5. Drug-AIDS hypothesis

Since drugs are the only new health risk of Americans and Europeans since the 1970s, and AIDS is the only new epidemic, it is proposed here that the drug epidemic is the cause of the American and European AIDS epidemic. The hypothesis is:

The key to the drug hypothesis is that with drugs, the dose makes the poison (211). Only long-term consumption accumulates sufficient dosage to cause AIDS-defining diseases. Occasional or short-term recreational drug use causes first the desired euphoria which is followed either by reversible diseases or by no diseases at all. That is why it takes 20 years of smoking to acquire the tabacco dose for lung cancer or emphysema, 20 years of drinking to acquire the alcohol dose for liver cirrhosis, and 10 years of drug use to acquire the toxic dose leading to AIDS. In other words, drugs used at recreational doses are slow pathogens.

In contrast to drugs, infectious agents are self-replicating, and hence (if at all) fast pathogens. By multiplying exponentially in the body pathogenic infectious agents generate sufficient doses of toxic substances to cause diseases within days or weeks (50, 212). Thus, microbes are either fast pathogens or no pathogens at all.

Hardly anybody remembers that from 1981 to 1984, before the HIV hypothesis became national dogma, recreational drugs such as nitrite and ethylchloride inhalants, cocaine, heroin, amphetamines, phenylcyclidine, and LSD, were proposed by epidemiologists and toxicologists as the causes of AIDS. The reason for the early suspicion of drugs was simple. Nearly all AIDS patients were either male homosexuals who had used these drugs as aphrodisiacs and psychoactive agents, or were heterosexual intravenous drug users (111, 130, 132, 138, 144, 213-218). Before April 1984 many independent investigators and even scientists from the CDC in Atlanta considered AIDS a collection of drug diseases.

For example, between 1981 and 1982 the former CDC head James Curran stated, "At this point our best clue to the cause of the disease was ‘poppers’" (219). Curran’s clue was gleaned from anecdotal evidence including the first two Kaposi’s sarcoma patients seen by Dr. Alvin Friedman-Kien, professor of dermatology at New York University. Both of these patients were male homosexuals who "had a multiplicity of sexual partners over an extended period of time as well as using a variety of recreational drugs cocaine, marijuana, LSD, THC, MDA, and amyl nitrite." Friedman-Kien regularly called CDC officials to report his experience with AIDS: "…as patients started coming in, it turned out that all of them, 100 percent, had been using amyl nitrite" (219). The CDC’s AIDS researcher Harold Jaffe, now director of the HIV/AIDS division, also reported, through information gathered anecdotally, that over 90% of the surviving AIDS patients he talked to admitted regular nitrite use (111, 219).

Evidence continued to mount strongly supporting a correlation between nitrite use and AIDS. This included two Lancet articles, one by NIH researchers James Goedert, William Blattner et al. (132), another by an English team (108), the data collected by Harry Haverkos of the CDC’s Kaposi’s sarcoma opportunistic infection (KSOI) task force, and an abundance of prior studies on the immunotoxic effects of nitrates and nitrites (130).

Drugs seemed to be the most plausible explanation for the restriction of AIDS to risk groups, because drug consumption was the only dangerous common denominator of male and female intravenous drug users and male homosexuals. This original drug-AIDS hypothesis was euphemistically called the "lifestyle hypothesis" (220).

The drug-AIDS hypothesis was just as plausible then as it is now. Drug toxicity provides chemically plausible causes of disease. Based on their intrinsic chemical properties drugs used by AIDS patients are either indirectly toxic, cytotoxic, mutagenic (genotoxic), carcinogenic, or a combination of these. And, since its appearance in 1981 AIDS coincides exactly, both chronologically and epidemiologically, with the American and European drug use epidemics (see 3. and 4.).

However, since the enthusiastic acceptance of the HIV hypothesis by the Secretary of HHS and the press in April 1984, the drug hypothesis has been suppressed and discredited by the medical and scientific establishment, by the public press and by AIDS activists, and all federal funding for the drug hypothesis has been terminated (6, 11, 12, 96, 221) (see 7.). Asked in 1996 about the CDC’s negligence in considering the drug-AIDS connection, Curran, now dean of the School of public Health at Emory University in Atlanta, told the Wall Street Journal, "treating drug addiction wasn’t directly part of the CDC’s mandate, stopping the spread of AIDS among needle-sharing addicts ‘fell between the cracks’" (28). In the preceeding paragraph the article reports that, "the CDC’s biggest single prevention program, AIDS prevention ... accounted for $589 million." But that was all spent on HIV, not a nickel was left for drugs.

In view of the popularity of the national HIV-AIDS dogma, five of the six early American proponents of the drug hypothesis, Blattner, Curran, Friedman-Kien, Goedert and Jaffe converted to the HIV hypothesis, without even offering a scientific refutation of the drug hypothesis. Haverkos survived as a semi-proponent of the drug hypothesis by adopting HIV as a cofactor (78).

But despite its poor press the drug hypothesis stands scientifically unrefuted. Indeed, the efforts to refute the drug hypothesis have instead provided new data to support it (114, 115, 222, 223) (see 7.).