The Cause of AIDS: Advanced Aging ...some history
James Howard
I have long thought that "AIDS" is really symptoms produced by severe
loss of DHEA. It is known that DHEA begins to decline soon after age
20, and declines to very low levels in old age. I, and others, think
that this loss of DHEA results in aging. I have often compared AIDS to
advanced aging. August 17, 1992, I sent a letter to EA Nunez, the last
author of the quotation below, that included this statement: "I intend
to demonstrate to you that DHEA is directly involved in immune system
function, and that reduced DHEA leads to vulnerability to the HIV and
the severely reduced DHEA results in AIDS, whether or not induced by the
HIV." December 7, 1992, Nunez responded to my letter. His letter
included: "I have read your thesis with great interest. It is
reassuring that our laboratory data can be integrated into such a broad
theoretical framework as the one you propose. Rest assured that your
thesis will be taken into account in our interpretation of future
experimental data. It is perhaps infortunate that we, who spend much of
our time with experimental manipulations do not always appreciate the
broader, integrated view of theoretical biology."
Psychoneuroendocrinology 1997;22 Suppl 1:S11-S18, "Serum cortisol and
DHEA concentrations during HIV infection," Christeff N, Gherbi N, Mammes
O, Dalle MT, Gharakhanian S, Lortholary O, Melchior JC, Nunez EA
'The progression of HIV infection is accompanied by severe
immunodepression and cachexia, particularly during advanced stages. The
immune depression is due largely to a dramatic drop in the number of CD4
cells. The loss of body weight is mainly due to a reduced fat-free mass
with no change in adipose tissue. We determined the serum concentrations
of cortisol and DHEA and their correlations with absolute CD4 cell
counts and changes in body weight of HIV-positive men. The results of
five retrospective and prospective studies indicate that the serum
concentrations of cortisol and DHEA in HIV-infected patients were
different from those of HIV-negative controls. Serum cortisol was
elevated at all stages of infection (+20 to +50%, p < .05 to p < .001)
particularly in AIDS patients (stage IV C). In contrast, the serum DHEA
concentrations were closely correlated with the stage of HIV-infection,
being higher in the early stages (stages II and III or > 500 CD4) than
in advanced stages (IV C or < 500 CD4)-in the latter being below those
of HIV-negative men-or in controls (+40 to 100%, p < .01 to p < .001).
There was a negative linear correlation between the CD4 cell counts and
cortisol (r = -0.4, p < .02) and a positive linear correlation with DHEA
(r = +0.36, p < .01). There was no significant correlation between delta
body weight and serum cortisol. In contrast, there was a negative
correlation between serum DHEA and delta body weight (%) (r = -0.69, p
<.0001) and a positive correlation with the cortisol/DHEA ratio
(r=+0.61, p < .0001). There is thus a link between the circulating
concentrations of adrenal steroids and the progression of
immunosuppression and cachexia during HIV-infection. This raises the
question of whether there is a cause-and-effect relationship between
clinical progression and circulating steroid concentrations. Further
investigations into the relationship between the ratio cortisol/DHEA and
the immune response and cachexia should indicate the contributions of
these steroids to the etiology of HIV infection and lead to the
development of new therapeutic strategies."
