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The ACTH response to dexamethasone in PTSD
Rachel Yehuda1, Julia A Golier, Sarah L Halligan
1Traumatic Stress Studies Program, Department of Psychiatry, Mount Sinai School of Medicine, and Bronx Veterans Affairs Medical Center, New York, USA. rachel.yehuda@med.va.gov
The American Journal of Psychiatry
|August 3, 2004
Summary
Individuals with posttraumatic stress disorder (PTSD) exhibit enhanced negative feedback regulation of the stress response. This suggests pituitary-level adjustments, not adrenal insufficiency, are key in PTSD.
Area of Science:
- Neuroendocrinology
- Psychiatry
Background:
- Posttraumatic stress disorder (PTSD) presents paradoxical endocrine findings, including increased corticotropin-releasing factor release despite low cortisol levels.
- Two models, enhanced negative feedback and reduced adrenal output, attempt to explain these observations.
Purpose of the Study:
- To differentiate between enhanced negative feedback and reduced adrenal output models in PTSD.
- To investigate adrenocorticotropic hormone (ACTH) and cortisol dynamics in response to dexamethasone suppression in PTSD.
Main Methods:
- Assessed ACTH and cortisol responses to 0.50 mg dexamethasone in 19 PTSD subjects and 19 healthy controls.
- Compared baseline and dexamethasone-suppressed ACTH-to-cortisol ratios between groups.
Main Results:
- No significant difference in ACTH-to-cortisol ratio between groups at baseline or after dexamethasone.
- PTSD subjects demonstrated greater suppression of both ACTH and cortisol following dexamethasone administration.
Conclusions:
- Findings support enhanced cortisol negative feedback inhibition of ACTH secretion at the pituitary level in PTSD.
- Suggests pituitary glucocorticoid receptor function, not low adrenal output, is the primary mechanism.