Physical disorders and neuroendocrine vulnerability in the development of posttraumatic stress disorder: A 2-year injury cohort study.

This study examined whether the association between early post-trauma cortisol levels and posttraumatic stress disorder (PTSD) onset is moderated by the burden of preexisting physical disorders (PDs), with attention to earlier- versus delayed-onset PTSD. Given evidence that earlier-onset and delayed-onset PTSD may involve distinct temporal and pathophysiological mechanisms, we hypothesized that cortisol and number of PDs would more strongly predict earlier-onset PTSD. Data were drawn from a prospective cohort of 895 adults hospitalized for traumatic injuries. Morning serum cortisol was measured within one month post-trauma. The number of PDs was assessed as a count of affected organ system categories, based on a 15-category system that integrated medical history, treatment records, and self/caregiver reports, without accounting for severity or functional impact. PTSD was evaluated at 3, 6, 12, and 24 months using the CAPS-5, and classified as earlier-onset (≤6 months) or delayed-onset (>6 months). Logistic regression models tested main and interaction effects of cortisol and number of PDs on PTSD onset, controlling for relevant covariates. Neither cortisol nor number of PDs independently predicted PTSD onset. However, lower cortisol predicted earlier-onset PTSD only among individuals with higher number of PDs (adjusted interaction p = 0.021). No association was found in those with lower number of PDs or for delayed-onset PTSD. Cortisol and number of PDs were modestly negatively correlated. number of PDs moderates the association between early post-trauma cortisol and earlier-onset PTSD. These findings highlight a context-dependent biological vulnerability and may help explain prior inconsistencies in cortisol-PTSD research. Integrating somatic health status into early PTSD risk models may improve prediction and prevention strategies.