How Much Longer Can We Afford the
AIDS Virus Monopoly?
To be published in the Genetica monograph, "AIDS:
Virus- or Drug-Induced?" (1995) Abstract
By Peter H. Duesberg
Until 1984 AIDS science was open. Initially, the
new epidemic of pneumonias and Kaposi's sarcomas, since called AIDS,
was considered a collection of non-infectious "lifestyle"
diseases. But the Centers for Disease Control in Atlanta published
that the pneumonias and Kaposi's sarcomas of male homosexuals, who
were addicted to recreational drugs, were caused by a common infectious
agent because patients had been "linked" by sexual contacts.
On the basis of the CDC's sexual linkage study, the Secretary of
Health and Human Services announced in 1984 the hypothesis that
the retrovirus HIV is the cause of AIDS. The HIV-AIDS hypothesis
currently holds a monopoly on all AIDS research and treatment. However,
the HIV hypothesis is scientifically unproven. It has failed each
of 15 testable predictions, as for example that AIDS would explode
via sexual transmission of HIV into the general population. Moreover,
HIV meets all classical criteria of a harmless passenger virus:
unpredictable intervals between infection and any subsequent disease,
and unpredictable presence and activity of the virus during a disease.
Since HIV is rare in the US, it is a marker of real AIDS risks,
frequent injection of intravenous drugs, thousands of drug-mediated
sexual contacts, and transfusions. Indeed, AIDS does not meet even
one of the classical criteria of an infectious disease, as for example
equal distribution between the sexes, disease within days or weeks
after infection, and exponential spread of the disease in an un-immunized
population (Farr's law).
Far from being beneficial, the HIV-AIDS hypothesis
has become a threat to public health in the last 10 years: It is
the sole basis for (1) the daily treatment of at least 200,000 HIV-positives
with cytotoxic DNA chain terminators originally designed to kill
growing human cells for chemotherapy, like AZT, that are now prescribed
as anti-HIV drugs; (2) the clean-needle programs that encourage
intravenous drug use, and the misinformation that HIV-infection
is the only health risk of recreational drug use. However, recreational
drugs, such as heroin, cocaine, amphetamines and nitrite inhalants,
have long been known to have immunotoxic, cytotoxic and/or carcinogenic
effects; and (3) the anxiety and the many restrictions of human
rights associated with a positive HIV-test.
Here it is proposed that American and European AIDS
is caused by the long-term consumption of recreational and of anti-HIV
drugs like AZT. The drug-AIDS hypothesis correctly predicts American/European
AIDS: (1) AIDS is restricted to intravenous and oral users of recreational
drugs and AZT; (2) AIDS is 87% male, because males consume this
share of recreational drugs; (3) AIDS occurs in newborns, because
mothers use recreational drugs during pregnancy; (4) AIDS is new
in America, because AIDS is a consequence of the recreational drug
use epidemic that started in the 1960s, and of AZT prescriptions
that started in 1987; (5) AIDS occurs only in a small fraction of
recreational drug users, because only the highest life-time dose
of drugs causes irreversible AIDS-defining diseases - likewise only
the heaviest smokers get emphysema or lung cancer; (6) AIDS manifests
as specific diseases in specific risk groups, because each group
has specific drug habits. For example, pulmonary Kaposi's sarcoma
is exclusively diagnosed in male homosexuals who inhale carcinogenic
alkyl nitrites; (7) AIDS does not occur in millions of HIV-positive
non-drug users, and there are thousands of HIV-free AIDS cases,
because AIDS is not caused by HIV; (8) AIDS is stabilized, even
cured, if patients stop using recreational drugs or AZT - regardless
of the presence of HIV. The drug hypothesis predicts that AIDS is
an entirely preventable and in part curable disease. The solution
to AIDS could be as close as a very testable and affordable alternative
to the HIV hypothesis - the drug-AIDS hypothesis.
Table of Contents
I. Fabricating the case for infectious AIDS
II. The HIV-AIDS hypothesis proves to be unprovable
III. HIV - a harmless passenger virus
IV. HIV - a marker for AIDS risks
V. The myth of infectious AIDS - unconfirmed
VI. The HIV-AIDS hypothesis is costly, unproductive
VII. The drug-AIDS hypothesis
VIII. The drug-AIDS hypothesis predicts American/European
AIDS - completely
IX. A possible solution - at last
The emperor marched in the procession under the
beautiful canopy, and all who saw him in the street and out of the
windows exclaimed: "Indeed, the emperor's new suit is incomparable!
What a long train he has!" ... "But he has nothing on
at all," said a little child at last.... "But he has nothing
on at all," cried at last the whole people. That made a deep
impression upon the emperor, for it seemed to him that they were
right; but he thought to himself, "Now I must bear up to the
end." And the chamberlains walked with still greater dignity,
as if they carried the train which did not exist.
Hans Christian Andersen, The Emperor's
I. Fabricating the case for infectious AIDS
Hardly anybody remembers that in its first three
years, from 1981 to 1984, AIDS science was open. The new epidemic
of pneumonias and Kaposi's sarcomas, that was called AIDS, was considered
infectious by some, but many independent investigators and even
scientists from the Centers for Disease Control (CDC) in Atlanta
considered AIDS behavioral diseases. Recreational drugs such as
nitrite and ethylchloride inhalants, cocaine, heroin, amphetamines,
phenylcyclidine, LSD, and some others were proposed by epidemiologists
and toxicologists as the causes of AIDS because in the early 1980s
nearly all AIDS patients were either male homosexuals who had used
these drugs as aphrodisiacs and psychoactive agents, or were heterosexual
intravenous drug users #(Goedert et al., 1982; Marmor et
al., 1982; Jaffe et al., 1983; Mathur-Wagh et al.,
1984; Haverkos et al., 1985; Newell et al., 1985a;
Newell et al., 1985b; Lauritsen and Wilson, 1986; Haverkos
and Dougherty, 1988). Drugs seemed to be the most plausible explanation
for the restriction of AIDS to these risk groups, because drug consumption
was their only specific common denominator-not shared with the general
population. This original drug-AIDS hypothesis was called the "lifestyle
hypothesis" #(Oppenheimer, 1992)#.
But in April 1984 the secretary of Health and Human
Services and AIDS researcher Robert Gallo from the National Institutes
of Health (NIH) announced at an international press conference in
Washington that a virus is the "probable cause of AIDS"
#(Altman, 1984)#. This "AIDS virus" #(Altman, 1984)# had
been discovered a year earlier in France, in a male homosexual without
AIDS #(Barré-Sinoussi et al., 1983)#. Within two
years after that announcement an international committee of retrovirologists
had named this virus, the Human Immunodeficiency Virus (HIV), to
indicate that it was the accepted cause of AIDS #(Coffin et al.,
The road for the ready acceptance of the "AIDS
virus" by the scientific community had been paved by epidemiologists
from the CDC. By tracing sexual contacts of male homosexual AIDS
patients the CDC claimed that it could "link patients,"
"who had sexual exposure with other AIDS patients within five
years of the onset of symptoms." #(Auerbach et al.,
1984)#. On that basis the CDC proposed that AIDS "may be caused
by an infectious agent that is transmissible from person to person
in a manner analogous to hepatitis B virus infection: through sexual
contacts; through parenteral exposure by intravenous drug abusers...;
through blood products; and, perhaps, through mothers who are ...
intravenous drug users to their infants." #(Auerbach et
However, compared to hepatitis B or any other authentic
infectious disease, the CDC's case for infectious AIDS was bizarre
with regard to the diversity of the diseases linked. The CDC had
"linked by sexual contact" the Kaposi's sarcomas of some
patients to the pneumonias of others and vice versa. The uncritical
acceptance by the scientific community of a common infectious cause
for such diametrically different diseases as cancer and pneumonia
allowed the CDC to fabricate infectious AIDS. Since cancer, pneumonia,
and by now about 30 different diseases were all said to have the
same cause, they would soon all be called by the same new name,
AIDS #(Institute of Medicine, 1988; Centers for Disease Control
and Prevention, 1992; National Institute of Allergy and Infectious
A second bizarre element in the CDCs case for infectious
AIDS was the assumption of an average "latency period"
from infection to AIDS of 10 months #(Auerbach et al., 1984)#,
now 10 years (see below). The assumption of a microbe that only
causes disease after an average latency period of 10 months
was without proven precedent. It was necessary, because prospective
patients "were asymptomatic at the time of sexual exposure,"
and only developed AIDS up to 5 years after a critical contact #(Auerbach
et al., 1984)#. Indeed, the carriers of the assumed infectious
agent had to be exceedingly healthy during the latency period, because
they had "large numbers" of "approximately 250 different
male sexual partners each year." In view of such large numbers
of sexual contacts and the long latency periods between infection
and AIDS, tracing the one contact that would cause a disease had
to be a masterpiece of epidemiological detective work. Therefore
the CDC's case for sexual transmission of AIDS was about as compelling
as the claim that one car had a flat tire at an intersection, because
another car had blown a head gasket at the same intersection in
the previous 5 years. Nevertheless, the sexual contact study was
accepted by the scientific community as proof for infectious AIDS
without further scrutiny.
The fact that "linked patients" "have
been frequent users of inhaled amyl and butyl nitrite" and
"of recreational drugs other than nitrite" was not considered
an AIDS risk by the CDC in 1984 #(Auerbach et al., 1984)#,
although CDC scientists had originally proposed recreational drugs
as the cause of AIDS #(Oppenheimer, 1992)#.
In 1984, the CDC also presented typical hemophilia
diseases, like pneumonia and candidiasis, as AIDS from parenteral
infection via blood transfusions-in support of its claim that AIDS
was infectious #(Curran et al., 1984; Evatt et al.,
1984; Duesberg, 1995b)#. The paradox that none of the CDC's hemophiliacs
with AIDS would have developed Kaposi's sarcoma from an infectious
agent that presumably caused Kaposi's sarcoma in homosexuals was
effectively hidden because all these entirely unrelated diseases
had been named AIDS #(Duesberg, 1992; Duesberg, 1994a; Duesberg,
Indeed the CDC, originally established to fight infectious
diseases, had grown desperate for a new infectious disease, because
ever since polio had been eliminated by vaccines over 30 years ago,
no new infectious diseases had plagued the Western World. In the
words of a Red Cross official, "... the CDC increasingly needs
a major epidemic to justify its existence" #(Associated Press,
1994)#. Infectious AIDS, but not the drug-AIDS hypothesis, offered
such an opportunity. A new infectious epidemic readily generates
fear and funding. But research on the toxicity of recreational drugs
is trivial, not likely to make headlines in the scientific literature.
As a possible investment in its future existence, the CDC has recently
launched a new journal, Emerging Infectious Diseases, to
raise "public awareness of exotic bugs." #(Kaiser, 1994)#.
For example, in 1994 the CDC promoted the Hanta virus -after it
presumably killed some Indians #(Denetclaw and Denetclaw, 1994a;
Denetclaw and Denetclaw, 1994b)#- into a threat to the nation, and
in 1995 the Ebola virus, that had apparently killed some Zairens,
was promoted into a global "killer virus" #(Associated
Press, 1995a)#. The CDC claimed that 108 people may have been killed
by the Ebola outbreak in Zaire in 1995 #(Centers for Disease Control,
1995)#. But it failed to mention that 20% of the 55 million Zairens
are Ebola virus antibody-positive, having survived the virus without
apparent disease #(Dietrich J., 1995)#.
As AIDS claimed ever more victims and gained ever
more media attention, the CDC's message that AIDS was a new infectious
disease was enthusiastically picked up by the stars of medical research,
particularly the virologists. A new infectious disease is a magnet
for virologists, microbiologists and immunologists because it holds
the promise for a new microbial pathogen and new vaccines. Since
the discovery of pathogenic microbes by Robert Koch and Louis Pasteur
in the 1880s, the identification of a new microbial pathogen has
been the key for many brilliant careers-like those of Walter Reed,
John Enders, and Albert Sabin. Stated the New York Times on
the search for an AIDS virus "... the greatest thrills for
a scientist are in discovering a new microbe, a new disease, cure
and prevention ..." #(Altman, 1992)#.
After decades of basic research in the War on Cancer,
an army of highly sophisticated virologists had failed to prove
that viruses can cause cancer in humans #(Greenberg, 1986; Booth,
1988)#. Among these were the current leaders of AIDS research, Luc
Montagnier from France, Robin Weiss from the U.K., David Baltimore,
Jay Levy, Robert Gallo and even Peter Duesberg from the U.S. among
others. Searching for other diseases for their viruses, most cancer
virologists welcomed AIDS as a new frontier to apply their considerable
skills #(Duesberg, 1987; Booth, 1988; Duesberg and Schwartz, 1992)#.
With an AIDS virus, the medical virologists could continue
their familiar research, and their companies could extend their
markets from the narrow confines of conventional virus tests and
vaccines to the new multi-billion dollar markets of HIV-antibody
tests, HIV vaccines, and anti-HIV drugs #(Weiss and Jaffe, 1990;
The AIDS virus also proved to be the politically
correct cause of AIDS. No AIDS risk group could be blamed for being
infected by a God-given egalitarian virus. A virus could reach all
of us. Nobody would be ostracized since "We are all in this
together." Not so with drugs: The consumption of illicit psychoactive
drugs implies individual and social responsibilities that nobody
wanted to face.
Once accepted as the politically correct explanation
of AIDS, the HIV hypothesis has become the central investment for
a whole generation of AIDS scientists, AIDS companies, AIDS journalists,
AIDS politicians and gay activists.
The perceived danger of an AIDS virus decimating
the general public also provided the scientific and moral arguments
for quick and unreflective action and for the complete dismissal
of the competing drug-AIDS hypothesis. The fear of nature's presumably
uncontrollable microbes created an unscientific war-mentality that
has since dominated the field #(Christie, 1994)#. Scientists, health
care workers, and journalists would rather be safe and fast in protecting
against HIV, than sorry and slow in reflecting about the clinical
and political consequences of drug use #(Lang, 1994)#. The confrontation
with man-made drugs, after all, would have to take second place
in urgency, as they would not reach the innocent public.
Claiming this priority, the virus-AIDS orthodoxy
justifies intolerance, even censorship, of all those who question
infectious AIDS #(San Francisco Project Inform, 1992; Maddox, 1993b;
Maddox, 1993a; Cohen, 1994a; Lang, 1994; see Chapter 12)#. Epidemiologists
from the CDC warn that to "ignore this [HIV-AIDS] concept would
result in an unconscionable tragedy." #(Garza, Drotman and
Jaffe, 1994)#. Virologists are quick to call those who question
the virus-AIDS hypothesis "irresponsible and pernicious"
#(Booth, 1988; Baltimore and Feinberg, 1989)#. And the New York
Times still calls all non-HIV science "cruelly irresponsible
anti-science" #(Lewis, 1994)#.
Therefore, the "AIDS virus" won unprecedented
popularity within a short time after its announcement.
But eleven years later, in 1995, the virus-AIDS hypothesis
has still failed to produce any public health benefits in the war
on AIDS. No vaccine, no antiviral drug, no cure, not even an effective
AIDS prevention have been developed. It cannot even be predicted
whether and when an infected person will get ill. And it cannot
predict which of the about 30 AIDS diseases it will be #(Duesberg,
1992; Benditt and Jasny, 1993; Cohen, 1994a; Cohen, 1994b; Wade,
1995)#. Moreover, the very basis of the virus-AIDS hypothesis, the
assumption that AIDS is infectious, has since become questionable
on several grounds. For example:
(1) Would you have believed AIDS is infectious 11
years ago, if you had known that until now not even one of the doctors
and health-care workers who have treated the over 400,000 American
AIDS patients since 1984 #(Centers for Disease Control and Prevention,
1994c)# is confirmed to have contracted AIDS from a patient? Even
if that would not have changed your mind, would you still believe
in infectious AIDS if you had considered that the health care workers
were neither protected by an anti-HIV vaccine nor by an antiviral
drug #(Duesberg, 1992)?
(2) Would you have believed that a sexually transmitted
virus was causing AIDS if you had known that none of the wives of
the 15,000 HIV-positive American hemophiliacs has contracted AIDS
from their husbands in the last 10 years? Their risk of developing
an AIDS-defining disease is the normal background of these diseases
in the U.S. #(Duesberg, 1992; Duesberg, 1995b)#.
(3) Would you have believed that AIDS was contagious
if you had known that after a marriage of 10 years, neither the
wife nor the 6-year old daughter of the late tennis star and AIDS
patient Arthur Ashe have developed AIDS or even become HIV-positive
#(Ashe and Rampersad, 1993)#; or that the long-term lover of the
movie star Rock Hudson has no AIDS symptoms, 10 years after Hudson
died from AIDS in 1985? Would you believe that AIDS was sexually
transmitted if you had known that, after a 13-year marriage and
2 children, the husband of the late AIDS patient Elizabeth Glaser
is healthy and HIV-free #(Champkin, 1994)#?
(4) Would you have believed in an AIDS virus if you
had known that nobody ever contracted Kaposi's sarcoma in the US
from a blood donor with Kaposi's sarcoma #(Haverkos, Drotman and
(5) Would you have believed AIDS is a sexually transmitted
disease in 1984 if you had known that 11 years later there is still
no AIDS in American heterosexuals, not even in prostitutes, unless
they are drug addicts #(Duesberg, 1992)#?
(6) Would you have believed in a sexually transmitted
AIDS virus if you had considered that such a virus would be incompatible
with life? Because sex is the only known source of human life, a
sexually transmitted, fatal virus would have exterminated itself
together with its host #(Duesberg, 1992)#.
Have we lost the war on AIDS because we have mistaken
a harmless virus for its real cause?
II. The HIV-AIDS hypothesis proves to be unprovable
The HIV-AIDS hypothesis #(Institute of Medicine,
1988; National Institute of Allergy and Infectious Diseases, 1994)#
1. HIV causes immunodeficiency by killing T-cells
2. immunodeficiency occurs on average only 10 years
after this virus has been neutralized by antiviral immunity-a condition
termed a "positive HIV test";
3. immunodeficiency is the basis for about 30 previously
known diseases, including pneumocystis pneumonia, tuberculosis,
candidiasis, Kaposi's sarcoma, dementia, diarrhea, >10% weight
loss, and many others (Table 1);
4. AIDS is a sexually transmitted disease, because
HIV is a sexually transmitted virus.
Owing to the immense popularity of this hypothesis,
over 100,000 scientific papers have been published on HIV since
1984. But not even one of these has been able to explain how
HIV causes AIDS. Worse yet, not one paper exists that proves
that HIV causes AIDS #(Duesberg, 1992; Dickson, 1994; Fields, 1994;
Schoch, 1994; Thomas Jr., Mullis and Johnson, 1994)#.
Circular Definition of Aids
In view of this proof-deficit, the HIV-AIDS establishment
cites the "perfect" correlation between HIV and AIDS as
support for the hypothesis that HIV causes AIDS #(Blattner, Gallo
and Temin, 1988; Weiss and Jaffe, 1990; San Francisco Project Inform,
1992; Maddox, 1993b; Garza, Drotman and Jaffe, 1994; National Institute
of Allergy and Infectious Diseases, 1994)#. However, this argument
is inadequate as an element of proof for three reasons:
(1) According to the HIV-AIDS hypothesis, the 30
AIDS-defining diseases are diagnosed as AIDS only when antibody
against HIV is present. In its absence these diseases are called
by their old name and caused by their old causes. In other words,
AIDS is defined entirely by its hypothetical cause, HIV. Therefore,
the perfect correlation is not a natural coincidence but a perfect
artifact of the definition of AIDS by its hypothetical cause, HIV.
It is one of the purest examples of circular logic.
(2) The HIV antibody-test for the detection of HIV
is indirect, because it does not assay for the virus. Moreover it
is not reliable; up to 90% false-positives are obtained, depending
on the subjects tested and on the tests used #(Duesberg, 1993f;
Papadopulos-Eleopulos, Turner and Papadimitriou, 1993)#.
(3) Even a perfect correlation is not sufficient
to prove causation. For example, perfect correlations between yellow
teeth and lung cancer, or between hospitalization and death do not
prove that one causes the other #(Duesberg, 1989; Smith and Phillips,
1992; Duesberg, 1993d).
Predictions of the HIV Hypothesis
In the absence of direct proof, the merit of a scientific
hypothesis is determined by the accuracy of its predictions. For
example, there is no direct proof for the hypothesis that smoking
causes lung cancer and emphysema, but the prediction that long-term
smoking causes these diseases has validated this hypothesis. In
the following we will analyze the predictions of the HIV-AIDS hypothesis
(1) HIV-infected persons will get AIDS, and otherwise
matched HIV-negatives will not. In the face of the relentless
propaganda for the HIV hypothesis, it comes as a big surprise to
almost everybody that there is not even one study to show that American,
heterosexual or homosexual men, who are HIV-positive but not drug
users or hemophiliacs ever get AIDS. More precisely, there is no
study to show that such men would get AIDS-defining diseases that
exceed the long-established, low background of these diseases in
otherwise matched, HIV-free counterparts #(Duesberg, 1995a, see
Chapter 10)#. There is not a single epidemiological study to support
the most frightening slogan of the HIV orthodoxy; that HIV-positives
develop AIDS-defining diseases because of HIV.
All studies that claim HIV causes AIDS have instead
analyzed the AIDS risks of HIV-positive people who were recreational
drug users, were treated with AZT or other anti-viral drugs, had
received transfusions, suffered from congenital diseases, or were
subject to exotic life styles as in Africa. The AIDS risks of such
groups were then determined by comparisons, either with normal HIV-free
people or with HIV-negative people from risk groups who were not
matched for drug use or other AIDS risks #(Duesberg, 1992; Duesberg,
1993a; Duesberg, 1993c; Duesberg, 1993d, see Chapter 8)#. In other
words, there is no epidemiological evidence properly controlled
for confounding factors that HIV is a "deadly virus" or
"the virus that causes AIDS."
In view of the enormous experimental difficulties
and costs in sorting out the possible role HIV plays in AIDS from
the roles that recreational drugs, AZT, transfusions, congenital
diseases and exotic life styles play, it is surprising that the
assumption that HIV causes AIDS has never been studied in people
who are free of confounding AIDS risks. There can only be one plausible
explanation for the absence of an epidemiological study that shows
that HIV causes AIDS in people who are not in risk groups: HIV does
not cause AIDS.
Indeed, there are 1 million HIV-positive Americans
#(National Institute of Allergy and Infectious Diseases, 1994)#
and 17 million HIV-positive humans #(Merson, 1993; World Health
Organization, 1995)# who are healthy, probably because they are
not subject to real AIDS risks other than the hypothetical AIDS
risk HIV. Moreover, HIV-positives who stop practicing risk behavior
or stop being subjected to AIDS risks even recover lost immunity-despite
the presence of HIV (see below Section VIII). For example, HIV-positive
hemophiliacs treated for 3 years with highly purified blood clotting
factor regained lost immunity, while controls treated with unpurified
blood products continued to lose immunity #(Seremetis et al.,
1993; Duesberg, 1995b and Chapter 11)#.
Thus HIV is only ever deadly for people who are at
risk for AIDS from toxic drugs or who depend on long-term blood
transfusions to treat underlying deadly diseases #(Duesberg, 1992,
see Chapter 6)#.
(2) American AIDS is new, because HIV is new in
America. However, in America HIV is a long-established
retrovirus #(Duesberg, 1992, see Chapter 6)#. Ever since the virus
could be detected in 1984, an unchanging 1 million Americans are
HIV-positive (Fig 1A) #(Curran et al., 1985; National Institute
of Allergy and Infectious Diseases, 1994, Farber, 1995b)#. By contrast,
a new microbe/virus spreads exponentially in a susceptible population
(see V). Thus the non-spread of HIV establishes it as an old virus
in America #(Duesberg, 1992)#.
(3) HIV is active and abundant in persons with
AIDS, and inactive and rare in healthy virus carriers. All
microbes cause diseases by killing or alterating a larger number
of target cells than the host can spare or regenerate during the
course of an infection. Thus HIV would have to infect and kill at
least 50% of all human T-cells to cause AIDS.
However, in AIDS patients HIV is found hibernating
in only 0.1% of T-cells, and biochemically active in less than 0.01%
of T-cells #(Duesberg, 1992; Duesberg, 1993e; Piatak et al.,
1993)#. Indeed, there are healthy HIV-positive people with 30- to
40-times more infected T-cells than in AIDS patients #(Simmonds
et al., 1990; Bagasra et al., 1992; Duesberg, 1992)#.
The fact that the vast majority of susceptible T-cells remain uninfected,
even in people dying from AIDS, is the definitive evidence that
there is no active HIV in HIV-antibody-positive persons. HIV is
neutralized by antiviral immunity, even in AIDS patients. If there
were un-neutralized HIV, all T-cells would be infected.
The fundamental problem for the HIV-hypothesis is
not just how HIV works, but how it causes fatal diseases when it
does not work at all. Since there is no rational explanation for
how HIV could cause AIDS, HIV researchers now postulate a multiplicity
of indirect mechanisms of pathogenesis #(Blattner, Gallo and Temin,
1988; Booth, 1988; Gallo, 1991; Maddox, 1991; Weiss et al.,
1992; Maddox, 1993b; Maddox, 1995; Wade, 1995; Wain-Hobson, 1995)#.
(4) HIV causes AIDS by killing T-cells. However,
viruses that integrate their genomes with that of the host, like
HIV, cannot kill the host cell. Since the genes of such viruses
are part of the host's genes, integrated viruses can only replicate
as long as the host survives integration and remains able to express
integrated viral genes. All integrated viruses survive from passive,
and some retroviruses also from active replication with the host.
This strategy only works if the host survives integration. If the
virus were to kill the cell as it is integrated, integration would
be a useless exercise and it would be undetectable. Indeed, HIV
is mass-produced for the "HIV test" in immortal T-cell
lines in cell culture at titers of 106 infectious units per ml #(Rubinstein,
1990; Karpas et al., 1992)#. Luc Montagnier, the discoverer
of HIV, and many other researchers have confirmed that HIV does
not kill T-cells #(Lemaitre et al., 1990; Duesberg, 1992)#.
(5) Since the generation time of HIV is two days,
HIV will cause AIDS two weeks after infection. The HIV-hypothesis
predicts AIDS within 2 weeks after infection, because HIV, like
all other retroviruses, replicates within two days. During that
time one infected cell produces at least 100 new viruses #(Weiss
et al., 1985)#. In the absence of antiviral immunity, these
100 viruses would in turn infect 100 cells producing 100 x 100 viruses,
or 104 infected cells within 4 days after infection. Within 14 days
of such exponential growth, 1014 cells -the equivalent of a human
body- would be infected. This is the typical latent period of proven
pathogenic retroviruses, like Rous sarcoma virus, and of pathogenic
human viruses like flu, measels, mumps, chicken pox, and herpes,
which all have generation times like HIV #(Fenner et al.,
1974; Mims and White, 1984)#.
However, if dated from the time of HIV infection,
AIDS occurs at totally unpredictable times. The latent period between
infection and AIDS was estimated to average 10 months in 1984 #(Auerbach
et al., 1984)#, 10 years in 1988 #(Institute of Medicine,
1988)# and over 20 years in HIV-positive hemophiliacs in 1994 #(Phillips
et al., 1994)#. A Berkeley mathematician recently has determined
the most accurate formula for the latent period of HIV, by subtracting
1984, the year when HIV was proposed to cause AIDS, from the current
calendar year. But blaming AIDS on a HIV infection that occured
10 years earlier is the logical equivalent of blaming today's broken
leg on stumbling over a crack in the sidewalk 10 years ago.
(6) Viral AIDS will spread exponentially ("explode"). The
AIDS orthodoxy has predicted that according to Farr's law #(Bregman
and Langmuir, 1990)#, AIDS would spread exponentially ("explode")
into the general, unimmunized population #(Duesberg, 1992)#-just
like all other new infectious diseases.
However, AIDS in America and Europe remained confined
to the original risk groups, i.e. male homosexuals practicing risk
behaviour and intravenous drug users #(National Commission on AIDS,
1991; Centers for Disease Control and Prevention, 1994b)#. Instead
of growing exponentially, AIDS in America (and Europe) has increased
slowly, over 15 years, far from reaching saturation of the susceptible
population of over 100 million sexually active adults (Fig. 1A).
AIDS behaved just like an occupational disease.
(7) The spread of AIDS will follow the dissemination
of HIV. However, there is no correlation between the spreads
of AIDS and HIV in America. In the last 10 years, AIDS increased
in America from a few hundred to about 100,000 cases annually (Fig.
1A) #(Centers for Disease Control and Prevention, 1994c)#. (The
burst of AIDS cases in 1993 is largely an artifact of the most recent
redefinition of AIDS, which nearly doubled the AIDS cases in one
year #(Centers for Disease Control and Prevention, 1994c)#.)
However, during those same 10 years HIV did not spread
at all (Fig. 1A). Ever since HIV became detectable in 1985, an unchanging
one million Americans have been HIV-positive up to 1994 (Fig. 1A)
#(Duesberg, 1992; Duesberg, 1994a; National Institute of Allergy
and Infectious Diseases, 1994)#. To hide this discrepancy, a latency
period of 10 years has been postulated between HIV and AIDS.
(8) Like all other sexually transmitted diseases,
AIDS in America will equilibrate between the sexes. However,
since 1981, AIDS has remained in the original risk groups in America,
i.e. male homosexuals, intravenous drug users of which over 75%
are males #(Duesberg, 1992)#, and hemophiliacs which are nearly
all males. Since 1981, 347,767 out of 401,749, or 87% of all American
AIDS cases, have been males #(Centers for Disease Control and Prevention,
(9) HIV is a sexually transmitted virus. However,
HIV could never survive in evolution from sexual transmission. Based
on studies of discordant couples, e.g. hemophiliacs with HIV and
spouses without, conducted by the CDC and others, it takes on average
1000 unprotected sexual contacts to transmit HIV #(Hearst and Hulley,
1988; Peterman et al., 1988; Rosenberg and Weiner, 1988;
Lawrence et al., 1990; Blattner, 1991)#. According to Rosenberg
and Weiner, "HIV infection in non-drug using prostitutes tends
to be low or absent, implying that sexual activity alone does not
place them at high risk." The efficiency of transmission in
homosexual contacts is also estimated at 1 in 1000 contacts #(Jacquez
et al., 1994)#.
Since about 10 to 30 sexual contacts are required
to generate a child, but 30 contacts are required to transmit HIV,
HIV could never survive natural selection on the basis of sexual
transmission, because the host would outgrow the parasite. Conventional
venereal microbes, like syphilis and gonorrhea, survive because
they are transmitted by about two sexual contacts #(Freeman, 1979)#.
HIV also could not survive from transmission to newborns if it were
fatally pathogenic to babies, as is claimed by the proponents of
the HIV hypothesis #(Blattner, Gallo and Temin, 1988; Institute
of Medicine, 1988)#.
The extremely low efficiency of sexual transmission
of HIV also predicts that the safe-sex-campaigns conducted by the
HIV orthodoxy will be of very limited value. Only those would benefit
who either have on average 1,000 sexual contacts with HIV positives
or those who have on average 250,000 contacts with average Americans,
of which only 1 million in 250 million is HIV positive (Fig. 1A)
#(Duesberg, 1992; National Institute of Allergy and Infectious Diseases,
(10) AIDS will be restricted by controlling sexual
transmission of HIV via "safe sex," and parenteral transmission
of HIV via "clean needles." But AIDS continues
to increase steadily despite the "safe sex" and "clean
needle" programs #(Centers for Disease Control and Prevention,
1994c)# (see Fig. 1A).
(11) Health-care workers will contract AIDS from
their patients, scientists from propagating virus, and prostitutes
from their clients. Not a single confirmed case exists
in the scientific literature of a health-care worker who contracted
AIDS #(Duesberg, 1992; Duesberg, 1994a)# from one of the over 400,000
American AIDS patients #(Centers for Disease Control and Prevention,
1994c)#. None of the tens of thousands of HIV researchers have developed
AIDS from propagating HIV. And no prostitutes picked up AIDS from
their clients-despite the absence of antiviral vaccines or effective
anti-HIV drugs #(Duesberg, 1992; Duesberg, 1994a)#.
A few unpublished cases have been claimed, but each
of these seemed to have been treated with the cytotoxic drug AZT
that is sufficient to cause immunodeficiency (see below) #(Cohen,
(12) Chimpanzees inoculated with HIV will develop
AIDS, and the 15,000 American hemophiliacs who were infected by
transfusions before 1984 will die from AIDS. Not one of
the 150 chimpanzees inoculated with HIV since 1983 has developed
AIDS #(Duesberg, 1992)#. Contrary to prediction, the median life
of American hemophiliacs has increased 2.5-fold from 11 to 27 years
between 1972 and 1987 #(Institute of Medicine, 1988; Stehr-Green
et al., 1989)#, although 75% (15,000) were infected with
HIV by transfusions received before 1984 #(Duesberg, 1992)#. However,
in 1987 the median life of HIV-positive hemophiliacs started to
decrease again #(Chorba et al., 1994)# because since then
they have been treated with the cytotoxic AZT #(Duesberg, 1995b,
See Chapter 11)# (see below).
(13) Natural or vaccine-induced anti-HIV immunity
will cure AIDS or protect against future AIDS. Natural
antiviral immunity, a positive HIV-test, is observed in many AIDS
patients, but does not protect against AIDS. Paradoxically, anti-HIV
immunity is by HIV-AIDS definition the only criterion to predict
who gets AIDS. With all other viruses and microbes -there is no
exception- immunity is the only criterion to predict who does not
get a disease. It is for this reason that antiviral/microbial immunity
is artificially induced by vaccination. It is also for this reason
that the HIV-AIDS establishment has called for an HIV vaccine since
(14) All AIDS diseases are consequences of HIV-mediated
T-cell deficiency. Indeed, up to 1992 about 61% of all
American AIDS diseases, the microbial diseases such as Pneumocystis
carinii, candida, tuberculosis, etc. were consequences of Acquired
ImmunoDeficiency (Table 1) #(Centers for Disease Control, 1993)#.
However, 39% were neither caused by, nor consistently
associated with, immunodeficiency. These include Kaposi's sarcoma,
lymphoma, >10% weight loss, and dementia (Table 1). Accordingly,
Kaposi's sarcoma and dementia have been diagnosed in male homosexuals
whose immune systems were normal #(Murray et al., 1988; Spornraft
et al., 1988; Gill et al., 1989; Friedman-Kien et
al., 1990; Duesberg, 1992; Kaldor et al., 1993; Bacellar
et al., 1994)#.
the CDC introduced, once more, a new AIDS definition #(Centers for
Disease Control and Prevention, 1992)#. This has shifted the balance
of immunodeficiency to non-immunodeficiency AIDS diseases significantly
in favour of immunodeficiency diseases, i.e. from 61% to 80% (Table
1) #(Centers for Disease Control and Prevention, 1994a)#. The critical
innovation of this new definition was that a healthy person with
less than 200 T-cells, but with no clinical disease, would now be
registered as an AIDS patient. The new AIDS definition nearly doubled
the new AIDS cases, thus adding new life to the sagging curves of
the American AIDS statistics (Fig. 1A). However, if one substracts
from the 1993 statistics the new AIDS cases with less than 200 T-cells,
the ratio of the remaining real immunodeficiency diseases to the
non-immunodeficiency diseases is almost the same as in 1992.
Imagine the rationalizations an unprejudiced virologist,
who is aware of the heterogeneity of AIDS-defining diseases, must
make to accommodate an AIDS virus. Ever since Koch and Pasteur,
microbiologists and virologists were taught that a specific microbe
or virus would cause a specific disease-e.g. polio, flu, measels,
chicken pox, hepatitis, etc.-just like a particular musical instrument
would make specific sounds.
To accommodate the AIDS virus, the concept of a specific
microbe causing a specific disease had to be abandoned for the following
bewildering scenario: By picking up the AIDS virus from a diarrhea
patient, a person would get Kaposi's sarcoma. The Kaposi patient
would then be able to cause dementia or pneumonia in others by passing
on the diarrhea virus, just as the CDC's sexual contact study had
claimed in 1984 #(Auerbach et al., 1984)#. As of 1993, any
one of these patients could have also caused a clinically undetectable
depletion of T-cells in others, again by passing on their diarrhea,
dementia, Kaposi's sarcoma and pneumonia virus.
Moreover, the unprejudiced virologist would have
to reconcile this bewildering pathogenic potential of HIV with the
fact that HIV is one of the most primitive viruses in terms of genetic
information that exist, carrying only 9,000 nucleotides. This is
the viral equivalent of a musical instrument that is said to sound
like an orchestra, although it only has the repertoire of a bell.
(15) If HIV is the cause of AIDS, the percent
incidence of AIDS diseases will be the same in all risk groups. However,
the percent incidence of AIDS-defining diseases is very different
in different risk groups. For example, Kaposi's sarcoma in America
and Europe is almost exclusively observed in male homosexuals #(Beral
et al., 1990)#. Intravenous drug users have a proclivity
for tuberculosis, weight loss, and pneumonia #(Duesberg, 1992)#
and a very high mortality dying at 30 years #(Lockemann et al.,
1995)#. Pneumonia and candidiasis are virtually the only AIDS diseases
ever diagnosed in hemophiliacs #(Duesberg, 1992; Duesberg, 1995b)#.
And bacterial infections other than tuberculosis are almost exclusively
diagnosed in babies with AIDS #(Centers for Disease Control, 1987;
Centers for Disease Control and Prevention, 1992; Duesberg, 1992,
see Chapter 6)#. Thus the percent incidence of an AIDS diseases
is very different in different AIDS risk groups.
In view of this, some AIDS researchers cite co-factors
of HIV, such as recreational drugs and immunosuppressive transfusions,
as explanations for risk group-specific diseases #(Evans, 1989;
Duesberg, 1992; Ludlam, 1992; Root-Bernstein, 1995a)#. However,
they fail to provide evidence that such cofactors depend on the
cofactor HIV to be pathogenic.
The CDC and other mainstream AIDS researchers insist
that recreational drugs and transfusions solely enhance the risk
to get infected by HIV, rather than playing causative roles in AIDS
#(Cohen, 1994a)#. It is for this reason that the CDC refers to drug-
or transfusion-risk groups as "exposure categories" #(Centers
for Disease Control and Prevention, 1994a)#. In fact, the CDC obscures
the existence of risk-group-specific AIDS diseases by reporting
only the percent incidence of AIDS diseases in all risk groups combined
#(Centers for Disease Control and Prevention, 1994a)#.
It is evident that the HIV-AIDS hypothesis is unable
to make even one verifiable prediction-the hallmark of a failed
Even if a hypothesis fails to make valid predictions
in terms of established scientific criteria, it could by chance
lead to a valid prevention or treatment. But the HIV-AIDS hypothesis
has not lead to any public health benefit. Instead it has harmed
not only AIDS patients but also healthy persons who are at risk
for AIDS or just antibody-positive (see VI).
III. HIV-a harmless passenger virus
Confronted with the evidence that the HIV-AIDS hypothesis
has failed to make valid predictions and failed to lead to public
health benefits, many agree that HIV may not cause AIDS. But then,
they wonder: What does HIV do?
Indeed, all viruses are generally assumed to be pathogenic
by an unsuspecting public, because a few of them actually are. Likewise,
a whole nation is often stereotyped by the characteristics of a
minority. For example the French are considered great lovers and
the Italians great singers, because a few of them are great lovers
and singers. The same is true for viruses.
In reality, most viruses cause no disease at all.
Viruses are not here to kill their hosts, not even to cause disease.
Instead, viruses are here for exactly the same reasons we are, to
continue their species. This goal can only be achieved by keeping
the host species alive, and it is achieved best if every host survives
the infection. That is the reason that most viruses never cause
a disease in their host. Therefore they are called passenger
viruses. Passenger viruses are those that take a ride on the
host, but demand no more from the host than a passenger demands
from an airplane (see Chapter 9).
Since HIV is not the cause of AIDS, the simplest
and most plausible HIV hypothesis postulates that HIV is just a
passenger virus #(Duesberg, 1994a)#. A passenger virus is defined
(1) The time of infection is irrelevant to the onset
of any disease.
(2) The passenger virus can be either active or passive,
either rare or abundant during any disease.
(3) The passenger virus can be entirely absent during
(4) If the passenger virus is de-repressed by a failing
immune system, as for example during a disease, the passenger virus
may or may not contribute to the disease. For example HHV-6 #(Cone
et al., 1994)# or cytomegalovirus may contribute their specific
pathogenic properties to an immunodeficient patient.
HIV meets all these criteria with regard to its relation
(1) HIV infects at totally unpredictable times prior
to or even after the onset of AIDS (see VIII below) or not at all
#(Duesberg, 1992; Phair et al., 1992; Duesberg, 1993f)#.
(2) HIV is typically passive and rare during AIDS-hence
the notorious difficulties of leading AIDS researchers in isolating
HIV from AIDS patients #(Duesberg, 1992, see Chapter 6)#.
(3) There are thousands of HIV-free AIDS cases, e.g.
HIV-free homosexuals with Kaposi's sarcoma and HIV-free intravenous
drug users with tuberculosis #(Duesberg, 1993f, see Chapter 7)#.
(4) There is no report in the literature that AIDS
patients are clinically distinguishable from each other because
HIV is active or passive or not present at all #(Duesberg, 1993b;
Duesberg, 1994a)#. Thus HIV is a harmless passenger virus, even
when it is active in some rare immunodeficient persons #(Duesberg,
If this is true, there should be many more HIV carriers
than AIDS patients. Indeed, there are 1 million healthy HIV-positive
Americans #(Duesberg, 1992; Duesberg, 1994a)# and there are 17 million
healthy HIV-positive humans #(Merson, 1993; National Institute of
Allergy and Infectious Diseases, 1994; World Health Organization,
Nevertheless, there is some tenuous evidence that
HIV can function as an autonomous pathogen, causing a mild flu-like
or mononucleosis-like condition, prior to antiviral immunity #(Albert
et al., 1987; Duesberg, 1987; Kessler et al., 1987;
Gaines et al., 1988; Marcus and the CDC Cooperative Needlestick
Surveillance Group, 1988; Tindall et al., 1988; Pedersen
et al., 1990; Duesberg, 1992; Niu, Stein and Schnittmann,
1993, see Chapters 1, 6)#. However, in millions of HIV-positives
HIV infection has gone unnoticed, because they do not experience
a characteristic HIV-disease prior to antiviral immunity-like measles,
mumps or flu which all occur prior to immunity against these viral
The rare cases in which HIV infections, prior to
antiviral immunity, have been linked with mononucleosis or flu-like
symptoms are restricted to prospective studies of male homosexuals
at risk for AIDS. These cases could either be coincidences with
a common cold or with intoxications from recreational drug use (see
below) #(Gaines et al., 1988; Tindall et al., 1988;
Pedersen et al., 1990)# rather than evidence for HIV disease.
IV. HIV-a marker for AIDS risks
Even those who understand all virological arguments
against HIV as the cause of AIDS, and for HIV as a passenger virus,
have misgivings about dismissing the HIV-AIDS hypothesis, because
HIV is more common in AIDS patients than in the healthy population.
This sounds like an ominous connection, but only if it is taken
out of its trivial microbiological context.
This trivial context is that AIDS risk behavior is
synonymous with collecting microbes. The common denominator
of all AIDS risk groups in America and Europe is that they collect
microbes either from unsterile drugs injected with unsterile equipment,
or from the thousands of drug-mediated sexual contacts, that are
required to transmit HIV sexually, or from transfusions received
for the treatment of illnesses #(Jaffe et al., 1983; Auerbach
et al., 1984; Lauritsen and Wilson, 1986; Haverkos and Dougherty,
1988; Rappoport, 1988; Adams, 1989; Callen, 1990; Lifson et al.,
1990; Archibald et al., 1992; Duesberg, 1992; Jones, 1994;
Mullis, 1995)#. This is the reason that numerous uncommon microbes
are common not only in AIDS patients but also in healthy persons
from AIDS risk groups. For example, the bacteria that cause syphilis,
gonorrhea, and tuberculosis, the hepatitis virus, rare strains of
herpes virus, putative leukemia virus, genital papilloma virus,
and even HIV are all common in AIDS risk groups and AIDS patients
but uncommon in the general population #(Duesberg, 1992, see Chapter
6)#. Thus HIV is just one of many microbial markers of AIDS risk
behavior. Since AIDS is defined as one of 30 diseases in the presence
of HIV, rather than any other microbial or viral marker, the correlation
between HIV and AIDS is in theory 100%.
V. The myth of infectious AIDS-unconfirmed
If a hypothesis is unproductive, and unable to make
verifiable predictions, the scientific method calls for alternative
hypotheses. To find the correct AIDS hypothesis, we need to decide
first whether to look for other viruses and microbes or for drugs
as causes of AIDS. In other words, we need to know whether AIDS
is infectious or not.
There are five classic criteria to define an infectious
(1) The causative microbe/virus is abundant and very
active in target tissues during the course of the disease.
(2) The disease follows within days or weeks after
infection, because microbes/viruses multiply exponentially with
generation times of 0.5 to 48 hrs, unless they are stopped by immunity
(3) The disease spreads, according to Farr's law,
exponentially in an un-immunized population within weeks or months,
and subsequently fades away as antiviral immunity builds up #(Bregman
and Langmuir, 1990)#. The bell shaped curve of a seasonal flu epidemic
is the model.
(4) Infectious diseases are equally distributed between
(5) Infectious diseases are most commonly observed
in those under 20 and over 60 years of age. This is because after
birth the immune system builds up a wide repertoire of antimicrobial
resistances that is nearly complete at 20, and over 60 the system
begins to decline.
But American/European AIDS does not fit one of these
(1) There is no abundant microbe common to all American
AIDS cases. If HIV is present, it is typically rare and hibernating.
(2) If dated from the time of HIV infection, AIDS
occurs at entirely unpredictable times ranging from less than 1
year to over 10 years or never. It has now been 10 years since 1
million Americans were found to be HIV-infected. Most of these and
17 million healthy, HIV-positive non-Americans are still waiting
for HIV to cause AIDS.
(3) American AIDS has slowly increased over 10 years.
Although AIDS affects annually only a small fraction of susceptible
persons-less than 100,000 out of a susceptible pool of 250 million
Americans-it has has now almost plateaued for 4 years [after adjusting
for new additions of diseases to the AIDS definition] #(Centers
for Disease Control and Prevention, 1994b)#. Thus AIDS in America
has increased steadily over years, just like an occupational disease,
as for example lung cancer from smoking. There is no evidence for
immunity and no evidence for a bell shaped AIDS curve.
(4) American AIDS is 87% male #(Centers for Disease
Control and Prevention, 1994c)#, which is epidemiologically as far
from equality between the sexes as the sun is from the earth. A
similar sexual bias has been observed early in the epidemic of smoking-related
diseases in the 1960s, before women picked up smoking at the same
rate as men.
(5) 98% of all American AIDS cases are over 20 and
under 60 #(Centers for Disease Control and Prevention, 1994c)#.
Only 1% each are under 20 and over 60! Such an age bias is typical
of occupational diseases, like bullet wounds for soldiers.
Thus AIDS in America and Europe #(Duesberg, 1992)#
does not meet even one of the criteria of infectious disease.
Indeed, even proponents of the HIV-AIDS hypothesis,
such as Jaap Goudsmit from the University of Amsterdam, grant that
"AIDS does not have the characteristics of an ordinary infectious
disease. This view is incontrovertible" #(Goudsmit, 1992)#.
The AIDS epidemiologists Eggers and Weyer from the University of
Cologne state that "the spread of AIDS does not behave like
the spread of a disease that is caused by a single sexually transmitted
agent" #(Eggers and Weyer, 1991)#. To reconcile AIDS with infectious
disease they "simulated a cofactor [that] cannot be identified
with any known infectious agent." The epidemiologists Anderson
and May from the University of London had to invent "assortative
scenarios" for different AIDS risk groups to match AIDS with
infectious disease #(Anderson and May, 1992)#.
Until we have scientific evidence, infectious AIDS
is just a myth-and, in view of the facts, a very implausible myth
VI. The HIV-AIDS hypothesis is costly,
unproductive and harmful
For 11 years now the world has fought the war on
AIDS united by the HIV-AIDS hypothesis. But despite its enormous
popularity, the virus-AIDS hypothesis has been a complete failure
in terms of public health benefits: no vaccine has been developed
that prevents AIDS, no drug that cures AIDS, no policy that stops
the spread of AIDS #(Benditt and Jasny, 1993; Fields, 1994; Swinbanks,
1994; Wade, 1995)#.
Whatever the reasons are for the complete failure
of the HIV-AIDS hypothesis to produce public health benefits, one
thing is clear: it was not for lack of trying. The passionate complaint
of Shilts' 1987 book, And the Band Played On, that indifference
was the only obstacle against a solution of AIDS #(Shilts, 1987)#
has long become profoundly obsolete. Since 1984, an unprecedented
$35 billion has been paid by the US taxpayer alone in support of
HIV-AIDS research and treatment-more than for all other viral and
microbial diseases combined #(AIDS Weekly, 1995; Gutknecht, 1995;
Henry, 1995; Stone and Cohen, 1995)#. With all this spending, more
research has been done on HIV than on any other virus in history,
but absolutely no progress has been made against AIDS. Time, at
least, has voted against the HIV-hypothesis. Traditionally, such
complete failures are the consequences of a flawed hypothesis.
But the HIV-AIDS establishment does not only cost
dearly and fails to produce positive results, it also causes irreparable
(1) clinical, (2) educational, and (3) psychological damage:
(1) Clinical damage. Worldwide about 200,000
HIV antibody-positive persons are prescribed, every six hours, the
highly toxic DNA chain terminator AZT or equivalents like ddI, ddC,
and d4T as anti-HIV drugs #(Duesberg, 1992; Thomas, 1995)#. Most
of these, ie. 200,000 minus the 50,000 to 80,000 annual AIDS patients
in America and Europe, are healthy HIV-positives given AZT to prevent
AIDS. Recently these include even unborn American and French children
and their HIV-positive mothers, although the risk of such children
to pick up HIV from their mothers is only about 25% #(The Lancet,
1994; Farber, 1995a)#.
AZT was designed 30 years ago to kill growing human
cells for cancer chemotherapy #(Horwitz, Chua and Noel, 1964; Duesberg,
1992)#. In view of its inevitable toxicity, AZT was approved as
an anti-HIV drug only tentatively in 1987 #(Kolata, 1987)#. See
the warnings of a non-medical manufacturer, Sigma, on the label
of an AZT bottle (Fig. 2). The label points out, with skull and
cross bones, AZTs toxicity to the bone marrow, the source of T-cells.
Indeed, AZT therapy of HIV appears harmful and irrational.
Since HIV is postulated to cause AIDS by killing T-cells (see above),
it is irrational to kill the same HIV-infected cells twice-once
with HIV and again with AZT. Moreover, it is harmful to kill numerous
uninfected cells with AZT collaterally #(Kolata, 1987; Lauritsen,
1990; Nussbaum, 1990; Wyatt, 1994)#.
Accordingly, AZT has failed to cure even one AIDS
patient or to prevent AIDS in HIV-infected persons #(Duesberg, 1992;
Oddone et al., 1993; Tokars et al., 1993; Bacellar
et al., 1994; Goedert et al., 1994; Lenderking et
al., 1994; Seligmann et al., 1994, Volberding, 1995,
Ho, 1995)#. Instead, evidence is growing that AZT causes AIDS-defining
and other diseases as expected from a chain terminator of DNA synthesis
(see below) #(Mir and Costello, 1988; Lauritsen, 1990; Duesberg,
1992; Lauritsen, 1992; Bacellar et al., 1994; Cohen, 1994a;
Duesberg, 1994a; Goedert et al., 1994; Lewis-Thorton, 1994)#.
Yet this evidence is either denied or belittled by the AIDS establishment
as the following examples document:
(i) The observation that "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" #(Bacellar
et al., 1994)#.
Goedert et al., explain their 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-by
saying this happened "probably because zidovudine was administered
first to those whom clinicians considered to be at highest risk"
#(Goedert et al., 1994)#.
(ii) 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..." #(Saah
et al., 1995)#. The fact that an inhibitor of DNA synthesis
designed to kill human cells would inhibit lymphocyte growth was
(iii) 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 #(Poznansky et al., 1995)#.
(iv) The largest test of AIDS prophylaxis with AZT
of its kind, the Concorde trial, found a 25% higher mortality in
AZT recipients than in untreated controls. In view of this Seligmann
et al., reached the conservative conclusion: "The results
of Concorde do not encourage the early use of zidovudine [AZT] in
symptom-free HIV-infected adults" #(Seligmann et al.,
(v) Five years after introducing AZT prophylaxis
to several hundred thousands of healthy HIV-positives, Paul Volberding
of the University of California at San Francisco, Anthony Fauci
of the National Institute of Allergy and Infectious Diseases and
over 100 scientific collaborators now publish in the New England
Journal of Medicine: "Zidovudine ... does not significantly
prolong either AIDS-free or overall survival. These results do not
encourage the routine use of Zidovudine" (Volberding et
al., 1995). In an accompanying editorial "Time to hit HIV,
early and hard" the "Journal" makes the forward recommendation
to treat HIV infection with AZT and other experimental drugs before
antiviral immunity restricts the virus to chronic latency (Ho, 1995).
The article suggests that current AZT prophylaxis is too little
too late. This is said although the ineffectiveness of the proposed
"early and hard" treatment is known since 1993 (Tokars
et al., 1993).
(vi) The occurence of 8 serious birth defects, 8
spontaneous abortions and 8 therapeutic abortions among 104 pregnancies
treated with AZT is interpreted as "not proving safety, thus
lending tenous support to the use of this drug." #(Kumar, Hughes
and Khurranna, 1994)#.
AZT must be considered the most toxic among legal
public health threats available to healthy persons, much more toxic
than alcohol and tobacco. For this reason I have termed AZT AIDS
by prescription #(Duesberg, 1992, see Chapter 6)#. Even Burroughs
Wellcome, the manufacturer of AZT, makes that same assessment, but
expresses it in different words: "It was often difficult to
distinguish adverse events possibly associated with zidovudine [AZT]
administration from underlying signs of HIV disease..." #(Physicians'
Desk Reference, 1994)#.
(2) Educational damage. Since HIV, but not drugs, is thought
to cause AIDS, the HIV-AIDS establishment educates the public to
use "clean needles" for the injection of unsterile (!)
street drugs and to wear condoms for sex under the influence of
aphrodisiac drugs #(Institute of Medicine, 1988; San Francisco Project
Inform, 1992; Benditt and Jasny, 1993; National Institute of Allergy
and Infectious Diseases, 1994)#. However, the disregard, in fact
explicit dismissal, of drug toxicity by the AIDS establishment #(Weiss
and Jaffe, 1990; Ascher et al., 1993; Duesberg, 1993d; Maddox,
1993a; Schechter et al., 1993b; Schechter et al.,
1993c; Cohen, 1994a)# encourages recreational drug use because it
eliminates the fear of drug toxicity. A popular joke illustrates
this point: "Two junkies are reminded by a friend not to share
a syringe full of cocaine. Their response: 'We wear condoms and
use a clean needle'."
Yet long-term use of recreational drugs, including cocaine, heroin,
amyl- and isobutyl nitrite inhalants, amphetamines, and others has
been documented in numerous studies to cause exactly the same diseases
that are now blamed on HIV #(Haverkos and Dougherty, 1988; Stoneburner
et al., 1988; Lerner, 1989; Duesberg, 1992, see Chapter 6)#.
The list of drug-induced diseases, established long before the discovery
of HIV, reads like a catalogue of AIDS-defining diseases: weight
loss, fever, dementia, tuberculosis, oral thrush, pneumonia, diarrhea,
mouth infections, night sweats, and many others (see below) #(Lerner,
1989; Duesberg, 1992)#.
(3) Psychological damage. According to the HIV-AIDS establishment,
nearly all HIV-infected, healthy persons are claimed to die from
AIDS on average 10 years after infection by HIV #(Institute of Medicine,
1988; Garza, Drotman and Jaffe, 1994; National Institute of Allergy
and Infectious Diseases, 1994; Thomas Jr., Mullis and Johnson, 1994).
In view of this, one million HIV-positive but healthy Americans,
and 17 million HIV-positive but healthy humans on this planet #(Merson,
1993; National Institute of Allergy and Infectious Diseases, 1994;
World Health Organization, 1995)#, are subjected to a multiplicity
of psychological and sociological pressures #(Anonymous, 1992; Duesberg,
1992; Schmalz, 1992b; Schmalz, 1992a; Miami Herald, 1994; Yarbo,
They are given a death sentence by the medical establishment for
being HIV-positive; they are denied coverage by health insurance
companies; they lose their jobs and social status; they are denied
entrance visas to many countries including the U.S.; they are denied
employment by the US Army; and worst of all they are pressured to
accept the toxic AZT therapy-all of this, only because they have
made antibodies against a virus that is presumed to cause AIDS.
If they refuse to submit to these pressures, they are charged with
denial (of the HIV-AIDS hypothesis) by the AIDS establishment
#(Moss, Osmond and Bacchetti, 1988; San Francisco Project Inform,
In sum, the public health record of the HIV-AIDS hypothesis in
America adds up to a staggering deficit: for $35 billion #(Duesberg,
1994b; AIDS Weekly, 1995; Gutknecht, 1995)# there is no cure, no
vaccine, no effective prevention, hundreds of thousands are subjected
to psychological pressures resulting from positive HIV-tests, and
several million American drug addicts are denied available information
that recreational drugs cause AIDS-defining and other diseases #(Drug
Strategies, 1995)#, and about 150,000 are subjected annually to
AZT poisoning-many just for being HIV-positive, not for having AIDS
VII. The drug-AIDS hypothesis
Given no evidence for infectious AIDS, the reasons
for the original "lifestyle hypothesis," and the logic
of Sherlock Holmes-that "when you have eliminated the impossible,
whatever remains however improbable must be the truth"-AIDS
must be non-infectious.
In view of this I propose that:
All AIDS diseases in America and
Europe that exceed their long-established, normal backgrounds are
caused by the long-term consumption of recreational drugs and by
AZT and its analogs.
Hemophilia-AIDS, transfusion-AIDS, and the extremely
rare AIDS cases of the general population reflect the normal incidence
plus the AZT-induced incidence of these diseases under a new name.
African AIDS is a new name for old diseases
caused by malnutrition, parasitic infections and poor sanitation
#(Duesberg, 1991; Duesberg, 1992; Duesberg, 1994a, see Chapters
6 and 9).
Indeed, the recreational drug use epidemics, that
started in America and Europe during the Vietnam war, are the only
new health risk of the Western World since World War II. Since its
beginnings the drug use and AIDS epidemics in the US and Europe
have coincided both epidemiologically and chronologically #(Duesberg,
1992)#. About 33% of all American AIDS patients, nearly all heterosexual
AIDS patients, are intravenous drug users #(Centers for Disease
Control and Prevention, 1994b)#. Over 60% are male homosexuals who
have used psychoactive and aphrodisiac drugs orally such as nitrite
inhalants, amphetamines, cocaine and phenylcyclidine (Table 2).
Many of these recreational drug users and most of the few AIDS patients
who have not used recreational drugs have used AZT and cytotoxic
DNA chain terminators as anti-HIV drugs (see below) #(Duesberg,
1992; Duesberg, 1994a)#. Allowing a "latent period of 10 years"
for chronic recreational drug use to cause AIDS, the beginning of
the American drug use epidemics in the late 1960s and 1970s predicts
exactly the origin of AIDS in the 1980s.
Unlike the virus-AIDS hypothesis, the drug hypothesis
has a plausible chemical and experimentally testable basis. The
recreational drugs postulated to cause AIDS have strong biochemical
and psychoactive effects every time they are taken-the reason for
their popularity (see Chapter 6).
By contrast, HIV is latent, and neither chemically nor clinically
detectable in "HIV antibody-positives" with and without
AIDS. Despite 11 years of unprecedented research efforts no biochemical
evidence has been found in support of the HIV-AIDS hypothesis (Cohen
The specific toxicity and dosages of recreational
and medical drugs used by American and European AIDS risk groups
can explain all AIDS diseases #(Duesberg, 1992)#. AIDS drugs are
either indirectly toxic, or cytotoxic, or genotoxic and cytotoxic.
(1) Indirectly toxic. Cocaine, amphetamines
and heroin are indirectly immunotoxic. All three function as catalysts
in the human body. Cocaine and heroin are natural compounds and
amphetamines are synthetic adrenalins first developed in Germany
during World War II to suppress fatigue and anxiety in pilots and
tank commanders #(Weil and Rosen, 1983)#.
Indirect toxicity is the result of malnutrition and
insomnia which in turn are consequences of drug-induced suppression
of appetite and fatigue #(Layon et al., 1984; Lerner, 1989;
Pillai, Nair and Watson, 1991; Duesberg, 1992; Larrat and Zierler,
1993; Mientjes et al., 1993; Sadownick, 1994)#. These problems
are compounded by poverty due to the enormous costs of illicit drugs.
Direct, long-term pathogenic effects of cocaine and heroin have
not been studied owing to the general disregard of drug toxicity
(2) Cytotoxic and genotoxic. Nitrite inhalants
are cytotoxic, and thus are immunotoxic in animals and humans #(Goedert
et al., 1982; Haverkos and Dougherty, 1988)#. A recreational
dose of 1 ml per day #(Haverkos and Dougherty, 1988; Duesberg, 1992)#
corresponds to about 15 ppm in a 75 kg-person, and corresponds to
107 nitrite molecules for everyone of the 1014 cells in the human
body. The cytotoxicity of nitrites on the epithelial tissues of
the lung are enhanced by the toxins of cigarette smoke, which also
suppresses the immunesystem #(Nieman et al., 1993).
In addition nitrite inhalants are among the best
established mutagens and carcinogens #(National Research Council,
1982; Lewis, 1989; Winter, 1989; Mirvish et al., 1993)#.
In view of the toxicity of nitrite inhalants, a prescription requirement
was instated by the US Food and Drug Administration in 1969 #(Newell
et al., 1985a)#, and because of an "AIDS link"
#(Cox, 1986)# the sale of nitrites was banned by the U.S. Congress
in 1988 (Public Law 100-690) #(Haverkos, 1990)# and by the "Crime
Control Act of 1990" #(Duesberg, 1992)#. Moreover, the US Food
and Drug Administration limits nitrites as food preservatives to
less than 200 ppm, because of direct toxicity and because "they
have been implicated in an increased incidence of cancer" #(Lewis,
1989, National Research Council, 1982)#.
(3) Genotoxic-cytotoxic. AZT, ddI and other
DNA chain terminators are directly toxic by killing all growing
cells, in particular the fastest growing ones-the hematopoietic
and epithelial cells (Fig. 2), #(Merck Research Laboratories, 1992;
Chiu and Duesberg, 1995)#. In addition, AZT prevents mitochondrial
DNA synthesis in non-growing cells, such as neurons or muscles,
and can be carcinogenic by mutating cells #(Pluda et al.,
1990; Duesberg, 1992; Parker and Cheng, 1994)#.
The key to the drug hypothesis is that only long-term
consumption causes irreversible AIDS-defining diseases. Occasional
or short-term recreational drug use causes reversible diseases or
no diseases at all. With drugs, the dose is the poison. Yet,
most studies investigating the effects of recreational drugs are
concerned with their short-term psychoactive rather with their long-term
clinical effects #(Duesberg, 1992). For example, it takes 20 years
of smoking to acquire irreversible lung cancer or emphysema,
and 20 years of drinking to acquire irreversible liver cirrhosis.
In contrast to drugs, infectious agents are self-replicating toxins.
By multiplying exponentially in the body infectious agents may generate
sufficient doses of toxic substances to cause diseases within days
Since currently no experiments are being done in
America to test the drug hypothesis, I have evaluated the drug-AIDS
hypothesis on the basis of its predictions. In contrast to the HIV-AIDS
hypothesis, the drug hypothesis can predict all parameters of American/European
IX. The drug-hypothesis predicts the American/European
(1) AIDS is restricted to intravenous and oral
users of recreational drugs and of AZT, because drugs cause AIDS.
Since 1981 94% of all American AIDS cases have been
from risk groups who had used such drugs #(Centers for Disease Control
and Prevention, 1994c)#. About one-third of these were intravenous
drug users #(Centers for Disease Control, 1993)# and two-thirds
were male homosexuals #(Centers for Disease Control and Prevention,
1994c; Centers for Disease Control and Prevention, 1994a)# who had
used oral recreational drugs and AZT #(Duesberg, 1992; Ascher et
al., 1993; Duesberg, 1993c; Duesberg, 1993a; Duesberg, 1993d;
Parke, 1993; Schechter et al., 1993b)#. HIV-positive hemophiliacs
and transfusion recipients also receive AZT as an antiviral drug
#(Duesberg, 1992; Duesberg, 1995b)#. (However, a small percentage
of hemophiliacs annually develop a specific subset of AIDS-defining
immunodeficiency diseases, mostly pneumonia and candidiasis, only
from the long-term transfusion of foreign proteins that contaminate
commercial factor VIII #(Duesberg, 1992; Duesberg, 1995b, see Chapter
11#). European AIDS also correlates with drug consumption #(Duesberg,
1992, see Chapter 6)#.
(2) American/European AIDS predominantly affects
adult males, because they are the predominant users of recreational
drugs and AZT.
The CDC reports that 87% of all American AIDS patients
are males #(Centers for Disease Control and Prevention, 1994c)#.
This number is the sum of the following constituents: The National
Institute on Drug Abuse and the Bureau of Justice Statistics report
that over 75% of hard, recreational drugs are consumed intravenously
by males #(Duesberg, 1992, see Chapter 6).
According to the federally supported Drug Strategies
program "women account for the fastest-growing population in
jails and prisons, in large part because of drug offenses"
#(Drug Strategies, 1995)#. Therefore the CDC reports that women
are now the fastest growing AIDS risk group #(Centers for Disease
Control, 1994; Centers for Disease Control and Prevention, 1994a)#.
The CDC and independent investigators report that
nearly all male homosexuals with AIDS and at risk for AIDS are long-term
users of oral drugs such as nitrite inhalants, ethylchloride inhalants,
amphetamines, cocaine, and others to facilitate sexual contacts,
particularly anal intercourse #(Lifson et al., 1990; Duesberg,
1992; Ascher et al., 1993; Duesberg, 1993d; Schechter et
al., 1993a; Schechter et al., 1993c)#. The drug use of
male homosexuals with AIDS or at risk for AIDS reported by the CDC
#(Jaffe et al., 1983; Darrow et al., 1987; Lifson
et al., 1990)# and others #(Ascher et al., 1993; Duesberg,
1993d; Schechter et al., 1993c; Ellison, Downey and Duesberg,
1995)# as of 1983 is listed in Table 2. Ostrow reported that nitrite
inhalant use in a cohort of over 5000 male homosexuals from Chicago,
Baltimore, Los Angeles and Pittsburgh showed a "consistent
and strong cross-sectional association with ... anal sex" #(Ostrow,
1994)#. In addition, many HIV-positive homosexuals are prescribed
AZT as an antiviral drug #(Duesberg, 1992; Duesberg, 1993d; Ellison,
Downey and Duesberg, 1995)#.
Since intravenous drug users, who are 75% male, make
up one-third of all AIDS patients, and male homosexuals make up
almost two-thirds of all American AIDS patients, the drug hypothesis
explains why 87% of all American AIDS patients are males.
(3) Pediatric AIDS coccurs because of maternal
Indeed about 80% of pediatric AIDS cases in America
and Europe are children born to mothers who were intravenous drug
users during pregnancy (see below (5) and (8)), #(Mok et al., 1987;
European Collaborative Study, 1991; Duesberg, 1992)#. The remainder
reflects the normal low incidence of AIDS-defining diseases among
AIDS is new and increasing steadily, because the American drug epidemic
is new and increasing steadily.
In the U.S. recreational drug use is epidemiologically
new, as it has increased over the last decades from statistically
undetectable levels to epidemic levels at about the same rate as
AIDS #(Duesberg, 1992)#.
For example, cocaine consumption increased 200-fold
from 1980 to 1990, based on cocaine seizures that increased from
500 kg in 1980 to 100,000 kg in 1990 #(Duesberg, 1992, see Chapter
6)#. During the same time cocaine-related hospital emergencies increased
from 3,296 cases in 1981, to 80,355 cases in 1990, and to 119,843
in 1992 and to over 120,000 in 1993 #(Duesberg, 1992; Meddis, 1994;
Drug Strategies, 1995)# (Fig. 1B).
In the last three years, the increase of cocaine
consumption has slowed down at the expense of increases in heroin
consumption, which were accompanied by increases in heroin-related
hospital emergencies #(Gettman, 1994; Meddis, 1994; Drug Strategies,
1995)#. Heroin-related hospital emergencies doubled, from over 30,000
in 1990 to over 60,000 in 1993 (Fig. 1B)#(Drug Strategies, 1995)#.
Amphetamine consumption has increased 100-fold from
1980 to 1990 #(Bureau of Justice Statistics, 1991)#. Non-scientific
reports describe new upsurges in the consumption of amphetamines
(Sadownick, 1994) and the "gay drug" (nitrite inhalants)
(Mirken, 1995) among male homosexuals. According to a recent report
from the National Institute on Drug Abuse and the CDC, "nitrite
use has increased in the 1990s in gay men in Chicago and San Francisco"
after a decline in the 1980s #(Haverkos and Drotman, 1995)#.
Drug offenders are now the "largest and fastest-growing
category in the Federal prisons population, accounting for 61% of
the total, compared with 38% in 1986." The number of Federal
drug offenders increased from about 5,000 in 1980 to about 55,000
in 1993. In 1993, between 60 and 80% of the 12 million prisoners
in the US had been on illicit drugs #(Drug Strategies, 1995)#.
The German "Rauschgiftbilanz" reports an
11.2% increase in the consumption of illicit recreational drugs
in 1994 compared to 1993 #(Rauschgiftbilanz 1994, 1995)#.
Consider a grace period of about 10 years to achieve
the dosage needed to cause irreversible disease, and you can date
the origin of AIDS in 1981 as a consequence of the drug use epidemic
that started in America in the late 1960s during the Vietnam War.
Indeed, AIDS increased from a few dozen cases annually in 1981 to
about 100,000 in 1993 (Fig. 1A) #(Centers for Disease Control and
Prevention, 1994c)#. Note the parallelisms between the spread of
AIDS and the spread of cocaine and cocaine-related hospital emergencies
since 1981 (Fig. 1A and B), and the contrast with the non-spread
of HIV, the hypothetical cause of AIDS, since 1984 (Fig. 1A). Thus
both, the newness and the increase of the AIDS epidemic are predictable
by the drug-AIDS hypothesis.
The growth of the epidemic has been accelerated by
AZT. Since its introduction in 1987, AZT is now prescribed to about
200,000 HIV-positives worldwide #(Duesberg, 1992; Thomas, 1995)#.
(5) Only a small fraction of drug users develop
AIDS, because only the highest cumulative drug doses cause irreversible
The cumulative total of 401,749 American AIDS cases
since 1981 that were reported in June 1994 #(Centers for Disease
Control and Prevention, 1994c)# have been recruited from a much
larger reservoir of drug users. There are currently between 3 #(Drug
Strategies, 1995)# and 8 million cocaine addicts #(Duesberg, 1992)#
and 0.6 million heroin addicts in the US #(Drug Strategies, 1995)#.
In 1980, 5 million Americans had used nitrite inhalants. In 1989,
100 million doses of amphetamines were consumed in the U.S. #(Duesberg,
According to a 1994-survey of the National Institute
on Drug Abuse, "more than 5 percent (221,000) of the 4 million
women who give birth each year use illicit drugs during their pregnancy."
#(Drug Strategies, 1995)#. These mothers are the reservoir from
which most of the 1017 pediatric AIDS cases reported in the US in
1994 were recruited #(Centers for Disease Control and Prevention,
1994b)# (see 10).
Unfortunately, scientific documentation of recreational
drug use is extremely sporadic and inaccessible, not only because
these drugs are illegal, but more importantly because the medical-scientific
community is totally uninterested in drugs as a cause of AIDS (see
In addition, about 150,000 HIV-positive Americans
were on AZT between 1992 and #1995 (Duesberg, 1992; Thomas, 1995)#.
Probably because drug toxicity is generally ignored, there are also
no national statistics available on how many HIV-positive Americans
are on AZT and other anti-HIV drugs, that, like AZT, are designed
to kill human cells #(Duesberg, 1992).
The small percentage of AIDS patients among the many
American drug users reflects the highest lifetime dose of drug use,
just like the lung cancer and emphysema patients reflect the highest
lifetime tobacco dose among the 50 million smokers in the U.S. The
long "latent period of HIV" is a euphemism for the time
needed to accumulate the drug dosage that is sufficient for AIDS.
Indeed it takes about 10 years of injecting heroin and cocaine to
develop weight loss, tuberculosis, bronchitis, pneumonia and other
drug-induced diseases #(Layon et al., 1984; Schuster, 1984;
Savona et al., 1985; Donahoe et al., 1987; Espinoza
et al., 1987; Weber et al., 1990)#.
The time lag from initiating a habit of inhaling
nitrites to acquire Kaposi's sarcoma has been determined
to be 7 to 10 years #(Newell et al., 1985a; Beral et al.,
1990; Lifson et al., 1990; Duesberg, 1992)#. Blaming Kaposi's
sarcoma on HIV after inhaling carcinogenic nitrites for 10 years
is like blaming lung cancer and emphysema on a "slow"
virus after smoking two packs of cigarettes a day for 20 years.
AZT, at the currently prescribed high doses of 0.5
to 1.5 grams per person per day, causes many of the above described
AZT-specific diseases faster than recreational drugs, i.e. within
weeks or months after administration #(Duesberg, 1992; Lewis-Thorton,
(6) Risk group-specific AIDS diseases occur, because
of risk group-specific drugs.
Group-specific drug use explains the following risk-group-specific
(i) Kaposi's sarcoma specific for male homosexuals.
Kaposi's sarcoma as an AIDS diagnosis is 20 times more common
among homosexuals who use nitrite inhalants than among AIDS patients
who are intravenous drug users, or hemophiliacs #(Haverkos and Dougherty,
1988; Beral et al., 1990)#. Due to the carcinogenic potential,
nitrites were originally proposed as causes of Kaposi's sarcoma
#(Marmor et al., 1982; Haverkos et al., 1985)#. "Aggressive
and life-threatening" Kaposi's sarcoma particularly pulmonary
Kaposi's sarcoma, is exclusively observed in male homosexuals (Sloand,
Kumar and Pierce, 1993; Meduri et al., 1986; Garay et
al., 1987; Gill et al., 1989). Since the lungs are the
primary site of exposure to nitrite inhalants, the evidence that
up to 32% of Kaposi's sarcomas of homosexual men can be diagnosed
as pulmonary Kaposi's sarcoma #(Gill et al., 1989; Irwin
and Kaplan, 1993)#, lends additional support to the nitrite-Kaposi's
sarcoma hypothesis. Pulmonary Kaposi's sarcoma has never been described
by Moritz Kaposi, nor anywhere else prior to the AIDS epidemic #(Kaposi,
It appears that the nitrite-induced AIDS Kaposi's
sarcoma and the classic Kaposi's sarcomas are entirely different
cancers under the same name. The "HIV-associated" Kaposi's
sarcomas observed in male homosexuals are "aggressive and life-threatening"
#(Sloand, Kumar and Pierce, 1993)#, fatal within 8-10 months after
diagnosis, and often located in the lung #(Meduri et al.,
1986; Garay et al., 1987; Gill et al., 1989; Irwin
and Kaplan, 1993)#. The classic "indolent and chronic"
Kaposi's sarcomas are diagnosed on the skin of the lower extremities
and hardly progress over many years #(Meduri et al., 1986;
Drotman and Haverkos, 1992; Cohen, 1994a)#. Meduri et al. point
out that the "pulmonary involvement by the neoplasma has been
an unusual clinical finding" in the Kaposi's sarcomas of male
homosexuals compared to all "classic" Kaposi's sarcomas
#(Meduri et al., 1986)#. Nevertheless, the distinction between
classic and AIDS Kaposi's sarcoma is hardly ever emphasized and
may have escaped many observers due to the "difficulty in pre-mortem
diagnosis," because "pulmonary Kaposi's sarcoma was indistinguishable
from opportunistic pneumonia ..." #(Garay et al., 1987)#.
The immunotoxicity and cytotoxicity of nitrites also
explains the proclivity of male homosexual nitrite users for pneumonia,
which is the most common AIDS disease in the U.S. and Europe #(Haverkos
and Dougherty, 1988; Duesberg, 1992)# (Table 1) (Chapter 6). Moreover
the immunotoxins and cytotoxins of cigarette smoke explain, why
in two groups of otherwise matched HIV-positive male homosexuals
cigarette smokers developed pneumonia twice as often as non-smokers
over a period of 9 months #(Nieman et al., 1993)#.
(ii) High mortality of intravenous drug users. Intravenous
drug users suffer from long-term malnutrition and insomnia, which
are primary causes of immunodeficiency worldwide #(Seligmann et
al., 1984)#. This explains the tuberculosis, pneumonia, and
weight loss that are typical of these risk groups #(Layon et
al., 1984; Stoneburner et al., 1988; Pillai, Nair and
Watson, 1991; Duesberg, 1992; Mientjes et al., 1993)#. Injection
of unsterile drugs combined with immunodeficiency also cause septicemia
and endocarditis that are common in AIDS patients who are intravenous
drug users #(Duesberg, 1992)#. As a result, intravenous drug users
only achieve a very low average age. A German study found the average
age at death to 29.6 years for HIV-free and 31.5 years for HIV-positive
addicts #(Lockemann et al., 1995)#; and an American study
showed that both HIV-positive and negative intravenous drug users
died from the same diseases #(Stoneburner et al., 1988)#.
(iii) Low birth weight and mental retardation
of AIDS babies. 80% of American/European babies with AIDS
are born to mothers who were intravenous drug users during pregnancy;
they acquire low birth weight, mental retardation and immunodeficiency
through maternal drug use #(Duesberg, 1992; Drug Strategies, 1995)#.
The B-cell deficiencies and certain bacterial infections-that are
both only considered AIDS-defining in children-are also specific
expressions of their acquired immunodeficiency #(Centers for Disease
Control, 1987; Centers for Disease Control and Prevention, 1992;
(iv) Anemia and wasting of AZT recipients. Anemia,
leukopenia, pancytopenia, diarrhea, weight loss, hair loss, impotence
#(Duesberg, 1992), hepatitis #(Freiman et al., 1993)#, and
pneumocystis pneumonia #(Saah et al., 1995)# that are observed
in recipients of AZT and other DNA chain terminators, are predictable
consequences of the cytotoxicity of these drugs (see Chapter 6).
In addition, non-renewal of mitochondrial DNA causes muscle atrophy,
hepatitis, and dementia; and carcinogenic activity causes cancers
such as lymphoma in AZT recipients #(Pluda et al., 1990;
Duesberg, 1992; McLeod and Hammer, 1992; Freiman et al.,
1993; Bacellar et al., 1994; Parker and Cheng, 1994; Physicians'
Desk Reference, 1994)#. Compared to untreated controls AZT recipients
die 2.4-times more often #(Goedert et al., 1994)#, 25% more
often #(Seligmann et al., 1994)#, or live only 2 years instead
of 3 years with AIDS #(Poznansky et al., 1995)#.
(7) Non-correlations between HIV and AIDS, because drugs, not
HIV, cause AIDS.
(i) Long-term survivors or "non-progressors." Persons
infected by HIV for more than the 10-year-latent-period-from-HIV-to-AIDS
who are studied by HIV researchers are termed long-term survivors
and more recently "non-progressors" #(Scolaro, Durham
and Pieczenik, 1991; Learmont et al., 1992; Cao et al.,
1995)#. David Ho et al. recently gave a key to long-term survival,
"none had received antiretroviral therapy" #(Cao et
al., 1995)#. Likewise Alvaro Munoz reported that not one of
the long-term survivors of the largest federally funded study of
male homosexuals at risk for AIDS, the MACS study, had used AZT
#(Munoz, 1995)#. And several survey studies document that in addition
to abstaining from antiviral drugs long-term survivors are those
who have given up or never taken recreational drugs #(Wells, 1993;
Gavzer, 1995; Root-Bernstein, 1995b)#.
Indeed, the vast majority of HIV-positives are long-term survivors!
Worldwide, they number 17 million, including 1 million HIV-positive
but healthy Americans and 0.5 million HIV-positive but healthy Europeans
#(Merson, 1993; World Health Organization, 1995)#. Most of these
have been HIV-positive for at least 10 years now, because their
numbers have not changed since the time between 1984 to 1988, when
the epidemic of HIV-testing began in the respective countries #(Duesberg,
Only about 6% (or 1,025,073) of these 17 million HIV-positives
have developed AIDS diseases since AIDS statistics are kept #(World
Health Organization, 1995)#. Since no more than 6% of HIV-carriers
worldwide have developed AIDS in 7 to 10 years, the annual AIDS
risk of an HIV-carrier is less than 1% per year. However, even this
low figure is not corrected for the normal occurence of the 29 AIDS-defining
diseases in HIV-free controls. There is no evidence that HIV-positive
people who are not drug users have a higher morbidity or mortality
than HIV-free controls #(Duesberg, 1995a, see Chapter 10).
(ii) Intravenous drug users and male homosexuals losing their
T-cells prior to HIV infection. Prospective studies of male
homosexuals using psychoactive and sexual stimulants have demonstrated
that their T-cells may decline prior to infection with HIV. For
example, the T-cells of 37 homosexual men from San Francisco declined
steadily prior to HIV infection for 1.5 years from over 1200 to
below 800 per µl #(Lang et al., 1989)#. In fact, some
had fewer than 500 T-cells 1.5 years before seroconversion #(Lang
et al., 1987)#. Although recreational drug use was not mentioned
in these articles, other studies of the same cohort of homosexual
men from San Francisco described extensive use of recreational drugs
including nitrites #(Darrow et al., 1987; Moss, 1987; Ascher
et al., 1993; Duesberg, 1993d; Ellison, Downey and Duesberg,
1995)#. Likewise 33 HIV-free male homosexuals from Vancouver, Canada,
had "acquired" immunodeficiency prior to HIV infection
#(Marion et al., 1989)#. Again this study did not mention
drug use, but in other articles the authors reported that all men
of this cohort had used nitrites, cocaine and amphetamines #(Archibald
et al., 1992; Duesberg, 1993f; Schechter et al., 1993c)#.
The largest study of its kind reported that about 450 (16% of
2795) HIV-free, homosexual American men of the MACS cohort from
Chicago, Baltimore, Pittsburgh and Los Angeles had acquired immunodeficiency,
having less than 600 T-cells per µl, prior to HIV infection
#(Kaslow et al., 1989)#. Many HIV-positive and -negative
men of this cohort had essentially the same degree of lymphadenopathy:
"Although seropositive men had a significantly higher mean
number of involved lymph node groups than seronegative men (5.7
compared to 4.5 nodes, p0.005), the numerical difference in the
means is not striking" #(Kaslow et al., 1987)#. According
to previous studies on this cohort 71% of these men had used nitrite
inhalants, in addition to other drugs #(Kaslow et al., 1987)#;
83% had used one drug, and 60% had used two or more drugs during
sex in the previous six months #(Ostrow et al., 1990)#.
Another study of the same cohort observed that the risk of developing
AIDS correlated with the frequency of receptive anal intercourse
prior to and after HIV infection #(Phair et al., 1992)#.
Other studies have shown that receptive anal intercourse correlates
directly with the use of nitrite vasodilaters #(Haverkos and Dougherty,
1988; Duesberg, 1992; Parke, 1993)#.
Thus in male homosexuals at risk for AIDS, AIDS often precedes
infection by HIV, not vice versa. Since the cause must precede the
consequence, drug use remains the only group-specific choice to
explain "acquired" immunodeficiencies prior to HIV. If
male homosexuality were to cause immunodeficiency, about 10% of
the adult American male population should have AIDS #(Duesberg,
1992; Seidman and Rieder, 1994)#.
Prospective studies of intravenous drug users also document T-cell
losses prior to infection by HIV. For example, among intravenous
drug users in New York "The relative risk for seroconversion
among subjects with one or more CD4 [T-cell] count <500 cells/µl
compared with HIV-negative subjects with all counts >500 cells/µl
was 4.53." #(Des Jarlais et al., 1993)#. A similar study
from Italy showed that a low number of T-cells was the highest risk
factor for HIV infection #(Nicolosi et al., 1990)#. Again,
a decrease in T-cells is a risk factor for HIV infection, and not
This confirms the hypothesis that HIV is a marker of drug consumption,
rather than the cause of AIDS (see IV): the more drugs are consumed
intravenously or for sex, the higher is the risk of HIV infection
(iii) HIV-free AIDS. One summary of the AIDS literature
describes over 4,621 clinically diagnosed AIDS cases who were not
infected by HIV #(Duesberg, 1993f, see Chapter 7)#. Additional cases
are described that were not in this summary #(Kaslow et al.,
1987; Lang et al., 1987; European Collaborative Study, 1991;
Weiss et al., 1992; Ellison, Downey and Duesberg, 1995; Moore
and Chang, 1995)#. They include intravenous drug users, male homosexuals
using aphrodisiac drugs like nitrite inhalants, and hemophiliacs
developing immune suppression from long-term transfusion of foreign
proteins contaminating factor VIII #(Duesberg, 1993f; Duesberg,
Each of these non-correlations between HIV and AIDS are predicted
by the hypothesis that recreational drugs and other non-contagious
risk factors cause AIDS.
(8) Discontinuation of drug use either stabilizes
or cures AIDS and other diseases-even in HIV-positives.
(i) AZT. Ten out of 11 HIV-positive, AZT-treated
AIDS patients recovered cellular immunity after discontinuing AZT
in favor of an experimental vaccine #(Scolaro, Durham and Pieczenik,
1991)#. Two weeks after discontinuing AZT, 4 out of 5 AIDS patients
recovered from myopathy #(Till and MacDonnell, 1990)#. Three of
four AIDS patients recovered from severe pancytopenia and bone marrow
aplasia 4-5 weeks after AZT was discontinued #(Gill et al.,
(ii) Heroin/cocaine. The incidence of AIDS
diseases among HIV-positive intravenous drug users over 16 months
was 19% (23/124) and only 5% (5/93) among those who stopped injecting
drugs #(Weber et al., 1990). The T-cell counts of HIV-positive
intravenous drug users from New York dropped 35% over 9 months,
compared to HIV-positive controls who had stopped injecting #(Des
Jarlais et al., 1987)#.
(iii) Recreational drugs and AZT. The health
of male homosexuals is stabilized or even improved by avoiding recreational
drugs. For example in August 1993 there was no mortality during
1.25 years in a group of 918 British HIV-positive homosexuals who
had "avoided the experimental medications on offer" and
chose to "abstain from or significantly reduce their use of
recreational drugs, including alcohol" #(Wells, 1993)#. Assuming
an average 10-year latent period from HIV to AIDS, the virus-AIDS
hypothesis would have predicted at least 58 (918/10 x 1.25 x 50%)
AIDS cases among 918 HIV-positives over 1.25 years. Indeed, the
absence of mortality in this group over 1.25 years corresponds to
a minimal latent period from HIV to AIDS of over 1,148 (918 x 1.25)
years. On July 1, 1994 there was still not a single AIDS case in
this group of 918 HIV-positive homosexuals (J. Wells, London, personal
The T-cells of 29% of 1,020 HIV-positive male homosexuals
and intravenous drug users in a clinical trial even increased over
2 years #(Hughes et al., 1994)#. These HIV-positives belonged
to the placebo arm of an AZT trial for AIDS prevention and thus
were not treated by AZT. It is probable that under clinical surveillance
the 29% whose T-cells increased, despite HIV, have given up or reduced
immunosuppressive recreational drug use in the hope that AZT would
(iv) AIDS babies, born to drug-addicted mothers,
recover after birth. HIV-positive babies, born to mothers who
were intravenous drug users during pregnancy, provide the best examples
for the prediction that termination of drug use prevents, or cures
AIDS-despite the presence of HIV. For example, Blanche et al.
have observed for three years 71 HIV-positive newborns who had
shared intravenous drugs with their mothers prior to birth. Ten
of these children developed encephalopathy and AIDS-defining diseases
of which 9 died during their first 18 months of life. The study
points out that the risk of a newborn to develop AIDS was related
"directly with the severity of the disease in the mother at
the time of delivery." Based on the severity of their symptoms
about 60% of the children were treated prophylactically, but apparently
briefly with AZT "for at least one month," and 50% were
treated with sulfa-drugs #(Blanche et al., 1994)#. Despite
HIV, 61 of the 71 HIV-positive children either developed only "intermittent"
diseases from which they recovered during their first 18 months
or developed no disease at all during the 3 years of observation.
The T-cells of these children increased after birth from low to
normal levels-despite the presence of HIV.
A very similar picture emerges from a collaborative
European study of HIV-positive newborns #(The European Collaborative
Study, 1994)#. The study reports that about 20% of the HIV-positive
children had died or developed long-term AIDS during the first year
after birth, and another 20% during the second and third year. About
10% of the children were "treated with zidovudine [AZT]"
before 6 months of age and 40% by 4 years #(The European Collaborative
Study, 1994)#. But over 60% of congenitally-infected children proved
to be healthy up to 6 years after birth-despite the presence of
HIV. Most of these had experienced transient AIDS diseases, such
as pneumonia, bacterial infections, candidiasis and cryptosporidial
infection during the first year after birth.
Although this study does not even mention the health
and health risks of the mothers, previous reports from the European
Collaborative Study group have documented that "nearly all
children were born to mothers who are intravenous drug users"
#(Mok et al., 1987; Duesberg, 1992)#. In 1991, the European
Collaborative Study group reported that 80% of the children with
pediatric AIDS were born to mothers who were intravenous drug users
#(European Collaborative Study, 1991)#. The 1991-study further points
out that "children with drug withdrawal symptoms" were
most likely to develop diseases, and that children with no withdrawal
symptoms but "whose mothers had used recreational drugs in
the final 6 months of pregnancy were intermediate" in their
risk to develop diseases #(European Collaborative Study, 1991)#.
According to the HIV hypothesis every infected baby
should have developed AIDS and progressively lost T-cells, and according
to an HIV plus cofactor hypothesis, at least all those with intermittent
diseases should have progressed to AIDS. This was not observed.
According to the drug hypothesis, the AIDS risk of
the children is a function of the drugs consumed. Those who received
the highest doses of drugs before birth would have acquired irreversible
diseases and those who acquired diseases from sublethal thresholds
would be able to recover after cessation of maternally administered
drugs. Indeed, both, the European Collaborative Study group and
Blanche et al. show that the majority of children gained
T-cells and recovered from transient diseases after discontinuation
of maternal drug input-despite the presence of HIV. The childrens
risk for AIDS was related "directly with the severity of the
disease in the mother" #(Blanche et al., 1994)#, which
is an expression for the extent of drug consumption by the mother.
Moreover, the harm of maternal drug consumption to
sick babies was compounded after birth, because "prophylactic
treatment [with] ... sulfamethoxazale and zidovudine [AZT] was started
earlier and was more frequent among the 16 children born to mothers
with class IV disease (AIDS)" #(Blanche et al., 1994)#.
(The Blanche study did include mothers with AIDS who were not intravenous
drug users). The European Collaborative Study group reports that
10 to 40% of HIV-positive children were treated with AZT.
It follows that discontinuation of recreational and
antiretroviral drug use stabilizes and even cures AIDS in HIV-positive
Likewise the T-cells of HIV-positive hemophiliacs
increase after removal of immunosuppressive foreign proteins from
their factor VIII therapy (Duesberg, 1995, see Chapter 11), and
the T-cells of African HIV-positive tuberculosis patients increase
after "standard anti-TB treatment" and improved nutrition
(Martin et al., 1995).
In sum, the drug-AIDS hypothesis correctly predicts
all aspects of American/European AIDS, while the HIV-hypothesis
X. A possible solution at last
Testing the drug hypothesis should have a very high
priority in AIDS research, because this hypothesis makes verifiable
predictions #(Cohen, 1994a; DeNoon, 1995)#. Drug toxicity could
be tested experimentally in animals, and in human cells in tissue
culture. In addition, drug toxicity could be tested epidemiologically
in humans who are addicted to recreational drugs or are prescribed
AZT. Such tests could be conducted at a fraction of the cost that
is now invested in the HIV hypothesis.
If the drug hypothesis proved to be correct, AIDS
would be an entirely preventable disease. Here is how:
(1) AZT use would be banned immediately.
(2) AIDS from illicit recreational drugs would be
reduced or prevented by education against drug use. (Hemophilia
AIDS would be prevented by the use of pure factor VIII (Chapter
(3) AIDS therapy would be achieved by termination
of recreational drug use and treating AIDS diseases for their specific
causes, e.g. tuberculosis with antibiotics, Kaposi's sarcoma with
conventional cancer therapy, and weight loss with good nutrition-rather
than treating each of these unrelated diseases with the same cell-killer
In addition to saving about 100,000 lives per year
from AIDS, the drug hypothesis could save the American tax payer
up to $20 billion annually. Currently the federal government spends
annually $7.5 billion on AIDS treatment, research and education
#(AIDS Weekly, 1995; Gutknecht, 1995)#. And the Federal drug budget
currently costs $13 billion, mainly for supply control, interdiction,
methadone treatment and "education" #(Drug Strategies,
But neither AIDS education nor drug education ever
target the health effects of long-term drug use. They focus on the
legal and social consequences of drug use and on the effects of
drug use on transmission of HIV via unsafe sex and without "clean
needles." Instead of studying the unknown, and warning against
the known health hazards of recreational drugs, the medical establishment
turns a blind eye to drug toxicity in its single-minded pursuit
of HIV with safe sex and clean needles #(Project Inform, 1992; Ascher
et al., 1993; Cohen, 1994a)#. The clean-needle program of
the AIDS-establishment would appear to encourage rather than discourage
intravenous drug use. Reflecting this state of mind, Science
recently rejected the drug-AIDS hypothesis, quoting a drug researcher
that "Heroin is a blessedly untoxic drug" #(Cohen, 1994a)#
and described nitrite inhalant-AIDS links as another "hatched"
theory #(Cohen, 1994b)#.
The failure to warn against the health risks of drug
addiction is certainly one of the reasons that "drug use among
young people has risen substantially for the first time in more
than a decade" #(Drug Strategies, 1995)#. Nitrite use continues
to remain popular and has even increased recently, particulary among
male homosexuals #(Ascher et al., 1993; Duesberg, 1993d;
Mansfield and Owen, 1993; Parke, 1993; Schechter et al.,
1993b; Schechter et al., 1993c; Bethell, 1994; Gorman, 1994;
Hodgkinson, 1994; Lauritsen, 1994; Sadownick, 1994; Vollbrechtshausen,
1994; Brandley, 1995; Haverkos and Drotman, 1995, Mirken, 1995).
There is no report that nitrite bans are ever enforced or that nitrite
warnings are taken seriously #(Bethell, 1994, Mirken, 1995)#. And
the number of intravenous drug-AIDS patients has increased steadily
for years in America #(Centers for Disease Control and Prevention,
1994b; Drug Strategies, 1995)#-probably because drug control in
America is "primarily focused on supply control efforts"
#(Drug Strategies, 1995)#.
However, if AIDS and drug education were based on
the health consequences of long-term drug use, it would be as successful
as the federal anti-smoking program. Based on education that smoking
causes lung cancer, emphysema and heart disease, smoking has dropped
in the US from 42% of the adult population in 1965 to 25% in 1995
#(Associated Press, 1995b)#.
The solution of AIDS could be as close as a very
testable, very affordable, and very practicable alternative hypothesis.
Ruhong Li for searching the AIDS literature and assistance with
computer programs, Prof. Phil Johnson, School of Law UC Berkeley,
for many references and critical commentary, Russell Schoch for
critical review of the manuscript, and Siggi Sachs for preparation
of, and review of the manuscript, and Claus Koehnlein (Kiel, Germany)
and Colman Jones (Toronto, Canada) for critical information. This
investigation was supported in part by the Council for Tobacco Research,
USA, and private donations from Thomas Boulger (Redondo Beach, Calif.,
USA), Glenn Braswell (Los Angeles, Calif., USA), Dr. Richard Fischer
(Annandale, Va., USA), Dr. Peter Paschen (Hamburg, Germany), Ruth
Sackman, president of the Foundation for the Advancement in Cancer
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