Some limitations are worth noting. First, although high-risk family-based samples have several benefits including enriched endorsement for AUD and other psychopathology, they may not generalize. Second, the PGS analyses were largely constrained to individuals of European ancestry due to the dearth of GWAS of these phenotypes in individuals of non-European ancestry and the poor portability of PGS prediction across ancestries (Martin et al., 2017). Despite our efforts to include PGS for those of African–American ancestry, the present null findings may be partially attributable to reduced power arising from smaller discovery GWASs in African ancestry populations. Our European ancestry-specific findings may thus contribute to the disparity in applicability of research findings to non-European populations (Martin et al., 2019). Third, ages of onsets of some symptoms for some participants were retrospectively reported and thus subject to recall bias, which we tried to minimize by choosing the first reported age of onset. Fourth, given insufficient assessments of dimensional psychopathology, we were unable to longitudinally evaluate subthreshold symptom development across waves, complicating the ability to distinguish predisposition from consequence. Fifth, despite covarying for tobacco
