How Much Longer Can We Afford the AIDS Virus Monopoly?

Peter H. Duesberg
Department of Molecular and Cell Biology, Stanley Hall, UC Berkeley, Berkeley, CA 94720, USA
P.H. Duesberg (ed.), AIDS; Virus or Drug Induced?, 241-270, 1996.

Abstract

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.

1. Fabricating the case for infectious AIDS

Hardly anybody remembers that in its first three years, from 1981 to 1984, AIDS science was open. The new epidemic of pneumonias and Kaposi's sarcomas, that was called AIDS, was considered infectious by some, but many independent investigators and even scientists from the Centers for Disease Control (CDC) in Atlanta considered AIDS behavioral diseases. Recreational drugs such as nitrite and ethylchloride inhalants, cocaine, heroin, amphetamines, phenylcyclidine, LSD, and some others were proposed by epidemiologists and toxicologists as the causes of AIDS because in the early 1980s nearly all AIDS patients were either male homosexuals who had used these drugs as aphrodisiacs and psychoactive agents, or were heterosexual intravenous drug users (Goedert et al., 1982; Marmor et al., 1982; Jaffe et al., 1983; Mathur-Wagh et al., 1984; Haverkos et al., 1985; Newell et al., 1985a; Newell et al., 1985b; Lauritsen and Wilson, 1986; Haverkos and Dougherty, 1988). Drugs seemed to be the most plausible explanation for the restriction of AIDS to these risk groups, because drug consumption was their only specific common denominator-not shared with the general population. This original drug-AIDS hypothesis was called the "lifestyle hypothesis" (Oppenheimer, 1992).

But in April 1984 the secretary of Health and Human Services and AIDS researcher Robert Gallo from the National Institutes of Health (NIH) announced at an international press conference in Washington that a virus is the "probable cause of AIDS" (Altman, 1984). This "AIDS virus" (Altman, 1984) had been discovered a year earlier in France, in a male homosexual without AIDS (Barré-Sinoussi et al., 1983). Within two years after that announcement an international committee of retrovirologists had named this virus, the Human Immunodeficiency Virus (HIV), to indicate that it was the accepted cause of AIDS (Coffin et al., 1986).

The road for the ready acceptance of the "AIDS virus" by the scientific community had been paved by epidemiologists from the CDC. By tracing sexual contacts of male homosexual AIDS patients the CDC claimed that it could "link patients," "who had sexual exposure with other AIDS patients within five years of the onset of symptoms." (Auerbach et al., 1984). On that basis the CDC proposed that AIDS "may be caused by an infectious agent that is transmissible from person to person in a manner analogous to hepatitis B virus infection: through sexual contacts; through parenteral exposure by intravenous drug abusers...; through blood products; and, perhaps, through mothers who are ... intravenous drug users to their infants." (Auerbach et al., 1984).

However, compared to hepatitis B or any other authentic infectious disease, the CDC's case for infectious AIDS was bizarre with regard to the diversity of the diseases linked. The CDC had "linked by sexual contact" the Kaposi's sarcomas of some patients to the pneumonias of others and vice versa. The uncritical acceptance by the scientific community of a common infectious cause for such diametrically different diseases as cancer and pneumonia allowed the CDC to fabricate infectious AIDS. Since cancer, pneumonia, and by now about 30 different diseases were all said to have the same cause, they would soon all be called by the same new name, AIDS (Institute of Medicine, 1988; Centers for Disease Control and Prevention, 1992; National Institute of Allergy and Infectious Diseases, 1994).

A second bizarre element in the CDCs case for infectious AIDS was the assumption of an average "latency period" from infection to AIDS of 10 months (Auerbach et al., 1984), now 10 years (see below). The assumption of a microbe that only causes disease after an average latency period of 10 months was without proven precedent. It was necessary, because prospective patients "were asymptomatic at the time of sexual exposure," and only developed AIDS up to 5 years after a critical contact (Auerbach et al., 1984). Indeed, the carriers of the assumed infectious agent had to be exceedingly healthy during the latency period, because they had "large numbers" of "approximately 250 different male sexual partners each year." In view of such large numbers of sexual contacts and the long latency periods between infection and AIDS, tracing the one contact that would cause a disease had to be a masterpiece of epidemiological detective work. Therefore the CDC's case for sexual transmission of AIDS was about as compelling as the claim that one car had a flat tire at an intersection, because another car had blown a head gasket at the same intersection in the previous 5 years. Nevertheless, the sexual contact study was accepted by the scientific community as proof for infectious AIDS without further scrutiny.

The fact that "linked patients" "have been frequent users of inhaled amyl and butyl nitrite" and "of recreational drugs other than nitrite" was not considered an AIDS risk by the CDC in 1984 (Auerbach et al., 1984), although CDC scientists had originally proposed recreational drugs as the cause of AIDS (Oppenheimer, 1992).

In 1984, the CDC also presented typical hemophilia diseases, like pneumonia and candidiasis, as AIDS from parenteral infection via blood transfusions-in support of its claim that AIDS was infectious (Curran et al., 1984; Evatt et al., 1984; Duesberg, 1995b). The paradox that none of the CDC's hemophiliacs with AIDS would have developed Kaposi's sarcoma from an infectious agent that presumably caused Kaposi's sarcoma in homosexuals was effectively hidden because all these entirely unrelated diseases had been named AIDS (Duesberg, 1992; Duesberg, 1994a; Duesberg, 1995b).

Indeed the CDC, originally established to fight infectious diseases, had grown desperate for a new infectious disease, because ever since polio had been eliminated by vaccines over 30 years ago, no new infectious diseases had plagued the Western World. In the words of a Red Cross official, "... the CDC increasingly needs a major epidemic to justify its existence" (Associated Press, 1994). Infectious AIDS, but not the drug-AIDS hypothesis, offered such an opportunity. A new infectious epidemic readily generates fear and funding. But research on the toxicity of recreational drugs is trivial, not likely to make headlines in the scientific literature. As a possible investment in its future existence, the CDC has recently launched a new journal, Emerging Infectious Diseases, to raise "public awareness of exotic bugs." (Kaiser, 1994). For example, in 1994 the CDC promoted the Hanta virus -after it presumably killed some Indians (Denetclaw and Denetclaw, 1994a; Denetclaw and Denetclaw, 1994b)- into a threat to the nation, and in 1995 the Ebola virus, that had apparently killed some Zairens, was promoted into a global "killer virus" (Associated Press, 1995a). The CDC claimed that 108 people may have been killed by the Ebola outbreak in Zaire in 1995 (Centers for Disease Control, 1995). But it failed to mention that 20% of the 55 million Zairens are Ebola virus antibody-positive, having survived the virus without apparent disease (Dietrich J., 1995).

As AIDS claimed ever more victims and gained ever more media attention, the CDC's message that AIDS was a new infectious disease was enthusiastically picked up by the stars of medical research, particularly the virologists. A new infectious disease is a magnet for virologists, microbiologists and immunologists because it holds the promise for a new microbial pathogen and new vaccines. Since the discovery of pathogenic microbes by Robert Koch and Louis Pasteur in the 1880s, the identification of a new microbial pathogen has been the key for many brilliant careers-like those of Walter Reed, John Enders, and Albert Sabin. Stated the New York Times on the search for an AIDS virus "... the greatest thrills for a scientist are in discovering a new microbe, a new disease, cure and prevention ..." (Altman, 1992).

After decades of basic research in the War on Cancer, an army of highly sophisticated virologists had failed to prove that viruses can cause cancer in humans (Greenberg, 1986; Booth, 1988). Among these were the current leaders of AIDS research, Luc Montagnier from France, Robin Weiss from the U.K., David Baltimore, Jay Levy, Robert Gallo and even Peter Duesberg from the U.S. among others. Searching for other diseases for their viruses, most cancer virologists welcomed AIDS as a new frontier to apply their considerable skills (Duesberg, 1987; Booth, 1988; Duesberg and Schwartz, 1992). With an AIDS virus, the medical virologists could continue their familiar research, and their companies could extend their markets from the narrow confines of conventional virus tests and vaccines to the new multi-billion dollar markets of HIV-antibody tests, HIV vaccines, and anti-HIV drugs (Weiss and Jaffe, 1990; Duesberg, 1992).

The AIDS virus also proved to be the politically correct cause of AIDS. No AIDS risk group could be blamed for being infected by a God-given egalitarian virus. A virus could reach all of us. Nobody would be ostracized since "We are all in this together." Not so with drugs: The consumption of illicit psychoactive drugs implies individual and social responsibilities that nobody wanted to face.

Once accepted as the politically correct explanation of AIDS, the HIV hypothesis has become the central investment for a whole generation of AIDS scientists, AIDS companies, AIDS journalists, AIDS politicians and gay activists.

The perceived danger of an AIDS virus decimating the general public also provided the scientific and moral arguments for quick and unreflective action and for the complete dismissal of the competing drug-AIDS hypothesis. The fear of nature's presumably uncontrollable microbes created an unscientific war-mentality that has since dominated the field (Christie, 1994). Scientists, health care workers, and journalists would rather be safe and fast in protecting against HIV, than sorry and slow in reflecting about the clinical and political consequences of drug use (Lang, 1994). The confrontation with man-made drugs, after all, would have to take second place in urgency, as they would not reach the innocent public.

Claiming this priority, the virus-AIDS orthodoxy justifies intolerance, even censorship, of all those who question infectious AIDS (San Francisco Project Inform, 1992; Maddox, 1993b; Maddox, 1993a; Cohen, 1994a; Lang, 1994; see Chapter 12). Epidemiologists from the CDC warn that to "ignore this [HIV-AIDS] concept would result in an unconscionable tragedy." (Garza, Drotman and Jaffe, 1994). Virologists are quick to call those who question the virus-AIDS hypothesis "irresponsible and pernicious" (Booth, 1988; Baltimore and Feinberg, 1989). And the New York Times still calls all non-HIV science "cruelly irresponsible anti-science" (Lewis, 1994).

Therefore, the "AIDS virus" won unprecedented popularity within a short time after its announcement.

But eleven years later, in 1995, the virus-AIDS hypothesis has still failed to produce any public health benefits in the war on AIDS. No vaccine, no antiviral drug, no cure, not even an effective AIDS prevention have been developed. It cannot even be predicted whether and when an infected person will get ill. And it cannot predict which of the about 30 AIDS diseases it will be (Duesberg, 1992; Benditt and Jasny, 1993; Cohen, 1994a; Cohen, 1994b; Wade, 1995). Moreover, the very basis of the virus-AIDS hypothesis, the assumption that AIDS is infectious, has since become questionable on several grounds. For example:

(1) Would you have believed AIDS is infectious 11 years ago, if you had known that until now not even one of the doctors and health-care workers who have treated the over 400,000 American AIDS patients since 1984 (Centers for Disease Control and Prevention, 1994c) is confirmed to have contracted AIDS from a patient? Even if that would not have changed your mind, would you still believe in infectious AIDS if you had considered that the health care workers were neither protected by an anti-HIV vaccine nor by an antiviral drug (Duesberg, 1992)?

(2) Would you have believed that a sexually transmitted virus was causing AIDS if you had known that none of the wives of the 15,000 HIV-positive American hemophiliacs has contracted AIDS from their husbands in the last 10 years? Their risk of developing an AIDS-defining disease is the normal background of these diseases in the U.S. (Duesberg, 1992; Duesberg, 1995b).

(3) Would you have believed that AIDS was contagious if you had known that after a marriage of 10 years, neither the wife nor the 6-year old daughter of the late tennis star and AIDS patient Arthur Ashe have developed AIDS or even become HIV-positive (Ashe and Rampersad, 1993); or that the long-term lover of the movie star Rock Hudson has no AIDS symptoms, 10 years after Hudson died from AIDS in 1985? Would you believe that AIDS was sexually transmitted if you had known that, after a 13-year marriage and 2 children, the husband of the late AIDS patient Elizabeth Glaser is healthy and HIV-free (Champkin, 1994)?

(4) Would you have believed in an AIDS virus if you had known that nobody ever contracted Kaposi's sarcoma in the US from a blood donor with Kaposi's sarcoma (Haverkos, Drotman and Hanson, 1994)?

(5) Would you have believed AIDS is a sexually transmitted disease in 1984 if you had known that 11 years later there is still no AIDS in American heterosexuals, not even in prostitutes, unless they are drug addicts (Duesberg, 1992)?

(6) Would you have believed in a sexually transmitted AIDS virus if you had considered that such a virus would be incompatible with life? Because sex is the only known source of human life, a sexually transmitted, fatal virus would have exterminated itself together with its host (Duesberg, 1992).

Have we lost the war on AIDS because we have mistaken a harmless virus for its real cause?

2. The HIV-AIDS hypothesis proves to be unprovable

The HIV-AIDS hypothesis (Institute of Medicine, 1988; National Institute of Allergy and Infectious Diseases, 1994) postulates that:

1. HIV causes immunodeficiency by killing T-cells (lymphocytes);

2. immunodeficiency occurs on average only 10 years after this virus has been neutralized by antiviral immunity-a condition termed a "positive HIV test";

3. immunodeficiency is the basis for about 30 previously known diseases, including pneumocystis pneumonia, tuberculosis, candidiasis, Kaposi's sarcoma, dementia, diarrhea, >10% weight loss, and many others (Table 1);

4. AIDS is a sexually transmitted disease, because HIV is a sexually transmitted virus.

Owing to the immense popularity of this hypothesis, over 100,000 scientific papers have been published on HIV since 1984. But not even one of these has been able to explain how HIV causes AIDS. Worse yet, not one paper exists that proves that HIV causes AIDS (Duesberg, 1992; Dickson, 1994; Fields, 1994; Schoch, 1994; Thomas Jr., Mullis and Johnson, 1994).

In view of this proof-deficit, the HIV-AIDS establishment cites the "perfect" correlation between HIV and AIDS as support for the hypothesis that HIV causes AIDS (Blattner, Gallo and Temin, 1988; Weiss and Jaffe, 1990; San Francisco Project Inform, 1992; Maddox, 1993b; Garza, Drotman and Jaffe, 1994; National Institute of Allergy and Infectious Diseases, 1994). However, this argument is inadequate as an element of proof for three reasons:

(1) According to the HIV-AIDS hypothesis, the 30 AIDS-defining diseases are diagnosed as AIDS only when antibody against HIV is present. In its absence these diseases are called by their old name and caused by their old causes. In other words, AIDS is defined entirely by its hypothetical cause, HIV. Therefore, the perfect correlation is not a natural coincidence but a perfect artifact of the definition of AIDS by its hypothetical cause, HIV. It is one of the purest examples of circular logic.

(2) The HIV antibody-test for the detection of HIV is indirect, because it does not assay for the virus. Moreover it is not reliable; up to 90% false-positives are obtained, depending on the subjects tested and on the tests used (Duesberg, 1993f; Papadopulos-Eleopulos, Turner and Papadimitriou, 1993).

(3) Even a perfect correlation is not sufficient to prove causation. For example, perfect correlations between yellow teeth and lung cancer, or between hospitalization and death do not prove that one causes the other (Duesberg, 1989; Smith and Phillips, 1992; Duesberg, 1993d).

In the absence of direct proof, the merit of a scientific hypothesis is determined by the accuracy of its predictions. For example, there is no direct proof for the hypothesis that smoking causes lung cancer and emphysema, but the prediction that long-term smoking causes these diseases has validated this hypothesis. In the following we will analyze the predictions of the HIV-AIDS hypothesis (Duesberg, 1994a):

(2.1) HIV-infected persons will get AIDS, and otherwise matched HIV-negatives will not.

In the face of the relentless propaganda for the HIV hypothesis, it comes as a big surprise to almost everybody that there is not even one study to show that American, heterosexual or homosexual men, who are HIV-positive but not drug users or hemophiliacs ever get AIDS. More precisely, there is no study to show that such men would get AIDS-defining diseases that exceed the long-established, low background of these diseases in otherwise matched, HIV-free counterparts (Duesberg, 1995a, see Chapter 10). There is not a single epidemiological study to support the most frightening slogan of the HIV orthodoxy; that HIV-positives develop AIDS-defining diseases because of HIV.

All studies that claim HIV causes AIDS have instead analyzed the AIDS risks of HIV-positive people who were recreational drug users, were treated with AZT or other anti-viral drugs, had received transfusions, suffered from congenital diseases, or were subject to exotic life styles as in Africa. The AIDS risks of such groups were then determined by comparisons, either with normal HIV-free people or with HIV-negative people from risk groups who were not matched for drug use or other AIDS risks (Duesberg, 1992; Duesberg, 1993a; Duesberg, 1993c; Duesberg, 1993d, see Chapter 8). In other words, there is no epidemiological evidence properly controlled for confounding factors that HIV is a "deadly virus" or "the virus that causes AIDS."

In view of the enormous experimental difficulties and costs in sorting out the possible role HIV plays in AIDS from the roles that recreational drugs, AZT, transfusions, congenital diseases and exotic life styles play, it is surprising that the assumption that HIV causes AIDS has never been studied in people who are free of confounding AIDS risks. There can only be one plausible explanation for the absence of an epidemiological study that shows that HIV causes AIDS in people who are not in risk groups: HIV does not cause AIDS.

Indeed, there are 1 million HIV-positive Americans (National Institute of Allergy and Infectious Diseases, 1994) and 17 million HIV-positive humans (Merson, 1993; World Health Organization, 1995) who are healthy, probably because they are not subject to real AIDS risks other than the hypothetical AIDS risk HIV. Moreover, HIV-positives who stop practicing risk behavior or stop being subjected to AIDS risks even recover lost immunity-despite the presence of HIV (see below Section VIII). For example, HIV-positive hemophiliacs treated for 3 years with highly purified blood clotting factor regained lost immunity, while controls treated with unpurified blood products continued to lose immunity (Seremetis et al., 1993; Duesberg, 1995b and Chapter 11).

Thus HIV is only ever deadly for people who are at risk for AIDS from toxic drugs or who depend on long-term blood transfusions to treat underlying deadly diseases (Duesberg, 1992, see Chapter 6).

(2.2) American AIDS is new, because HIV is new in America. 

However, in America HIV is a long-established retrovirus (Duesberg, 1992, see Chapter 6). Ever since the virus could be detected in 1984, an unchanging 1 million Americans are HIV-positive (Fig 1A) (Curran et al., 1985; National Institute of Allergy and Infectious Diseases, 1994, Farber, 1995b). By contrast, a new microbe/virus spreads exponentially in a susceptible population (see V). Thus the non-spread of HIV establishes it as an old virus in America (Duesberg, 1992).

(2.3) HIV is active and abundant in persons with AIDS, and inactive and rare in healthy virus carriers. 

All microbes cause diseases by killing or alterating a larger number of target cells than the host can spare or regenerate during the course of an infection. Thus HIV would have to infect and kill at least 50% of all human T-cells to cause AIDS.

However, in AIDS patients HIV is found hibernating in only 0.1% of T-cells, and biochemically active in less than 0.01% of T-cells (Duesberg, 1992; Duesberg, 1993e; Piatak et al., 1993). Indeed, there are healthy HIV-positive people with 30- to 40-times more infected T-cells than in AIDS patients (Simmonds et al., 1990; Bagasra et al., 1992; Duesberg, 1992). The fact that the vast majority of susceptible T-cells remain uninfected, even in people dying from AIDS, is the definitive evidence that there is no active HIV in HIV-antibody-positive persons. HIV is neutralized by antiviral immunity, even in AIDS patients. If there were un-neutralized HIV, all T-cells would be infected.

The fundamental problem for the HIV-hypothesis is not just how HIV works, but how it causes fatal diseases when it does not work at all. Since there is no rational explanation for how HIV could cause AIDS, HIV researchers now postulate a multiplicity of indirect mechanisms of pathogenesis (Blattner, Gallo and Temin, 1988; Booth, 1988; Gallo, 1991; Maddox, 1991; Weiss et al., 1992; Maddox, 1993b; Maddox, 1995; Wade, 1995; Wain-Hobson, 1995).

(2.4) HIV causes AIDS by killing T-cells. 

However, viruses that integrate their genomes with that of the host, like HIV, cannot kill the host cell. Since the genes of such viruses are part of the host's genes, integrated viruses can only replicate as long as the host survives integration and remains able to express integrated viral genes. All integrated viruses survive from passive, and some retroviruses also from active replication with the host. This strategy only works if the host survives integration. If the virus were to kill the cell as it is integrated, integration would be a useless exercise and it would be undetectable. Indeed, HIV is mass-produced for the "HIV test" in immortal T-cell lines in cell culture at titers of 106 infectious units per ml (Rubinstein, 1990; Karpas et al., 1992). Luc Montagnier, the discoverer of HIV, and many other researchers have confirmed that HIV does not kill T-cells (Lemaitre et al., 1990; Duesberg, 1992).

(2.5) Since the generation time of HIV is two days, HIV will cause AIDS two weeks after infection. The HIV-hypothesis predicts AIDS within 2 weeks after infection, because HIV, like all other retroviruses, replicates within two days. During that time one infected cell produces at least 100 new viruses (Weiss et al., 1985). In the absence of antiviral immunity, these 100 viruses would in turn infect 100 cells producing 100 x 100 viruses, or 104 infected cells within 4 days after infection. Within 14 days of such exponential growth, 1014 cells -the equivalent of a human body- would be infected. This is the typical latent period of proven pathogenic retroviruses, like Rous sarcoma virus, and of pathogenic human viruses like flu, measels, mumps, chicken pox, and herpes, which all have generation times like HIV (Fenner et al., 1974; Mims and White, 1984).

However, if dated from the time of HIV infection, AIDS occurs at totally unpredictable times. The latent period between infection and AIDS was estimated to average 10 months in 1984 (Auerbach et al., 1984), 10 years in 1988 (Institute of Medicine, 1988) and over 20 years in HIV-positive hemophiliacs in 1994 (Phillips et al., 1994). A Berkeley mathematician recently has determined the most accurate formula for the latent period of HIV, by subtracting 1984, the year when HIV was proposed to cause AIDS, from the current calendar year. But blaming AIDS on a HIV infection that occured 10 years earlier is the logical equivalent of blaming today's broken leg on stumbling over a crack in the sidewalk 10 years ago.

(2.6) Viral AIDS will spread exponentially ("explode"). 

The AIDS orthodoxy has predicted that according to Farr's law (Bregman and Langmuir, 1990), AIDS would spread exponentially ("explode") into the general, unimmunized population (Duesberg, 1992)-just like all other new infectious diseases.

However, AIDS in America and Europe remained confined to the original risk groups, i.e. male homosexuals practicing risk behaviour and intravenous drug users (National Commission on AIDS, 1991; Centers for Disease Control and Prevention, 1994b). Instead of growing exponentially, AIDS in America (and Europe) has increased slowly, over 15 years, far from reaching saturation of the susceptible population of over 100 million sexually active adults (Fig. 1A). AIDS behaved just like an occupational disease.

(2.7) The spread of AIDS will follow the dissemination of HIV. 

However, there is no correlation between the spreads of AIDS and HIV in America. In the last 10 years, AIDS increased in America from a few hundred to about 100,000 cases annually (Fig. 1A) (Centers for Disease Control and Prevention, 1994c). (The burst of AIDS cases in 1993 is largely an artifact of the most recent redefinition of AIDS, which nearly doubled the AIDS cases in one year (Centers for Disease Control and Prevention, 1994c).)

However, during those same 10 years HIV did not spread at all (Fig. 1A). Ever since HIV became detectable in 1985, an unchanging one million Americans have been HIV-positive up to 1994 (Fig. 1A) (Duesberg, 1992; Duesberg, 1994a; National Institute of Allergy and Infectious Diseases, 1994). To hide this discrepancy, a latency period of 10 years has been postulated between HIV and AIDS.

(2.8) Like all other sexually transmitted diseases, AIDS in America will equilibrate between the sexes. 

However, since 1981, AIDS has remained in the original risk groups in America, i.e. male homosexuals, intravenous drug users of which over 75% are males (Duesberg, 1992), and hemophiliacs which are nearly all males. Since 1981, 347,767 out of 401,749, or 87% of all American AIDS cases, have been males (Centers for Disease Control and Prevention, 1994c).

(2.9) HIV is a sexually transmitted virus.

However, HIV could never survive in evolution from sexual transmission. Based on studies of discordant couples, e.g. hemophiliacs with HIV and spouses without, conducted by the CDC and others, it takes on average 1000 unprotected sexual contacts to transmit HIV (Hearst and Hulley, 1988; Peterman et al., 1988; Rosenberg and Weiner, 1988; Lawrence et al., 1990; Blattner, 1991). According to Rosenberg and Weiner, "HIV infection in non-drug using prostitutes tends to be low or absent, implying that sexual activity alone does not place them at high risk." The efficiency of transmission in homosexual contacts is also estimated at 1 in 1000 contacts (Jacquez et al., 1994).

Since about 10 to 30 sexual contacts are required to generate a child, but 30 contacts are required to transmit HIV, HIV could never survive natural selection on the basis of sexual transmission, because the host would outgrow the parasite. Conventional venereal microbes, like syphilis and gonorrhea, survive because they are transmitted by about two sexual contacts (Freeman, 1979). HIV also could not survive from transmission to newborns if it were fatally pathogenic to babies, as is claimed by the proponents of the HIV hypothesis (Blattner, Gallo and Temin, 1988; Institute of Medicine, 1988).

The extremely low efficiency of sexual transmission of HIV also predicts that the safe-sex-campaigns conducted by the HIV orthodoxy will be of very limited value. Only those would benefit who either have on average 1,000 sexual contacts with HIV positives or those who have on average 250,000 contacts with average Americans, of which only 1 million in 250 million is HIV positive (Fig. 1A) (Duesberg, 1992; National Institute of Allergy and Infectious Diseases, 1994).

(2.10) AIDS will be restricted by controlling sexual transmission of HIV via "safe sex," and parenteral transmission of HIV via "clean needles." 

But AIDS continues to increase steadily despite the "safe sex" and "clean needle" programs (Centers for Disease Control and Prevention, 1994c) (see Fig. 1A).

(2.11) Health-care workers will contract AIDS from their patients, scientists from propagating virus, and prostitutes from their clients. 

Not a single confirmed case exists in the scientific literature of a health-care worker who contracted AIDS (Duesberg, 1992; Duesberg, 1994a) from one of the over 400,000 American AIDS patients (Centers for Disease Control and Prevention, 1994c). None of the tens of thousands of HIV researchers have developed AIDS from propagating HIV. And no prostitutes picked up AIDS from their clients-despite the absence of antiviral vaccines or effective anti-HIV drugs (Duesberg, 1992; Duesberg, 1994a).

A few unpublished cases have been claimed, but each of these seemed to have been treated with the cytotoxic drug AZT that is sufficient to cause immunodeficiency (see below) (Cohen, 1994a).

(2.12) Chimpanzees inoculated with HIV will develop AIDS, and the 15,000 American hemophiliacs who were infected by transfusions before 1984 will die from AIDS. 

Not one of the 150 chimpanzees inoculated with HIV since 1983 has developed AIDS (Duesberg, 1992). Contrary to prediction, the median life of American hemophiliacs has increased 2.5-fold from 11 to 27 years between 1972 and 1987 (Institute of Medicine, 1988; Stehr-Green et al., 1989), although 75% (15,000) were infected with HIV by transfusions received before 1984 (Duesberg, 1992). However, in 1987 the median life of HIV-positive hemophiliacs started to decrease again (Chorba et al., 1994) because since then they have been treated with the cytotoxic AZT (Duesberg, 1995b, See Chapter 11) (see below).

(2.13) Natural or vaccine-induced anti-HIV immunity will cure AIDS or protect against future AIDS. 

Natural antiviral immunity, a positive HIV-test, is observed in many AIDS patients, but does not protect against AIDS. Paradoxically, anti-HIV immunity is by HIV-AIDS definition the only criterion to predict who gets AIDS. With all other viruses and microbes -there is no exception- immunity is the only criterion to predict who does not get a disease. It is for this reason that antiviral/microbial immunity is artificially induced by vaccination. It is also for this reason that the HIV-AIDS establishment has called for an HIV vaccine since 1984.

(2.14) All AIDS diseases are consequences of HIV-mediated T-cell deficiency. 

Indeed, up to 1992 about 61% of all American AIDS diseases, the microbial diseases such as Pneumocystis carinii, candida, tuberculosis, etc. were consequences of Acquired ImmunoDeficiency (Table 1) (Centers for Disease Control, 1993).

However, 39% were neither caused by, nor consistently associated with, immunodeficiency. These include Kaposi's sarcoma, lymphoma, >10% weight loss, and dementia (Table 1). Accordingly, Kaposi's sarcoma and dementia have been diagnosed in male homosexuals whose immune systems were normal (Murray et al., 1988; Spornraft et al., 1988; Gill et al., 1989; Friedman-Kien et al., 1990; Duesberg, 1992; Kaldor et al., 1993; Bacellar et al., 1994).

In 1993, the CDC introduced, once more, a new AIDS definition (Centers for Disease Control and Prevention, 1992). This has shifted the balance of immunodeficiency to non-immunodeficiency AIDS diseases significantly in favour of immunodeficiency diseases, i.e. from 61% to 80% (Table 1) (Centers for Disease Control and Prevention,1994a). The critical innovation of this new definition was that a healthy person with less than 200 T-cells, but with no clinical disease, would now be registered as an AIDS patient. The new AIDS definition nearly doubled the new AIDS cases, thus adding new life to the sagging curves of the American AIDS statistics (Fig. 1A). However, if one substracts from the 1993 statistics the new AIDS cases with less than 200 T-cells, the ratio of the remaining real immunodeficiency diseases to the non-immunodeficiency diseases is almost the same as in 1992.

Imagine the rationalizations an unprejudiced virologist, who is aware of the heterogeneity of AIDS-defining diseases, must make to accommodate an AIDS virus. Ever since Koch and Pasteur, microbiologists and virologists were taught that a specific microbe or virus would cause a specific disease-e.g. polio, flu, measels, chicken pox, hepatitis, etc.-just like a particular musical instrument would make specific sounds.

To accommodate the AIDS virus, the concept of a specific microbe causing a specific disease had to be abandoned for the following bewildering scenario: By picking up the AIDS virus from a diarrhea patient, a person would get Kaposi's sarcoma. The Kaposi patient would then be able to cause dementia or pneumonia in others by passing on the diarrhea virus, just as the CDC's sexual contact study had claimed in 1984 (Auerbach et al., 1984). As of 1993, any one of these patients could have also caused a clinically undetectable depletion of T-cells in others, again by passing on their diarrhea, dementia, Kaposi's sarcoma and pneumonia virus.

Moreover, the unprejudiced virologist would have to reconcile this bewildering pathogenic potential of HIV with the fact that HIV is one of the most primitive viruses in terms of genetic information that exist, carrying only 9,000 nucleotides. This is the viral equivalent of a musical instrument that is said to sound like an orchestra, although it only has the repertoire of a bell.

(215) If HIV is the cause of AIDS, the percent incidence of AIDS diseases will be the same in all risk groups. 

However, the percent incidence of AIDS-defining diseases is very different in different risk groups. For example, Kaposi's sarcoma in America and Europe is almost exclusively observed in male homosexuals (Beral et al., 1990). Intravenous drug users have a proclivity for tuberculosis, weight loss, and pneumonia (Duesberg, 1992) and a very high mortality dying at 30 years (Lockemann et al., 1995). Pneumonia and candidiasis are virtually the only AIDS diseases ever diagnosed in hemophiliacs (Duesberg, 1992; Duesberg, 1995b). And bacterial infections other than tuberculosis are almost exclusively diagnosed in babies with AIDS (Centers for Disease Control, 1987; Centers for Disease Control and Prevention, 1992; Duesberg, 1992, see Chapter 6). Thus the percent incidence of an AIDS diseases is very different in different AIDS risk groups.

In view of this, some AIDS researchers cite co-factors of HIV, such as recreational drugs and immunosuppressive transfusions, as explanations for risk group-specific diseases (Evans, 1989; Duesberg, 1992; Ludlam, 1992; Root-Bernstein, 1995a). However, they fail to provide evidence that such cofactors depend on the cofactor HIV to be pathogenic.

The CDC and other mainstream AIDS researchers insist that recreational drugs and transfusions solely enhance the risk to get infected by HIV, rather than playing causative roles in AIDS (Cohen, 1994a). It is for this reason that the CDC refers to drug- or transfusion-risk groups as "exposure categories" (Centers for Disease Control and Prevention, 1994a). In fact, the CDC obscures the existence of risk-group-specific AIDS diseases by reporting only the percent incidence of AIDS diseases in all risk groups combined (Centers for Disease Control and Prevention, 1994a).

It is evident that the HIV-AIDS hypothesis is unable to make even one verifiable prediction-the hallmark of a failed hypothesis.

Even if a hypothesis fails to make valid predictions in terms of established scientific criteria, it could by chance lead to a valid prevention or treatment. But the HIV-AIDS hypothesis has not lead to any public health benefit. Instead it has harmed not only AIDS patients but also healthy persons who are at risk for AIDS or just antibody-positive (see VI).

3. HIV-a harmless passenger virus

Confronted with the evidence that the HIV-AIDS hypothesis has failed to make valid predictions and failed to lead to public health benefits, many agree that HIV may not cause AIDS. But then, they wonder: What does HIV do?

Indeed, all viruses are generally assumed to be pathogenic by an unsuspecting public, because a few of them actually are. Likewise, a whole nation is often stereotyped by the characteristics of a minority. For example the French are considered great lovers and the Italians great singers, because a few of them are great lovers and singers. The same is true for viruses.

In reality, most viruses cause no disease at all. Viruses are not here to kill their hosts, not even to cause disease. Instead, viruses are here for exactly the same reasons we are, to continue their species. This goal can only be achieved by keeping the host species alive, and it is achieved best if every host survives the infection. That is the reason that most viruses never cause a disease in their host. Therefore they are called passenger viruses. Passenger viruses are those that take a ride on the host, but demand no more from the host than a passenger demands from an airplane (see Chapter 9).

Since HIV is not the cause of AIDS, the simplest and most plausible HIV hypothesis postulates that HIV is just a passenger virus (Duesberg, 1994a). A passenger virus is defined as follows:

(1) The time of infection is irrelevant to the onset of any disease.

(2) The passenger virus can be either active or passive, either rare or abundant during any disease.

(3) The passenger virus can be entirely absent during any disease.

(4) If the passenger virus is de-repressed by a failing immune system, as for example during a disease, the passenger virus may or may not contribute to the disease. For example HHV-6 (Cone et al., 1994) or cytomegalovirus may contribute their specific pathogenic properties to an immunodeficient patient.

HIV meets all these criteria with regard to its relation to AIDS:

(1) HIV infects at totally unpredictable times prior to or even after the onset of AIDS (see VIII below) or not at all (Duesberg, 1992; Phair et al., 1992; Duesberg, 1993f).

(2) HIV is typically passive and rare during AIDS-hence the notorious difficulties of leading AIDS researchers in isolating HIV from AIDS patients (Duesberg, 1992, see Chapter 6).

(3) There are thousands of HIV-free AIDS cases, e.g. HIV-free homosexuals with Kaposi's sarcoma and HIV-free intravenous drug users with tuberculosis (Duesberg, 1993f, see Chapter 7).

(4) There is no report in the literature that AIDS patients are clinically distinguishable from each other because HIV is active or passive or not present at all (Duesberg, 1993b; Duesberg, 1994a). Thus HIV is a harmless passenger virus, even when it is active in some rare immunodeficient persons (Duesberg, 1993e).

If this is true, there should be many more HIV carriers than AIDS patients. Indeed, there are 1 million healthy HIV-positive Americans (Duesberg, 1992; Duesberg, 1994a) and there are 17 million healthy HIV-positive humans (Merson, 1993; National Institute of Allergy and Infectious Diseases, 1994; World Health Organization, 1995).

Nevertheless, there is some tenuous evidence that HIV can function as an autonomous pathogen, causing a mild flu-like or mononucleosis-like condition, prior to antiviral immunity (Albert et al., 1987; Duesberg, 1987; Kessler et al., 1987; Gaines et al., 1988; Marcus and the CDC Cooperative Needlestick Surveillance Group, 1988; Tindall et al., 1988; Pedersen et al., 1990; Duesberg, 1992; Niu, Stein and Schnittmann, 1993, see Chapters 1, 6). However, in millions of HIV-positives HIV infection has gone unnoticed, because they do not experience a characteristic HIV-disease prior to antiviral immunity-like measles, mumps or flu which all occur prior to immunity against these viral infections.

The rare cases in which HIV infections, prior to antiviral immunity, have been linked with mononucleosis or flu-like symptoms are restricted to prospective studies of male homosexuals at risk for AIDS. These cases could either be coincidences with a common cold or with intoxications from recreational drug use (see below) (Gaines et al., 1988; Tindall et al., 1988; Pedersen et al., 1990) rather than evidence for HIV disease.

4. HIV-a marker for AIDS risks

Even those who understand all virological arguments against HIV as the cause of AIDS, and for HIV as a passenger virus, have misgivings about dismissing the HIV-AIDS hypothesis, because HIV is more common in AIDS patients than in the healthy population. This sounds like an ominous connection, but only if it is taken out of its trivial microbiological context.

This trivial context is that AIDS risk behavior is synonymous with collecting microbes. The common denominator of all AIDS risk groups in America and Europe is that they collect microbes either from unsterile drugs injected with unsterile equipment, or from the thousands of drug-mediated sexual contacts, that are required to transmit HIV sexually, or from transfusions received for the treatment of illnesses (Jaffe et al., 1983; Auerbach et al., 1984; Lauritsen and Wilson, 1986; Haverkos and Dougherty, 1988; Rappoport, 1988; Adams, 1989; Callen, 1990; Lifson et al., 1990; Archibald et al., 1992; Duesberg, 1992; Jones, 1994; Mullis, 1995). This is the reason that numerous uncommon microbes are common not only in AIDS patients but also in healthy persons from AIDS risk groups. For example, the bacteria that cause syphilis, gonorrhea, and tuberculosis, the hepatitis virus, rare strains of herpes virus, putative leukemia virus, genital papilloma virus, and even HIV are all common in AIDS risk groups and AIDS patients but uncommon in the general population (Duesberg, 1992, see Chapter 6). Thus HIV is just one of many microbial markers of AIDS risk behavior. Since AIDS is defined as one of 30 diseases in the presence of HIV, rather than any other microbial or viral marker, the correlation between HIV and AIDS is in theory 100%.

5. The myth of infectious AIDS-unconfirmed

If a hypothesis is unproductive, and unable to make verifiable predictions, the scientific method calls for alternative hypotheses. To find the correct AIDS hypothesis, we need to decide first whether to look for other viruses and microbes or for drugs as causes of AIDS. In other words, we need to know whether AIDS is infectious or not.

There are five classic criteria to define an infectious disease.

In individuals:

(1) The causative microbe/virus is abundant and very active in target tissues during the course of the disease.

(2) The disease follows within days or weeks after infection, because microbes/viruses multiply exponentially with generation times of 0.5 to 48 hrs, unless they are stopped by immunity (see above).

In populations:

(3) The disease spreads, according to Farr's law, exponentially in an un-immunized population within weeks or months, and subsequently fades away as antiviral immunity builds up (Bregman and Langmuir, 1990). The bell shaped curve of a seasonal flu epidemic is the model.

(4) Infectious diseases are equally distributed between the sexes.

(5) Infectious diseases are most commonly observed in those under 20 and over 60 years of age. This is because after birth the immune system builds up a wide repertoire of antimicrobial resistances that is nearly complete at 20, and over 60 the system begins to decline.

But American/European AIDS does not fit one of these criteria:

(1) There is no abundant microbe common to all American AIDS cases. If HIV is present, it is typically rare and hibernating.

(2) If dated from the time of HIV infection, AIDS occurs at entirely unpredictable times ranging from less than 1 year to over 10 years or never. It has now been 10 years since 1 million Americans were found to be HIV-infected. Most of these and 17 million healthy, HIV-positive non-Americans are still waiting for HIV to cause AIDS.

(3) American AIDS has slowly increased over 10 years. Although AIDS affects annually only a small fraction of susceptible persons-less than 100,000 out of a susceptible pool of 250 million Americans-it has has now almost plateaued for 4 years [after adjusting for new additions of diseases to the AIDS definition] (Centers for Disease Control and Prevention, 1994b). Thus AIDS in America has increased steadily over years, just like an occupational disease, as for example lung cancer from smoking. There is no evidence for immunity and no evidence for a bell shaped AIDS curve.

(4) American AIDS is 87% male (Centers for Disease Control and Prevention, 1994c), which is epidemiologically as far from equality between the sexes as the sun is from the earth. A similar sexual bias has been observed early in the epidemic of smoking-related diseases in the 1960s, before women picked up smoking at the same rate as men.

(5) 98% of all American AIDS cases are over 20 and under 60 (Centers for Disease Control and Prevention, 1994c). Only 1% each are under 20 and over 60! Such an age bias is typical of occupational diseases, like bullet wounds for soldiers.

Thus AIDS in America and Europe (Duesberg, 1992) does not meet even one of the criteria of infectious disease.

Indeed, even proponents of the HIV-AIDS hypothesis, such as Jaap Goudsmit from the University of Amsterdam, grant that "AIDS does not have the characteristics of an ordinary infectious disease. This view is incontrovertible" (Goudsmit, 1992). The AIDS epidemiologists Eggers and Weyer from the University of Cologne state that "the spread of AIDS does not behave like the spread of a disease that is caused by a single sexually transmitted agent" (Eggers and Weyer, 1991). To reconcile AIDS with infectious disease they "simulated a cofactor [that] cannot be identified with any known infectious agent." The epidemiologists Anderson and May from the University of London had to invent "assortative scenarios" for different AIDS risk groups to match AIDS with infectious disease (Anderson and May, 1992).

Until we have scientific evidence, infectious AIDS is just a myth-and, in view of the facts, a very implausible myth indeed.

6. The HIV-AIDS hypothesis is costly, unproductive and harmful

For 11 years now the world has fought the war on AIDS united by the HIV-AIDS hypothesis. But despite its enormous popularity, the virus-AIDS hypothesis has been a complete failure in terms of public health benefits: no vaccine has been developed that prevents AIDS, no drug that cures AIDS, no policy that stops the spread of AIDS (Benditt and Jasny, 1993; Fields, 1994; Swinbanks, 1994; Wade, 1995).

Whatever the reasons are for the complete failure of the HIV-AIDS hypothesis to produce public health benefits, one thing is clear: it was not for lack of trying. The passionate complaint of Shilts' 1987 book, And the Band Played On, that indifference was the only obstacle against a solution of AIDS (Shilts, 1987) has long become profoundly obsolete. Since 1984, an unprecedented $35 billion has been paid by the US taxpayer alone in support of HIV-AIDS research and treatment-more than for all other viral and microbial diseases combined (AIDS Weekly, 1995; Gutknecht, 1995; Henry, 1995; Stone and Cohen, 1995). With all this spending, more research has been done on HIV than on any other virus in history, but absolutely no progress has been made against AIDS. Time, at least, has voted against the HIV-hypothesis. Traditionally, such complete failures are the consequences of a flawed hypothesis.

But the HIV-AIDS establishment does not only cost dearly and fails to produce positive results, it also causes irreparable (1) clinical, (2) educational, and (3) psychological damage:

(1) Clinical damage.

Worldwide about 200,000 HIV antibody-positive persons are prescribed, every six hours, the highly toxic DNA chain terminator AZT or equivalents like ddI, ddC, and d4T as anti-HIV drugs (Duesberg, 1992; Thomas, 1995). Most of these, ie. 200,000 minus the 50,000 to 80,000 annual AIDS patients in America and Europe, are healthy HIV-positives given AZT to prevent AIDS. Recently these include even unborn American and French children and their HIV-positive mothers, although the risk of such children to pick up HIV from their mothers is only about 25% (The Lancet, 1994; Farber, 1995a).

AZT was designed 30 years ago to kill growing human cells for cancer chemotherapy (Horwitz, Chua and Noel, 1964; Duesberg, 1992). In view of its inevitable toxicity, AZT was approved as an anti-HIV drug only tentatively in 1987 (Kolata, 1987). See the warnings of a non-medical manufacturer, Sigma, on the label of an AZT bottle (Fig. 2). The label points out, with skull and cross bones, AZTs toxicity to the bone marrow, the source of T-cells.

Indeed, AZT therapy of HIV appears harmful and irrational. Since HIV is postulated to cause AIDS by killing T-cells (see above), it is irrational to kill the same HIV-infected cells twice-once with HIV and again with AZT. Moreover, it is harmful to kill numerous uninfected cells with AZT collaterally (Kolata, 1987; Lauritsen, 1990; Nussbaum, 1990; Wyatt, 1994).

Accordingly, AZT has failed to cure even one AIDS patient or to prevent AIDS in HIV-infected persons (Duesberg, 1992; Oddone et al., 1993; Tokars et al., 1993; Bacellar et al., 1994; Goedert et al., 1994; Lenderking et al., 1994; Seligmann et al., 1994, Volberding, 1995, Ho, 1995). Instead, evidence is growing that AZT causes AIDS-defining and other diseases as expected from a chain terminator of DNA synthesis (see below) (Mir and Costello, 1988; Lauritsen, 1990; Duesberg, 1992; Lauritsen, 1992; Bacellar et al., 1994; Cohen, 1994a; Duesberg, 1994a; Goedert et al., 1994; Lewis-Thorton, 1994). Yet this evidence is either denied or belittled by the AIDS establishment as the following examples document:

(i) The observation that "HIV dementia among those reporting any antiretroviral use (AZT, ddI, ddC, or d4T) was 97% higher than among those not using this antiretroviral therapy" is interpreted by its authors with little concern for percentages: "This effect was not statistically significant" (Bacellar et al., 1994).

Goedert et al., explain their stunning results-that HIV-positive hemophiliacs on AZT have 4.5-times more AIDS and have a 2.4-times higher mortality than untreated HIV-positive hemophiliacs-by saying this happened "probably because zidovudine was administered first to those whom clinicians considered to be at highest risk" (Goedert et al., 1994).

(ii) Saah et al. explain their observation that male homosexuals on AZT have a two- to four-fold higher risk of Pneumocystis pneumonia than untreated controls as follows: "Zidovudine was no longer significant after T-helper lymphocyte count was considered, primarily because nonusers had higher cell counts..." (Saah et al., 1995). The fact that an inhibitor of DNA synthesis designed to kill human cells would inhibit lymphocyte growth was not mentioned.

(iii) The blunt result that AZT prophylaxis reduced survival from 3 to 2 years, and caused "wasting syndrome, cryptosporidiosis, and cytomegalovirus infection ... almost exclusively" in AZT-treated AIDS patients, was interpreted like this: "The study of patients who progress from primary HIV infection to AIDS without receiving medical intervention gives insights into the effects of medical intervention on presentation and survival after developing an AIDS defining illness." But the nature of these "insights" was not revealed by the authors (Poznansky et al., 1995).

(iv) The largest test of AIDS prophylaxis with AZT of its kind, the Concorde trial, found a 25% higher mortality in AZT recipients than in untreated controls. In view of this Seligmann et al., reached the conservative conclusion: "The results of Concorde do not encourage the early use of zidovudine [AZT] in symptom-free HIV-infected adults" (Seligmann et al., 1994).

(v) Five years after introducing AZT prophylaxis to several hundred thousands of healthy HIV-positives, Paul Volberding of the University of California at San Francisco, Anthony Fauci of the National Institute of Allergy and Infectious Diseases and over 100 scientific collaborators now publish in the New England Journal of Medicine: "Zidovudine ... does not significantly prolong either AIDS-free or overall survival. These results do not encourage the routine use of Zidovudine" (Volberding et al., 1995). In an accompanying editorial "Time to hit HIV, early and hard" the "Journal" makes the forward recommendation to treat HIV infection with AZT and other experimental drugs before antiviral immunity restricts the virus to chronic latency (Ho, 1995). The article suggests that current AZT prophylaxis is too little too late. This is said although the ineffectiveness of the proposed "early and hard" treatment is known since 1993 (Tokars et al., 1993).

(vi) The occurence of 8 serious birth defects, 8 spontaneous abortions and 8 therapeutic abortions among 104 pregnancies treated with AZT is interpreted as "not proving safety, thus lending tenous support to the use of this drug." (Kumar, Hughes and Khurranna, 1994).

AZT must be considered the most toxic among legal public health threats available to healthy persons, much more toxic than alcohol and tobacco. For this reason I have termed AZT AIDS by prescription (Duesberg, 1992, see Chapter 6). Even Burroughs Wellcome, the manufacturer of AZT, makes that same assessment, but expresses it in different words: "It was often difficult to distinguish adverse events possibly associated with zidovudine [AZT] administration from underlying signs of HIV disease..." (Physicians' Desk Reference, 1994).

(2) Educational damage.

Since HIV, but not drugs, is thought to cause AIDS, the HIV-AIDS establishment educates the public to use "clean needles" for the injection of unsterile (!) street drugs and to wear condoms for sex under the influence of aphrodisiac drugs (Institute of Medicine, 1988; San Francisco Project Inform, 1992; Benditt and Jasny, 1993; National Institute of Allergy and Infectious Diseases, 1994). However, the disregard, in fact explicit dismissal, of drug toxicity by the AIDS establishment (Weiss and Jaffe, 1990; Ascher et al., 1993; Duesberg, 1993d; Maddox, 1993a; Schechter et al., 1993b; Schechter et al., 1993c; Cohen, 1994a) encourages recreational drug use because it eliminates the fear of drug toxicity. A popular joke illustrates this point: "Two junkies are reminded by a friend not to share a syringe full of cocaine. Their response: 'We wear condoms and use a clean needle'."

Yet long-term use of recreational drugs, including cocaine, heroin, amyl- and isobutyl nitrite inhalants, amphetamines, and others has been documented in numerous studies to cause exactly the same diseases that are now blamed on HIV (Haverkos and Dougherty, 1988; Stoneburner et al., 1988; Lerner, 1989; Duesberg, 1992, see Chapter 6). The list of drug-induced diseases, established long before the discovery of HIV, reads like a catalogue of AIDS-defining diseases: weight loss, fever, dementia, tuberculosis, oral thrush, pneumonia, diarrhea, mouth infections, night sweats, and many others (see below) (Lerner, 1989; Duesberg, 1992).

(3) Psychological damage.

According to the HIV-AIDS establishment, nearly all HIV-infected, healthy persons are claimed to die from AIDS on average 10 years after infection by HIV (Institute of Medicine, 1988; Garza, Drotman and Jaffe, 1994; National Institute of Allergy and Infectious Diseases, 1994; Thomas Jr., Mullis and Johnson, 1994). In view of this, one million HIV-positive but healthy Americans, and 17 million HIV-positive but healthy humans on this planet (Merson, 1993; National Institute of Allergy and Infectious Diseases, 1994; World Health Organization, 1995), are subjected to a multiplicity of psychological and sociological pressures (Anonymous, 1992; Duesberg, 1992; Schmalz, 1992b; Schmalz, 1992a; Miami Herald, 1994; Yarbo, 1994).

They are given a death sentence by the medical establishment for being HIV-positive; they are denied coverage by health insurance companies; they lose their jobs and social status; they are denied entrance visas to many countries including the U.S.; they are denied employment by the US Army; and worst of all they are pressured to accept the toxic AZT therapy-all of this, only because they have made antibodies against a virus that is presumed to cause AIDS. If they refuse to submit to these pressures, they are charged with denial (of the HIV-AIDS hypothesis) by the AIDS establishment (Moss, Osmond and Bacchetti, 1988; San Francisco Project Inform, 1992).

In sum, the public health record of the HIV-AIDS hypothesis in America adds up to a staggering deficit: for $35 billion (Duesberg, 1994b; AIDS Weekly, 1995; Gutknecht, 1995) there is no cure, no vaccine, no effective prevention, hundreds of thousands are subjected to psychological pressures resulting from positive HIV-tests, and several million American drug addicts are denied available information that recreational drugs cause AIDS-defining and other diseases (Drug Strategies, 1995), and about 150,000 are subjected annually to AZT poisoning-many just for being HIV-positive, not for having AIDS (Duesberg, 1992).

7. The drug-AIDS hypothesis

Given no evidence for infectious AIDS, the reasons for the original "lifestyle hypothesis," and the logic of Sherlock Holmes-that "when you have eliminated the impossible, whatever remains however improbable must be the truth"-AIDS must be non-infectious.

In view of this I propose that: 

All AIDS diseases in America and Europe that exceed their long-established, normal backgrounds are caused by the long-term consumption of recreational drugs and by AZT and its analogs.

Hemophilia-AIDS, transfusion-AIDS, and the extremely rare AIDS cases of the general population reflect the normal incidence plus the AZT-induced incidence of these diseases under a new name.

African AIDS is a new name for old diseases caused by malnutrition, parasitic infections and poor sanitation (Duesberg, 1991; Duesberg, 1992; Duesberg, 1994a, see Chapters 6 and 9).

Indeed, the recreational drug use epidemics, that started in America and Europe during the Vietnam war, are the only new health risk of the Western World since World War II. Since its beginnings the drug use and AIDS epidemics in the US and Europe have coincided both epidemiologically and chronologically (Duesberg, 1992). About 33% of all American AIDS patients, nearly all heterosexual AIDS patients, are intravenous drug users (Centers for Disease Control and Prevention, 1994b). Over 60% are male homosexuals who have used psychoactive and aphrodisiac drugs orally such as nitrite inhalants, amphetamines, cocaine and phenylcyclidine (Table 2). Many of these recreational drug users and most of the few AIDS patients who have not used recreational drugs have used AZT and cytotoxic DNA chain terminators as anti-HIV drugs (see below) (Duesberg, 1992; Duesberg, 1994a). Allowing a "latent period of 10 years" for chronic recreational drug use to cause AIDS, the beginning of the American drug use epidemics in the late 1960s and 1970s predicts exactly the origin of AIDS in the 1980s.

Unlike the virus-AIDS hypothesis, the drug hypothesis has a plausible chemical and experimentally testable basis. The recreational drugs postulated to cause AIDS have strong biochemical and psychoactive effects every time they are taken-the reason for their popularity (see Chapter 6). By contrast, HIV is latent, and neither chemically nor clinically detectable in "HIV antibody-positives" with and without AIDS. Despite 11 years of unprecedented research efforts no biochemical evidence has been found in support of the HIV-AIDS hypothesis (Cohen 1995).

The specific toxicity and dosages of recreational and medical drugs used by American and European AIDS risk groups can explain all AIDS diseases (Duesberg, 1992). AIDS drugs are either indirectly toxic, or cytotoxic, or genotoxic and cytotoxic.

(1) Indirectly toxic. Cocaine, amphetamines and heroin are indirectly immunotoxic. All three function as catalysts in the human body. Cocaine and heroin are natural compounds and amphetamines are synthetic adrenalins first developed in Germany during World War II to suppress fatigue and anxiety in pilots and tank commanders (Weil and Rosen, 1983).

Indirect toxicity is the result of malnutrition and insomnia which in turn are consequences of drug-induced suppression of appetite and fatigue (Layon et al., 1984; Lerner, 1989; Pillai, Nair and Watson, 1991; Duesberg, 1992; Larrat and Zierler, 1993; Mientjes et al., 1993; Sadownick, 1994). These problems are compounded by poverty due to the enormous costs of illicit drugs. Direct, long-term pathogenic effects of cocaine and heroin have not been studied owing to the general disregard of drug toxicity (Duesberg, 1992).

(2) Cytotoxic and genotoxic. Nitrite inhalants are cytotoxic, and thus are immunotoxic in animals and humans (Goedert et al., 1982; Haverkos and Dougherty, 1988). A recreational dose of 1 ml per day (Haverkos and Dougherty, 1988; Duesberg, 1992) corresponds to about 15 ppm in a 75 kg-person, and corresponds to 107 nitrite molecules for everyone of the 1014 cells in the human body. The cytotoxicity of nitrites on the epithelial tissues of the lung are enhanced by the toxins of cigarette smoke, which also suppresses the immunesystem (Nieman et al., 1993).

In addition nitrite inhalants are among the best established mutagens and carcinogens (National Research Council, 1982; Lewis, 1989; Winter, 1989; Mirvish et al., 1993). In view of the toxicity of nitrite inhalants, a prescription requirement was instated by the US Food and Drug Administration in 1969 (Newell et al., 1985a), and because of an "AIDS link" (Cox, 1986) the sale of nitrites was banned by the U.S. Congress in 1988 (Public Law 100-690) (Haverkos, 1990) and by the "Crime Control Act of 1990" (Duesberg, 1992). Moreover, the US Food and Drug Administration limits nitrites as food preservatives to less than 200 ppm, because of direct toxicity and because "they have been implicated in an increased incidence of cancer" (Lewis, 1989, National Research Council, 1982).

(3) Genotoxic-cytotoxic. AZT, ddI and other DNA chain terminators are directly toxic by killing all growing cells, in particular the fastest growing ones-the hematopoietic and epithelial cells (Fig. 2), (Merck Research Laboratories, 1992; Chiu and Duesberg, 1995). In addition, AZT prevents mitochondrial DNA synthesis in non-growing cells, such as neurons or muscles, and can be carcinogenic by mutating cells (Pluda et al., 1990; Duesberg, 1992; Parker and Cheng, 1994).

The key to the drug hypothesis is that only long-term consumption causes irreversible AIDS-defining diseases. Occasional or short-term recreational drug use causes reversible diseases or no diseases at all. With drugs, the dose is the poison. Yet, most studies investigating the effects of recreational drugs are concerned with their short-term psychoactive rather with their long-term clinical effects (Duesberg, 1992). For example, it takes 20 years of smoking to acquire irreversible lung cancer or emphysema, and 20 years of drinking to acquire irreversible liver cirrhosis. In contrast to drugs, infectious agents are self-replicating toxins. By multiplying exponentially in the body infectious agents may generate sufficient doses of toxic substances to cause diseases within days or weeks.

Since currently no experiments are being done in America to test the drug hypothesis, I have evaluated the drug-AIDS hypothesis on the basis of its predictions. In contrast to the HIV-AIDS hypothesis, the drug hypothesis can predict all parameters of American/European AIDS.

9. The drug-hypothesis predicts the American/European AIDS epidemic-completely

(9.1) AIDS is restricted to intravenous and oral users of recreational drugs and of AZT, because drugs cause AIDS.

Since 1981 94% of all American AIDS cases have been from risk groups who had used such drugs (Centers for Disease Control and Prevention, 1994c). About one-third of these were intravenous drug users (Centers for Disease Control, 1993) and two-thirds were male homosexuals (Centers for Disease Control and Prevention, 1994c; Centers for Disease Control and Prevention, 1994a) who had used oral recreational drugs and AZT (Duesberg, 1992; Ascher et al., 1993; Duesberg, 1993c; Duesberg, 1993a; Duesberg, 1993d; Parke, 1993; Schechter et al., 1993b). HIV-positive hemophiliacs and transfusion recipients also receive AZT as an antiviral drug (Duesberg, 1992; Duesberg, 1995b). (However, a small percentage of hemophiliacs annually develop a specific subset of AIDS-defining immunodeficiency diseases, mostly pneumonia and candidiasis, only from the long-term transfusion of foreign proteins that contaminate commercial factor VIII (Duesberg, 1992; Duesberg, 1995b, see Chapter 11). European AIDS also correlates with drug consumption (Duesberg, 1992, see Chapter 6).

(9.2) American/European AIDS predominantly affects adult males, because they are the predominant users of recreational drugs and AZT.

The CDC reports that 87% of all American AIDS patients are males (Centers for Disease Control and Prevention, 1994c). This number is the sum of the following constituents: The National Institute on Drug Abuse and the Bureau of Justice Statistics report that over 75% of hard, recreational drugs are consumed intravenously by males (Duesberg, 1992, see Chapter 6).

According to the federally supported Drug Strategies program "women account for the fastest-growing population in jails and prisons, in large part because of drug offenses" (Drug Strategies, 1995). Therefore the CDC reports that women are now the fastest growing AIDS risk group (Centers for Disease Control, 1994; Centers for Disease Control and Prevention, 1994a).

The CDC and independent investigators report that nearly all male homosexuals with AIDS and at risk for AIDS are long-term users of oral drugs such as nitrite inhalants, ethylchloride inhalants, amphetamines, cocaine, and others to facilitate sexual contacts, particularly anal intercourse (Lifson et al., 1990; Duesberg, 1992; Ascher et al., 1993; Duesberg, 1993d; Schechter et al., 1993a; Schechter et al., 1993c). The drug use of male homosexuals with AIDS or at risk for AIDS reported by the CDC (Jaffe et al., 1983; Darrow et al., 1987; Lifson et al., 1990) and others (Ascher et al., 1993; Duesberg, 1993d; Schechter et al., 1993c; Ellison, Downey and Duesberg, 1995) as of 1983 is listed in Table 2. Ostrow reported that nitrite inhalant use in a cohort of over 5000 male homosexuals from Chicago, Baltimore, Los Angeles and Pittsburgh showed a "consistent and strong cross-sectional association with ... anal sex" (Ostrow, 1994). In addition, many HIV-positive homosexuals are prescribed AZT as an antiviral drug (Duesberg, 1992; Duesberg, 1993d; Ellison, Downey and Duesberg, 1995).

Since intravenous drug users, who are 75% male, make up one-third of all AIDS patients, and male homosexuals make up almost two-thirds of all American AIDS patients, the drug hypothesis explains why 87% of all American AIDS patients are males.

(9.3) Pediatric AIDS coccurs because of maternal drug addiction.

Indeed about 80% of pediatric AIDS cases in America and Europe are children born to mothers who were intravenous drug users during pregnancy (see below (5) and (8)), (Mok et al., 1987; European Collaborative Study, 1991; Duesberg, 1992). The remainder reflects the normal low incidence of AIDS-defining diseases among newborns.

(9.4) American AIDS is new and increasing steadily, because the American drug epidemic is new and increasing steadily.

In the U.S. recreational drug use is epidemiologically new, as it has increased over the last decades from statistically undetectable levels to epidemic levels at about the same rate as AIDS (Duesberg, 1992).

For example, cocaine consumption increased 200-fold from 1980 to 1990, based on cocaine seizures that increased from 500 kg in 1980 to 100,000 kg in 1990 (Duesberg, 1992, see Chapter 6). During the same time cocaine-related hospital emergencies increased from 3,296 cases in 1981, to 80,355 cases in 1990, and to 119,843 in 1992 and to over 120,000 in 1993 (Duesberg, 1992; Meddis, 1994; Drug Strategies, 1995) (Fig. 1B).

In the last three years, the increase of cocaine consumption has slowed down at the expense of increases in heroin consumption, which were accompanied by increases in heroin-related hospital emergencies (Gettman, 1994; Meddis, 1994; Drug Strategies, 1995). Heroin-related hospital emergencies doubled, from over 30,000 in 1990 to over 60,000 in 1993 (Fig. 1B)(Drug Strategies, 1995).

Amphetamine consumption has increased 100-fold from 1980 to 1990 (Bureau of Justice Statistics, 1991). Non-scientific reports describe new upsurges in the consumption of amphetamines (Sadownick, 1994) and the "gay drug" (nitrite inhalants) (Mirken, 1995) among male homosexuals. According to a recent report from the National Institute on Drug Abuse and the CDC, "nitrite use has increased in the 1990s in gay men in Chicago and San Francisco" after a decline in the 1980s (Haverkos and Drotman, 1995).

Drug offenders are now the "largest and fastest-growing category in the Federal prisons population, accounting for 61% of the total, compared with 38% in 1986." The number of Federal drug offenders increased from about 5,000 in 1980 to about 55,000 in 1993. In 1993, between 60 and 80% of the 12 million prisoners in the US had been on illicit drugs (Drug Strategies, 1995).

The German "Rauschgiftbilanz" reports an 11.2% increase in the consumption of illicit recreational drugs in 1994 compared to 1993 (Rauschgiftbilanz 1994, 1995).

Consider a grace period of about 10 years to achieve the dosage needed to cause irreversible disease, and you can date the origin of AIDS in 1981 as a consequence of the drug use epidemic that started in America in the late 1960s during the Vietnam War. Indeed, AIDS increased from a few dozen cases annually in 1981 to about 100,000 in 1993 (Fig. 1A) (Centers for Disease Control and Prevention, 1994c). Note the parallelisms between the spread of AIDS and the spread of cocaine and cocaine-related hospital emergencies since 1981 (Fig. 1A and B), and the contrast with the non-spread of HIV, the hypothetical cause of AIDS, since 1984 (Fig. 1A). Thus both, the newness and the increase of the AIDS epidemic are predictable by the drug-AIDS hypothesis.

The growth of the epidemic has been accelerated by AZT. Since its introduction in 1987, AZT is now prescribed to about 200,000 HIV-positives worldwide (Duesberg, 1992; Thomas, 1995).

(9.5) Only a small fraction of drug users develop AIDS, because only the highest cumulative drug doses cause irreversible diseases.

The cumulative total of 401,749 American AIDS cases since 1981 that were reported in June 1994 (Centers for Disease Control and Prevention, 1994c) have been recruited from a much larger reservoir of drug users. There are currently between 3 (Drug Strategies, 1995) and 8 million cocaine addicts (Duesberg, 1992) and 0.6 million heroin addicts in the US (Drug Strategies, 1995). In 1980, 5 million Americans had used nitrite inhalants. In 1989, 100 million doses of amphetamines were consumed in the U.S. (Duesberg, 1992).

According to a 1994-survey of the National Institute on Drug Abuse, "more than 5 percent (221,000) of the 4 million women who give birth each year use illicit drugs during their pregnancy." (Drug Strategies, 1995). These mothers are the reservoir from which most of the 1017 pediatric AIDS cases reported in the US in 1994 were recruited (Centers for Disease Control and Prevention, 1994b) (see 10).

Unfortunately, scientific documentation of recreational drug use is extremely sporadic and inaccessible, not only because these drugs are illegal, but more importantly because the medical-scientific community is totally uninterested in drugs as a cause of AIDS (see above).

In addition, about 150,000 HIV-positive Americans were on AZT between 1992 and 1995 (Duesberg, 1992; Thomas, 1995). Probably because drug toxicity is generally ignored, there are also no national statistics available on how many HIV-positive Americans are on AZT and other anti-HIV drugs, that, like AZT, are designed to kill human cells (Duesberg, 1992).

The small percentage of AIDS patients among the many American drug users reflects the highest lifetime dose of drug use, just like the lung cancer and emphysema patients reflect the highest lifetime tobacco dose among the 50 million smokers in the U.S. The long "latent period of HIV" is a euphemism for the time needed to accumulate the drug dosage that is sufficient for AIDS. Indeed it takes about 10 years of injecting heroin and cocaine to develop weight loss, tuberculosis, bronchitis, pneumonia and other drug-induced diseases (Layon et al., 1984; Schuster, 1984; Savona et al., 1985; Donahoe et al., 1987; Espinoza et al., 1987; Weber et al., 1990).

The time lag from initiating a habit of inhaling nitrites to acquire Kaposi's sarcoma has been determined to be 7 to 10 years (Newell et al., 1985a; Beral et al., 1990; Lifson et al., 1990; Duesberg, 1992). Blaming Kaposi's sarcoma on HIV after inhaling carcinogenic nitrites for 10 years is like blaming lung cancer and emphysema on a "slow" virus after smoking two packs of cigarettes a day for 20 years.

AZT, at the currently prescribed high doses of 0.5 to 1.5 grams per person per day, causes many of the above described AZT-specific diseases faster than recreational drugs, i.e. within weeks or months after administration (Duesberg, 1992; Lewis-Thorton, 1994).

(9.6) Risk group-specific AIDS diseases occur, because of risk group-specific drugs.

Group-specific drug use explains the following risk-group-specific AIDS diseases:

(i) Kaposi's sarcoma specific for male homosexuals. Kaposi's sarcoma as an AIDS diagnosis is 20 times more common among homosexuals who use nitrite inhalants than among AIDS patients who are intravenous drug users, or hemophiliacs (Haverkos and Dougherty, 1988; Beral et al., 1990). Due to the carcinogenic potential, nitrites were originally proposed as causes of Kaposi's sarcoma (Marmor et al., 1982; Haverkos et al., 1985). "Aggressive and life-threatening" Kaposi's sarcoma particularly pulmonary Kaposi's sarcoma, is exclusively observed in male homosexuals (Sloand, Kumar and Pierce, 1993; Meduri et al., 1986; Garay et al., 1987; Gill et al., 1989). Since the lungs are the primary site of exposure to nitrite inhalants, the evidence that up to 32% of Kaposi's sarcomas of homosexual men can be diagnosed as pulmonary Kaposi's sarcoma (Gill et al., 1989; Irwin and Kaplan, 1993), lends additional support to the nitrite-Kaposi's sarcoma hypothesis. Pulmonary Kaposi's sarcoma has never been described by Moritz Kaposi, nor anywhere else prior to the AIDS epidemic (Kaposi, 1872).

It appears that the nitrite-induced AIDS Kaposi's sarcoma and the classic Kaposi's sarcomas are entirely different cancers under the same name. The "HIV-associated" Kaposi's sarcomas observed in male homosexuals are "aggressive and life-threatening" (Sloand, Kumar and Pierce, 1993), fatal within 8-10 months after diagnosis, and often located in the lung (Meduri et al., 1986; Garay et al., 1987; Gill et al., 1989; Irwin and Kaplan, 1993). The classic "indolent and chronic" Kaposi's sarcomas are diagnosed on the skin of the lower extremities and hardly progress over many years (Meduri et al., 1986; Drotman and Haverkos, 1992; Cohen, 1994a). Meduri et al. point out that the "pulmonary involvement by the neoplasma has been an unusual clinical finding" in the Kaposi's sarcomas of male homosexuals compared to all "classic" Kaposi's sarcomas (Meduri et al., 1986). Nevertheless, the distinction between classic and AIDS Kaposi's sarcoma is hardly ever emphasized and may have escaped many observers due to the "difficulty in pre-mortem diagnosis," because "pulmonary Kaposi's sarcoma was indistinguishable from opportunistic pneumonia ..." (Garay et al., 1987).

The immunotoxicity and cytotoxicity of nitrites also explains the proclivity of male homosexual nitrite users for pneumonia, which is the most common AIDS disease in the U.S. and Europe (Haverkos and Dougherty, 1988; Duesberg, 1992) (Table 1) (Chapter 6). Moreover the immunotoxins and cytotoxins of cigarette smoke explain, why in two groups of otherwise matched HIV-positive male homosexuals cigarette smokers developed pneumonia twice as often as non-smokers over a period of 9 months (Nieman et al., 1993).

(ii) High mortality of intravenous drug users. Intravenous drug users suffer from long-term malnutrition and insomnia, which are primary causes of immunodeficiency worldwide (Seligmann et al., 1984). This explains the tuberculosis, pneumonia, and weight loss that are typical of these risk groups (Layon et al., 1984; Stoneburner et al., 1988; Pillai, Nair and Watson, 1991; Duesberg, 1992; Mientjes et al., 1993). Injection of unsterile drugs combined with immunodeficiency also cause septicemia and endocarditis that are common in AIDS patients who are intravenous drug users (Duesberg, 1992). As a result, intravenous drug users only achieve a very low average age. A German study found the average age at death to 29.6 years for HIV-free and 31.5 years for HIV-positive addicts (Lockemann et al., 1995); and an American study showed that both HIV-positive and negative intravenous drug users died from the same diseases (Stoneburner et al., 1988).

(iii) Low birth weight and mental retardation of AIDS babies. 80% of American/European babies with AIDS are born to mothers who were intravenous drug users during pregnancy; they acquire low birth weight, mental retardation and immunodeficiency through maternal drug use (Duesberg, 1992; Drug Strategies, 1995). The B-cell deficiencies and certain bacterial infections-that are both only considered AIDS-defining in children-are also specific expressions of their acquired immunodeficiency (Centers for Disease Control, 1987; Centers for Disease Control and Prevention, 1992; Duesberg, 1992).

(iv) Anemia and wasting of AZT recipients. Anemia, leukopenia, pancytopenia, diarrhea, weight loss, hair loss, impotence (Duesberg, 1992), hepatitis (Freiman et al., 1993), and pneumocystis pneumonia (Saah et al., 1995) that are observed in recipients of AZT and other DNA chain terminators, are predictable consequences of the cytotoxicity of these drugs (see Chapter 6). In addition, non-renewal of mitochondrial DNA causes muscle atrophy, hepatitis, and dementia; and carcinogenic activity causes cancers such as lymphoma in AZT recipients (Pluda et al., 1990; Duesberg, 1992; McLeod and Hammer, 1992; Freiman et al., 1993; Bacellar et al., 1994; Parker and Cheng, 1994; Physicians' Desk Reference, 1994). Compared to untreated controls AZT recipients die 2.4-times more often (Goedert et al., 1994), 25% more often (Seligmann et al., 1994), or live only 2 years instead of 3 years with AIDS (Poznansky et al., 1995).

(9.7) Non-correlations between HIV and AIDS, because drugs, not HIV, cause AIDS.

(i) Long-term survivors or "non-progressors." Persons infected by HIV for more than the 10-year-latent-period-from-HIV-to-AIDS who are studied by HIV researchers are termed long-term survivors and more recently "non-progressors" (Scolaro, Durham and Pieczenik, 1991; Learmont et al., 1992; Cao et al., 1995). David Ho et al. recently gave a key to long-term survival, "none had received antiretroviral therapy" (Cao et al., 1995). Likewise Alvaro Munoz reported that not one of the long-term survivors of the largest federally funded study of male homosexuals at risk for AIDS, the MACS study, had used AZT (Munoz, 1995). And several survey studies document that in addition to abstaining from antiviral drugs long-term survivors are those who have given up or never taken recreational drugs (Wells, 1993; Gavzer, 1995; Root-Bernstein, 1995b).

Indeed, the vast majority of HIV-positives are long-term survivors! Worldwide, they number 17 million, including 1 million HIV-positive but healthy Americans and 0.5 million HIV-positive but healthy Europeans (Merson, 1993; World Health Organization, 1995). Most of these have been HIV-positive for at least 10 years now, because their numbers have not changed since the time between 1984 to 1988, when the epidemic of HIV-testing began in the respective countries (Duesberg, 1992).

Only about 6% (or 1,025,073) of these 17 million HIV-positives have developed AIDS diseases since AIDS statistics are kept (World Health Organization, 1995). Since no more than 6% of HIV-carriers worldwide have developed AIDS in 7 to 10 years, the annual AIDS risk of an HIV-carrier is less than 1% per year. However, even this low figure is not corrected for the normal occurence of the 29 AIDS-defining diseases in HIV-free controls. There is no evidence that HIV-positive people who are not drug users have a higher morbidity or mortality than HIV-free controls (Duesberg, 1995a, see Chapter 10).

(ii) Intravenous drug users and male homosexuals losing their T-cells prior to HIV infection. Prospective studies of male homosexuals using psychoactive and sexual stimulants have demonstrated that their T-cells may decline prior to infection with HIV. For example, the T-cells of 37 homosexual men from San Francisco declined steadily prior to HIV infection for 1.5 years from over 1200 to below 800 per µl (Lang et al., 1989). In fact, some had fewer than 500 T-cells 1.5 years before seroconversion (Lang et al., 1987). Although recreational drug use was not mentioned in these articles, other studies of the same cohort of homosexual men from San Francisco described extensive use of recreational drugs including nitrites (Darrow et al., 1987; Moss, 1987; Ascher et al., 1993; Duesberg, 1993d; Ellison, Downey and Duesberg, 1995). Likewise 33 HIV-free male homosexuals from Vancouver, Canada, had "acquired" immunodeficiency prior to HIV infection (Marion et al., 1989). Again this study did not mention drug use, but in other articles the authors reported that all men of this cohort had used nitrites, cocaine and amphetamines (Archibald et al., 1992; Duesberg, 1993f; Schechter et al., 1993c).

The largest study of its kind reported that about 450 (16% of 2795) HIV-free, homosexual American men of the MACS cohort from Chicago, Baltimore, Pittsburgh and Los Angeles had acquired immunodeficiency, having less than 600 T-cells per µl, prior to HIV infection (Kaslow et al., 1989). Many HIV-positive and -negative men of this cohort had essentially the same degree of lymphadenopathy: "Although seropositive men had a significantly higher mean number of involved lymph node groups than seronegative men (5.7 compared to 4.5 nodes, p0.005), the numerical difference in the means is not striking" (Kaslow et al., 1987). According to previous studies on this cohort 71% of these men had used nitrite inhalants, in addition to other drugs (Kaslow et al., 1987); 83% had used one drug, and 60% had used two or more drugs during sex in the previous six months (Ostrow et al., 1990).

Another study of the same cohort observed that the risk of developing AIDS correlated with the frequency of receptive anal intercourse prior to and after HIV infection (Phair et al., 1992). Other studies have shown that receptive anal intercourse correlates directly with the use of nitrite vasodilaters (Haverkos and Dougherty, 1988; Duesberg, 1992; Parke, 1993).

Thus in male homosexuals at risk for AIDS, AIDS often precedes infection by HIV, not vice versa. Since the cause must precede the consequence, drug use remains the only group-specific choice to explain "acquired" immunodeficiencies prior to HIV. If male homosexuality were to cause immunodeficiency, about 10% of the adult American male population should have AIDS (Duesberg, 1992; Seidman and Rieder, 1994).

Prospective studies of intravenous drug users also document T-cell losses prior to infection by HIV. For example, among intravenous drug users in New York "The relative risk for seroconversion among subjects with one or more CD4 [T-cell] count <500 cells/µl compared with HIV-negative subjects with all counts >500 cells/µl was 4.53." (Des Jarlais et al., 1993). A similar study from Italy showed that a low number of T-cells was the highest risk factor for HIV infection (Nicolosi et al., 1990). Again, a decrease in T-cells is a risk factor for HIV infection, and not vice versa.

This confirms the hypothesis that HIV is a marker of drug consumption, rather than the cause of AIDS (see IV): the more drugs are consumed intravenously or for sex, the higher is the risk of HIV infection (Duesberg, 1992).

(iii) HIV-free AIDS. One summary of the AIDS literature describes over 4,621 clinically diagnosed AIDS cases who were not infected by HIV (Duesberg, 1993f, see Chapter 7). Additional cases are described that were not in this summary (Kaslow et al., 1987; Lang et al., 1987; European Collaborative Study, 1991; Weiss et al., 1992; Ellison, Downey and Duesberg, 1995; Moore and Chang, 1995). They include intravenous drug users, male homosexuals using aphrodisiac drugs like nitrite inhalants, and hemophiliacs developing immune suppression from long-term transfusion of foreign proteins contaminating factor VIII (Duesberg, 1993f; Duesberg, 1995b).

Each of these non-correlations between HIV and AIDS are predicted by the hypothesis that recreational drugs and other non-contagious risk factors cause AIDS.

(9.8) Discontinuation of drug use either stabilizes or cures AIDS and other diseases-even in HIV-positives.

(i) AZT. Ten out of 11 HIV-positive, AZT-treated AIDS patients recovered cellular immunity after discontinuing AZT in favor of an experimental vaccine (Scolaro, Durham and Pieczenik, 1991). Two weeks after discontinuing AZT, 4 out of 5 AIDS patients recovered from myopathy (Till and MacDonnell, 1990). Three of four AIDS patients recovered from severe pancytopenia and bone marrow aplasia 4-5 weeks after AZT was discontinued (Gill et al., 1987).

(ii) Heroin/cocaine. The incidence of AIDS diseases among HIV-positive intravenous drug users over 16 months was 19% (23/124) and only 5% (5/93) among those who stopped injecting drugs (Weber et al., 1990). The T-cell counts of HIV-positive intravenous drug users from New York dropped 35% over 9 months, compared to HIV-positive controls who had stopped injecting (Des Jarlais et al., 1987).

(iii) Recreational drugs and AZT. The health of male homosexuals is stabilized or even improved by avoiding recreational drugs. For example in August 1993 there was no mortality during 1.25 years in a group of 918 British HIV-positive homosexuals who had "avoided the experimental medications on offer" and chose to "abstain from or significantly reduce their use of recreational drugs, including alcohol" (Wells, 1993). Assuming an average 10-year latent period from HIV to AIDS, the virus-AIDS hypothesis would have predicted at least 58 (918/10 x 1.25 x 50%) AIDS cases among 918 HIV-positives over 1.25 years. Indeed, the absence of mortality in this group over 1.25 years corresponds to a minimal latent period from HIV to AIDS of over 1,148 (918 x 1.25) years. On July 1, 1994 there was still not a single AIDS case in this group of 918 HIV-positive homosexuals (J. Wells, London, personal communication).

The T-cells of 29% of 1,020 HIV-positive male homosexuals and intravenous drug users in a clinical trial even increased over 2 years (Hughes et al., 1994). These HIV-positives belonged to the placebo arm of an AZT trial for AIDS prevention and thus were not treated by AZT. It is probable that under clinical surveillance the 29% whose T-cells increased, despite HIV, have given up or reduced immunosuppressive recreational drug use in the hope that AZT would prevent AIDS.

(iv) AIDS babies, born to drug-addicted mothers, recover after birth. HIV-positive babies, born to mothers who were intravenous drug users during pregnancy, provide the best examples for the prediction that termination of drug use prevents, or cures AIDS-despite the presence of HIV. For example, Blanche et al. have observed for three years 71 HIV-positive newborns who had shared intravenous drugs with their mothers prior to birth. Ten of these children developed encephalopathy and AIDS-defining diseases of which 9 died during their first 18 months of life. The study points out that the risk of a newborn to develop AIDS was related "directly with the severity of the disease in the mother at the time of delivery." Based on the severity of their symptoms about 60% of the children were treated prophylactically, but apparently briefly with AZT "for at least one month," and 50% were treated with sulfa-drugs (Blanche et al., 1994). Despite HIV, 61 of the 71 HIV-positive children either developed only "intermittent" diseases from which they recovered during their first 18 months or developed no disease at all during the 3 years of observation. The T-cells of these children increased after birth from low to normal levels-despite the presence of HIV.

A very similar picture emerges from a collaborative European study of HIV-positive newborns (The European Collaborative Study, 1994). The study reports that about 20% of the HIV-positive children had died or developed long-term AIDS during the first year after birth, and another 20% during the second and third year. About 10% of the children were "treated with zidovudine [AZT]" before 6 months of age and 40% by 4 years (The European Collaborative Study, 1994). But over 60% of congenitally-infected children proved to be healthy up to 6 years after birth-despite the presence of HIV. Most of these had experienced transient AIDS diseases, such as pneumonia, bacterial infections, candidiasis and cryptosporidial infection during the first year after birth.

Although this study does not even mention the health and health risks of the mothers, previous reports from the European Collaborative Study group have documented that "nearly all children were born to mothers who are intravenous drug users" (Mok et al., 1987; Duesberg, 1992). In 1991, the European Collaborative Study group reported that 80% of the children with pediatric AIDS were born to mothers who were intravenous drug users (European Collaborative Study, 1991). The 1991-study further points out that "children with drug withdrawal symptoms" were most likely to develop diseases, and that children with no withdrawal symptoms but "whose mothers had used recreational drugs in the final 6 months of pregnancy were intermediate" in their risk to develop diseases (European Collaborative Study, 1991).

According to the HIV hypothesis every infected baby should have developed AIDS and progressively lost T-cells, and according to an HIV plus cofactor hypothesis, at least all those with intermittent diseases should have progressed to AIDS. This was not observed.

According to the drug hypothesis, the AIDS risk of the children is a function of the drugs consumed. Those who received the highest doses of drugs before birth would have acquired irreversible diseases and those who acquired diseases from sublethal thresholds would be able to recover after cessation of maternally administered drugs. Indeed, both, the European Collaborative Study group and Blanche et al. show that the majority of children gained T-cells and recovered from transient diseases after discontinuation of maternal drug input-despite the presence of HIV. The childrens risk for AIDS was related "directly with the severity of the disease in the mother" (Blanche et al., 1994), which is an expression for the extent of drug consumption by the mother.

Moreover, the harm of maternal drug consumption to sick babies was compounded after birth, because "prophylactic treatment [with] ... sulfamethoxazale and zidovudine [AZT] was started earlier and was more frequent among the 16 children born to mothers with class IV disease (AIDS)" (Blanche et al., 1994). (The Blanche study did include mothers with AIDS who were not intravenous drug users). The European Collaborative Study group reports that 10 to 40% of HIV-positive children were treated with AZT.

It follows that discontinuation of recreational and antiretroviral drug use stabilizes and even cures AIDS in HIV-positive persons.

Likewise the T-cells of HIV-positive hemophiliacs increase after removal of immunosuppressive foreign proteins from their factor VIII therapy (Duesberg, 1995, see Chapter 11), and the T-cells of African HIV-positive tuberculosis patients increase after "standard anti-TB treatment" and improved nutrition (Martin et al., 1995).

In sum, the drug-AIDS hypothesis correctly predicts all aspects of American/European AIDS, while the HIV-hypothesis predicts none.

10. A possible solution at last

Testing the drug hypothesis should have a very high priority in AIDS research, because this hypothesis makes verifiable predictions (Cohen, 1994a; DeNoon, 1995). Drug toxicity could be tested experimentally in animals, and in human cells in tissue culture. In addition, drug toxicity could be tested epidemiologically in humans who are addicted to recreational drugs or are prescribed AZT. Such tests could be conducted at a fraction of the cost that is now invested in the HIV hypothesis.

If the drug hypothesis proved to be correct, AIDS would be an entirely preventable disease. Here is how:

(1) AZT use would be banned immediately.

(2) AIDS from illicit recreational drugs would be reduced or prevented by education against drug use. (Hemophilia AIDS would be prevented by the use of pure factor VIII (Chapter 10)).

(3) AIDS therapy would be achieved by termination of recreational drug use and treating AIDS diseases for their specific causes, e.g. tuberculosis with antibiotics, Kaposi's sarcoma with conventional cancer therapy, and weight loss with good nutrition-rather than treating each of these unrelated diseases with the same cell-killer AZT.

In addition to saving about 100,000 lives per year from AIDS, the drug hypothesis could save the American tax payer up to $20 billion annually. Currently the federal government spends annually $7.5 billion on AIDS treatment, research and education (AIDS Weekly, 1995; Gutknecht, 1995). And the Federal drug budget currently costs $13 billion, mainly for supply control, interdiction, methadone treatment and "education" (Drug Strategies, 1995).

But neither AIDS education nor drug education ever target the health effects of long-term drug use. They focus on the legal and social consequences of drug use and on the effects of drug use on transmission of HIV via unsafe sex and without "clean needles." Instead of studying the unknown, and warning against the known health hazards of recreational drugs, the medical establishment turns a blind eye to drug toxicity in its single-minded pursuit of HIV with safe sex and clean needles (Project Inform, 1992; Ascher et al., 1993; Cohen, 1994a). The clean-needle program of the AIDS-establishment would appear to encourage rather than discourage intravenous drug use. Reflecting this state of mind, Science recently rejected the drug-AIDS hypothesis, quoting a drug researcher that "Heroin is a blessedly untoxic drug" (Cohen, 1994a) and described nitrite inhalant-AIDS links as another "hatched" theory (Cohen, 1994b).

The failure to warn against the health risks of drug addiction is certainly one of the reasons that "drug use among young people has risen substantially for the first time in more than a decade" (Drug Strategies, 1995). Nitrite use continues to remain popular and has even increased recently, particulary among male homosexuals (Ascher et al., 1993; Duesberg, 1993d; Mansfield and Owen, 1993; Parke, 1993; Schechter et al., 1993b; Schechter et al., 1993c; Bethell, 1994; Gorman, 1994; Hodgkinson, 1994; Lauritsen, 1994; Sadownick, 1994; Vollbrechtshausen, 1994; Brandley, 1995; Haverkos and Drotman, 1995, Mirken, 1995). There is no report that nitrite bans are ever enforced or that nitrite warnings are taken seriously (Bethell, 1994, Mirken, 1995). And the number of intravenous drug-AIDS patients has increased steadily for years in America (Centers for Disease Control and Prevention, 1994b; Drug Strategies, 1995) - probably because drug control in America is "primarily focused on supply control efforts" (Drug Strategies, 1995).

However, if AIDS and drug education were based on the health consequences of long-term drug use, it would be as successful as the federal anti-smoking program. Based on education that smoking causes lung cancer, emphysema and heart disease, smoking has dropped in the US from 42% of the adult population in 1965 to 25% in 1995 (Associated Press, 1995b).

The solution of AIDS could be as close as a very testable, very affordable, and very practicable alternative hypothesis.*

Acknowledgments

I thank Ruhong Li for searching the AIDS literature and assistance with computer programs, Prof. Phil Johnson, School of Law UC Berkeley, for many references and critical commentary, Russell Schoch for critical review of the manuscript, and Siggi Sachs for preparation of, and review of the manuscript, and Claus Koehnlein (Kiel, Germany) and Colman Jones (Toronto, Canada) for critical information. This investigation was supported in part by the Council for Tobacco Research, USA, and private donations from Thomas Boulger (Redondo Beach, Calif., USA), Glenn Braswell (Los Angeles, Calif., USA), Dr. Richard Fischer (Annandale, Va., USA), Dr. Peter Paschen (Hamburg, Germany), Ruth Sackman, president of the Foundation for the Advancement in Cancer Therapy (New York, USA).

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