Associations between PRS and individual substances were only partially attributable to GENSUB, indicating specificity of certain relationships (e.g., ADHD PRS and nicotine involvement). This is significant, considering that twin studies implicate GENSUB as the primary source of genetic variance in individual substance use disorders (Kendler et al., 2003, 2007, 2012). Our factor loadings support this high degree of cohesiveness, with the possible exception of nicotine, also consistent with a prior twin study (Kendler et al., 2007). Notably, unlike prior research which has heavily relied on binary measures of substance use or dependence, we capitalized on the range of substance involvement present in our target sample due to the ascertainment strategy (Table 2), including non-problem use (i.e., use with no dependence symptoms) as well as multiple levels of problematic use (i.e., 1–2 vs. 3–5 vs. 6–7 dependence symptoms). Not only did this coding allow us to differentiate between early/casual and later/maladaptive levels of substance involvement, but it also allowed us to test whether PRS were associated with specific levels of substance involvement (i.e., to compare across groups). Despite factorial architecture suggesting
