Refutation of Duesberg and Rasnick on AIDS

James Michael Howard jmhoward at
Mon Aug 14 07:49:21 EST 2000

A Response to Duesberg and Rasnick (Genetica 1998;104(2):85-132)

An Explanation of Differential HIV Infection and Other AIDS Phenomena that
Refutes the Duesberg and Rasnick Hypotheses

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

Duesberg and Rasnick suggest: "The drug hypothesis predicts that AIDS: (1) is
non-contagious; (2) is non-random, because 85% of AIDS causing drugs are used by
males, particularly sexually active homosexuals between 25 and 49 years of age,
and (3) would follow the drug epidemics chronologically."  (Genetica 1998; 104:

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.  

More information about the Immuno mailing list