I just found the following citation which supports my theory of
reduced DHEA and AIDS (http://www.naples.net/~nfn03605).
James Howard
Khorram O, et al., "Activation of immune function by
dehydroepiandrosterone (DHEA) in age-advanced men," J Gerontol A Biol
Sci Med Sci 52 (1): M1-M7 (1997)
"BACKGROUND: Substantial data from animal studies have demonstrated a
stimulatory effect of dehydroepiandrosterone (DHEA) on immune
function. However, little is known about the effects of DHEA on the
human immune system. Since aging is associated with a decline in
immune function and in DHEA production, we proposed that oral
administration of DHEA to elderly men would result in activation of
their immune system. METHODS: Nine healthy age-advanced men (mean age
of 63 years) with low DHEA-sulfate levels participated in this study.
They were treated nightly with an oral placebo for 2 weeks followed by
DHEA (50 mg) for 20 weeks. Fasting (0800h-0900h) blood samples were
obtained at 4- to 8-week intervals for immune function studies and
hormone determinations. Freshly isolated peripheral lymphocytes were
used for flow cytometric identification of lymphocyte subsets, cells
expressing the IL-2 receptor (IL-2R), mitogen stimulation studies, and
for determining natural killer (NK) cell number and cytotoxicity.
Levels of interleukin-2 (IL-2) and IL-6 secreted from cultured
lymphocytes were determined under basal and mitogen stimulated
conditions. Sera were analyzed for soluble IL-2 Receptor (sIL-2R)
levels, insulin-like growth factor-I (IGF-I) and IGF binding protein-I
(IGFBP-I) concentrations. RESULTS: Baseline levels of serum DHEA
sulfate (DHEAS), a stable marker of circulating DHEA levels, were 2
standard deviations below young adult values and increased 3-4 fold
within 2 weeks. These levels were sustained throughout the duration of
DHEA administration. When compared with placebo, DHEA administration
resulted in a 20% increase (p < .01) in serum IGF-I, a decreasing
trend in IGFBP-I, and a 32% increase in the ratio of IGF-I/IGFBP-I (p
< .01). Activation of immune function occurred within 2-20 weeks of
DHEA treatment. The number of monocytes increased significantly (p <
01) after 2 (45%) and 20 (35%) weeks of treatment. The population of
B cells fluctuated with increases (p < .05) at 2 (35%) and 10 (29%)
weeks of treatment. B cell mitogenic response increased 62% (p < .05)
by 12 weeks unaccompanied by changes in serum IgG, IgA, and IgM
levels. Total T cells and T cell subsets were unaltered. However, a
40% increase (p < .05) in T cell mitogenic response, 39% increase in
cells expressing the IL-2R (CD25+) (p < .05), and 20% increase in
serum sIL-2R levels (p < .01) were found at 12-20 weeks of DHEA
treatment, suggesting a functional activation of T lymphocytes
occurred. In vitro mitogen stimulated release of IL-2 and IL-6 was
enhanced 50% (p < .05) and 30% (p < .01) respectively by 20 weeks of
treatment without basal secretion being affected. NK cell number
showed a 22-37% increase (p < .01) by 18-20 weeks of treatment with a
concomitant 45% increase (p < .01) in cytotoxicity. There were no
adverse effects noted with DHEA administration. CONCLUSION:
Administration of oral DHEA at a daily dose of 50 mg to age-advanced
men with low serum DHEAS levels significantly activated immune
function. The mechanism(s) to account for the immunoenhancing
properties of DHEA are unclear. Consideration is given to the
potential role of an increase in bioavailable IGF-I, which by virtue
of its mitogenic effects on immune cell function, may mediate the DHEA
effects. While extended studies are required, our findings suggest
potential therapeutic benefits of DHEA in immunodeficient states."