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.

中文翻译：

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青春期期间创伤事件和药物滥用是否同时发生？检验三个因果病因学假设

背景为什么潜在创伤事件（PTE）和物质使用（SU）在青春期如此常见地同时发生？从成人创伤后应激障碍 (PTSD) 和物质使用障碍 (SUD) 研究中得出的因果假设尚未在具有这些疾病先兆的青少年中进行严格的理论分析或实证检验：PTE 和 SU。建立因果关系需要考虑各种因素（例如遗传、家长教育、种族/民族），这些因素将支持 PTE 和 SU 的青少年与不支持 PTE 和 SU 的青少年区分开来，这一步骤在之前的研究中经常被忽视。 方法我们利用了来自社会人口学多样化青年样本的全国数据（氮= 11,468）在青少年大脑和认知发展研究中。每年评估 PTE 和物质使用流行率。为了解释有和没有 PTE/SU 的青少年之间许多预先存在的差异（即混杂偏差）并提供对因果假设的严格检验，我们通过重复测量将 PTE 和 SU（酒精、大麻、尼古丁）的内部变化联系起来并根据时变因素（例如年龄、内化症状、外化症状和朋友使用物质）进行调整。结果在使用人内模型调整混杂因素之前，PTE 和 SU 表现出显着的并发关联（βs = 0.46–1.26，ps < .05) 和 PTE 前瞻性预测更大的 SU (βs = .55–1.43,ps < .05)，但反之则不然。调整混杂因素后，PTE 表现出与酒精显着的并发关联（βs = .14–.23，ps < .05) 和尼古丁 (βs = .16,ps < .05) 但不是大麻 (βs = ‐.01,ps > .05)，PTE 前瞻性地预测了更大的 SU (βs = .28–.55，ps > .05），但反之则不然。结论当在全国青少年样本中进行严格测试时，我们发现支持 PTE 后面跟着 SU 的模型，但不支持 SU 后面跟着 PTE 的模型。在扩展到青少年之前，解释为什么 PTSD 和 SUD 在成人中同时发生可能需要进一步的理论分析和调整。