THE DRUG-AIDS HYPOTHESIS

Peter Duesberg and David Rasnick

7. How the HIV/AIDS orthodoxy divorces drugs from AIDS

Despite abundant evidence for drug pathogenicity, the orthodox medical literature almost unanimously disregards diseases from recreational drugs. Wearing their HIV/AIDS blinkers, AIDS researchers even fail to make the drug connection when matched groups of drug users, differing only in HIV, have the same diseases and high motrtality. Whereas, the diseases and high mortality of HIV-positive drug users are credited to HIV, those of HIV-negatives are credited to other microbes and even to contaminants of street drugs rather than to the psychoactive drugs themselves (39, 40, 86, 302, 324) (see 3. and below).

But even when drug use is recognized as a direct AIDS risk, the role of drugs is divorced from AIDS by unscientific manipulations including misrepresentations, double-standards, omissions of facts and controls and outright censorship. The following examples substantiate these assertions:

7.1. Disregarding drugs.
Although 3.6 million Americans are regular users of cocaine and at least 0.6 million are addicted to heroin (see 3.) and a third of the 500,000 American AIDS patients are confirmed long-term intravenous drug users (3, 11, 26), the pathogenic effects of long-term cocaine and heroin use are not studied anywhere in the US and Europe (11, 16, 26, 121). But at least 100,000 American PhDs and MDs are studying the hypothetical pathogen HIV (11, 121).

A tendentious article in Science described the mood perfectly in 1994 with the quote from a distinguished HIV/AIDS toxicologist, heroin is a "blessedly untoxic drug" (16). But unbeknown to Science and its readers, growing numbers of American entertainment stars and junkies are dying from heroin. In the same year in which Science described the "blessedly untoxic" heroin, the US Dept. of HHS recorded 2910 male and 601 female heroin "decedents" (see 3.1 and Table 4) (61). The stories of some were just described in the San Francisco Chronicle under the title "Heroin is in fashion and death statistics prove it" (325).

Uninformed or even misinformed (see below) by the trusted medical orthodoxy, the general public and even those who have a direct interest or mandate to warn against drug use are unaware of drug diseases. For example, the Bureau of Justice Stastistics, the Drug Strategies foundation and drug control officials from the White House who publish The National Drug Control Strategy: 1996 never warn about the medical consequences of drug use, except that they might lower vigilance against infection by HIV and other microbes (28, 52, 53, 55, 74) (see 3.3).

Although the National Drug Control Study: 1996 is concerned about the safety of "America’s [non-drug using] citizens" because "Hardcore drug users frequently are ‘vectors’ for the spread of infectious diseases such as hepatitis, tuberculosis, and HIV." (53), the Study misses the point that drugs cause the immunodeficiency necessary for these microbes to be pathogenic. It is for this reason that hardcore drug users are virtually the only "American citizens" who are victims of these microbes.

Although inhaling nitrites has been illegal in the US since 1988, because of an "AIDS link" (see 3.), inhaling has been practised by at least 4.2 million Americans in 1992, according to a survey of the National Institute of Drug Abuse (81). In spite of this, nitrites are not listed as an illegal drug category of their own by the Bureau of Justice Statistics (52), Drug Strategies (51), the Drug Abuse Warning Network (DAWN) of the US Department of HHS (61, 85), or the President’s National Drug Control Study: 1996 (53).

Although the majority of American AIDS patients male homosexuals, and probably all Kaposi's sarcoma patients have been using cytotoxic and carcinogenic nitrite inhalants and many other toxic recreational drugs, non-injected drugs are not reported as an AIDS risk category by the CDC’s HIV/AIDS Surveillance Reports. But no HIV infection "category" is too small to be left out of the Surveillance Reports, as for example the less than 10 annual male AIDS cases that reportedly result from "sex with a person with hemophilia" (326).

The San Francisco Chronicle just demonstrated the consequences of the orthodox blindness to the drug-AIDS connection Under the title "HIV hits former USSR a small city’s story," (327). The journal is shocked that "half of the town’s drug-injecting subculture is believed to be infected [by HIV]" and that "AIDS will be more common here than America". But neither the journal nor the journalist even gave a thought to the possibility that "to shoot raw opium" may be the cause of the predicted AIDS epidemic.

7.2. Misrepresentation of facts, example 1.
The CDC provides the first example of misrepresenting facts to dissociate drugs from AIDS. After the publication in April 1983 of two different AIDS viruses in Science, one by Gallo (HTLV-I) (328) the other by Montagnier (329) (now termed HIV), the CDC was ready to abandon the drug hypothesis. But in view of the overwhelming correlations between drugs (particularly nitrites) and AIDS, functional evidence was necessary to discard the drug hypothesis in favor of viral AIDS.

To accomplish this transition the CDC commissioned a study of the immune effects of nitrite inhalants on mice and published the results in an anonymous one-page-paper in the CDC’s house journal, the Morbidity Mortality Weekly Reports (330). The study concluded that, "None of the animals exposed to IBN (isobutyl nitrite) showed any evidence of immunotoxic reactions. Methemaglobinemia [oxidation of hemoglobin] was noted in animals exposed to 300 ppm (parts per million) of IBN, and some evidence of thymic atrophy, possibly stress-related..." The study was apparently published in a hurry because "...detailed histologic examinations have not been completed." Yet the CDC concluded with the authority of its office that, "…these drugs are not responsible for the basic immune defects characteristic of AIDS."

The CDC’s action was exceptional on several grounds:

1) Rather than following its usual practice of reporting AIDS information supplied by other researchers and institutes this time the CDC conducted its own experimental study on AIDS.

2) The CDC study referenced two Lancet papers as the initial evidence of a correlation between nitrites and AIDS. But until then the CDC had not refuted or attempted to refute publications from others.

3) The CDC’s anonymous investigators exposed mice to a concentration of nitrites that is orders of magnitude below that inhaled recreationally (131). According to a reporter who interviewd one of the investigators of the CDC study in 1994, "Lewis explained that, in determining the dose, they had to adjust it below the level where they were ‘losing’ the mice... (96) a fact that might have been useful to include in the text of a paper that concluded that, drugs are not responsible for ... AIDS" (330).

4) Considering that T-cell deficiency is the hallmark of AIDS, it is hard to understand how the CDC could dismiss "thymic atrophy" in nitrite exposed mice as "stress related".

7.3. Misrepresentation of facts, example 2.
In an effort to dissociate the new American drug epidemic from the new AIDS epidemic the office of the director of AIDS research of the NIAID, Anthony Fauci, also published an anonymous paper, "The relationship between the Human immunodeficiency Virus and the Acquired Immunodeficiency Syndrome," (14). The paper claims that drugs cannot cause AIDS, because AIDS is new but drug use is old. The NIAID asserts that, "a temporal association between the onset of the extensive use of recreational drugs and the AIDS epidemic is also lacking. The wide-spread use of opiates in the United States has existed since the middle of the 19th century. ... the number of individuals aged 25 to 44 years reporting current use of marijuana, cocaine, inhalants, hallucinogens and cigarettes declined between 1974 and 1992, while the AIDS epidemic worsened."

However, the NIAID’s information is hard to reconcile with information from the Bureau of Justice Statistics, the White House, the Deparment of HHS Drug Abuse Warning System, the NIDA and even private investigators (see Tables 2 and 3, Fig. 2). These and other sources document that:

1) The American drug epidemic of the "middle of the 19th century" had declined after World War I and completely ended during World War II (52).

2) The percentage of drug users at the peak of the early American drug epidemic was significantly smaller than the current one, namely 250,000 addicts out of 75 million Americans in 1900 (52, 55) compared to 20 million addicts out of 250 million now (51, 52).

3) The amounts consumed in the early epidemic were much lower, about 11 tons of cocaine for 90 million Americans in 1906, compared to about 400 tons for 250 million now (see 3.).

4) Before World War I, nearly a third of all Americans died from pneumonia, tuberculosis and other AIDS defining diseases, and the average age at death of Americans was about the same as that of AIDS patients now (1, 331). Thus, drug-AIDS mortality would have been hidden in the normal background mortality from the dominant infectious diseases of that time.

It follows that either the NIAID, or many others including the Bureau of Jusice Statistics, the Department of HHS, the NIDA, the White House as well as non-governmental sources misrepresent the facts. Even the major source of drug use in the NIAID’s anonymous report, David Courtwright’s Dark Paradise: Opiate Addiction in America Before 1940, documents that the number of American opium addicts had dwindled to a few thousand, mostly doctors, by 1940, and that drug arrests had fallen below 3000 per year by that time (54).

7.4. Different standards of verification for HIV and drugs.
Since infectious HIV is virtually never detectable in AIDS patients, AIDS epidemiologists accept antibodies against the virus as evidence for the virus (26, 31, 47). However, antibodies signal virus neutralization the reason why infectious HIV is undetectable in most AIDS patients. Thus evidence for a prior defeat of the virus with antiviral immunity, is taken as evidence for a current or future viral disease. However, the principle of vaccination teaches just the opposite: antiviral immunity is the only current and future protection against viruses. The search for HIV is further biased in favor of being positive, because antibodies against many other microbes will register as anti-HIV antibodies due to the inherent false positive rate of all antibody tests (48, 300, 301). Thus antibodies are grossly exaggerated standards for the presence of a virus.

AIDS epidemiologists rely only on "self-reporting" to determine recreational drug use, instead of using standard drug tests (229, 275). This epidemiological honor system is certain to minimize drug-AIDS connections because people tend to forget and to deny socially unacceptable behavior like drug use. Indeed, denial is one of the first indications of all addictions. According to drug treatment experts: "deception is the rule in the illicit drug market place..." (126). Thus, unverified questionnaires are underestimates of drug use.

Moreover, comparisons between HIV and other possible causes of AIDS are 100% biased in favor of HIV because of the HIV-based AIDS definition (see 2.). According to this definition HIV/AIDS researchers are entitled to exclude HIV-free AIDS cases from their AIDS statistics. Thus, citing 100% HIV-AIDS correlations as proof for the HIV hypothesis is not only misleading, but is in fact deceptive (35).

It is, therefore, not surprising that even the most popular recreational drugs of a given risk group, like nitrite inhalants among male homosexuals (Table 5), lose out against HIV when studied by HIV/AIDS epidemiologists. Indeed, based on the presumptuous HIV-AIDS definition and the double standards of verification for drug use and HIV, two articles have recently refuted Duesberg’s drug-use hypothesis (80) (see 7.5.). One of these was even commissioned as a commentary by Nature (80), and was sponsored by the NIAID, the other was published in The Lancet (105). For further emphasis the articles were accompanied by international press releases to enhace their impact on unsuspecting non-AIDS professionals and the general public (221, 332-334).

An unbiased search for the cause or causes of AIDS would first define AIDS diseases clinically, and then report the coincidences of all the suspects.

7.5. Omission of facts and controls.
But refutation of the drug hypothesis by the Nature commentary was not only based on questionable standards of verification, but also on the omission of crucial facts and controls (80). For example:

1) The authors proudly display, on a blue colored background, a graph of "drug-free", HIV-positive AIDS patients losing their T cells over time. The graph demonstrates that the authors are clearly aware that a drug-free control group of HIV-positive AIDS patients is necessary to refute the drug hypothesis of AIDS, while at the same time supporting the orthodox view that HIV causes AIDS. However, the drug-free group reported by the authors proved to be an empty set, as no drug-free AIDS patients were recorded in the Nature commentary (114, 335). Our independent analysis of the data base also failed to identify the missing group of drug-free AIDS patients (115, 221). Despite our challenge in The Lancet (223), Genetica (115), and Science (336) , to this date the authors have failed to come up with an explanation as to the origin of their drug-free group (337).

2) The re-investigation of the database of the Nature commentary further revealed that 45 drug-using, HIV-free patients had been omitted from the paper, although they had AIDS defining diseases (115). This brazen manipulation of the facts was legitimised with the CDC’s HIV antibody-based AIDS definition (337) (see 2.).

3) The Nature commentary also omitted the fact that 73% of the HIV-positive AIDS patients were on AZT. However, in response to our challenge the authors acknowledged the AZT prescriptions 2 years later (303).

Thus the drug hypothesis was refuted by claiming non-existing, drug-free AIDS patients, by hiding HIV-free AIDS patients, and by omitting widespread AZT use by AIDS patients.

Numerous other epidemiologists have also investigated "HIV disease progression" (102) to AIDS in drug users (87, 88, 91-93, 101, 104, 106, 279) without offering drug-free controls. Indeed, there is not a single epidemiological study in the bulging AIDS literature that ever described a group of HIV-positive people, without confounding health risks like drug use or hemophilia, progressing from HIV to AIDS (11, 225). This absence of drug-free controls is the single most damaging flaw of AIDS epidemiology.

For example, Alcabes et al. conclude from a study of HIV-positive intravenous drug users from New York that, "The results of this analysis provide evidence for a mechanism by which the clinical factors that predict more rapid progression to AIDS, such as bacterial infection, might work, and why other factors, such as drug injection, are unrelated to AIDS risk" (87). But no control is offered for drug-free AIDS.

Based on analyses of HIV-positive intravenous drug users, "with 45% injecting at least once per day," Margolick et al. conclude "that progression of HIV-1 infection in IV drug users, as reflected in the decline of CD4 cell counts, is no more rapid than that reported for other risk groups" (91). In an effort to exclude the role of drugs in AIDS, the authors pointed out that in a particular 6 month survey interval there was no "effect of active vs inactive drug use" on T cell loss. However, there was no verification for "inactive" drug use, and no informatiom as to whether "inactive" street drug use was substituted by methadone, which is itself immune suppressive (338). Moreover there was no effort to determine the cumulative lifetime drug dose of active or "inactive" drug users that is essential to evaluate drug pathogenicity. There was also no information as to whether "other risk groups" included drug-free controls.

It is also claimed that cohorts of HIV-positive male homosexuals using batteries of recreational drugs including, "alcohol, tobacco, cannabis, nitrites, cocaine and amphetamines" in addition to AZT developed AIDS from HIV infection alone without offering a population of drug-free HIV-patients as a control. For example, a Tricontinental study from San Francisco, Vancouver, Amsterdam and Sydney that was sponsored by the American NIAID concluded that, "None of the presented hazards is significant." Although the study acknowledged that, "there were no appreciable differences in the use of alcohol, tobacco or nitrites," it insisted that, "Notably, nitrite use was not associated with disease progression, and the use of tobacco appears not to be related to progression to AIDS or P. carinii pneumonia (data for the latter not shown)" (102). A remarkable "Tricontinental" conclusion!

Likewise, the NIAID-sponsored MAC study of male homosexuals published that there is "No evidence for a role of alcohol or other psychoactive drugs in accelerating immunodeficiency in HIV-1 positive individuals" (103) although it had never identified even one drug-free, HIV-positive homosexual with AIDS in 10 years (109). Indeed, a recent report from the MAC study, published in the Journal of Substance Abuse seems to contradict their earlier message: "Men who combined volatile nitrite (popper) use with other recreational drugs were at highest risk both behaviorally and in terms of human immunodeficiency virus-1 (HIV) seroconversion throughout the study." All of the 500-800 homosexual men at "highest risk" studied had used nitrites, in addition to various combinations of 12 other recreational drugs (104).

Because of their complete disregard for the medical consequences of drug use, most AIDS epidemiologists do not even look for a drug-free AIDS case although many acknowledge bewildering drug use (see Tables 4 and 6). An event at a conference on the role of nitrites in Kaposi’s sarcoma in 1994 illustrates this bias perfectly. Asked whether there was even one AIDS patient who never used drugs, an investigator of the largest group of male homosexuals ever studied for "HIV disease progression," the MACS cohort, responded, "I never looked at the data in this way" (96, 109). But the MAC study, which is supported by the NIAID with several million dollars annually, has repeatedly recorded heavy drug use for over 10 years (Table 5) (103, 104, 279).

However, until drug-free controls are available, conclusions that HIV rather than drugs cause AIDS are un-informed speculations. In fact the sheer multiplicity of epidemiological studies describing "HIV-disease progression" only in drug users from San Francisco (80, 102), Vancouver (102, 339), Chicago Los Angeles Baltimore Pittsburgh (103, 104), Sydney (102), Milan (93), Amsterdam (102), London (106) can hardly be an accident. It suggests that drugs are causing AIDS.

To avoid the pitfalls of confounding variables of HIV, matched groups must be compared that differ only in one variable (340). Thus an appropriate statistical analysis of the role of drugs in AIDS would compare two groups of HIV-positives (or two groups of HIV-negatives) matched for all variables but drug use. Based on Feynman’s standards of science, there are three contending explanations why so many AIDS-epidemiologists have omitted drug-free controls: (a) either they are ignorant of drug toxicity, or (b) they are ignorant of confounding variables in epidemiological studies, or (c) there are no drug-free AIDS cases, because drugs cause AIDS.

7.6. Confounding confounding viariables.
The Nature commentary also demonstrates the "proper methods" used by HIV researchers to eliminate confounding variables such as drug use from the non-confounding variable HIV (80).

In view of the "fact" that homosexual men who were "heavy" nitrite users had twice as much Kaposi’s sarcoma as those who were "light" users, the authors argued as follows: "This crude association is apparently the basis for Duesberg’s hypothesis. Further analysis of the data reveals a similar association between drug use and HIV positivity, and when controlled for HIV serostatus, there is no overall effect of drug use on AIDS. A similar effect, a marginal association that drops after controlling for HIV serostatus, is seen in cases which end in Kaposi’s sarcoma. Thus when proper methods are used to assess the role of confounding variables, there is no evidence of a drug effect" (80). With this reasoning the article proudly rejected the drug hypothesis with, "such claims have no basis in fact." The anti-drug bias of Nature is so pervasive that the editor openly censored (341) all critics pointing out confounding by drug use (114, 115, 222, 342). However, The Lancet allowed two critical letters (47, 223).

Called to task on the possibility of confounding two years later in Science, the authors simply restated their conclusion without lifting the secret of their "proper methods": "The standard statistical methods that we used to differentiate cause from confounding factors showed, in this case, that HIV was the cause and that drug-use association was spurious" (337).

In short, Nature has refuted the drug hypothesis by first commissioning a commentary that relied on AIDS patients who had all (!) used a multiplicity of recreational drugs in addition to AZT, and then by openly censoring all objections to its methodological flaws and unscientific manipulations a bewildering achievement coming from the world’s oldest science journal.

7.7. Grouping drug-using with non-drug using HIV-positives.
This manipulation credits the diseases of drug users to non-drug users within the same study group of HIV-positive people. For example, HIV-positive babies who either shared recreational drugs with their mothers or received AZT from their doctors are grouped with babies who neither received drugs from their mothers nor AZT, and the diseases of the HIV-positive "group" as a whole are then compared to those of HIV-free babies (205, 314, 322) (see 6.9.). But mothers of HIV-free babies typically have not used cocaine, nor are HIV-free babies ever treated with AZT 26.

Likewise, the mortality of groups of HIV-positive hemophiliacs who on average have received many more immunosuppressive transfusions than HIV-negatives and of which most are now treated with AZT and other toxic antiviral drugs, is compared to that of untreated, HIV-free hemophiliacs (see 7.8.) (22-24, 38, 183). Naturally, all excess mortality from immunosuppressive transfusions, AZT and other anti-HIV/AIDS drugs is credited to HIV. This practice obscures the role of drugs and other non-contagious risk factors in AIDS in favor of HIV.

7.8. Hiding evidence that AZT accelerates death, eleven examples.
In an effort to hide the emerging tragedy, the medical establishment either trivializes or disclaims the evidence that AZT causes diseases and accelerates death. An analysis of several of the above cited examples of AZT-accelerated morbidity and mortality (see 4.) documents this assertion:

1) The observation that among male homosexuals, "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" (117).

2) The 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, is excused by the NIH researcher James Goedert, the former proponent of the nitrite-AIDS hypothesis (see 3.), with the casual explanation, "probably because zidovudine was administered first to those whom clinicians considered to be at highest risk" (204). But, although AZT apparently increased the morbidity and mortality of hemophiliacs significantly, Goedert et al. did not question the appropriateness of AZT therapy.

3) Darby et al. report in Nature in 1995 that the mortality of HIV-positive British hemophiliacs increased 10-fold since the introduction of AZT in 1987 (183). The authors acknowledge that "treatment, by prophylaxis against Pneumocystis carinii pneumonia or with zidovudine [AZT] has been widespread" in HIV-positive hemophiliacs. But instead of even considering that these drugs could play a role in accelerating the deaths of hemophiliacs, they argued that "HIV-associated mortality has not been halted by these treatments" (183). They failed to explain why HIV-associated mortality would have risen 10-fold only after the introduction of AZT and other anti-AIDS therapies in 1987, rather than in the two decades before 1985 when HIV was unknowingly transfused into hemophiliacs together with clotting factor (24).

4) 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..." (201). The fact that an inhibitor of DNA synthesis designed to kill human cells would reduce lymphocyte counts was not mentioned.

5) An evaluation of AIDS prophylaxis with AZT produced in 1994 the following results: "the average time with neither a progression of disease nor adverse event was 15.7, 15.6, and 14.8 months for patients receiving placebo, 500 mg zidovudine, and 1500 mg zidovudine, respectively. …After 18 months, the 500-mg group gained an average of 0.5 month without disease progression, as compared with the placebo group, but had severe adverse events 0.6 month sooner." On this basis the authors concluded that, "…a reduction in the quality of life due to severe side effects of therapy approximately equals the increase in the quality of life associated with a delay in the progression of HIV disease" (202). It remains unclear, however, how one gains 0.5 months "without disease progression" while one has "severe adverse effects" 0.6 months sooner.

In view of this one wonders why since 1994 at least 220,000 mostly healthy, HIV-positive people continue to receive AZT, either by itself or combined with other drugs like protease inhibitors, all of which have no therapeutic value and cost the patient or tax payer over $12,000 per year (26).

6) 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 (203).

7) The largest test of AIDS prophylaxis with AZT of its kind, the Concorde trial, found no prophylactic value, but instead revealed a 25% higher mortality in AZT recipients than in untreated controls (343). In view of these awkward results Seligmann et al. reached the patronizing conclusion: "The results of Concorde do not encourage the early use of zidovudine [AZT] in symptom-free HIV-infected adults" (160).

8) A study that treated HIV-positive, intravenous drug users from New York with AZT observed: "The rate of CD4 lymphocyte depletion did not appear to slow after the initiation of zidovudine therapy….". This led to the conclusion: "Our data failed to provide evidence for an effect of zidovudine on the depletion of CD4+ lymphocytes, but the direction of the modeling results suggested that zidovudine users in this sample may have experienced more rapid CD4+ cell depletion" (87).

9) As of 1994 the American NIAID and the CDC promoted the prevention of maternal HIV transmission with AZT (45, 184, 185, 344). But the costs of the hypothetical triumph of reduced HIV transmission in terms of birth defects and abortions were omitted from the reports of the original trial (184, 185, 344-347). However a study from outside the US reported 8 spontaneous abortions, 8 therapeutic abortions and 8 serious birth defects, including holes in the chest, abnormal indentations at the base of the spine, misplaced ears, triangular faces, heart defects, extra digits and albinism among the babies born to 104 AZT-treated women. But these bewildering results were interpreted as just "not proving safety, thus lending tenuous support to the use of this drug" (200).

Indeed, "spontaneous" or therapeutic abortion as a result of AZT was not an unforseeable accident. A review in The Lancet on "non-surgical abortion" documents that chemotherapeutic drugs, like methotrexate, have been used to abort normal and ectopic pregnancies since 1952 (188). The article concedes early "concerns over teratogenicity, but concludes: used correctly, the method could bring great benefits" (188).

10) In 1996, the American National Institute of Child Health and Human Development reported the consequences of AIDS prophylaxis with AZT for HIV-positive babies: "In contrast with anecdotal clinical observations and other studies indicating that zidovudine favorably influences weight-growth rates, our analysis suggests the opposite. Because our analysis of zidovudine effect on standardized growth outcomes was based on limited numbers of patients (no more than 10 at any one visit with prior zidovudine use) and because we could not control for stage of HIV disease in the study design, the result indicating no effect or a negative effect of zidovudine on growth should be interpreted with caution. Presumably, zidovudine use is confounded by progression of HIV disease. The observation that standardized LAZs [length for age scores] were lower after the start of zidovudine therapy than before may suggest merely that sicker infants received zidovudine. However, our findings suggest that the widely held view that antiretroviral treatment improves growth in children with HIV disease needs further study" (205). Thus AZT toxicity was shifted to HIV.

But if the lower health standards of AZT-treated babies were due to prior "HIV disease", it would have been necessary to conclude that AZT failed to reverse or even maintain the "HIV disease" of these babies. But that possibility was not mentioned nor apparently even considered by the AZT-doctors. Moreover, the likelihood that AZT was the cause of the babies’ diseases was obscured by averaging the diseases of AZT-treated with those of untreated HIV-positive babies (see 7.7.).

11) The disquieting observation that AZT increases the annual lymphoma risk of HIV-positives 50-fold, from 0.3 to 14.5%, per year was resolved by the NCI director, Samuel Broder and his collaborators, by claiming a victory for AZT: "Therefore, patients with profound immunodeficiency are living longer [on AZT], theoretically allowing more time for the development of non-Hodgkin lymphoma or other malignancies" (198).

7.9. Conclusions.
The extent of the evasions, obfuscations, and outright censorship of the abundant drug-AIDS connections suggests that AIDS researchers must at least suspect that recreational drugs and AZT cause AIDS. Considering that most AIDS researchers have graduated from university with at least some appreciation of the central importance of DNA synthesis, somewhere in the Richard Feyman-recesses of their minds they must be aware of the high toxicity of DNA chain-terminators. Even if they did not understand that life depends on continued DNA synthesis, the complete failure of drugs like AZT to cure or prevent AIDS should have inspired concern.

Thus HIV/AIDS scientists fall far short of Feynman’s standard, "to try to give all the information to help others to judge the value of your contribution". HIV/AIDS scientists ought to inform others that the overwhelming correlation between drugs and AIDS can not be just a coincidence, and that the literature already documents that the drugs used by AIDS patients can cause each of the 30 AIDS-defining diseases and deaths.

CONTINUE