Patients with posttraumatic stress disorder (PTSD) have numerous endocrine abnormalities. Several involve the "stress hormone" cortisol, but the hypothalamic-pituitary-adrenal (HPA) system includes internal feedback, and it is difficult to pinpoint where problems begin. Yehuda et al. (p.
1397) tested two possibilities: one, that negative feedback within the HPA axis is exaggerated in PTSD, thereby inhibiting overall activity, and two, that the adrenal glands of PTSD patients produce reduced amounts of cortisol. The findings supported the first hypothesis. The cortisone-like agent dexamethasone decreased both cortisol and adrenocorticotropic hormone (ACTH) more in PTSD patients than in healthy subjects. ACTH is thought to respond to dexamethasone upstream of the adrenal glands, and so the parallel responses of ACTH and cortisol suggest an overall effect, rather than adrenal insufficiency, which would affect cortisol only.
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