The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and holocaust survivors with and without posttraumatic stress disorder

@article{Yehuda2002TheCA,
  title={The cortisol and glucocorticoid receptor response to low dose dexamethasone administration in aging combat veterans and holocaust survivors with and without posttraumatic stress disorder},
  author={R. Yehuda and S. Halligan and R. Grossman and J. Golier and Cheryl M. Wong},
  journal={Biological Psychiatry},
  year={2002},
  volume={52},
  pages={393-403}
}
BACKGROUND Because alterations in cortisol negative feedback inhibition associated with aging are generally opposite of those observed in posttraumatic stress disorder (PTSD), we examined the cortisol and glucocorticoid receptor (GR) response to dexamethasone (DEX) in older trauma survivors. METHODS Twenty-three Holocaust survivors (9 men, 14 women), 27 combat veterans (all male), and 10 comparison subjects (7 men, 3 women) provided samples for plasma or salivary cortisol and glucocorticoid… Expand
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The results suggest that trauma exposure is sufficient to induce changes in GR binding characteristics, whereas resistance of T-cell proliferation to DEX only occurs in PTSD. Expand
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The ACTH response to dexamethasone in PTSD.
TLDR
The data support the hypothesis of enhanced cortisol negative feedback inhibition of ACTH secretion at the level of the pituitary in PTSD, which is implicated as a likely mechanism for this effect. Expand
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TLDR
Comparison of basal cortisol levels in adults with current PTSD and in people without psychiatric disorder revealed that studies assessing plasma or serum showed significantly lower levels in people with PTSD than in controls not exposed to trauma. Expand
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Maternal PTSD associates with greater glucocorticoid sensitivity in offspring of Holocaust survivors
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Findings are consistent with the hypothesis that epigenetic programming may be involved in the intergenerational transmission of trauma-related effects on glucocorticoid regulation. Expand
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