Our findings should be interpreted in light of some limitations. First, the smaller sample of AA twins may have limited our power to detect racial/ethnic differences between EAs and AAs, and to examine specific factors that might contribute to racial/ethnic differences (e.g., socioeconomic status). Second, we noted a negative individual-specific environmental correlation (Table 4, rE=−0.55) between cannabis initiation and problems in AAs, which might plausibly be related to compensatory environmental mechanisms that decelerate progression from early to problem use in AAs, after accounting for common genetic risk. Given the limited exploration of cannabis use in AAs, it is difficult to speculate what these environmental factors may be. Alternatively, the modest association between early cannabis use and cannabis problems in AAs relative to EAs may have resulted in sparseness of data in cross-twin cross-trait correlations, yielding statistical compensation for these estimates. Third, although the majority of the sample was ascertained in the peak years for cannabis initiation and early-to-peak years for problem onset, not all participants had passed through the age of risk for the cannabis outcomes. Fourth, although we attempted
