interactions for all variables included in the model (Table 3). Interactions among trauma exposure and PRS with p < 0.05 and p < 0.10 thresholds were observed for cannabis ever use but not DSM-5 CUDsx (Table 3). Both PRS had a greater influence on cannabis ever use and DSM-5 CUDsx among those exposed to trauma (R2: 0.011–0.014; AUC: 0.58 (0.53, 0.62)) as compared to those who were not exposed to trauma (R2: 0.001–0.002; AUC: 0.49 (0.43, 0.54), Fig. 2a). Trauma exposure was not predicted by cannabis use PRS (p > 0.26).Table 3Moderation of cannabis use and DSM-5 CUD symptom count by trauma exposure and frequency of religious service attendance among COGA participants of European ancestry; results from Model 1 that includes the following covariates: age, sex, birth cohort, genotype array, and PCs 1–3PRS thresholdCannabis use ever (lifetime)DSM-5 cannabis use disorder Sx count R 2 Betap value R 2 Betap valueTrauma exposure × PRS p < 0.0001—————— p < 0.001—————— p < 0.01—————— p < 0.05 0.005 0.181 0.009 a 0.0010.0980.148 p < 0.1 0.004 0.341 0.016 0.0010.1150.406 p < 0.2—————— p < 0.3—————— p < 0.4—————— p < 0.5——————Frequency of service attendance × PRS p < 0.0001—————— p < 0.001——————
