THE DRUG-AIDS HYPOTHESIS

Peter Duesberg and David Rasnick

6. Predictions are proving the drug-hypothesis

A good hypothesis must predict and explain the outcome of man’s or nature’s experiments. According to Feynman, "nature’s phenomena will agree or disagree with your theory". The following examples document that the drug hypothesis predicts and explains the American and European AIDS epidemic exactly.

6.1. American and European AIDS restricted to recreational drugs and AZT.
The drug hypothesis predicts that all AIDS-defining diseases that exceed their long-established normal background (i.e. >95%) are restricted to recreational and anti-HIV drug users. The rare AIDS cases from the general population, including hemophiliacs and transfusion recipients (224), represent the spontaneous and AZT-induced incidence of AIDS defining diseases in these groups under the new name AIDS (23, 24, 26) (see 5.).

Indeed, the following positive and negative evidence confirms this prediction. Even the CDC acknowledges that a third of the over 500,000 American AIDS patients are intravenous drug users (3). Prior to 1984 the CDC had also confirmed that the remaining two thirds of American AIDS patients were male homosexuals who had all used a multiplicity of recreational drugs, above all nitrite inhalants, amphetamines and cocaine (111) (Table 5). After 1984, by which time the CDC had adopted the HIV hypothesis, independent publications continued to document illicit recreational drug use by American and European homosexual AIDS patients (see 3. and Table 5). Since 1987 a large percentage of HIV-positive male homosexuals also took anti-HIV drugs, above all AZT, as AIDS prophylaxis or therapy (see 4. and 7. and Table 7).

Furthermore, negative evidence supports this assessment. Despite the over 100,000 papers published on HIV and AIDS, the AIDS establishment has never been able to demonstrate that even a small group of healthy HIV-positive Americans or Europeans, who had neither used recreational drugs nor antiviral drugs such as AZT ever developed AIDS (225). No controlled study in the medical literature has found any HIV-positives any sicker or dying sooner than matched HIV-negative controls (11, 26). Yet, such groups could be easily recruited from the US Army that annually rejects 1 out of 1000 healthy applicants just for having antibodies against HIV (225). All studies linking HIV to AIDS investigate people with life-threatening health risks such as drug addiction, hemophilia or exotic lifestyles.

Although the CDC offers rare, anecdotal AIDS cases outside the drug risk groups as examples for drug-free AIDS, that institution has never been able to provide the control statistics to prove that these cases exceed the normal low background in the drug-free population (3, 11). If matched groups that only differ in HIV are ever compared, the mortality of the HIV-positives is exactly the same as that of the HIV-negatives, as for example American transfusion recipients (226), sub-Saharan Africans (42), and intravenous drug users (39, 41, 86).

Thus drugs explain the restriction of AIDS to risk groups, precisely.

6.2. Nine out of ten American/European AIDS patients are males.
The drug hypothesis predicts that American and European AIDS is predominantly male, because males consume over 78% of the hard injected drugs (Table 4) (53, 61), over 98% of nitrite inhalants (79, 80) and most of the AZT (see 3., 4. and 7.).

Indeed, the CDC reports that 87% of all American AIDS patients are males (227). And the sex ratio of the European AIDS epidemic is a mirror image of the American drug epidemic (26). This sex distribution is the sum of the following constituents:

1) The CDC reports that a third of all American AIDS patients are intravenous drug users (3). According to the NIDA, the US Department of HHS and the Bureau of Justice Statistics, and the White House 75-78% of drug users are males (26, 52, 53, 61, 85) (see 3. and Table 4).

2) The CDC also reports that nearly two thirds, over 60%, of all American AIDS patients are male homosexuals (228). Based on self-answered questionnaires (229) (of the CDC and independent investigators) all of these were frequent users of nitrite inhalants, ethylchloride inhalants, amphetamines, cocaine, and other drugs that facilitate sexual contacts, particularly anal intercourse. Indeed, not a single drug-free homosexual AIDS case has ever been documented in the literature (see 3. and Table 5).

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. The same applies to the European AIDS epidemic.

6.3. AIDS and deaths from recreational drugs have the same age distribution.
The drug hypothesis predicts that the age distributions of deaths from AIDS and from recreational drugs coincide.

Indeed, this prediction is already proved. In 1994, 89% of all American AIDS cases (3), and 82% of all American drug deaths fell into the age group between 25 and 54 years (61). In 1990, 82% of the cocaine-related and 75% of the morphine-related hospital emergencies were 20-39 years old, again overlapping very closely with the age distribution of AIDS patients (230). Moreover, according to the same sources, 77% of the drug deaths and 82% of the AIDS cases in 1994 were males a remarkable coincidence (Table 4).

6.4. Pediatric AIDS caused by maternal drug addiction.
The drug hypothesis predicts AIDS in babies who shared intravenous drugs and AZT with their mothers regardless of HIV.

In fact, over 80% of pediatric AIDS cases in America and Europe are babies born to mothers who were intravenous drug users (26, 205, 231-233). Since 1989, many were also prescribed AZT and other anti-HIV drugs after birth (see 4. and 6.9.). The remainder reflects the normal low incidence of AIDS-defining diseases among newborns, particularly among newborns of poor and homeless mothers.

6.5. Why AIDS now?
The drug hypothesis predicts that American and European AIDS is new because it is a direct consequence of the drug use epidemics that spiraled after the Vietnam war, from negligible numbers in the 1970s to currently about 20 million illict drug users in America (see 3.). Allow a grace period of about 10 years for recreational drugs to achieve the dosage needed to cause irreversible disease (26) and you can date the origin of AIDS in 1981 (see 3. and 6.7.). In addition, the drug hypothesis predicts that additional AIDS cases were generated since 1987 by the epidemic of AZT prescriptions for 220,000 HIV-positives (26) (see 4.).

According to the CDC’s HIV/AIDS Surveillance Reports, AIDS in America increased from a few dozen cases annually in 1981 to about 50,000-75,000 since 1990 (224) (Fig. 1). The peak in 1992 and 1993 reflects in part yet another increase in the list of AIDS-defining diseases; this time to about 30 (17) (Fig. 1). After 1993 the annual incidence of AIDS cases has leveled off and even appears to decline (Fig 1). A comparison of Figures 1 and 2 graphically underscores the parallels between the AIDS and drug epidemics since 1981. Thus American and European AIDS is new because the drug epidemic is new. In fact, both the newness and the growth of the AIDS epidemic are predicted by the newness and the growth of the drug epidemic, as postulated by the drug-AIDS hypothesis.

6.6. Risk group-specific AIDS diseases.
The drug hypothesis predicts drug-specific AIDS diseases and explains the following risk-group-specific AIDS diseases as drug-specific AIDS diseases:

1) Kaposi’s sarcoma specific for male homosexual nitrite users. 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 (36, 130).

According to the drug hypothesis Kaposi’s sarcoma is a nitrite-specific AIDS disease. Indeed, male homosexuals are 58-times more likely to use nirite inhalants as sexual and mental stimulants than heterosexuals (79) (see 3.). Due to their carcinogenic potential, nitrites were originally proposed as causes of Kaposi's sarcoma (215, 217). The fact that up to 32% of Kaposi's sarcomas of homosexual men can be diagnosed as pulmonary Kaposi's sarcoma (234, 235), lends additional support to the nitrite-Kaposi's sarcoma hypothesis, because the lungs are the primary site of exposure to nitrite inhalants. 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 (236). This agrees with the fact that "aggressive and life-threatening" Kaposi's sarcoma, particularly pulmonary Kaposi’s sarcoma, is exclusively observed in male homosexuals (235-238). Pulmonary Kaposi’s sarcoma had never been observed by Moritz Kaposi, nor by anyone else prior to the AIDS epidemic (239).

Moreover, it appears that the nitrite-induced AIDS-Kaposi's sarcoma and the classic, spontaneous 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" (237), often located in the lung and fatal within 8-10 months after diagnosis (234-236, 238). The classic "indolent and chronic" Kaposi's sarcomas are only diagnosed on the skin of the lower extremities and hardly progress over many years (16, 236, 240). Nevertheless, the distinction between classic and AIDS-Kaposi's sarcoma is rarely ever emphasized and may have escaped many observers due to the "difficulty in pre-mortem diagnosis", and because "pulmonary Kaposi's sarcoma was indistinguishable from opportunistic pneumonia..." (238).

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 US and Europe (26, 130) (Table 1). The cytotoxic effects of nitrites are compounded by the immunotoxins and cytotoxins of cigarette smoke. For example, 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 (133).

2) High mortality and specific diseases of intravenous drug users. High mortality and tuberculosis, pneumonia, mouth infections, immunodeficiency, lymphadenopathy, candidiasis, fever, weight loss and dementia are each characteristic of intravenous drug users (26, 86, 120, 122, 124, 125) (see 3.) and AIDS patients.

A recent review article has tried to resolve the "confusion [that] may arise as to the aetiology of specific symptoms" from intravenous drug use and from HIV, "since they may mimic each other" (40). But, after confirming that drug use causes lymphadenopathy, diarrhea, dementia, epileptic seizures, impotence, tuberculosis and other clinical features by itself, the article fails to resolve the confusion (see 3.). Since it lacks drug-free HIV-infected patients with the specific diseases of intravenous drug users, the confusion remained. In other words, the article confirmed, despite its intent, once more that AIDS diseases of intravenous drug users are drug diseases.

Because of drug-induced diseases intravenous drug users only reach a very low average age. A German study found the average age at death of intravenous drug users was 29.6 years for HIV-free and 31.5 years for HIV-positive addicts in 1995 (39). American studies show that both HIV-positive and negative intravenous drug users die between the ages of 25 and 48 years (41), and from the same AIDS-defining and other diseases in 1988 (86). The average age at death of amphetamine addicts was also determined to be about 30 years (118). Thus drugs, not HIV, determine the specific diseases and high mortality of intravenous drug users.

3) Low birth weight and mental retardation of AIDS babies. Low birth weight, mental retardation and immunodeficiency for lack of B-cells are specific AIDS diseases of AIDS babies (224).

According to the drug hypothesis these are drug diseases because 80% of American/European babies with AIDS are born to mothers who were intravenous drug users during pregnancy (26, 51, 205, 233). Moreover, HIV-free "crack babies" of drug-addicted mothers have exactly the same diseases as HIV-positive infants (241) (see 6.8.). The remaining 20% are due to congenital diseases such as hemophilia, and infant morbidity and mortality due to poverty (26).

4) Anemia, wasting, lymphoma and high mortality of AZT recipients. Anemia, leukopenia, lymphoma, pancytopenia, diarrhea, weight loss, hair loss, impotence (26), muscle atrophy, dementia, hepatitis (195), and pneumocystis pneumonia (201) are specific AIDS diseases typical of those prescribed AZT and other DNA chain terminators. They are all predictable consequences of the termination of DNA synthesis (see 4.).

Indeed, compared to untreated controls AZT recipients have 50-times more often lymphoma (198), die either 2.4-times more often (204) or 25% more often (160), or live only 2 years instead of 3 with AIDS with the above diseases (203) (see 4.1., 7.8.). And babies treated with AZT before birth develop birth defects or are aborted, and those treated after birth experience "a negative effect on growth" (205) (see 4., 7.8.).

6.7. Not all drug users develop AIDS.
The drug hypothesis predicts that drug diseases only occur after a pathogenic threshold of drug toxicity has been accumulated over a lifetime. Short term users of drugs at recreational doses will experience either no diseases or reversible diseases.

In adults it takes about 10 years of injecting or oral use of heroin, cocaine and amphetamines to develop tuberculosis, bronchitis, pneumonia, irreversible or hardly reversible weight loss, and other drug-induced diseases (118, 120, 122, 242-246). The time lag from initiating a habit of inhaling nitrites to acquire Kaposi's sarcoma has also been determined to be 7 to 10 years (26, 36, 113, 138). Clearly, irreversible damage is achieved much faster in a developing fetus than in a fully developed adult.

Since most recreational drug users give up drugs for personal, economic, and health reasons before they experience serious medical consequences, only a fraction will develop drug diseases (126). Thus the 500,000 individuals annually delivered to hospitals for reversible drug diseases, and the 50,000 to 75,000 for irreversible AIDS diseases (51) are only a small fraction of the over 20 million American illict drug users. Likewise, the 600-800 annual American AIDS babies (3) are only a small fraction of the 221,000 that are born to American mothers who use drugs during pregnancy (51) (see 3.).

In addition, only a fraction of the 220,000 HIV-positive persons on daily prescriptions of AZT and other anti-HIV drugs, that, like AZT, are designed to kill human cells, are annually converted to AIDS patients (160). The annual percentage of healthy AZT-recipients developing AIDS is not published, but can be estimated at 25 to 35% considering that out of 220,000 on AZT between 50,000 and 75,000 Americans each year develop AIDS (Fig. 1).

Thus the American AIDS patients are those 50,000 to 75,000 of the 20 million recreational drug users and the 220,000 AZT recipients who have achieved the highest lifetime doses of toxicity just like the lung cancer and emphysema patients reflect the highest lifetime tobacco dose among the 50 million smokers in the US (247).

6.8. Non-correlations between HIV and AIDS.
The drug hypothesis predicts (a) HIV without AIDS, (b) AIDS before HIV, and (c) AIDS without HIV. Each of these predictions is confirmed.

1) Long-term survivors or "non-progressors". In view of the appearance of growing numbers of HIV carriers who are healthy even 15 years after infection, the HIV orthodoxy has created a new category of HIV carriers, termed long-term survivors or "long-term non-progressors" (248). The first mainstream paper on long-term survivors described a healthy male homosexual blood donor and five blood recipients who by 1992 had survived HIV for 10 to 12 years (249). The HIV orthodoxy has therefore proposed that the existence of the non-progressors is due to non-virulent, mutant strains of HIV and that such viruses would be ideal vaccine strains. However, these optimistic proposals were not backed up by functional evidence for non-virulent HIV (248, 250).

According to the drug hypothesis the non-progressors should be HIV-positive people who have stopped using or never used recreational drugs or AZT. Indeed, the HIV-researchers David Ho et al. inadvertantly provided the key to long-term survival: "none had received antiretroviral therapy" (251). 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 MAC study, had used AZT (252). Another orthodox HIV study acknowledged "only 38% of the HLP [healthy long-term HIV-positives] had ever used zidovudine or other nucleoside analogues compared with 94% progressors". Clearly the wording "had ever used" implies that AZT had been discontinued after a short traumatic, but reversible experience.

Independent scientists document that in addition to abstaining from antiviral drugs long-term survivors are those who have given up or never taken recreational drugs (253-255). Timothy Hand, from the Ogelthorpe University in Atlanta GA, adds much weight to this view:

While healthy, ‘non-progressing’ HIV carriers are considered rare (and doomed), they may in fact vastly outnumber the sick and dying. This is certainly implied by the ubiquitous estimate of HIV prevalence in America of one million. Long-term AIDS survival is now a hot topic in the literature, and anecdotal reports (256, 257) as well as numerous scientific studies (101, 251, 258-264) suggest that most long-term survivors have shunned antiviral drugs. This point is often understated in these studies, and is not made in the titles or abstracts. In David Baltimore’s editorial on 2 of these studies, avoidance of antivirals was not mentioned at all (265). Needless to say, none of these studies was funded by a pharmaceutical firm.

Interestingly, nearly all of these studies suggest a protective role of cytotoxic CD8+ T-cells and/or natural killer cells in healthy survivors. Many focus on the importance of maintaining cell-mediated immunity, rather than on "killing HIV". Thus HIV infection per se seems to entail little danger, unless it is followed by antiviral therapy (266).

Similar observations have been made by the late homosexual AIDS activist Michael Callen:

In researching his 1990 book Surviving AIDS, Callen interviewed nearly fifty people who had lived for many years not just after being pronounced HIV-positive, but after an AIDS diagnosis. He found that only four had ever used AZT; three of those had since died, and one was dying of AZT-induced lymphoma. But the overwhelming majority of long-term survivors had somehow managed to resist the enormous pressure to take AZT.

The pressure did not just come from doctors, Callen told the Amsterdam meeting (7, 267), but from a certain segment of AIDS activism that seemed driven by a ‘drugs-into-bodies’ mentality. ‘I feel many AIDS activist friends who are in the forefront of this frenzy are very misleading to people with AIDS, who are frightened and desperate. They only seem to talk about two possible outcomes of taking experimental drugs: one is that it works and one that it does not work. There is a third, apparently much more common possibility, which is that you will be worse off than if you did nothing at all. And nobody likes to talk about that because it is so unpleasant’. He had seen the devastation wreaked by AZT, watching with horror as friends with AIDS ‘turn the colour of boiled ham from AZT poisoning, endure the melting away of their muscles, become transfusion dependent, and experience drug-induced psychosis’. Yet his perception of a person diagnosed with AIDS in 1992 was that ‘they would sell their grandmother into slavery to get a slot in the latest drug-of-the-month clinical trial’.

Another feature of the long-term survivors was that they rejected the predominant scientific view that HIV-positivity meant inevitable decline of the immune system towards an early death (7).

In December 1995 The Advocate, the largest national gay magazine, published the story of Dennis Leoutsakas, a man who is HIV-positive "for at least 17 years [but] doesn’t have AIDS and no one knows why" (268). According to the article, "most HIV researchers have insisted that HIV infection will, in almost every case, eventually lead to AIDS" a belief underscored by their preferred term for nonprogressors: slow progressors.

Wearing his HIV blinkers the author of the article fails to see the formula for Leoutsakas’ "slow progression": "Leoutsakas, 47: A former IV-drug user who last shared a needle in 1978 ... first tested positive in 1987. He has a T-cell count ... between 650 and 950. In addition, Leoutsakas has had none of the opportunistic infections that define AIDS no pneumonia, no Kaposi’s sarcoma, no fungal infections, nada. Leoutsakas says doctors have attempted to explain his case by theorizing that, like the Australians (249), he is infected with a weakened form of HIV but it’s really just speculation." ... "Leoutsakas has no theory of his own and no special formula for his well-being. He’s never taken AZT or any other antiretroviral drugs." No more IV-drugs, no antiretroviral drugs but "no formula for his well-being"!

And in October 1996 even an orthodox professor of medicine at the University of California at San Francisco taught his medical students the secret of long-term survival with HIV (see 4.): "I have a large population of people who have chosen not to take any antivirals since I’ve been following them since the very beginning... They’ve watched all of their friends go on the antiretroviral bandwagon and die, so they’ve chose to remain naive to therapy. More and more, however, are now succumbing to pressure that protease inhibitors are it ... We are in the middle of the honeymoon period, and whether or not this is going to be an enduring marriage is unclear to me at this time, so I’m advising my patients if they still have time, to wait."(180)

Unknowingly the vast majority of HIV-positives are long-term survivors! Worldwide, they number 17 million, including 1 million HIV-positive, healthy Americans and 0.5 million HIV-positive, healthy Europeans (269, 270). Most of these must have been HIV-positive for at least 10 years now because the numbers of the HIV-positive Americans and Europeans have not changed during the period 1984 to 1988 when the epidemic of HIV-testing began in the respective countries (26, 29) (Fig.1).

Since no more than 6% of the 17 million people worldwide with antibodies to HIV have developed AIDS over the last 7 to 10 years, the risk of AIDS to an HIV-carrier is less than 1% per year (270). However, even this low figure is not corrected for the normal occurence of the 30 AIDS-defining diseases in HIV-free controls. There is not a single controlled study in the vast AIDS literature proving that HIV-positive people who are not drug users have a higher morbidity or mortality than HIV-free controls (11, 225). (See 7., Table 4 and 5)

To save the reputation of the "deadly virus" in the face of long-term survivors, orthodox HIV researchers have already posted warnings that "regrettably ... the proportion of individuals who might demonstrate such a benign course is very small" (271). Others have postulated rare HIV attenuating mutations without providing functional evidence (248, 250). Gallo et al. went even further by postulating human mutants, who fall victim of HIV because they lack "major HIV-suppressive factors" (272). According to Gallo’s hypothesis most American homosexuals, hemophiliacs and intravenous drug users are mutants!

2) Drug users developing AIDS prior to HIV infection. Prospective studies have demonstrated that the T-cells of male homosexuals using psychoactive drugs and sexual stimulants 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 (273). Some even had fewer than 500 T-cells 1.5 years before seroconversion (274). 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 (80, 112, 114, 145, 275). Likewise, 33 HIV-free male homosexuals from Vancouver, Canada, had "acquired" immunodeficiency prior to HIV infection (276). 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 (48, 105, 277).

The MAC study reported that about 450 (16% of 2795) HIV-free, homosexual American men from Chicago, Baltimore, Pittsburgh and Los Angeles had acquired immunodeficiency, having less than 600 T-cells per µl, prior to HIV infection (103). 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 lymphnode groups than seronegative men (5.7 compared to 4.5 nodes, p<0.005), the numerical difference in the means is not striking" (278). According to previous studies on this cohort, 71% of these men had used - based on self reporting - nitrite inhalants, in addition to other drugs (278); 83% had used one drug, and 60% had used two or more drugs during sex in the previous six months (279).

Indeed, not a single prospective study of male homosexual cohorts at risk for AIDS ever measured drug use directly. Instead, each relied only on self reporting, using questionnaires that focused on recent use of a few selective drugs (32, 48, 229, 275) (see 7.). By contrast, all HIV tests were based on experimental methods that maximize positivity such as antibodies against the virus instead of the virus itself, or amplification of fragments of viral nucleic acid instead of standard infectivity tests (see 7.).

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 (280), which correlates directly with the use of nitrite vasodilaters (26, 100, 104, 130, 281) (see 3.).

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 plausible, 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 (26, 282), and the disease should have been well established long before 1981.

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" (283). A similar study from Italy showed that a low number of T-cells was the highest risk factor for HIV infection (284). 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: the more drugs are consumed intravenously or as an aid to sex, the higher is the risk of HIV infection (26).

3) HIV-free AIDS. Intravenous drug users, their babies, male homosexuals consuming aphrodisiac and psychoactive drugs, hemophiliacs, and poor Africans develop the same AIDS-defining diseases with or without HIV. One summary of the AIDS literature describes over 4,621 clinically diagnosed AIDS cases who were not infected by HIV (48). Additional cases are described that are not in this summary (232, 274, 275, 278, 285, 286). They include intravenous drug users, male homosexuals using aphrodisiac drugs like nitrite inhalants, hemophiliacs developing immune suppression from long-term transfusion of foreign proteins contaminating factor VIII, and Africans subject to malnutrition, parasitic infection and poor sanitation (24, 48).

The following examples of clinical AIDS in HIV-free male homosexuals (1-9), and in intravenous drug users and their babies (10-26) illustrate this point:

1) The first five AIDS cases, diagnosed in 1981 before HIV was known (i.e. presence of HIV is speculative), were male homosexuals who had all consumed nitrite inhalants and presented with Pneumocystis pneumonia and cytomegalovirus infection (287).

2) In 1985, and again in 1988, Haverkos analyzed the AIDS risks of 87 male homosexual AIDS patients with Kaposi’s sarcoma [47], Kaposi’s sarcoma plus pneumonia [20] and pneumonia only [20] (217, 288). All men had used several sexual stimulants, 98% had used nitrites. Those with Kaposi’s sarcomas reported 2 times more sexual partners and 4.4 times more receptive anal intercourse than those with only pneumonia. The median number of sexual partners in the year prior to the illness was 120 for those with Kaposi’s and 22 for those with pneumonia only. The Kaposi’s cases reported 6-times more amylnitrite and ethylchloride use, 4-times more barbiturate use, and 2-times more methaqualone, lysergic acid and cocaine use than those with pneumonia only. Since no statistically significant differences were found for sexually transmitted diseases among the patients, the authors concluded that the drugs had caused Kaposi’s sarcoma.

Although the data for Haverkos’ analysis had been collected before HIV was known, Haverkos’ conclusion is valid. This is because the development of AIDS was drug dose dependent, and thus was either sufficient or at least necessary for AIDS. Indeed, HIV was found in only 31% (289), 43% (290, 291), 48% (292), 49% (293), 56% (276), and 67% (112) of cohorts of homosexuals at risk for AIDS in Amsterdam, Chicago-Washington DC-Los Angeles-Pittsburgh, Boston, San Francisco and Canada respectively, that developed the same AIDS diseases as described by Haverkos.

3) A 4.5 year tracking study of 42 homosexual men with lymphadenopathy but not AIDS reported that 8 had developed AIDS within 2.5 years (214) and 12 within 4.5 years of observation (294). All of these men had used nitrite inhalants and other recreational drugs including amphetamines and cocaine, but they were not tested for HIV. The authors concluded that "a history of heavy or moderate use of nitrite inhalant before study entry was predictive of ultimate progression to AIDS" (214). Thus drug doses of 2.5 to 4.5 years were necessary for AIDS.

4) Before HIV was known, three controlled studies compared 20 homosexual AIDS patients to 40 AIDS-free controls (215), 50 patients to 120 controls (111) and 31 patients to 29 controls (216) to determine AIDS risk factors. Each study reported that multiple "street drugs" were used as sexual stimulants. And each study concluded that the "lifetime use of nitrites" (111) were 94% to 100% (!) consistent risk factors for AIDS (216).

5) A 27-58-fold higher consumption of nitrites by male homosexuals compared to heterosexuals and lesbians (79, 295) correlates with a 20-fold higher incidence of Kaposi’s sarcoma (36, 296) and a higher incidence of all other AIDS diseases in male homosexuals compared to most other risk groups (Tables 3 and 4). Again, drug use proved to be necessary for AIDS.

6) After the discovery of HIV, 5 out of 6 HIV-free male homosexuals from New York with Kaposi’s sarcoma reported the use of nitrite inhalants (297). Soon after, another 6 cases of HIV-free Kaposi’s sarcoma were reported in an HIV-free "high risk population" from New York (298). This indicates directly that HIV is not necessary and suggests that drugs are sufficient for AIDS.

7) In 1992, two HIV-free, male homosexuals, erroneously treated with AZT because of a false positive HIV-antibody test, developed fatal AIDS including pneumonia and muscle atrophy. Their case was described in the Oakland Tribune and in the New York Native because of a malpractice suit against Kaiser Hospital and the manufacturer of AZT, but was not followed up by the media, suggestive of a settlement (299). One of us has testified in three legal cases against AZT therapy, and in each case settlements were reached that barred further publicity. In view of the inherent false-positive rate of HIV-antibody tests (48, 300, 301), many more such cases are likely to exist that have never been identified (see 7.4.)

8) A rare, recent publication describes 4 HIV-free, male homosexual AIDS patients with Kaposi’s sarcoma in the New England Journal of Medicine (285). This publication was published in the orthodox literature at the same time as a "new Kaposi’s sarcoma virus" was considered by the AIDS establishment. This shows that the HIV orthodoxy can accept HIV-free AIDS cases, but only at the expense of substituting another AIDS virus in the place of HIV (302).

9) An independent re-analysis of the database of male homosexual AIDS patients from San Francisco who had used nirtrite inhalants, amphetamines, cocaine, and other recreational drugs in addition to AZT originally described in 1993 (80, 303), identified 45 HIV-free patients with AIDS defining diseases that had been omitted from the original study (115).

10) Among intravenous drug users in New York representing a "spectrum of HIV-related diseases," HIV was only observed in 22 out of 50 pneumonia deaths, 7 out of 22 endocarditis deaths, and 11 out of 16 tuberculosis deaths (86).

11) Pneumonia was diagnosed in 6 out of 289 HIV-free and in 14 out of 144 HIV-positive intravenous drug users in New York (304).

12) Among 54 prisoners with tuberculosis in New York state, 47 were street-drug users, but only 24 were infected with HIV (305).

13) In a group of 21 long-term heroin addicts, the ratio of helper to suppresser T-cells declined during 13 years from a normal of 2 to less than 1, which is typical of AIDS (5, 306), but only 2 of the 21 were infected by HIV (244).

14) Thrombocytopenia and immunodeficiency were diagnosed in 15 intravenous drug users on average 10 years after they became addicted, but 2 were not infected with HIV (243).

15) The annual mortality of 108 HIV-free Swedish heroin addicts was similar to that of 39 HIV-positive addicts, i.e. 3–5%, over several years (307).

16) A survey of over a thousand intravenous drug addicts from Germany reported that the percentage of HIV-positives among drug deaths (10%) was exactly the same as that of HIV-positives among living intravenous drug users (308). Another study from Berlin also reported that the percentage of HIV-positives among intravenous drug deaths was essentially the same as that among living intravenous drug users, i.e. 20–30% (309). This indicates that drugs are sufficient for and that HIV does not contribute to AIDS-defining diseases and deaths of drug addicts.

17) Lymphocyte reactivity and abundance was depressed by the absolute number of injections of drugs not only in 111 HIV-positive, but also in 210 HIV-free drug users from Holland (310).

18) The same lymphadenopathy, weight loss, fever, night sweats, diarrhea and mouth infections were observed in 49 out of 82 HIV-free, and in 89 out of 136 HIV-positive, long-term intravenous drug users in New York (311).

19) Among intravenous drug users in France, lymphadenopathy was observed in 41 and an over 10% weight loss in 15 out of 69 HIV-positives. The numbers were 12 and 8, respectively, out of 44 HIV-negatives (245). The French group had used drugs for an average of 5 years, but the HIV-positives had injected drugs about 50% longer than the negatives.

20) Among 97 intravenous drug users in New York with active tuberculosis, 88 were HIV-positive and 9 were HIV-negative; and among 6 "crack" (cocaine) smokers with tuberculosis, 3 were HIV-negative (312).

21) Among heroin addicts from New York, having injected an average of 5.7 years, natural killer cell activity was reduced 2-fold and T4/T8-cell ratios from 2 to 1.5 (90).

22) A survey of the causes of death of 412 intravenous drug users from New Jersey, revealed many HIV-free cases, including at least 48 pneumonias, 35 tuberculoses, and 6 encephalopathies (41).

23) Similar neurological deficiencies were observed among 12 HIV-infected and 16 uninfected infants of drug-addicted mothers (Thomas Koch, UC San Francisco, personal communication) (313). However, babies with and without HIV, but from HIV-positive mothers, had lower psychomotor indices than babies from HIV-free mothers. The probable reason is that HIV is again a marker for the cumulative dose of intravenous drugs consumed by the mother (26).

24) The psychomotor indices of infants "exposed to substance abuse in utero" were "significantly" lower than those of controls, "independent of HIV status." Their mothers were all drug users but differed with regard to drug use during pregnancy. The mean indices of 70 children exposed to drugs during pregnancy were 99 and those of 25 controls were 109. Thus maternal drug use during pregnancy impairs children independent of HIV (314).

The same study also reports a "significant difference" based on the HIV status of these children. The mean score of 12 HIV-positives was 88 and that of 75 negatives was 102. As is typical for the AIDS establishment, HIV-positive babies of non-drug using mothers were grouped with those from drug-using mothers (see 7.). But although the study did not break down the scores of the HIV-positive infants based on "exposure to substance abuse in utero", it documented that 4 of the 12 HIV-infected infants were "above average," i.e. 100-114 and that 4 of the 12 mothers did not inject drugs during pregnancy!

25) Ten HIV-free infants born to intravenous drug-addicted mothers had the following AIDS-defining diseases "failure to thrive, persistent generalized lymphadenopathy, persistent oral candidiasis, and developmental delay..." (315).

26) One HIV-positive and 18 HIV-free infants born to intravenous drug-addicted mothers had only half as many leukocytes at birth than normal controls. At 12 months after birth, the capacity of their lymphocytes to proliferate was 50- 70% lower than that of lymphocytes from normal controls (316).

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

6.9. Discontinuation of drug use either stabilizes or cures AIDS.
The drug hypothesis predicts that termination of drug use stabilizes or cures AIDS diseases, except for those that have reached a critical threshold of no return. Indeed, this has been documented in several examples:

1) AZT-recipients. Ten out of 11 HIV-positive, AZT-treated AIDS patients recovered cellular immunity after discontinuing AZT in favour of an experimental vaccine (317). Two weeks after discontinuing AZT, 4 out of 5 AIDS patients recovered from myopathy (318). Three of four AIDS patients recovered from severe pancytopenia and bone marrow aplasia 4-5 weeks after AZT was discontinued (319).

2) Heroin/cocaine-addicts. 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 (246). 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 (89).

3) Recreational and anti-HIV/AIDS drugs. 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" (254). Assuming an average 10-year latent period from HIV to AIDS, and a random distribution of infection times prior to AIDS, the virus-AIDS hypothesis would have predicted about 116 (918/10 x 1.25) 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).

Another "good example that medicines hurt more than they help is the story of Roger Cobb, co-chairman of the consumer caucus for the Commission on AIDS Care, Service and Treatment for Philadelphia and nine surrounding counties. ‘Sixty days after I started substance abuse treatment, I learned that I was HIV-positive,’ recalls Cobb, who had used crack and cocaine, among a smorgasbord of other drugs, for more than 21 years. ‘A little while later I started treatment with AZT for about 14 months.’ It was during this time that he developed what he calls ‘the look.’ ‘I had the sunken face, the ashy skin; I lost weight everything. Against my doctor’s advice, I decided AZT was not for me, so I decided to try something else.’ And ‘the look’? ‘The look is fabulous now,’ says the 40-year-old, who is working on his master’s degree in social work. ‘I’m back to me’" (320).

4) Recreational drug users.  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 (321). 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 (see 4.2).

5) AIDS babies, born to drug-addicted mothers, recover. HIV-positive babies, born to mothers who were intravenous drug users during pregnancy, provide the best controlled examples for the prediction that termination of recreational 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. After three years, 61 of these HIV-positive children were healthy, although some had developed "intermittent" diseases from which they had recovered during their first 18 months. Contrary to the HIV hypothesis, the T-cells of these children increased after birth from low to normal levels despite the presence of HIV.

Only 10 of these children developed encephalopathy and other AIDS-defining diseases of which 9 died during their first 18 months of life. The study points out that the baby’s risk of developing AIDS was related "directly with the severity of the disease in the mother at the time of delivery".

The potential recovery of babies from congenital AIDS diseases acquired as a result of maternal drug use was apparently impaired by iatrogenic intoxication with AZT and other anti-AIDS drugs, "prophylactic treatment [with] ... sulfamethoxazale and zidovudine [AZT] was started earlier and was more frequent among the children born to mothers with class IV disease (AIDS)" (322). Based on the severity of their symptoms about 60% of the children were treated prophylactically with AZT for at least one month, and 50% were treated with sulfa-drugs (322).

A very similar picture emerges from a collaborative European study of HIV-positive newborns (323). The study reports that over 60% of congenitally-infected children were healthy at 6 years after birth although many had experienced transient AIDS diseases, such as pneumonia, bacterial infections, candidiasis and cryptosporidial infection during the first year after birth. 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 years and that is exactly the percentage that was "treated with zidovudine [AZT]", 10% before 6 months of age and 40% by 4 years (323).

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" (26, 231). 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 (232). 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 (232).

An American study reports that during the first 18 months after birth a group of HIV-positive babies lagged on average behind a control group of HIV-free infants in all developmental parameters (205). But the study also reports intravenous and other drug use by the mothers, and that "up to 60% at 18 months" of HIV-posities were on AZT. By 18 months 40% of the HIV-positive babies had apparently completely recovered from maternal drugs, despite HIV, because they were nor treated with AZT nor were any deaths reported. However, up to 60% apparently had suffered intermittent diseases from AZT and residual damage of maternal drug use. Thus the normal performance of 40% of the HIV-positive group, 18 months after withdrawl from maternal drugs, was hidden by the subnormal performance of the HIV-group that was an average of AZT recipients and untreated babies (see 7.7.).

It follows that discontinuation of recreational and antiretroviral drugs before a critical threshold is reached prevents or even cures AIDS in HIV-positives.

In sum, this chapter documents that the drug-AIDS hypothesis correctly predicts all facts of American/European AIDS, while the HIV-hypothesis predicts none.

CONTINUE