The present study is informed by the theory of allostatic load to examine how multiple stress responsive biomarkers are related to mental health outcomes. Data are from the TRAILS study, a large prospective population study of 715 Dutch adolescents (50.9 % girls), assessed at 16.3 and 19.1 years. Reactivity measures of the hypothalamic pituitary-adrenal (HPA) axis and autonomic nervous system (ANS) biomarkers (heart rate, HR; respiratory sinus arrhythmia, RSA; and pre-ejection period, PEP) to a social stress task were used to predict concurrent and longitudinal changes in internalizing and externalizing symptoms. Hierarchical linear modeling revealed relatively few single effects for each biomarker with the exception that high HR reactivity predicted concurrent internalizing problems in boys. More interestingly, interactions were found between HPA-axis reactivity and sympathetic and parasympathetic reactivity. Boys with high HPA reactivity and low RSA reactivity had the largest increases in internalizing problems from 16 to 19 years. Youth with low HPA reactivity along with increased ANS activation characterized by both decreases in RSA and decreases in PEP had the most concurrent externalizing problems, consistent with broad theories of hypo-arousal. Youth with high HPA reactivity along with increases in RSA but decreases in PEP also had elevated concurrent externalizing problems, which increased over time, especially within boys. This profile illustrates the utility of examining the parasympathetic and sympathetic components of the ANS which can act in opposition to one another to achieve, overall, stress responsivity. The framework of allostasis and allostatic load is supported in that examination of multiple biomarkers working together in concert was of value in understanding mental health problems concurrently and longitudinally. Findings argue against an additive panel of risk and instead illustrate the dynamic interplay of stress physiology systems.

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.