Original Theory of Low DHEA and AIDS

James Howard phis at sprynet.com
Sat Nov 30 11:31:51 EST 1996

In 1985, I copyrighted the following statements: "Identification and
motivation cannot be separated in either the nervous system or the immune
system.  That these two systems are induced and stimulated to growth by
DHEA is one of the major ideas of this theory.  In the homosexual men just
discussed, the paramount idea is that their levels of DHEA are reduced due
to split conversion to estrone in the adrenal gland.  ...I implicated abnormally
low levels of DHEA production due to estrone production in the adrenal
gland in the discussion of homosexuality.  I decided that the behavioral
result is a loss of the nervous system to properly monitor.  I suggest that this
reduced level of DHEA is responsible for AIDS since the immune system of
these people is compromised."    pages 103-104  of "A Theory of the Control
of the Ontogeny and Phylogeny of Homo sapiens by the Interaction of
Dehydroepiandrosterone and the Amygdala,"  copyright 1985, James
Michael Howard, registered with the U.S. Copyright office: Registration No.
TXu 220 580.  The first connection of low DHEA in AIDS in the literature is in
1989, out of N.I.H. In my copyrighted book, above, I also suggested that
Alzheimer's disease is due to low DHEA.  The same group that reported low
DHEA in AIDS, also reported in 1989, that DHEA is low in Alzheimer's.

Among many documents I have from the period 1985 through 1989, are the
following letters from Eddie Reed, M.D., Executive Secretary, NCI/NIAID
Drug Selection Committee,  July 3, 1986, and one from Robert C. Gallo,
M.D.,  January 24, 1987.  These are simply to show my connection to DHEA
and AIDS.

I responded to an ad entitled "NIH Program for Developing Treatments for
Acquired Immunodeficiency Syndrome," in the May 16, 1986, Science.
(Science 232: 905)  with may ideas about DHEA; at the time my focus was
on receptors used by DHEA.

Dr. Reed wrote me to say:

"Thank you for providing us with data which suggest that DHEA receptors
may play a role in the devlopment of AIDS.  The data you submitted have
been forwarded to expert members of our committee for discussion and
evaluation.  You will be contacted shortly regarding the Committee's
deliberations and to solicit any additional suggestions you might have
regarding further studies of DHEA." [sic]

Dr. Gallo wrote me to say:

"Dr. [James D.] Watson has been thoughtful enough to send your
correspondence to me regarding AIDS.  I am not an expert in steroid
metabolism.  Your speculations on various hormone-receptor interactions
are expansive and intriguing.  I really think you fall down when you
generalize about either hormonal or environmental influences that risk
groups might share.  I think that the evidence is very direct that infection by
HTLV-III (Hiv) alone is necessary and sufficient to produce the disease.  In
the brain the major infected cell is a monocyte/macrophage and the receptor
remains the T-4 molecule itself.  It is apparent that either parenteral sexual
exposure to the virus may result in infection without regard for sex, age, or
nationality.  It is probably that a number of other factors, especially those
that activate the immune system with an infection, or possibly hormonal
influences, may modulate the extent of viral expression on an individual
bases." [sic]

It was reported in 1992, that "The serum E1 [estrone] and E2 [estradiol]
concentrations were elevated 30-50% (p<0.01) in all groups of HIV+
patients.  In contrast, the E2 levels were significanlly  high only in group IVD
(50%, p<0.01) and group IVC2 (25%, NS)."  Journal of Acquired Immune
Deficiency Syndromes 1992; 5: 841.  Please read my theory of AIDS at
http://www.naples.net/~nfn03605 on the web.
James Howard

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