Response to Duesberg and Rasnick on AIDS

James Howard jameshoward950 at
Sat Jul 29 09:13:15 EST 2000

A Response to Duesberg and Rasnick (Genetica 1998;104(2):85-132): An
Explanation of Differential HIV Infection and Other Phenomena

James Michael Howard
Fayetteville, Arkansas, U.S.A.

In 1985, I suggested vulnerability to infection by the HIV is due to
lowered levels of dehydroepiandrosterone (DHEA).  Following puberty, as
a group, male homosexuals produce less DHEA than heterosexual men
(Biological Psychiatry 1973; 6: 31).  (It is my hypothesis that male
homosexuality results from low DHEA during brain development, in
utero.)  Therefore, male homosexuals are more vulnerable to infection.
When the HIV entered the United States, this group was first hit.
Since there is overlap in DHEA levels between homosexual men and
heterosexual men, this would predict that some men will be infected,
and continue to AIDS, some will be infected, but not continue to AIDS,
and some will not be infected.  This is the case in the male homosexual
community.  DHEA starts to decline around age 25 and continues to very
low levels in old age.  Nearly 75% of AIDS-related mortality is in men
25 to 44 years of age (Science 1988; 239: 611).

Now, I later deduced that the hormone, testosterone, reduces
availability of DHEA.  Therefore, men should exhibit greater infection
rates than women.  "More than 90% of AIDS-related premature mortality
occurs in men" (Science 1988; 239: 611).  In an animal model, it is
demonstrated that testosterone is directly involved in infection and
persistence of a virus, the equine arteritis virus ((Journal of
Comparative Pathology 1994; 111: 383 and J Comp Pathol 1993; 109: 29).
Black men produce significantly more testosterone than white men
(Journal of the National Cancer Institute 1986; 76: 45) and black women
produce "moderately, but significantly" more testosterone than white
women (Journal of Clinical Endocrinology and Metabolism 1996; 81:
1108).  Viral persistence according to race was recently reported in
humans.  "Persistent viremia" occurs more in blacks than
whites.  "Although the basis for this racial difference [in persistent
viremia] is unknown, the magnitude of the association and its
independence from other factors suggest host genetics may be important
in the outcome of acute hepatitis C.  …Further research is needed to
explain the less frequent clearance of HCV [Hepatitis C Virus]
infection among black persons and to improve utilization of treatment
for those infected in the context of injection drug use." (Journal of
the American Medical Association 2000; 284: 450).  Therefore, the least
HIV infection rates should occur in white women, followed by black
women, then white men, then black men.  This is the case (Science 1995;
270: 1372).  The ratio of testosterone in these four groups produces
the differences in HIV infection rates in the heterosexual population.
This also explains why Africa exhibits so much greater infection rates.

HIV infection is connected to drug use.  However, this is not
necessarily connected to needle sharing.  Again, the connection to
higher testosterone is supported.  "While blacks and Hispanics had a
greater HIV seroprevalence rate than whites, whites reported sharing
[needles] more.  Further, sharing needles was more frequent among white
HIV-seropositive IVDAs [intravenous drug abusers] than among their
minority counterparts." (Journal of the American Medical Association
1987; 258: 1475).  I suggest testosterone contributes to this
difference.  The connection of HIV infection is very high in drug
abusing communities.  There is more to this difference than differences
in testosterone levels.  For years I have thought that all drugs of
abuse produce effects on DHEA production: (1) they first stimulate
DHEA, which (2) increases dependence, then (3) DHEA production
eventually wanes and results in tolerance.  The drug abuser, over time,
must use drugs to try to keep DHEA levels up.  At first DHEA is
involved in the effectiveness of the drugs, then, as DHEA production
declines because of over-use of the adrenal glands, the effectiveness
declines.  The drug abuser seeks only to maintain declining levels of
DHEA, while drug effects decline.  I have found little support in this
area of my theory of DHEA function, but there is one citation that fits
well.  In the following study, chronic methadone produced significant
decreases in DHEA, only, compared to other hormones.

"The effect of chronic methadone treatment upon the serum levels of
Estradiol (E2), Progesterone (P), Prolactin (Prl), monkey chorionic
gonadotropin (mCG), dehydroepiandrosterone sulfate (DHEAS) and Cortisol
(C) in pregnant Cynomolgus monkeys (Macaca fascicularis) is described
in comparison with the hormone levels in a control group. Only DHEAS
was significantly decreased in late pregnancy in the methadone group.
>From these data it can not be concluded that methadone treatment
compromises (feto)placental function. The observed intra-uterine growth
retardation in the methadone treated group might be a result of a
direct influence of methadone upon growth." (European Journal of
Obstetrics, Gynecology, and Reproductive Biology 1991; 38: 145).

(Since my work suggests all growth, development, and maintenance of all
tissues depends on DHEA, I suggest "intra-uterine growth retardation in
the methadone treated group" was due to the significant decrease in
DHEAS (the background supply of DHEA).  It was this assumption, in
1985, that resulted in my prediction of low DHEA in AIDS in 1985.)

So, drug abuse, at least methadone and probably other drugs of abuse,
may reduce the availability of DHEA and impair immune function.
Therefore, I suggest that the connection of drugs of abuse and HIV/AIDS
results from the ultimate decline of DHEA.  When this occurs in people
of higher testosterone, the result intensifies.  I suggest this is why
HIV infection appears to be caused by drugs of abuse.

I mentioned above that I think all tissue maintenance depends on DHEA.
DHEA first surges during HIV infection, then declines.  This is a surge
of DHEA which stimulates the immune system.  Because of the decline of
DHEA during progression to AIDS, I have suggested for many years that
the symptoms of AIDS actually represent loss of DHEA.  This was
recently supported: "This study confirms that low serum DHEAS is
associated with HIV illness markers, including viral load, and carries
a negative prognostic value." (Journal of Acquired Immune Deficiency
Syndrome 1999; 22: 146).  Now, the loss of DHEA will produce effects in
different tissues according to vulnerabilities.  Therefore, AIDS will
produce symptoms typical of other diseases and phenomena that cause
DHEA declines will produce symptoms of AIDS.  This is why some diseases
mimic AIDS.

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