Do traumatic events and substance use co‐occur during adolescence? Testing three causal etiologic hypotheses

Author:

Patel Herry1ORCID,Tapert Susan F.1,Brown Sandra A.12,Norman Sonya B.134,Pelham William E.1

Affiliation:

1. Department of Psychiatry University of California San Diego La Jolla CA USA

2. Department of Psychology University of California San Diego La Jolla CA USA

3. National Center for PTSD White River Junction VT USA

4. Department of Veterans Affairs Medical Center La Jolla CA USA

Abstract

BackgroundWhy do potentially traumatic events (PTEs) and substance use (SU) so commonly co‐occur during adolescence? Causal hypotheses developed from the study of posttraumatic stress disorder (PTSD) and substance use disorder (SUD) among adults have not yet been subject to rigorous theoretical analysis or empirical tests among adolescents with the precursors to these disorders: PTEs and SU. Establishing causality demands accounting for various factors (e.g. genetics, parent education, race/ethnicity) that distinguish youth endorsing PTEs and SU from those who do not, a step often overlooked in previous research.MethodsWe leveraged nationwide data from a sociodemographically diverse sample of youth (N = 11,468) in the Adolescent Brain and Cognitive Development Study. PTEs and substance use prevalence were assessed annually. To account for the many pre‐existing differences between youth with and without PTE/SU (i.e. confounding bias) and provide rigorous tests of causal hypotheses, we linked within‐person changes in PTEs and SU (alcohol, cannabis, nicotine) across repeated measurements and adjusted for time‐varying factors (e.g. age, internalizing symptoms, externalizing symptoms, and friends' use of substances).ResultsBefore adjusting for confounding using within‐person modeling, PTEs and SU exhibited significant concurrent associations (βs = .46–1.26, ps < .05) and PTEs prospectively predicted greater SU (βs = .55–1.43, ps < .05) but not vice versa. After adjustment for confounding, the PTEs exhibited significant concurrent associations for alcohol (βs = .14–.23, ps < .05) and nicotine (βs = .16, ps < .05) but not cannabis (βs = ‐.01, ps > .05) and PTEs prospectively predicted greater SU (βs = .28–.55, ps > .05) but not vice versa.ConclusionsWhen tested rigorously in a nationwide sample of adolescents, we find support for a model in which PTEs are followed by SU but not for a model in which SU is followed by PTEs. Explanations for why PTSD and SUD co‐occur in adults may need further theoretical analysis and adaptation before extension to adolescents.

Funder

National Institute on Drug Abuse

National Institute on Alcohol Abuse and Alcoholism

Canadian Institutes of Health Research

Brain and Behavior Research Foundation

Publisher

Wiley

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