One plausible hypothesis about the nature of the genetic variation in humans that influences risk for drug abuse is that it should arise largely from genes that code for the primary sites of action of the psychoactive drugs themselves (e.g., Guindalini et al., 2006). If this were the case, we would expect most of the genetic variation to be substance specific as current evidence suggests that the principal receptor sites for the major drug classes such as cannabis, stimulants and sedatives, are largely distinct (Koob and Le Moal, 2006). However, prior twin studies based on personal interviews have found that a large proportion of the genetic influences on the abuse of specific classes of illicit substances were non-specific (Kendler et al., 2003, 2007; Tsuang et al., 1998). The main goal of this report was to determine whether we could replicate this pattern of results using a quite different methodological approach based on objective nation-wide data on DA from medical, mortality and criminal registries.
