Patterns, Predictors, and Correlates of Problematic Alcohol Use and Remission From Adolescence to Early Midlife

ABSTRACT Background The goal of this paper is to identify environmental, behavioral, and genetic predictors and early midlife correlates of problematic alcohol Use ( PAU ) patterns from adolescence to early midlife. Methods The data are from 1463 twin individuals (60.5% female) in the population‐based FinnTwin12 cohort born 1983–1987. PAU was assessed at ages 14, 22 and 37 using symptoms of alcohol use disorder ( AUD ) obtained from psychiatric interviews, mmMAST scores, and the AUDIT . Self‐reported health and well‐being were assessed at age 37. A behavioral and environmental risk index ( BERI ) was created by summing six risk factors: low socioeconomic status in childhood, family history of AUD , childhood externalizing and internalizing behaviors, adolescent substance use, peer substance use, and stressful life events in adolescence. The twins' genetic predispositions were indexed using polygenic scores for externalizing behavior ( PGS EXT ), PAU ( PGS PAU ), and depression ( PGS MDD ). Results Twins were classified into four PAU groups: Never ( n = 599, reference), Remitted ( n = 480), Persistent ( n = 271), and Late‐onset ( n = 113). When included in the same model, both BERI and PGS EXT were significantly associated with Remitted PAU , while BERI scores and PGS PAU were significantly associated with Persistent PAU . Compared to the Never PAU group, individuals in the Persistent and Late‐onset PAU groups reported lower educational attainment, poorer physical health, lower relationship satisfaction, lower life satisfaction, a worse financial situation, more depressive symptoms, recurrent pain, and sleep problems, and were less likely to be partnered or have children. Conclusions Persistent PAU was associated with the most negative outcomes in early midlife, and childhood and adolescent risk factors and genetic risk as indexed by PGS PAU were strong predictors of group membership. Late‐onset PAU may be the result of novel stressors in adulthood, given the lack of association with childhood and adolescent environmental risk or genetic risk.