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Foreword P.H. Duesberg. A Critical Analysis of the HIV-T4-cell-AIDS Hypothesis E. Papadopulos-Eleopulos, et al. Factor VIII, HIV and Aids in Haemophiliacs: An Analysis of their Relationship E. Papadopulos-Eleopulos, et al. Foreign-Protein-Mediated Immunodeficiency in Hemophiliacs with and without HIV P.H. Duesberg. Critical Analysis of the Current Views on the Nature of AIDS V.L. Koliadin. Some Mathematical Considerations on HIV and AIDS M. Craddock. HIV as a Surrogate Marker for Drug Use: A Re-analysis of the San Francisco Men's Health Study B.J. Ellison, et al. A Critical Appraisal of the Vancouver Men's Study Does it Refute the Drugs/AIDS Hypothesis? M. Craddock. Duesberg and the Right of Reply According to Maddox-Nature P.H. Duesberg, H. Bialy. HIV: Science by Press Conference M. Craddock. AZT Toxicity and AIDS Prophylaxis: Is AZT Beneficial for HIV+ Asymptomatic Persons with 500 or More T4 Cells per Cubic Millimeter? M.D. Zaretsky. The Toxicity of Azidothymidine (AZT) on Human and Animal Cells in Culture at Concentrations Used for Antiviral Therapy D.T. Chui, P.H. Duesberg. Measuring Inhalant Nitrite Exposure in Gay Men: Implications for Elucidating the Etiology of AIDS-Related Kaposi's Sarcoma H.W. Haverkos, D.P. Drotman. A Hypothetical Disease of the Immune System That May Bear Some Relation to the Acquired Immune Deficiency Syndrome K.B. Mullis. The Epidemiology and Transmission of AIDS: A Hypothesis Linking Behavioural and Biological Determinants to Time, Person and Place G.T. Stewart. Five Myths About AIDS that have Misdirected Research and Treatment R.S. Root-Bernstein. Semen Alloantigens and Lymphocytotoxic Antibodies in AIDS and ICL R.S. Root-Bernstein, S. Hobbs de Witt. AIDS and Good Theory-Making S. Harris. How Much Longer Can We Afford the AIDS Virus Monopoly? P.H. Duesberg. HIV and AIDS: Have we Been Misled? Questions of Scientific and Journalistic Responsibility S. Lang. To Fund or Not to Fund, That is the Question: Proposed Experiments on the Drug--AIDS Hypothesis To Inform or Not to Inform, That is Another Question S. Lang. HIV Symposium at AAAS Conference J. Lauritsen. AIDS and Poppers T. Bethell. NIDA Meeting Calls for Research into the Poppers--Kaposi's Sarcoma Connection J. Lauritsen. The Thinking Problem in HIV-Science P.E. Johnson. The Incidence Quagmire J. Lauritsen. The HIV Test C. Farber. Cry, Beloved Country: How Africa Became the Victim of a Non-Existent Epidemic of HIV/AIDS N. Hodgkinson.
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Chapters (15)

It is commonly accepted that HIV is both necessary and sufficient to cause the immunodeficiency and multiple diseases seen in patients diagnosed with AIDS. In other words it is accepted that HIV is the cause of AIDS. Upon this basis public health decisions in all Western countries regarding AIDS are made. However, many scientists now question the role of the virus (Root-Bernstein, 1993). Questions that have arisen about the virus include whether or not it is present in sufficient quantities to cause disease and whether or not AIDS is infectious. The former question has been applied to by new studies using the Polymerase Chain Reaction (PCR) technique that claim to detect very large quantities of virus in HIV+ patients at all stages of disease progression. I will examine these studies and show that they do not truly answer the criticisms that have been levelled. They in fact give rise to more questions than they answer. Predictions that one can make from them contradict the observed pattern of the disease. I will also argue that data based upon the so called Quantitative Competitive PCR need to be treated with caution.
The Vancouver cohort study of Schechter et al. (1993a) claiming to refute the drugs/AIDS hypothesis made by Peter Duesberg is critically examined. It is argued that the data as reported do not refute the Duesberg theory. Further, the data may in fact be taken as experimental confirmation of the drugs/AIDS hypothesis. It is concluded that research needs to be done so that the drugs/AIDS hypothesis can be correctly tested, and that the Vancouver research group should release more of its data so that a proper evaluation of their results can be made.
In 1993 John Maddox, the editor of Nature, commissioned a commentary refuting the hypothesis that drugs cause AIDS (Ascher et al., 1993). The piece described 215 patients each of which had used drugs (Duesberg, 1993a; Duesberg, 1993b; Duesberg, 1993c). In view of this Duesberg sent a letter to Nature arguing that the perfect correlation between drug use and AIDS confirmed, rather than refuted, the drug hypothesis. Maddox censored the letter and wrote an editorial ‘Has Duesberg a Right of Reply?’ (Maddox, 1993). The editorial pointed out that the world’s oldest science journal could not afford an open scientific debate on the cause of AIDS because of the perceived dangers of infectious AIDS.
One of the most disturbing aspects of what passes for AIDS research these days, is the separation between what researchers actually find, what they tell the press conference and what the media tells the public. To assume that these three are identical or even similar would be pure folly. The press conference has a venerable history in AIDS science. When Robert Gallo’s group ‘found’ that 26 out of 72 AIDS patients had small amounts of newly discovered retrovirus in their bodies, this interesting but unconvincing work was transformed by the magic of an officially sanctioned press conference into the announcement of the ‘probable cause of AIDS’. And Gallo’s modest findings became ‘compelling evidence’ that this new retrovirus was the cause of AIDS. Ten years later nothing has changed.
Since the writings of the 18th century philosopher David Hume it has been known that certainty about physical causes and effects is not to be had from mere association, even if the temporal sequence is correct. In fact, according to Hume, absolute certainty about positive causation is not to be had, even when we can do direct experiments — but most scientists ignore this most extremely pessimistic view of causal knowledge (or else they view the high degree of inductive certainty gainable with experiment to be ‘good enough’).
Until 1984 AIDS science was open. Initially the new epidemic of pneumonias and Kaposi’s sarcomas, since called AIDS, was considered a collection of non-infectious ‘lifestyle’ diseases. But the Centers for Disease Control in Atlanta published that the pneumonias and Kaposi’s sarcomas of male homosexuals, who were addicted to recreational drugs, were caused by a common infectious agent because patients had been ‘linked’ by sexual contacts. On the basis of the CDC’s sexual linkage study, the Secretary of Health and Human Services announced in 1984 the hypothesis that the retrovirus HIV, is the cause of AIDS. The HIV-AIDS hypothesis currently holds a monopoly on all AIDS research and treatment. However, the HIV hypothesis is scientifically unproven. It has failed each of 15 testable predictions, as for example that AIDS would explode via sexual transmission of HIV into the general population. Moreover HIV meets all classical criteria of a harmless passenger virus: unpredictable intervals between infection and any subsequent disease, and unpredictable presence and activity of the virus during a disease. Since HIV is rare in the US, it is a marker of real AIDS risks, frequent injection of intravenous drugs, thousands of drug-mediated sexual contacts, and transfusions. Indeed, AIDS does not meet even one of the classical criteria of an infectious disease, as for example equal distribution between the sexes, disease within days or weeks after infection, and exponential spread of the disease in an un-immunized population (Farr’s law). Far from being beneficial, the HIV-AIDS hypothesis has become a threat to public health in the last 10 years: It is the sole basis for (1) the daily treatment of at least 200 000 HIV-positives with cytotoxic DNA chain terminators originally designed to kill growing human cells for chemotherapy, like AZT, that are now prescribed as anti-HIV drugs; (2) the clean-needle programs that encourage intravenous drug use, and the misinformation that HIV-infection is the only health risk of recreational drug use. However, recreational drugs, such as heroin, cocaine, amphetamines and nitrite inhalants, have long been known to have immunotoxic, cytotoxic and/or carcinogenic effects; and (3) the anxiety and the many restrictions of human rights associated with a positive HIV-test. Here it is proposed that American and European AIDS is caused by the long-term consumption of recreational and of anti-HIV drugs like AZT. The drug-AIDS hypothesis correctly predicts American/European AIDS: (1) AIDS is restricted to intravenous and oral users of recreational drugs and AZT; (2) AIDS is 87% male, because males consume this share of recreational drugs; (3) AIDS occurs in newborns because mothers use recreational drugs during pregnancy; (4) AIDS is new in America, because AIDS is a consequence of the recreational drug use epidemic that started in the 1960s, and of AZT prescriptions that started in 1987; (5) AIDS occurs only in a small fraction of recreational drug users, because only the highest life-time dose of drugs causes irreversible AIDS-defining diseases — likewise only the heaviest smokers get emphysema or lung cancer; (6) AIDS manifests as specific diseases in specific risk groups, because each group has specific drug habits. For example, pulmonary Kaposi’s sarcoma is exclusively diagnosed in male homosexuals who inhale carcinogenic alkyl nitrites; (7) AIDS does not occur in millions of HIV-positive non-drug users, and there are thousands of HIV-free AIDS cases, because AIDS is not caused by HIV; (8) AIDS is stabilized, even cured, if patients stop using recreational drugs or AZT — regardless of the presence of HIV. The drug hypothesis predicts that AIDS is an entirely preventable and in part curable disease. The solution to AIDS could be as close as a very testable and affordable alternative to the HIV hypothesis — the drug-AIDS hypothesis.
For a decade, there has been increasing concern about ‘AIDS’ and a virus called ‘HIV’ which is said to cause ‘AIDS’. Having named this virus ‘HIV’ — Human Immunodeficiency Virus — contributes to making people accept that ‘HIV is the cause of AIDS’. However, to an extent which undermines classical standards of science, some purported scientific results concerning ‘HIV’ and ‘AIDS’ have been handled by press releases, by disinformation, by low quality studies, and by some suppression of information, manipulating the media and people at large. I am not here concerned with intent, but with scientific standards, especially the ability to tell the difference between a fact, an opinion, a hypothesis, and a hole in the ground. As we shall see shortly, there does not even exist a single proper definition of ‘AIDS’ on which discourse can reliably be based. One difficulty of which most people are not aware, lies in faulty terminology and different impressions by different people of what ‘AIDS’ means. Thus a morass about HIV and AIDS has been created.
Since Gallo’s press conference with HHS Secretary Margaret Heckler in 1984, the HIV-AIDS hypothesis that ‘HIV is the virus that causes AIDS’ has generally been accepted. Some people, notably Peter Duesberg, have pointed to serious difficulties about the scientific basis for this hypothesis, and have proposed another hypothesis, the drug hypothesis, that under certain conditions, involving the quantity and nature of drugs taken over certain periods of time, drug use may be a cause of certain diseases which have been listed by the CDC as AIDS related diseases. I take no position at this time concerning the validity of any of these hypotheses, but I am concerned here with the history of a proposal by Duesberg to perform some experiments to test the drug hypothesis. The bottom line is that the NIH Center for Drug Abuse refused the funding, and the matter was not reported in the scientific press, notably Science, at the time, thus raising two issues: one about the legitimacy of refusing such funding, and the other about the way the scientific community is not informed properly of some events which some scientists regard as important.The documentation I shall provide can also be used to evaluate the verdicts of sci?entific reviewers concerning the funding of a proposal that goes against accepted ideas.
The HIV-AIDS hypothesis was debated on 21 June 1994, at a day-long symposium in San Francisco, sponsored by the Pacific Division of the American Association for the Advancement of Science (AAAS).
Once a week, Dr. Harry Haverkos puts on the white uniform of the Public Health Service, and goes to work at the National Institute on Drug Abuse in Rockville, Maryland. It is one of over 40 divisions comprising the National Institutes of Health. Dr. Haverkos, 43, is the director of the Office of AIDS at NIDA, and although he is a cautious man, not given to dramatic statements, he is persistent, and for over ten years he has been pursuing a line of inquiry about AIDS that has received remarkably little attention considering its potential importance.
When the first cases of AIDS, or the predecessor cases of GRID (Gay Related Immune Deficiency) were identified in 1981, the nitrite inhalants known as ‘poppers’ were high on the list of etiological suspects. Here was a drug used heavily and almost exclusively by the people getting sick: a subset of gay men. It was especially plausible that the nitrites, as powerful mutagens, might be responsible for Kaposi’s sarcoma (KS), which was then believed to be a rare form of cancer.
Other contributors to this collection will be discussing the scientific evidence regarding HIV and AIDS in detail. To avoid duplicating their efforts, and to make a contribution appropriate for a Professor of Law, I will concentrate on the quality of the reasoning employed in AIDS research. I have a healthy respect for scientific methodology in its proper sphere. If I were persuaded that the scientific method had been properly employed to determine what AIDS is, how it is caused, and how many people are at risk for AIDS, I would happily accept the judgement of the scientific profession on such matters. Unfortunately, however, the scientific method has never been properly directed to determining the cause of AIDS or the extent of the claimed epidemic. Instead of real science we have had only HIV-science, which is something very different.
The incidence of AIDS has concerned me ever since the spring of 1987, when I reviewed the Institute of Medicine’s book, Confronting AIDS (Lauritsen, 1987). In that review I criticized the CDC’s AIDS projections through 1991 as being grossly exaggerated and based on little if any evidence. As the years passed it became painfully obvious that the CDC’s projections had indeed been far too high, even after they had greatly expanded their surveillance definition of AIDS in late 1987.
Whether or not people ought to submit to taking an ‘AIDS test’ has long been the subject of furious debate. The impact of the life or lives of the people who do take the test — if it comes back positive — is incalculable, since HIV is still largely associated with surefire death.
It has become increasingly clear during the 1990s that in prosperous, developed countries, AIDS is remaining almost exclusively confined to people with clearly defined risks to their immune system regardless of HIV. These risks include heavy drug use, promiscuous receptive anal intercourse, or, as with the injections given to patients with haemophilia before the arrival of high purity Factor 8, repeated exposure to other people’s blood. In Britain, out of a cumulative total of 6929 cases of AIDS in the first ten years of the epidemic, only 63 were in heterosexuals who were not obvious members of one of the known risk groups. In the United States, a 1992 National Research Council report found that many geographical areas and population groups were virtually untouched by AIDS, and would probably remain so.
... Furthermore, scientists should be cautious about launching ad hominem attacks against other scientists (maybe in an adjacent field of study) and researchers because there have been quite a few documented instances in history when scientists have been wrong. One such example can be seen in Subacute Myelo-Optic Neuropathy (SMON), wherein Virologists, for 15-25 years, believed that SMON was caused by a particular virus when it was indeed iatrogenically induced (Duesberg 1996). ...
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This chapter deals with the issue of reliance on scientific claims in contexts other than scientific ones. Both social and natural sciences are supposed to be able to provide decision-making processes with objective and neutral points of view on the natural order. Nevertheless, several factors—such as the constant evolution of scientific research, scientific uncertainty, and social implications of scientific debates—make increasingly difficult to access clearly reliable scientific knowledge. The thirty-year scientific- public dispute between the official hypothesis on HIV/AIDS and the so-called ‘AIDS denialism’ allows us to corroborate this general observation. Taking this example as a starting point and common thread, the author discusses the importance of improving experts’ communication towards society and the need to provide lay-persons with reasonable explanations. Indeed, paradigmatic comparative case-law confirm that also judges have to independently decide whether to admit scientific evidence in court, determining which claims are (more) reliable (than others). In his conclusions, the author points out that better scientific communication requires accepting complexity and constant variability characterising scientific matters. Instead, over-reliance on science might induce a lack of trust in scientific institutions, inevitably increasing relativism, confusion, and manipulation.
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