Neuroendocrine aspects of post-traumatic stress disorder

This chapter discusses how endocrine findings in post-traumatic stress disorder (PTSD) potentially inform hypothalamic-pituitary-adrenal (HPA) axis alterations associated with the disorder. Findings on basal cortisol levels, as well as 24-h excretion and circadian rhythm of cortisol, are presented, with the most common finding (low basal cortisol) discussed as a possible pretraumatic risk factor for developing PTSD. Also discussed are data on other factors that are likely to be involved in PTSD risk and pathology (i.e., CRF, ACTH, cortisol-binding globulin, and glucocorticoid receptors), and findings from endocrine challenge studies (such as the dexamethasone suppression test). These empirical findings on biologic alterations in PTSD are then compared with various models of HPA-axis dysfunction (notably enhanced negative feedback inhibition vs. adrenal insufficiency). The authors conclude that enhanced negative feedback inhibition seems most consistent with the range of findings that have been reported on PTSD, and therefore, is likely to play an important role in the disorder's pathology and pathogenesis. The chapter closes with a discussion of challenges and open questions in endocrine research on PTSD.