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Ascher et al.(1)
challenge my hypothesis that injected and orally consumed recreational
drugs and AZT cause AIDS.(2,3) Based on a one-time inquiry about
the use of marijuana, nitrite inhalants, cocaine and amphetamines
"for the 24-month period before entry into the study"
of mostly homosexual men from San Francisco, they claim that the
incidence of AIDS diseases over 8 years is independent of drugs.
However, their
study is worthless for a scientific appraisal of the drug-AlDS hypothesis,
because it fails i) to study the AIDS risk of HlV-positive, drug-free
controls, ii) to quantify recreational drug use, iii) to observe
drug use long enough to detect toxicity, and iv) to report AZT use
altogether.
Ascher et al.
claim that "when controlled for HIV serostatus, there is no
overall effect of drug use on AIDS," and that a "group"
of "seropositive no-drug" users have lost T-cells at the
same rates as "seropositive-heavy drug" users. However
there were no HIV-positive no-drug users in Ascher's study, although
the text implies that there were "homosexual/bisexual men reporting
none [drug use]."
This is documented
as follows. According to Table 1 all HIV-positives were homosexuals.
All heterosexuals were HIV-negative, except one who was a drug addict
(Ascher personal communication). According to Table 2 100% of the
homosexual men were either "heavy" or "light"
nitrite users, namely 144 plus 668 (Table 2) out of 812 (text).
An unreported percentage of these men had also used other illicit
recreational drugs, such as cocaine and amphetamines, in addition
to AZT (see below). It follows that there are no HIV positives who
did not use drugs. Thus Ascher et al. directly confirm my drug-AlDS
hypothesis. The association of drug use with all AIDS cases voids
all of Ascher et al.'s claims of HIV-positive drug-free AIDS. Moreover
if the data given elsewhere in the paper are correct, the curve
in the Figure said to represent a "group" of "seropositive-no
drug" users represents in fact nobody and is therefore a fabrication.
Ascher et al.
also did not record how many drugs were consumed over any period.
Although the cohort was examined at "6-monthly intervals,"
they based their drug-AlDS correlations on information "for
the 24-month period before entry into the study." However with
drugs "the dose is the poison." For example, lung cancer
and emphysema are only acquired after at least 10 years of heavy
smoking. If one were to correlate information on smoking for only
24 months with lung cancer, the results would be as inconclusive
as Ascher et al.'s on drugs and AIDS. The 10 years of recreational
drug use that is necessary to cause AIDS is a rational explanation
for what is claimed to be the 10-year latent period of HIV by proponents
of the HIV-AIDS hypothesis.(2) Indeed, Ascher et al. also confirm
this aspect of the drug hypothesis with the observation that "heavy"
drug users had twice as much AIDS and particularly Kaposi sarcoma
as "light" users (Table 2). They correctly suggest that
"this crude association is apparently the basis for Duesberg's
hypothesis."
Moreover, the
AIDS cases that Ascher et al. blame on HIV can instead be blamed
on drugs because HIV is a marker for drug consumption. As they acknowledge,
homosexuals at risk for AIDS use drugs as aphrodisiacs. Their data
also confirm this point, as 72.9% of the heavy drug users but only
50.9% of the light users are HIV positive (Table 2). Since it takes
about 1000 frequently drug-promoted sexual contacts to pick up HIV2,
HlV-positives have consumed the drug-equivalent of 1000 contacts
more than have the negatives. This is one reason why HlV-positives
are more likely to develop diseases from drug toxicity than negatives.
HIV positivity
is also an indication for AZT therapy, which they fail to report
altogether. AZT is prescribed as AIDS prophylaxis and therapy to
HIV-positives but not to HIV-negatives.(2) As a chain terminator
of DNA synthesis AZT is particularly toxic for the bone marrow (2,4,5),
the source of T-cells. Indeed one of Ascher's coauthors (Winkelstein)
confirms the widespread use of AZT in the San Francisco study.(6)
This plus recreational drug use readily explains the decline of
T-cells in HIV positives, which Ascher et al. blame on HIVI. To
properly evaluate the drug-AlDS hypothesis, they must compare the
numbers of T-cells over time in two groups of HIV-positives, those
who use recreational drugs, AZT or both and those who do not.
Ascher et al.
also fail to explain why "recreational drug use was considered
an aetiological factor" by epidemiologists before 1984 and
why since 1984 they find HIV to be the only cause of AIDS.(7) Epidemiologists
seemed to have changed their perspective at exactly the time when
the Department of Health and Human Services restricted funding for
AIDS to HIV research.
Considering
that AZT was developed to kill human cells by DNA chain termination
for cancer chemotherapy, and that nitrites are among the best known
mutagens and carcinogens, and can cause exactly the same Kaposi
sarcomas in HIV-free homosexuals as in those with HIV (7,3), it
is surprising that AIDS epidemiologists prefer the "enigmatic
mechanisms of HIV pathogenesis to AIDS" over straightforward,
chemical drug toxicity. But even solving all enigmas of HIV would
not explain the over 3000 HIV-free AIDS cases recorded in the literature
(2,8).
Peter Duesberg
Prof. of
molecular biology, UC Berkeley
References
1. Archer,
M.S., Sheppherd, H.W., Winkelstein Jr., W. & Villinghoff, E.
Nature 362, 103-104 (1993).
2. Duesberg,
P.H. Pharmacology & Therapeutics 55, 201-277 (1992).
3. Duesberg,
P.H. Biomed. Pharmacother. 46, 3-15 (1992).
4. Kolata,
G. Science 235,1462-1463 (1987).
5. Harnilton,
J.D., et al. N. Engl. J. Med. 326, 437-443 (1992).
6 Lang, W.,
el al. JAIDS 4 713-716 (1991).
7. Oppenheimer,
G.M. in AIDS: The Making of a Chronic Disease (eds. Fee,
E. & Fox, D.M.) 49-83 (University of California Press, Berkeley,
1992).
8. Duesberg,
P. Science 257,1848 (1992).
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