Dehydroepiandrosterone and Persistent 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.