may bias genetic and shared environmental effects (Lessov et al., 2004). When we estimated these covariances, we observed attenuation of the unique environmental correlations in men and women. The genetic and shared environmental correlations remained largely unchanged. (The shared environmental correlation among men became positive; however, the correlation obtained prior to accounting for residual variation was highly unreliable (rC=−.96 [−1.00, 1.00])). The residual unique environmental estimates include environmental variation and error that is (a) specific to each substance and (b) common to pairs of substances, but not all three. Accounting for this variation appeared to explain part – but not all – of the potentially direct association between the timing of tobacco, alcohol, and cannabis initiation and later abuse/dependence on these substances.
