The associations between traumatic experiences and trajectories of substance use in adolescence and young adulthood – the role of acute neuroendocrine and subjective stress reactivity

Abstract

Adolescents exposed to traumatic events, including physical and sexual abuse, are at higher risk of developing problematic substance use behaviours. This study investigates associations between traumatic experiences and trajectories of substance use in adolescence and young adulthood, focusing in particular on differences in neuroendocrine and subjective stress reactivity as potential explanatory mechanisms. Using data from the TRacking Adolescents’ Individual Lives Survey (TRAILS) (N = 715), we assessed whether traumatic experiences up to age 16 were associated with differences in acute neuroendocrine stress reactivity (in terms of heart rate (HR), high-frequency heart rate variability (HF-HRV), pre-ejection period (PEP), and cortisol reactivity), as well as subjective stress reactivity, assessed in the context of a standardized stress test conducted around age 16. We then analysed whether these stress reactivity measures predicted substance use trajectories (tobacco, alcohol, and cannabis) from around age 16 to around age 22. Results showed that traumatic experiences increased the risk of following trajectories characterized by an early initiation and escalation of tobacco, alcohol, and cannabis use (vs. no use or low use trajectories). Traumatic experiences were additionally associated with a higher probability of belonging to cannabis use trajectories characterized by consistently relatively low levels of use (vs. no use) or a later escalation of use in young adulthood. Regarding mechanisms, blunted neuroendocrine stress reactivity, but not subjective stress reactivity, was inconsistently linked to trajectories of higher substance use. However, differences in acute stress reactivity did not contribute to associations between traumatic experiences and substance use trajectories, as associations between traumatic experiences and acute stress reactivity were absent. Our findings emphasize the need to explore mechanisms beyond acute stress reactivity that may explain the association between trauma and adolescent and young adult substance use.