Aim 1: Biobehavioral pathways of development: Test biological-environmental pathways for adolescent substance use. Hypotheses are that (1) increased prenatal risk and earlier pubertal timing will partially mediate genetic influences on internalizing and externalizing problems and subsequent substance use, and (2) earlier pubertal timing will partially mediate parenting influences on internalizing and externalizing problems and subsequent substance use.

Aim 2: Biological-Environmental Interactions: Test biological (genetic, endocrine) X environmental (prenatal, parenting) interactions for adolescent substance use. Hypotheses include that (1) genetic influences, as measured by polygenic scores, will moderate associations between prenatal risk exposure and adolescent substance use, (2) genetic influences, as measured by polygenic scores, will moderate associations between parenting and adolescent substance use, (3) prenatal risk will moderate associations between pubertal timing and adolescent substance use, and (4) parenting will moderate associations between pubertal timing and adolescent substance use.