Genetic and shared environmental factors explain the association between adolescent polysubstance use and high school noncompletion

Psychol Addict Behav. 2024 Feb;38(1):114-123. doi: 10.1037/adb0000915. Epub 2023 Mar 13.

Abstract

Objective: Examine the nature of the relationship between adolescent polysubstance use and high school noncompletion.

Method: Among a sample of 9,579 adult Australian twins (58.63% female, Mage = 30.59), we examined the association between the number of substances used in adolescence and high school noncompletion within a discordant twin design and bivariate twin analysis.

Results: In individual-level models controlling for parental education, conduct disorder symptoms, childhood major depression, sex, zygosity, and cohort, each additional substance used in adolescence was associated with a 30% increase in the odds of high school noncompletion (OR = 1.30 [1.18, 1.42]). Discordant twin models found that the potentially causal effect of adolescent use on high school noncompletion was nonsignificant (OR = 1.19 [0.96, 1.47]). Follow-up bivariate twin models suggested genetic (35.4%, 95% CI [24.5%, 48.7%]) and shared environmental influences (27.8%, 95% CI [12.7%, 35.1%]) each contributed to the covariation in adolescent polysubstance use and early school dropout.

Conclusions: The association between polysubstance use and early school dropout was largely accounted for by genetic and shared environmental factors, with nonsignificant evidence for a potentially causal association. Future research should examine whether underlying shared risk factors reflect a general propensity for addiction, a broader externalizing liability, or a combination of the two. More evidence using finer measurement of substance use is needed to rule out a causal association between adolescent polysubstance use and high school noncompletion. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

MeSH terms

  • Adolescent
  • Adult
  • Australia / epidemiology
  • Child
  • Depressive Disorder, Major*
  • Female
  • Humans
  • Male
  • Parents
  • Risk Factors
  • Twins* / genetics