Neuroendocrine and neuroimmune markers in PTSD: pre-, peri- and post-trauma glucocorticoid and inflammatory dysregulation

- Low cortisol, enhanced GR function and a pro-inflammatory state have been repeatedly observed in subpopulations of PTSD patients.
- Biological dysregulation may precede trauma exposure and PTSD development.
- Post-trauma dysregulation may become more apparent over time.
- Effective therapy may attenuate dysregulation.
- Pre-treatment neurobiological functioning may predict treatment outcome.

We review current knowledge on how posttraumatic stress disorder (PTSD) is associated with dysregulation of the most commonly studied markers of the endocrine and immune systems pre-, peri- and post-trauma. Lower basal cortisol output, enhanced glucocorticoid receptor function, and a proinflammatory state have been most consistently found in PTSD, with considerable variability among studies and participants. Longitudinal research is scarce, but there is converging evidence that biological dysregulation is present before PTSD onset. Biological dysregulation may become more apparent with increasing time since trauma, and may be reversible with and predict effective treatment. However, considering the variability of findings and the complex interplay of these systems with other factors, the current clinical application of these findings remains limited.

Hypothesized routes toward PTSD versus prevention and/or recovery for individuals with dysregulated glucocorticoid-signaling and immune function as underlying biological mechanism.209