Læknaneminn


Læknaneminn - 01.04.1997, Side 126

Læknaneminn - 01.04.1997, Side 126
Peter Duesberg and David Rasnick demonstrates that the authors are clearly aware that a drug-free control group of HlV-positive AIDS patients is necessary to refute the drug hypothesis of AIDS, while at the same time supporting the orthodox view that HIV causes AIDS. However, the drug-free group reported by the authors proved to be an empty set, as no drug-free AIDS patients were recorded in the Nature commentary 11‘1’335. Our independent analysis of the data base also failed to identify the missing group of drug-free AIDS patients 115’221. Despite our chal- lenge in The Lancet 223, Genetica '15, and Science 3,6, to this date the authors have failed to come up with an explanation as to the origin of r/;«Vdrug-free group 337. 2) The re-investigation of the database of the Nature commentary further revealed that 45 drug-using, HIV- free patients had been omitted from the paper, although they had AIDS defining diseases "5. This brazen manipulation of the facts was legitimised with the CDC’s HIV antibody-based AIDS defmition 337 (see 2.). 3) The Nature commentary also omitted the fact that 73% of the HlV-positive AIDS patients were on AZT. However, in response to our challenge the authors acknowledged the AZT prescriptions 2 years later 303. Thus the drug hypothesis was refuted by claiming non-existing, drug-free AIDS patients, by hiding HIV- free AIDS patients, and by omitting widespread AZT use by AIDS patients. Numerous other epidemiologists have also investi- gated “HIV disease progression” 102 to AIDS in drug users 87,88,91‘93'101-104'106'279 without offering drug-free controls. Indeed, there is not a single epidemiological study in the bulging AIDS literature that ever described a group of HlV-positive people, without confounding health risks like drug use or hemophilia, progressing from HIV to AIDS n'225. This absence of drug-free controls is the single most damaging flaw of AIDS epidemiology. For example, Alcabes et al. conclude from a study of HlV-positive intravenous drug users from New York that, “The results of this analysis provide evidence for a mechanism by which the clinical factors that predict more rapid progression to AIDS, such as bacterial infection, might work, and why other factors, such as drug injection, are unrelated to AIDS rislc” 87. But no control is offered for drug-free AIDS. Based on analyses of HlV-positive intravenous drug users, “with 45% injecting at least once per day,” Margolick et al. conclude “that progression of HIV-1 infecdon in IV drug users, as reflected in the decline of CD4 cell counts, is no more rapid than that reported for other risk groups” 91. In an effort to exclude the role of drugs in AIDS, the authors pointed out that in a particular 6 month survey interval there was no “effect of active vs inactive drug use” on T cell loss. However, there was no verification for “inactive” drug use, and no informatiom as to whether “inactive” street drug use was substituted by methadone, which is itself immune suppressive 33S. Moreover there was no effort to determine the cumulative lifetime drug dose of active or “inactive” drug users that is essential to evalu- ate drug pathogenicity. There was also no information as to whether “other risk groups” included drug-free controls. It is also claimed that cohorts of HlV-positive male homosexuals using batteries of recreational drugs including, “alcohol, tobacco, cannabis, nitrites, cocaine and amphetamines” in addition to AZT developed AIDS from HIV infection alone without offering a population of drug-free HlV-patients as a control. For example, a “Tricontinental” study from San Francisco, Vancouver, Amsterdam and Sydney that was sponsored by the American NIAID concluded that, “None of the presented hazards is significant.” Although the study acknowledged that, “there were no appreciable differ- ences in the use of alcohol, tobacco or nitrites,” it insisted that, “Notably, nitrite use was not associated with disease progression, and the use of tobacco appears not to be related to progression to AIDS or P. carinii pneuntonia (data for the latter not shown)” 102. A remarkable “Tricontinental” conclusion! Likewise, the NIAID-sponsored MAC study of male homosexuals published that there is “No evidence for a role of alcohol or other psychoactive drugs in accelerat- ing immunodeficiency in HIV-1 positive individuals” 103 although it had never identified even one drug-free, HlV-positive homosexual with AIDS in 10 years 109. Indeed, a recent report from the MAC study, published in the Journal of Substance Abuse seems to contradict their earlier message: “Men who combined volatile nitrite (popper) use with other recreational drugs were at highest risk both behaviorally and in terms of human immunodeficiency virus-1 (HIV) seroconver- sion throughout the study.” All of the 500-800 homo- LÆKNANEMINN 124 1 ■ tbl. 1997, 50. árg.
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