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
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
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"
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
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"
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,
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
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
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
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"
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).
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.