| James Michael Howard 2005-03-23, 5:38 pm |
| Dehydroepiandrosterone and Persistant Vegetative States or Coma
Copyright 2005, James Michael Howard, Fayetteville, Arkansas, U.S.A.
It is my hypothesis that dehydroepiandrosterone (DHEA) is necessary
for proper brain function. Therefore, I have thought for some time
that comas may exhibit low DHEA. The literature does not directly
support my hypothesis, however, there are indications that I may be
correct. Head trauma results in significant reductions in DHEA, among
some other hormones (Clin Endocrinol (Oxf). 1986 Sep;25(3):265-74). A
case may be made that reduced DHEA may be the significant cause.
I suggest that when DHEA is not produced in sufficient amounts, the
DHEA-stimulator, prolactin, should be increased. That is, if DHEA is
available in proper amounts, DHEA feedback reduces prolactin.
Hyperprolactinemia has been found in a persistent vegetative state
along with a return to normal prolactin in patients who emerged from
coma (Immunopharmacol Immunotoxicol. 1998 Nov;20(4):519-29). It is
known that DHEA levels are often inversely related to interleukin-6
(IL-6) and TNF-alpha levels. IL-6 and TNF-alpha levels increase
following brain trauma in brain injury in rats (J Surg Res. 2005
Feb;123(2):188-93). People who suffer head trauma exhibit elevated
levels of IL-6 and "pronounced increase in IL-6 levels" upon
development of "brain death" (Metabolism. 1995 Jun;44(6):812-6).
C-reactive protein (CRP) is also elevated in head trauma and coma.
DHEA levels are also inversely related to CRP.
I suggest persistent vegetative states and / or coma may benefit from
treatment with DHEA.
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