Dehydroepiandrosterone and Persistant Vegetative States or Coma

James Michael Howard jmhoward at
Tue Mar 22 13:35:15 EST 2005

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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