12, pp. 627-635
Can Epidemiology Determine Whether Drugs or
HIV Cause AIDS?
Peter H. Duesberg
Professor Dr. Peter H. Duesberg, Department of
Molecular and Cell Biology, 229 Stanley Hall, University of California,
Berkeley, CA 94720, USA.
Two recent 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.
What is observed will always depend on the hypothesis held
by the observer.
-David Horrobin (1)
Two longitudinal 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 (Table 1).
Table 1: Drug use, AIDS and health among HIV positives reported
by the San Francisco and Vancouver surveys (2, 3).
positives Drug use* AIDS Healthy
San Francisco 445 100 % 215 230
Vancouver 365 >98 % 136 229
*Drug use among HIV-positives is documented below.
Thus both 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
The epidemiologists 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."
Although my 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 AIDS
1. Limits of the Epidemiological Method
i) Epidemiology 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.
Because of 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.
ii) Epidemiology 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 causation.
iii) Epidemiology 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.
iv) Disease 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
2. Correlation between HIV and AIDS Does Not Prove Causation
The surveys 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.
Since both 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
Moreover, 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 AIDS.
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.
3. Failure to Identify Drug-Free AIDS, the Absolute Argument against
the Drug-AIDS Hypothesis
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
In response 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 AIDS.
Despite a 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 (Table 1).
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 reality.
In response 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).
Thus, neither 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.
4. Failure 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.
Indeed, the 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
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.
Other epidemiological 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 (27).
The casual 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).
Unlike the 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, 5).
Moreover, 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).
In response 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).
However, a 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
Likewise the 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.
5. Censoring HIV-Free AIDS with the HIV-Based AIDS Definition?
By adhering 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).
Adherence 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.
Furthermore 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).
The following 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).
However, it 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.
6. Drug Data from San Francisco and Vancouver Confirm the Drug-AIDS
Data from 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.
i) Dose 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 AIDS.
However, since 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.
Indeed, studies 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 HIV-negatives.
Indeed, the 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
(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 hypothesis.
ii) Drug-specific 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).
However Kaposi's 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.
Since HIV 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.
Moreover, 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.
Ten years 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 antibodies.
Therefore, 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
i) AIDS must be determined clinically, independent of
HIV. All AIDS-defining diseases must be identified in order to detect drug-specific
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.
iii) Drug 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. *
With Viewpoint, 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.
The drug-AIDS 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 these challenges.
-The editor of AIDS-Forschung
I thank Lars Chapsky, Bryan Ellison, Phil Johnson, Harry
Rubin, Siggi Sachs, Jody Schwartz, Richard Strohman and Yue Wu for critical
review and discussions. I am supported by The Council For Tobacco Research-USA,
Inc. and by private donations from Bill Bowie (New York), Glenn Braswell
(Los Angeles), Dr. Richard Fischer (Annandale, VA), Dr. Fabio Franchi (Trieste,
Italy), Dr. Friedrich Luft (Berlin).
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