Epidemiology Determine Whether Drugs or HIV Cause AIDS?
Peter H. Duesberg
AIFO (AIDS-Forschung) has created a forum for scientific controversies.
To date Viewpoint has covered diverse topics including measures
to control AIDS-on which no consensus has been reached.
hypothesis (in contrast to the HIV-AIDS hypothesis) of Duesberg
has been a source of several controversies over the last year. AIFO
has contributed several articles of Duesberg to this controversy
(AIFO 4, 115-126; 507-515; 517-521 ; AIFO 6,
299-306 ; AIFO 7, 619-641 ).
Early in 1993 several articles appeared in the international press
that appeared to refute Duesberg's theses (Ascher et al., Nature
362, 103; Schechter et al., Lancet 341, 658; Piatak et al.,
Science 259, 1749; Pantaleo et al., Nature 362, 355;
Embretson, Nature 362, 359). Therefore AIFO has invited
Duesberg to critically review and discuss his theses in view of
Determine Whether Drugs or HIV Cause AIDS?
By Peter H. Duesberg
(AIFO), 12, pp. 627-635, December 1993
longitudinal surveys of homosexual men, one from San Francisco,
the other from Vancouver, have reinvestigated the question whether
AIDS is caused by HIV or drugs. During 8-year observation periods
the San Francisco survey observed that 215 out of 445 HIVpositive
drug users developed AIDS and the Vancouver survey that 136 out
of 365 HIV antibody-positive drug users developed AIDS. On the basis
of these correlations both surveys have concluded that HIV causes
AIDS, and have rejected my hypothesis that recreational drugs and
anti-HIV drugs, like AZT, cause AIDS. However, these conclusions
are worthless because the authors failed to recognize that: i) even
a perfect correlation with HIV (Koch's first postulate) does not
prove causation without functional tests; ii) positive antibody
tests do not prove HIV infection due to false-positives, e.g. 17%
in the Vancouver group; iii) they lacked the only absolute epidemiological
argument against the drug-AIDS hypothesis, drug-free AIDS cases;
iv) drug toxicity is dosage dependent, i.e. "the dose is the
poison." Since short-term drug users were not distinguished
from long-term users, no drug dose-AIDS response relationships emerged;
v) AZT, prescribed as an anti-HIV drug to HIV-positives, is immunotoxic
and lymphomagenic. Contrary to the authors' conclusion, data of
both surveys confirm the drug-AIDS hypothesis with consistent drug
AIDS correlations, drug-AIDS dose-response relationships, and even
drug-specific diseases. A definitive test to distinguish between
HIV and drugs as causes of AIDS would: i) define all AIDS diseases
clinically, independent of HIV; ii) test clinically defined AIDS
cases (a) for HIV, not antibodies against HIV, and (b) for their
lifetime dosage of recreational drugs and AZT; iii) conduct functional
tests with drugs or HIV, if no drug-free or HIV-free AIDS cases
can be found.
recreational drugs-AZT-clinical AIDS definition-drug-dose AIDS dependence-drug-specific
observed will always depend on the hypothesis held by the observer.
surveys, one of 812 homosexual men and 215 heterosexual controls
from San Francisco (2), the other of 715 homosexual men from Vancouver
(3), have recently reinvestigated the question whether recreational
and aphrodisiac drugs or HIV cause AIDS. Both surveys took aim at
my hypothesis that recreational drugs and AZT cause AIDS (4, 5).
But the Vancouver team also credited me erroneously with the hypothesis
that "chronic promiscuous male homosexual activity" causes
AIDS (3). After an 8-year observation period the San Francisco survey
had observed 215 AIDS cases out of 445 HIV-positive drug users (Table
1). The Vancouver survey had observed 136 AIDS cases out of 365
HIV-positive drug users after an observation period of 8.6 years
Drug use, AIDS and health among HIV positives reported by the San
Francisco and Vancouver surveys (2, 3).
Drug use* AIDS Healthy
445 100 % 215 230 Vancouver 365 >98 % 136 229
among HIV-positives is documented below.
surveys report perfect correlations between drug use and AIDS (see
below), but claim to have refuted my hypothesis that injected and
orally consumed recreational drugs and AZT cause AIDS (4, 5).
from San Francisco state that "substance abuse as a main cause
of AIDS has ... no basis in fact," and the epidemiologists
from Vancouver state that "the hypothesis that AIDS in homosexual
men is caused ... by drugs ... is rejected by these data,"
and that "HIV has an integral role in the pathogenesis of AIDS"
but it "does not rule out a role for cofactors ..." (3).
The Vancouver survey even warns that my drug hypothesis is "a
hindrance to public health initiatives" (3), and the San Francisco
survey advises "The energies of Duesberg and his followers
could better be applied to unraveling the enigmatic mechanism of
the HIV pathogenesis of AIDS."
name was cited 13 times by the authors of the San Francisco survey
in their 2-page Nature Commentary, the editor of Nature
denied me the right of reply because I had asked "unanswerable
rhetorical questions" (78). Two HIV researchers have seconded
this decision and have even submitted procedures how I "should
be stopped" (79).
Here I will
demonstrate that inherent limitations of the epidemiological method,
biases due to the HIV-based AIDS definition and the failures of
both surveys to recognize the dosage dependence of drug toxicity
and of drug-specific AIDS diseases invalidate their conclusions.
Indeed, data of both teams confirm the drug hypothesis with consistent
correlations, drug-AIDS dose-response relationships and drug-specific
of the Epidemiological Method
not sufficient to prove that a microbe causes disease. Because
a microbe can be pathogenic when it is active and abundant, and
is harmless when it is inactive and rare, documenting the presence
of a microbe is not sufficient to prove causation. The necessary
tests to prove causation have been defined by Robert Koch and since
termed Koch's postulates. According to these postulates i) the agent
must be present in every case of the disease in amounts sufficient
to cause disease; ii) it must be isolated in pure form; and iii)
it must cause the disease if inoculated into a suitable host.
its descriptive nature, epidemiological search for an infectious
pathogen is restricted to correlations and thus only relevant for
an appraisal of Koch's first postulate. Epidemiology can at best
confirm Koch's first postulate and hence never prove that an infectious
agent causes a disease.
sufficient to prove that drugs cause disease, if dosage is determined.
Clearly if drugs were to cause AIDS, the risk of a short-term user
would be much lower than that of a long-term user. The toxicity
of drugs depends on the dose that is consumed over a lifetime because
"the dose is the poison." One year of smoking or drinking
does not cause lung cancer or liver cirrhosis, but 10 to 20 years
may do so (6). Thus, a drug dose-response relationship must be established
to distinguish a toxic drug from other non-toxic agents. For this
purpose groups controlled for the dosage of drug use must be compared
to otherwise matched non-drug users. Final proof of causation is
obtained by causing toxin-specific disease in animals. Thus, demonstrating
unquantified drug use by AIDS patients is not sufficient to prove
can exclude possible causes of a disease. Epidemiology can exclude
both an infectious and a noninfectious agent as a cause, if the
disease occurs in its absence. Thus, drug-free AIDS cases must be
identified to exclude drugs, or HIV-free AIDS cases to exclude HIV
as causes of AIDS.
must be definable independent of a putative cause. In studies
designed to find the cause of a disease, the disease must be clinically
definable, independent of its putative cause. If A and B are investigated
as possible causes, it must be possible to define the disease independent
of A and B. The disease cannot be defined as A-disease, because
such a definition would exclude all A-negative cases, and would
bias the investigation in favour of a 100% correlation with A. Thus,
AIDS cases must be first diagnosed clinically and only then analysed
for the presence of drugs or HIV in order to study the roles of
drugs and HIV in AIDS.
between HIV and AIDS Does Not Prove Causation
from San Francisco and Vancouver have stated that HIV causes AIDS
because all of their AIDS cases were HIV antibody-positive (Table
1). However, this conclusion is flawed for three reasons.
i) Even a
perfect correlation with HIV does not prove causation without functional
evidence. It confirms only the first but not the third of Koch's
postulates. Indeed, other microbes have been proposed as causes
of AIDS on the basis of high or perfect correlations, as for example
human T-cell leukemia virus I (7) and cytomegalovirus (8-12). Thus,
it was arbitrary to single out HIV as the cause of AIDS, because
other microbes also correlate with AIDS.
surveys report perfect correlations not only between AIDS and HIV
but also between AIDS and drugs (see below), the choice of HIV as
the causative correlate was even more arbitrary than if it had been
the only known AIDS correlate. This is because the epidemiological
method cannot by itself distinguish between three consistent alternatives:
HIV alone, drugs and HIV, and drugs alone.
ii) A positive
HIV antibody test is not a rational prognosis for a viral disease,
because antibodies are the classical indicator for a virus that
has been rejected by the immune system. In response to antibodies,
which of necessity include cellular immunity, the virus is either
eliminated or restricted to latency-the reason why HIV is exceedingly
difficult to isolate from antibody-positive carriers with and without
AIDS (13-16). Thus, a positive antibody test is in general a counter-indication
for future viral pathogenicity.
a positive antibody test is not a reliable indicator for the presence
of a virus (17, 18). According to a recent review entitled "HIV
Testing: State of the Art," "depending on the population
tested, 20 to 70% of ... two successive ELISAs are confirmed by
Western blot [two variant antibody tests]," i.e. 30 to 80%
are false positives (19). But even in groups with a high probability
of infection, such as the San Francisco and Vancouver groups, significant
numbers of false positive Western blots have been recorded (18).
For example, Schechter et al. reported in 1991, that 33 out of 158
(17%) of Western blot-confirmed, antibody-positives in their Vancouver
cohort were HIV-free, based on HIV DNA testing with the polymerase
chain reaction (20). Two of these 33 had AIDS, the remainder had
various degrees of immunodeficiency and lymphadenopathy, but not
sufficient for a diagnosis for AIDS. The report also cites further
studies documenting that 14 to 17% of antibody-positive homosexuals
are HIV-provirus free.
Since a 100%
correlation with antibody-positivity does not mean 100 % infection,
it is probable that the AIDS cases from the San Francisco survey,
and certain that the cases from the Vancouver survey included HIV-free
iii) At least
4621 HIV-free AIDS cases have been documented in the literature,
indicating that HIV is not necessary to cause AIDS (18).
Thus the conclusion
of both surveys that HIV causes AIDS, because all AIDS cases appeared
antibody-positive, is not valid.
to Identify Drug-Free AIDS, the Absolute Argument against the Drug-AIDS
The most critical
argument against the drug-AIDS hypothesis would be a group of drug-free
AIDS patients. However neither the Vancouver nor the San Francisco
survey provided drug-free AIDS cases.
All 136 AIDS
patients from Vancouver belonged to a group of 365 HIV-positive
drug users (Table 1). This is documented as follows: Among the 365
HIV-positive men surveyed, 88% reported consumption of nitrites
and 80% the use of other "illicit" recreational drugs
including cocaine, heroin, amphetamines, methylene amphetamines,
lysergic acid, and diethylamide (3). Thus, assuming no specific
linkages between the use of these different drugs, 98% have used
at least one drug, because only 2% (12% x 20%) reported no use of
recreational drugs. And 70% (88 x 80) have used at least two drugs.
Even this high drug use may be an underestimate because illicit
drug use is known to be underreported and because the Vancouver
survey did not ever verify self-reported drug use by any tests.
Indeed, a recent article by the Vancouver team reports that 100%
of 87 AIDS patients had used nitrites (21). I followed their suggestion
to "reread" their article for a statement that this group
"includes some whose use was zero" (22), but I failed
to find that statement. In addition the Vancouver survey failed
to consider AZT use by HIV-positives (see below), but acknowledged
it upon request (22) and in previous publications (20). Thus, the
Vancouver survey lacks the most critical epidemiological argument
to refute the drug-AIDS hypothesis-a group of verified non-drug
users who developed AIDS.
to this critique (23), the Vancouver team has recently claimed that
19, or 5%, of the 365 HIV-positive men surveyed "... reported
no recreational drug use ..." and that " ... their CD4
counts fell a mean of 138/microliter per year ..." (22). However
there was no verification that these men were indeed recreational
drug-free and no mention whether they were on AZT. Moreover, no
claim was made that these presumably drug-free men ever developed
claim to the contrary, the San Francisco survey also lacked drug-free
AIDS. The survey reported that 100% of their 215 AIDS cases had
used nitrites in its table 2 (2). Additional undetermined percentages
of these cases had also used other illicit recreational drugs, such
as cocaine and amphetamines (2). Moreover, since the introduction
of AZT in 1987, 132 (84%) of the 157 AIDS cases observed by the
San Francisco survey were on AZT (Ascher et al., personal communication,
9 April 1993). AZT is generally prescribed before AIDS, once T-cell
counts drop below 500 per microliter (24). Thus, it is safe to conclude
that all 215 AIDS patients from San Francisco were on multiple drugs
including nitrites, one or more other recreational drugs and AZT
Yet the San
Francisco survey claims a "group" of "seropositive
no-drug" users who lost T-cells, although there are no data
for such a group in their paper. This is documented as follows.
According to the paper's table 1, all AIDS patients were HIV-positive
homosexuals, and all HIV-positives were homosexuals (2). All heterosexuals
were HIV-negative, except one who was a drug addict (Ascher, personal
communication). According to Table 2, 100% of the homosexual men
were either "heavy" or "light" nitrite users,
namely 144 plus 668 out of 812 (text) (2). Thus, all AIDS patients
and all HIV-positives in this study had used at least nitrites.
In addition they had used cocaine, amphetamines, other recreational
drugs and AZT. However, the corresponding figure purports, in color
(!), to give data on "average adjusted" T-cell losses
of three seropositive groups, with "no drug use," with
"moderate drug use" and "heavy drug use," respectively.
Three curves in that figure correspond to these three groups. Yet
based on tables 1 and 2 the category "seropositive-no drug
use" is an empty set representing nobody. Clearly the curve
labeled "seropositive-no drug use" needs to be "adjusted"
to this critique (23), the San Francisco epidemiologists "acknowledge
that it might have been clearer ... if we had labeled the latter
group as 'none/light' in the table ..." (25).
the San Francisco nor the Vancouver survey provided the absolute
epidemiological argument to exclude drugs as causes of AIDS, i.e.
drug-free AIDS cases.
to Quantitate Drug Dosage- the Key to Drug Toxicity
The San Francisco
team relied for drug use information on statements "for the
24-month period before entry into the study" (2), and the Vancouver
team on "ever versus never" statements. Thus the epidemiologists
from San Francisco and Vancouver failed to quantitate drug consumption
in three ways: i) They did not determine the cumulative lifetime
drug dose of their subjects; ii) They did not verify self-reported
drug use by any tests, although they acknowledged that illicit drug
use is generally underreported (22); iii) They ignored AZT use altogether.
failure to quantitate drug consumption did not reflect a lack of
suitable data, but a genuine disregard for drug toxicity. For example,
the San Francisco survey stated "We examined the cohort at
6-month intervals for 96 months ..." But for correlations with
AIDS over the 8-year study period "We compared heavy drug use
for the 24-month period before entry into the study ..." (2).
The Vancouver survey asked study subjects for drug use on an "ever
versus never" basis, "once every six months" according
to their 1993 study (3), and "on an annual basis" according
to an earlier study (20). Clearly such efforts shed little light
on the lifetime drug dosage of study subjects.
If one were
to correlate lung cancer with information on smoking for only 24
months or on an "ever versus never" smoking statement
the results would be as inconclusive as the results on drugs and
AIDS described by the San Francisco and Vancouver teams. Drug use
would indeed be as "casually [sic] associated with AIDS"
as the San Francisco team writes in its paper (2). By not quantifying
and by not verifying drug use, both teams missed the most relevant
parameter of drug toxicity, the lifetime dosage.
studies aimed at distinguishing between drugs and HIV as causes
of AIDS in homosexuals from San Francisco (26) have likewise been
invalidated by the failure to quantitate and verify drug consumption
disregard for drug toxicity by the San Francisco and Vancouver surveys
is hard to reconcile with the solid documentation of drug toxicity
in the literature. Toxicity has been documented empirically for
all and mechanistically for many psychoactive drugs (4). For example,
alkylnitrites are directly toxic as they are rapidly hydrolyzed
in vivo to yield nitrite ions which react with all biological macromolecules
(28). Toxicity for the immune system, the central nervous system,
the hematological system and pulmonary organs has been observed
after short exposure to nitrites in humans and animals (28-33).
In addition, nitrites were among the first known mutagens and carcinogens,
the reason they are considered health hazards in food (34, 35).
The toxicity of the long-term use of cocaine, amphetamines and other
illicit neurotropic, psychoactive drugs has been documented since
1909. It includes nearly all AIDS-defining diseases such as lymphopenia,
lymphadenopathy, fever, weight loss, septicemia, increased susceptibility
to infections, low T4 to T8 cell ratios and profound neurological
disorders (4, 36-49). These drugs are neurotoxic directly and immunotoxic
indirectly via malnutrition, insomnia and poor sanitation (4).
toxicity of psychoactive drugs consumed by AIDS patients, the toxicity
of the DNA chain terminator AZT is not a side effect, but a design.
AZT was designed for chemotherapy over 30 years ago to kill all
growing cells in cancer patients by terminating DNA synthesis (50).
Since this is its only known function, its cytotoxic effects on
the fast growing cells of the bone marrow (50-55), the source of
T-cells, are equivalent to "AIDS by prescription" (4,
recreational drugs and AZT are used in sufficient quantities to
explain fatal AIDS diseases. An approximate daily psychoactive dose
of amyl nitrite is 1 ml (or 0.01 mol) (55, 56). This represents
about 6 x 1021 molecules and corresponds to 6 x 107 molecules for
every one of the 1014 cells of the human body, enough for abundant
toxicity. The daily prescription of 500-1500 mg AZT also corresponds
to 2-6 x 1021 molecules or 2-6 x 107 for every cell in the human
body, more than enough to kill every cell that takes it up (4).
to this critique (23), the San Francisco and the Vancouver team
now claim in letters to The Lancet that drugs do not cause
AIDS because 39 (25) and 78 (22) HIV-free drug users did not develop
AIDS. Again the self-reported drug use of these subjects was not
quantitated and is likely to have been lower than in HIV-positives
because HIV is a marker for drug use (see below). Another clear
reason why they might not have developed AIDS diseases is that HIV-negatives
are not prescribed the immunotoxic AZT (see above).
negative representing a limited number of cases does not disprove
any scientific hypothesis, including the drug-AIDS hypothesis. For
example, subjects who have smoked for 20 years and not developed
lung cancer do not disprove the smoke-cancer hypothesis, and subjects
who have been drinking for 20 years and have no cirrhosis do not
disprove the alcohol-cirrhosis hypothesis.
absence of AIDS in 1 million healthy HIV-positive Americans and
in 0.5 million healthy HIV-positive Europeans and in 8 million healthy
HIV-positive Africans (57) does not disprove the HIV-AIDS hypothesis.
The San Francisco survey even reported 230 healthy subjects, and
the Vancouver survey reported 229 healthy subjects who were drug
users and were HIV-positive but did not develop AIDS (Table 1).
Indeed, the majority of the HIV-positive drug users remained healthy
for 8 years (Table 1). Again these negatives neither disprove the
drug nor the HIV-AIDS hypothesis.
HIV-Free AIDS with the HIV-Based AIDS Definition?
to the HIV-based AIDS definition AIDS researches bias against HIV-free
AIDS. Indeed, American AIDS statistics from the Centers for Disease
Control do not list the incidence of HIV-free AIDS cases (18).
to the HIV-based AIDS definition appears to be the reason why the
survey from San Francisco did not distinguish between the 30 AIDS-defining
diseases including dementia, diarrhea, lymphoma and pneumonia, except
for Kaposi's sarcoma. In an effort to provide HIV-independent diagnoses
of AIDS both surveys report T-cell depletion (3), as "a more
objective and, indeed, the primary pathognomonic feature of AIDS"
(2). However, both surveys fail to indicate how T-cell depletion
relates to the incidence of AIDS in their cohorts, e.g. whether
any of their AIDS cases was just diagnosed by a low T-cell count.
both surveys fail to recognize that not all AIDS diseases are based
on immunodeficiency (4). For example, in 1992, 39% of all American
AIDS patients developed such non-immunodeficiency AIDS diseases
as Kaposi's sarcoma (10%), wasting (20%), dementia (6%), and lymphoma
(3%) (58). These diseases are not caused by and often not associated
with immunodeficiency (4). This may be the reason why the San Francisco
survey has listed AIDS and Kaposi's sarcoma as separate items in
its table 2 (2).
examples suggest that the HIV-based AIDS definition (59, 60) has
biased AIDS diagnoses from San Francisco and Vancouver against HIV-free
AIDS. The Vancouver survey reports no AIDS in 350 HIV-negative homosexual
men in 8.6 years ("no AIDS illnesses occurred in men who remained
persistently negative for HIV-1 antibody") (3) and the San
Francisco survey reports "0" cases of AIDS in 367 HIV-negative
men in 8 years (2).
is improbable that no AIDS-defining disease-e.g. diarrhea, pneumonia,
candidiasis, herpes infection, dementia, >10% weight loss, fever
for several weeks, toxoplasmosis, cryptococcosis, cryptosporidiosis,
cytomegalovirus infection, mycobacterial infection and "other
illnesses" (3)-would have occurred in 717 male drug users in
over 8 years, since the very same diseases have been described in
drug addicts since 1909 (see above). According to table 2 of the
San Francisco survey, 100% of HIV-negative homosexual men had used
nitrites and an unknown percentage had also used cocaine, amphetamines
and other recreational drugs (2), and according to the Vancouver
survey, 56% had used nitrites, and 58% had also used cocaine, amphetamines,
heroin, lysergic acid, diethylamide and other illicit drugs (3).
Thus, it appears that the reported absence of AIDS in these HIV-free
groups reflects the bias of either not diagnosing or not reporting
AIDS-defining diseases in HIV-negatives.
Data from San Francisco and Vancouver Confirm the Drug-AIDS Hypothesis
the San Francisco and Vancouver surveys confirm the drug hypothesis
not only with perfect correlations but also with (i) quantitative
and (ii) qualitative arguments for the drug hypothesis-despite the
authors conclusions-on several grounds.
response relationships (a-c). (a) The HIV-AIDS hypothesis and
the authors of the surveys from San Francisco and Vancouver assume
that AIDS follows HIV infection with an average lag of currently
10 years (20, 60). This lag is termed the latent period of HIV.
According to this hypothesis healthy HIV carriers are those who
have not accumulated sufficient HIV lag time to experience HIV-mediated
HIV is not active during this lag period and rarely even active
during AIDS (4, 61-64), while the HIV carriers, as for example those
from AIDS risk groups in San Francisco and Vancouver, are actively
using recreational drugs and also AZT, this lag period in fact appears
to be a quantitative measure for 10 years of drug use.
that have measured toxicity of recreational drugs over time, have
documented that about 10 years of nitrite use are necessary to cause
Kaposi's sarcoma or pneumonia (29), even in persons without HIV
(65). Likewise other recreational drugs cause in 10 years immunodeficiency
diseases in persons with and without HIV (37, 47, 66-69). This toxicity
threshold provides a rational explanation for the 10-year "enigmatic
mechanism of the HIV pathogenesis of AIDS." (2).
(b) The claims
that HIV-negatives from San Francisco and Vancouver did not develop
AIDS diseases can also be illuminated in the light of the dosage
argument. Drug use and HIV infection are linked via sexual activity.
Recreational drugs are used by homosexuals at risk for AIDS as psychological
and physiological aphrodisiacs. They generate euphoria and facilitate
anal intercourse, particularly the nitrites which have been prescribed
as vasodilators against angina since the 19th century (28, 29, 70).
Since it takes about 1000 sexual contacts to pick up HIV (4), and
since these contacts are frequently drug-promoted, HIV antibody-positives
have consumed the drug the equivalent of 1000 contacts more than
Vancouver team acknowledges that "risk behaviors are known
to correlate to HIV-1 infection ..." (3). And the San Francisco
team reports that 72.9 % of the heavy drug users but only 50.9 %
of the light users are HIV positive (see table 2, 2). Thus, HIV-positives
are likely to have used more recreational drugs than HIV-negatives.
It is for this reason that I have proposed HIV as a marker of AIDS
risks, rather than the cause of AIDS: the more drug-mediated sexual
contacts the more likely is infection by HIV (4). In addition, HIV-negatives
were spared AIDS-diseases resulting from AZT, which is only prescribed
to HIV-positives. Therefore in addition to biases due to the HIV-based
AIDS definition (see above), a lower dosage of recreational drugs
and the absence of AZT shed light on the observation that HIV-negatives
were not reportedly developing AIDS diseases.
(c) The San
Francisco survey confirms the quantitative aspect of the drug hypothesis
even more directly with the observation that "heavy" drug
users had 1.6 times as much AIDS and had 2 times as much Kaposi's
sarcoma as "light" users (see table 2, 2). The authors
correctly suggest that "this crude association is apparently
the basis for Duesberg's hypothesis." The Vancouver team even
acknowledged one HIV-positive death from drug overdose "excluding
AIDS-related mortality" (3). Thus both teams provide drug-AIDS
dose-response relationships-a definitive argument for the drug-AIDS
diseases. The surveys from San Francisco and Vancouver also
provide qualitative evidence in support of the drug-AIDS hypothesis.
The San Francisco epidemiologists report that 43% (92/215) and the
Vancouver epidemiologists that 25% (34/136) of their AIDS victims
had Kaposi's sarcoma. This is 4.3 and 2.5 times higher than the
U.S. national average of 10% (58). This result is compatible with
national statistics indicating that Kaposi's sarcoma is about 20-times
more common in male homosexuals than in all other risk groups (71).
The fact that
Kaposi's sarcoma occurs almost exclusively in homosexuals but not
in other risk groups is hard to reconcile with the claims of the
San Francisco and Vancouver teams that HIV, contracted by "receptive
anal intercourse," causes Kaposi's sarcoma (3, 72). Indeed,
a controlled study has just excluded HIV, but not anal intercourse,
as the cause of AIDS. The study showed that among two HIV-positive
groups of homosexuals those who developed AIDS had practiced receptive
anal intercourse more than twice as much as those who remained healthy
(73). In view of such discrepancies with the virus hypothesis, its
followers, including the Vancouver team (21), have postulated a
second, as yet unknown sexually transmitted agent, to explain the
restriction of Kaposi's sarcoma to homosexuals (71, 73, 74).
sarcoma in homosexuals is totally consistent with the hypothesis
that nitrites inhaled to facilitate anal intercourse cause pulmonary
and epithelial Kaposi's sarcoma irrespective of the presence of
HIV (4, 28). Indeed, 100 % of the AIDS patients from San Francisco
and 100 % of the Kaposi cases from Vancouver (21) had inhaled nitrites.
replicates via a DNA intermediate, DNA chain terminators, like AZT,
are considered antiviral drugs and are prescribed as AIDS prophylaxis
to healthy HIV-positives (53) and as therapy to HIV-positive AIDS
patients (4). Since AZT kills all dividing human cells by DNA chain
termination, it is particularly toxic to the rapidly proliferating
bone marrow, the source of T-cells (4, 50-54). Thus, the widespread
use of AZT by HIV-positives from the San Francisco and Vancouver
groups (see above) explains the decline of T-cells in HIV-positives
as AZT-specific disease.
the widespread AZT use also sheds light on the 8% incidence of lymphoma
among HIV-positive AIDS patients from Vancouver (3). This is high
compared to the national average of 3% in the U.S. (58), but is
normal for AZT recipients who have an annual lymphoma incidence
of 9% (75).
The most urgent
and growing problem facing the HIV-AIDS hypothesis is its total
failure in terms of public health benefits. Despite enormous efforts
over the last 10 years, costing the US taxpayer alone $4 billion,
no vaccine has been developed, no AIDS patient has been cured, no
prevention has slowed the spread of AIDS. These are the hallmarks
of a flawed hypothesis.
of intensive research have failed to demonstrate that HIV causes
AIDS or is even toxic to human cells (4, 76). Indeed HIV is mass-produced
in indefinitely growing human T-cell lines at titers of up to 106
infectious units per ml (4, 77). Therefore the primary argument
for the HIV-AIDS hypothesis is just HIV/AIDS correlations of the
kind analysed here (59, 60, 74).
In the face
of a 10-year history of scientific and public health failures, the
scientific method calls for alternatives to the prevailing HIV-AIDS
hypothesis such as the drug-AIDS hypothesis. This hypothesis is
based on excellent correlations, e.g. according to the Centers for
Disease Control, 30% of all American AIDS patients including nearly
all heterosexuals with AIDS are intravenous drug users (58), and
about 60% are male homosexuals who have used aphrodisiac drugs as
has been demonstrated here and previously (4). Furthermore drug
toxicity has been documented and dose-response relationships and
drug-specific AIDS diseases have been described here and previously
confirming the drug-AIDS hypothesis (4).
If both AIDS-correlates,
drugs and HIV, were given unbiased consideration, the choice between
drugs and HIV, or antibodies against HIV, would be easy. It would
appear more rational to conclude that drug intake "has an integral
role in CD4 depletion ... and AIDS" (3) than HIV or antiviral
I call for a reinvestigation of whether in the predominant AIDS
risk groups in the U.S. and Europe, male homosexuals and intravenous
drug users, HIV or drugs cause AIDS based on the following criteria:
i) AIDS must
be determined clinically, independent of HIV. All AIDS-defining
diseases must be identified in order to detect drug-specific diseases.
ii) HIV must
be identified by virus tests, rather than antibody tests. A positive
antibody test would be considered tentative until it is confirmed
by HIV isolation.
use must be quantitated to determine dose-response relationships.
Both recreational drug use and AZT use must be compounded.
iv) If no
drug-free AIDS can be found to eliminate drugs, and no HIV-free
AIDS to eliminate HIV, functional tests must be developed to identify
the causative correlate. HIV toxicity could be tested in susceptible
cells in culture, in animals and in accidentally infected humans
who lack other risk factors. Drug toxicity could be tested in cells
in culture, experimental animals or in HIV-free drug addicts.
I thank Lars
Chapsky, Bryan Ellison, Phil Johnson, Harry Rubin, Siggi Sachs,
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