The twin design is particularly useful for partitioning the liability across multiple substance related outcomes into their genetic and environmental components. The benefit of the extension of the univariate twin model to the multivariate case is that it provides a test of different hypotheses regarding the nature of comorbidity. As seen in the aforementioned studies, researchers may test the hypothesis that there is a single underlying process as opposed to multiple correlated processes. Given the similarity in the neurological response to addictive substances (Goldman and Bergen, 1998; Volkow et al., 2002) and the generalized effect of pharmacological treatments for addiction (Basavarajappa, 2007, Rösner et al., 2010), individual differences in lifetime reports of drug dependence symptoms for multiple drugs could be attributable to common biological (i.e., genetic) factors. In fact, several studies (Vanyukov et al., 2003) have calculated the genetic correlation across dependence on multiple substances and have found them to be in excess of 0.5. However, despite the phenotypic indications of a latent risk, we are unaware of any twin studies that have explicitly tested a model indicating a generalized
