Observational cohort analysis demonstrates that early, severe threat exposure alters baseline cortisol and recovery in adolescents, highlighting threat-specific developmental programming.
Early life adversity (ELA) is associated with alterations in hypothalamic-pituitary-adrenal (HPA)-axis functioning, yet findings regarding cortisol responses to stress remain inconsistent. These inconsistencies, in part, reflect differences in how ELA is conceptualized, including its dimensions (i.e., threat versus deprivation), timing, and severity, which may differentially shape long-term stress regulation through calibration of the HPA axis. Thus, the present study examined whether dimensions, timing, and severity of ELA differentially predicted baseline cortisol, cortisol reactivity, and cortisol recovery in a community sample of N = 75 adolescents. Four complementary operationalizations of adversity dimensions, timing, and severity were examined using piecewise multilevel growth models. Timing of first threat and deprivation exposure alone did not predict any phase of the cortisol stress response. In contrast, earlier occurrence of the most severe threat exposure was associated with elevated baseline cortisol, while earlier and more frequent threat exposures were associated with prolonged cortisol recovery. Timing-weighted cumulative severity was not associated with HPA-axis functioning. Across all analyses, significant results were specific to threat rather than deprivation. Together, these findings suggest that the timing of threat-based ELA confers distinct yet interdependent alterations to HPA-axis functioning depending on how adversity severity is conceptualized, advancing our understanding of the biological embedding of ELA. As such, this work provides a foundation for identifying developmentally sensitive targets for prevention and intervention aimed at mitigating the long-term psychobiological consequences of ELA.
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Taylyn Jameson (2026) studied this question.
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