VIRUSMYTH HOMEPAGE
DUESBERG REPLIES
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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