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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



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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