symptoms. Our estimates of overlap in heritable influences on dependence symptoms are highly consistent with Xian et al. (2008), who found that 42.4% of the variance in AD and 33.7% of the variance in cannabis dependence were accounted for by a shared genetic factor (that also loaded on nicotine dependence), but less so with two other known studies in this area. Notably, these two investigations included additional phenotypes not examined in studies that produced results more similar to ours, which likely influenced the identification of common factors in these models and thus the estimated overlap in genetic influences specific to AD and cannabis dependence. For example, Kendler et al.’s (2007) study in which two distinct but correlated genetic factors emerged, with alcohol loading on one and cannabis on the other, included cocaine and caffeine dependence. Similarly, True et al. (1999)’s finding that the genetic factor common to AD symptoms and cannabis dependence symptoms accounted for only 7.6% of the total variance (and 17% of the genetic variance) in cannabis dependence symptoms may be attributable in part to the inclusion of conduct disorder in the models. In short, our study adds to a limited literature that has thus far produced mixed
