Alexander S Weigard1, Jillian E Hardee2, Robert A Zucker3, Mary M Heitzeg2, Adriene M Beltz4. 1. University of Michigan, Department of Psychiatry, Rachel Upjohn Building, 4250 Plymouth Road, Ann Arbor, MI, 48109, United States; University of Michigan, Department of Psychology, East Hall, 530 Church Street, Ann Arbor, MI, 48109, United States. Electronic address: asweigar@med.umich.edu. 2. University of Michigan, Department of Psychiatry, Rachel Upjohn Building, 4250 Plymouth Road, Ann Arbor, MI, 48109, United States. 3. University of Michigan, Department of Psychiatry, Rachel Upjohn Building, 4250 Plymouth Road, Ann Arbor, MI, 48109, United States; University of Michigan, Department of Psychology, East Hall, 530 Church Street, Ann Arbor, MI, 48109, United States. 4. University of Michigan, Department of Psychology, East Hall, 530 Church Street, Ann Arbor, MI, 48109, United States.
Abstract
BACKGROUND: Youth who experience puberty earlier than their peers are at heightened risk for substance use during adolescence. However, little is known about whether pubertal timing exacerbates effects of relevant early risk factors, such as family substance use history, as predicted by the "accentuation hypothesis". Using longitudinal data from youth with and without a family history of alcohol use disorder (AUD FHx), we evaluated whether pubertal timing intensifies preexisting familial risk effects on late adolescent substance use. METHODS: Participants were 568 males and 245 females from the Michigan Longitudinal Study. Pubertal timing was indexed by fitting mixed-effects linear models to repeated measures of self-reported Tanner stage. Multilevel models then tested: (a) whether AUD FHx predicted pubertal timing, and (b) whether AUD FHx, pubertal timing, or their interaction predicted alcohol and marijuana use at ages 16-18. RESULTS: AUD FHx was unrelated to pubertal timing in either males or females. In males, alcohol and marijuana use in late adolescence were predicted by AUD FHx and timing, but not their interaction. In females, AUD FHx predicted alcohol-related outcomes, but there were no main or interaction effects of timing. CONCLUSIONS: Pubertal timing does not moderate the link between AUD FHx and late adolescent substance use, in contrast to the accentuation hypothesis. In males, measures of pubertal maturation and familial risk provide unique information for prediction of use. Females displayed no link between pubertal timing and use, which may suggest different risk pathways, or may have been due to the female sample's smaller size.
BACKGROUND: Youth who experience puberty earlier than their peers are at heightened risk for substance use during adolescence. However, little is known about whether pubertal timing exacerbates effects of relevant early risk factors, such as family substance use history, as predicted by the "accentuation hypothesis". Using longitudinal data from youth with and without a family history of alcohol use disorder (AUD FHx), we evaluated whether pubertal timing intensifies preexisting familial risk effects on late adolescent substance use. METHODS:Participants were 568 males and 245 females from the Michigan Longitudinal Study. Pubertal timing was indexed by fitting mixed-effects linear models to repeated measures of self-reported Tanner stage. Multilevel models then tested: (a) whether AUD FHx predicted pubertal timing, and (b) whether AUD FHx, pubertal timing, or their interaction predicted alcohol and marijuana use at ages 16-18. RESULTS: AUD FHx was unrelated to pubertal timing in either males or females. In males, alcohol and marijuana use in late adolescence were predicted by AUD FHx and timing, but not their interaction. In females, AUD FHx predicted alcohol-related outcomes, but there were no main or interaction effects of timing. CONCLUSIONS: Pubertal timing does not moderate the link between AUD FHx and late adolescent substance use, in contrast to the accentuation hypothesis. In males, measures of pubertal maturation and familial risk provide unique information for prediction of use. Females displayed no link between pubertal timing and use, which may suggest different risk pathways, or may have been due to the female sample's smaller size.