The big advantage of this paper, compared to Duesberg’s book already posted in this thread, is that it’s much shorter (“only” 30 pages)…
My biggest criticism on this paper is that it offers nothing new since his 1996 book. Another criticism on this paper is that the other AIDS-toxics (besides AZT) to “treat” AIDS-victims, aren’t paid enough attention to. This is also a flaw in this thread.
Below are some excerpts from the paper, which show that:
1) AIDS isn’t caused by any virus;
2) In Africa there is a correlation between malnutrition and AIDS;
3) There is a correlation between “recreational” drugs use and AIDS.
Please note that I’m not convinced that “recreational” drugs cause AIDS. Maybe drugs users can be more easily poisoned with chemical and biological weapons...
However, the plethora of AIDS diseases was not, and still is not randomly distributed even among the different risk groups (table 2). For example, Kaposi’s sarcoma was exclusively diagnosed in male homosexual risk groups using nitrite inhalants and other psychoactive drugs as aphrodisiacs (Newell et al 1984; Haverkos et al 1985; Selik et al 1987; Duesberg 1988; Haverkos and Dougherty 1988; Beral et al 1990). Bacterial pneumonia was primarily diagnosed in children from mothers using psychoactive drugs during pregnancy (Novick and Rubinstein 1987; Duesberg 1988, 1992; Centers for Disease Control and Prevention 1997). Tuberculosis and pneumonia were, and still are more prevalent in intravenous drug users and “crack” (cocaine) smokers than in other risk groups (Lerner 1989; Duesberg 1992; Duesberg and Rasnick 1998).
In sharp contrast to its US/European namesakes, the African AIDS epidemic is randomly distributed between the sexes and not restricted to behavioural risk groups (Blattner et al 1988; Duesberg 1988; World Health Organization 2001a). Hence sub-Saharan African AIDS is compatible with a random, either microbial or chemical cause.
But, only 1 in 1000 unprotected sexual contacts transmits HIV (32–34) , and only 1 of 275 US citizens is HIV-infected (29, 30), (figure 1b). Therefore, an average un-infected US citizen needs 275,000 random “sexual contacts” to get infected and spread HIV – an unlikely basis for an epidemic!
But, in the peer-reviewed literature there is not one doctor or nurse who has ever contracted AIDS (not just HIV) from the over 816,000 AIDS patients recorded in the US in 22 years (30). Not one of over ten thousand HIV researchers has contracted AIDS. Wives of hemophiliacs do not get AIDS (35). And there is no AIDS-epidemic in prostitutes (36–38). Thus AIDS is not contagious (39, 40).
According to the article “the state’s top AIDS and HIV prevention officials came up with the smoking gun of all statistics: Gay men in California who use speed are twice as likely to be HIV-positive . . .” (Heredia 2003a).
The case for malnutrition and lack of drinkable water as the common denominator and probable cause of African AIDS in the HIV-era has been made by scientific (Mims and White 1984; Seligmann et al 1984; Konotey-Ahulu 1987a, b, 1989; Fiala 1998; Oliver 2000; Stewart et al 2000; Ross 2003) and non-scientific observers (Hodgkinson 1996; Shenton 1998; Malan 2001). The non-scientific observers even include the United Nations (Namango and World Food Program of the United Nations 2001) and president Mbeki of South Africa (Cherry 2000; Gellman 2000).
For example, the Lancet published in 1993 a Canadian epidemiological study, “HIV and the etiology of AIDS”, which found that 88% of AIDS cases in a cohort of male homosexuals at risk for AIDS had used nitrite inhalants and that 75–80% of the same cohort had also used “cocaine, heroin, amphetamines, lysergic acid dimethyl amide, or methylenedioxy amphetamine” (Schechter et al 1993). One of the subjects even passed away on an “overdose” of recreational drugs during the study. In addition an undisclosed percentage (but in 1993 certainly a high percentage, see above) was also prescribed the DNA chain-terminator AZT as anti-HIV drug (Duesberg 1993a, c). Thus not a single drug-free AIDS patient was identified. But, the study concluded, “drugs and sexual activity is rejected by these data” as causes of AIDS. Nevertheless, the authors acknowledged that their study “does not rule out a role for cofactors . . .”.
A sudden 10-fold increase in the mortality of HIV-positive British hemophiliacs, right after the introduction of AZT in 1987, made scientific headlines in 1995, because the increased mortality was attributed to HIV by the authors of the study, i.e. Darby et al (1995), as well as by the editor of Nature, “More conviction on HIV and AIDS” (Maddox 1995). Even the editor of the Lancet wrote an editorial asking, “Will Duesberg now concede defeat” (Horton 1995)? Darby et al based their conclusion on the sudden 10-fold increase of the hemophiliacs’ mortality in 1987, shown in figure 5, on the facts that the increased mortality was restricted to HIVpositive hemophiliacs and that the increase was independent of the degree of hemophilia (which is inversely proportional to the life expectancy of the patient).
Moreover, the mortality of hemophiliacs was steadily decreasing since the 1970s until 1987 – despite the presence of HIV (Duesberg 1995c)! Thus the only new risk of mortality, in and after 1987, was not HIV, but AZT. Darby et al even acknowledged “treatment, by prophylaxis against P. carinii pneumonia or with zidovudine (AZT), has been widespread for HIV-infected haemophiliacs since about 1989 (more accurately since 1987)”. The editor of Nature also pointed out that, “Darby et al failed to provide full details of the drug regimen followed” (Maddox 1995). The AZT-mortality hypothesis would of course also explain why the new hemophilia mortality was independent of the severity of the hemophilia, as Darby et al observed.