I just sent the following to the New England Journal of Medicine regarding,
"A Reevaluation of the Duration of Survival after the Onset of Dementia,"
which is in the most recent issue
(http://www.nejm.org/content/2001/0344/0015/1111.asp ). I thought you might
be interested in reading it.
"I suggest the findings of Wolfson, et al., represent excessive loss of
dehydroepiandrosterone (DHEA). It is my hypothesis that DHEA evolved to
optimize transcription and replication of DHEA and cortisol evolved as the
chief antagonist to DHEA. This follows from my hypothesis that nervous
tissue uses DHEA more than other tissues. Loss of DHEA would undermine
maintenance of the nervous system while continued, or increased cortisol,
would exert antagonistic effects on the nervous system. (It is known that
continued, high levels of cortisol damage nervous tissues.) Since the brain
is most sensitive to levels of DHEA, the maintenance defect, called
dementia, represents severe loss of DHEA. This is directly supported in
vascular dementia and dementia of the Alzheimer's type in the levels of DHEA
and the ratio of DHEA to cortisol. "By comparison to vascular dementia,
patients with Alzheimer's disease exhibited the highest cortisol
concentrations throughout the 24h. …The serum DHEAS levels were
significantly lower in elderly subjects and even more in demented patients
than in young controls. Consequently, a significant increase of the
cortisol/DHEAS molar ratio was evident when going from young controls to
healthy elderly subjects and to demented patients." Exp Gerontol 2000; 35:
1239-50.
I suggest shorter survival times in the study subjects, who exhibited
dementia of the Alzheimer's type or vascular dementia, represent severe
reduction of DHEA."
