The Chemical Basis of the Various AIDS Epidemics: Recreational Drugs,
Anti-viral Chemotherapy and Malnutrition
Peter Duesberg, Claus Koehnlein and David Rasnick
Donner Laboratory, University of California, Berkeley, CA 94720, USA
Internistische Praxis, Koenigsweg 14, 24103 Kiel, Germany
Corresponding author Email, duesberg@uclink4.berkeley.edu
MS received 22 January 2003; accepted 8 April 2003
Corresponding editor: Athel Cornish-Bowden
Abbreviations used: CDC, US Centers for Disease Control; NIH, US National
Institutes of Health; FDA, US Food and Drug Administration; WHO, World
Health Organization.
J. Biosci. | Vol. 28 | No. 4 | June 2003 | Indian Academy of Sciences
________________________________________________________________________
In 1981 a new epidemic of about two-dozen heterogeneous diseases began
to strike non-randomly growing numbers of male homosexuals and mostly male
intravenous drug users in the US and Europe. Assuming immunodeficiency as
the common denominator the US Centers for Disease Control (CDC) termed the
epidemic, AIDS, for acquired immunodeficiency syndrome. From 1981-1984
leading researchers including those from the CDC proposed that recreational
drug use was the cause of AIDS, because of exact correlations and of
drug-specific diseases. However, in 1984 US government researchers proposed
that a virus, now termed human immunodeficiency virus (HIV), is the cause of
the non-random epidemics of the US and Europe but also of a new, sexually
random, (though limited to poor people) epidemic in Africa.
The virus-AIDS hypothesis was instantly accepted, but it is burdened with
numerous paradoxes, none of which could be resolved by 2003: Why is there no
HIV in most AIDS patients, only antibodies against it? Why would HIV take 10
years from infection to AIDS? Why is AIDS not self-limiting via antiviral
immunity? Why is there no vaccine against AIDS? Why is AIDS in the US and
Europe not random like other viral epidemics? Why did AIDS not rise and then
decline exponentially owing to antiviral immunity like all other viral
epidemics? Why is AIDS not contagious? Why would only HIV carriers get AIDS
who use either recreational or anti-HIV drugs or are subject to malnutrition?
Why is the mortality of HIV-antibody-positives treated with anti-HIV drugs
7-9%, but that of all (mostly untreated) HIV-positives globally is only 1.4%?
Here we propose that AIDS is a collection of chemical epidemics, caused by
recreational drugs, anti-HIV drugs, and malnutrition. According to this
hypothesis AIDS is not contagious, not immunogenic, not treatable by vaccines
or antiviral drugs, and HIV is just a passenger virus. The hypothesis
explains why AIDS epidemics strike non-randomly if caused by drugs and
randomly among poor people if caused by malnutrition, why they manifest in
drug and malnutrition specific diseases, and why they are not self-limiting
via anti-viral immunity. The hypothesis predicts AIDS prevention by adequate
nutrition and abstaining from drugs, and even cures by treating AIDS diseases
with proven medications.
____________________________
1. Origins of the AIDS epidemics of the US, Europe and Africa
1.1 AIDS in the US and Europe
In the spring of 1981 the US Centers for Disease Control (CDC), the
nation's sentinel of infectious diseases, first reported a mysterious
epidemic of previously known diseases that selectively affected growing
numbers of young male homosexuals, intravenous drug users and a few minor
risk groups such as hemophiliacs and recipients of blood transfusions
(Centers for Disease Control 1981a, b, 1986).
The diseases of the new AIDS epidemic included Kaposi's sarcoma,
bacterial and fungal (pneumocystis and candida) pneumonia, oral yeast
infections, dementia, diarrhea, herpes, tuberculosis, lymphoma, weight loss,
toxoplasmosis, chronic fevers, etc. (table 1), (Centers for Disease Control
1986). A similar, non-random epidemic was soon also reported in Europe by
the World Health Organization (WHO), (Downs et al 1987). The selective
distribution of these epidemics in the US and European population
immediately suggested risk group or lifestyle specific causes.
However, the plethora of AIDS diseases was not, and still is not randomly
distributed even among the different risk groups (table 2). For example,
Kaposi's sarcoma was exclusively diagnosed in male homosexual risk groups
using nitrite inhalants and other psychoactive drugs as aphrodisiacs (Newell
et al 1984; Haverkos et al 1985; Selik et al 1987; Duesberg 1988; Haverkos
and Dougherty 1988; Beral et al 1990). Bacterial pneumonia was primarily
diagnosed in children from mothers using psychoactive drugs during pregnancy
(Novick and Rubinstein 1987; Duesberg 1988, 1992; Centers for Disease
Control and Prevention 1997). Tuberculosis and pneumonia were, and still are
more prevalent in intravenous drug users and "crack" (cocaine) smokers than
in other risk groups (Lerner 1989; Duesberg 1992; Duesberg and Rasnick
1998). Pneumocystis pneumonia and dementia are common in both of these risk
groups (Selik et al 1987; Duesberg 1992; Duesberg and Rasnick 1998).
Hemophiliacs and other transfusion recipients from the US and Europe
exclusively present with pneumonia and yeast infections (Curran et al 1984;
Duesberg 1992, 1995c). The non-random distribution of these diseases in
different risk groups, then and now, again suggests risk group-specific
causes, rather than a common one.
Only 3 months after first detecting the new epidemics of old diseases,
the CDC named all of them, AIDS, for Acquired Immune Deficiency Syndrome,
assuming that immunodeficiency was their common denominator (Centers for
Disease Control 1981b). According to their most recent AIDS definition of
1993, there are now 26 AIDS defining diseases (Centers for Disease Control
1986, 1992). However, about one third of the CDC's collection of AIDS
diseases are neither caused by, nor necessarily associated with
immunodeficiency (table 1), (Duesberg and Rasnick 1998). Examples are
Kaposi's sarcoma, lymphoma, dementia, and weight loss (see table 1 for the
share of these among the AIDS diseases of the US in 1997). Although the rest
of the CDC's AIDS diseases are indeed microbial diseases, they are typically
opportunistic microbial diseases, in which the causative microbe depends on
a defective immune system to cause disease. Examples are tuberculosis, yeast
infections and pneumocystis pneumonia (Duesberg 1992), (table 1).
Table 1. CDC-defined AIDS diseases and "conditions" in the US in 1997, the
last year the Centers for Disease Control published the distribution of AIDS
diseases.
Total of 60,161 cases
Disease AIDS-diagnosis Percentage of cases* Case numbers
No disease < 200 T cells and 61 36,634
antibody against HIV
_________________________
Microbial Pneumocystis 38 9,145
disease Candidiasis 16 3,846
Tuberculosis and Mycobacteria 15 3,537
Cytomegalovirus 7 1,638
Pneumonia 5 1,347
Herpes virus 5 1,250
Cryptococcus 5 1,168
Toxoplasmosis 4 1,073
Non-microbial Weight loss/wasting 18 4,212
disease Kaposi's sarcoma 7 1,500
Dementia 6 1,409
Lymphoma/leukemia 4 850
Cervical cancer 1 144
*According to the CDC, "The sum of percentages is greater than 100
because some patients are reported with more than one illness [disease or
condition]. Of persons reported with AIDS-defining opportunistic illnesses,
65% also were reported with severe HIV-related immunosuppression
[corresponding almost exactly to the share of the microbial diseases among
the total of 23,527 people with AIDS-defining diseases]. . . . The 36,634
adults/adolescents presented on this table are those persons reported with
immunosuppression as their only AIDS-indicator condition [rather than
disease]" (Centers for Disease Control and Prevention 1997).
Table 2. Risk group-specific AIDS diseases.
+ and ++ represent common and highly representative diseases respectively.
Risk groups
_____________________________________________________________
Male Intravenous AZT US, Europe Hemophilia,
Diseases homosexual drugs recipient child transfusion African
Kaposi's ++
sarcoma
Lymphoma + +
Bacterial ++ +
pneumonia
Tuberculosis ++ ++ ++
Dementia + + + +
Weight loss + + + + ++
Yeast + + + + + +
Pneumocystis ++ + + + +
pneumonia
By contrast, in a normal immune system, opportunistic microbes are
harmless passengers - the reason why such diseases are not transmitted to
healthy contacts, as for example to the doctors that treat AIDS patients
(see below in part 3 and table 4).
Since 1981 the AIDS epidemics of the US and Europe have increased
steadily for a decade and, after reaching peaks in the early 1990s, they
have all decreased to about 1/2 of their peak levels now (figure 1a), (World
Health Organization 2001b). By 2001 the US epidemic had generated a total of
816,149 AIDS cases and the European epidemic 251,021 AIDS cases (Centers for
Disease Control and Prevention 2001; World Health Organization 2001b). To
this day, the AIDS epidemics of the US and Europe have remained highly
non-random: 80% of all patients from the US and 80% from Europe are males
(World Health Organization 2001a). In the US about 2/3 of all AIDS cases are
male homosexuals and about 1/3 are male and female intravenous drug users.
In Europe about 1/2 are male homosexuals and about 1/2 are intravenous drug
users [note that over 75% of intravenous drug users are males (Duesberg and
Rasnick 1998)]. In addition both epidemics include fringe groups of
hemophiliacs and other transfusion recipients (1%) and children born to
drug-addicted mothers (1%) (World Health Organization 2001a).
_________________________
1.2 African epidemic
A new AIDS epidemic was also claimed to have emerged in sub-Saharan
Africa in 1984 (Bayley 1984; Piot et al 1984; Seligmann et al 1984; Van de
Perre et al 1984; Quinn et al 1986, 1987). In sharp contrast to its
US/European namesakes, the African AIDS epidemic among the poor is randomly
distributed between the sexes and not restricted to behavioural risk groups
(Blattner et al 1988; Duesberg 1988; World Health Organization 2001a). Hence
sub-Saharan African AIDS is compatible with a random, either microbial or
chemical cause.
The African epidemic is also a collection of long established, indigenous
diseases, such as chronic fevers, weight loss, alias "slim disease",
diarrhea and tuberculosis (table 2), (Colebunders et al 1987; Konotey-Ahulu
1987a, b, 1989; Pallangyo et al 1987; Duesberg 1992). However, the
distribution of AIDS-defining diseases in Africa differs strongly from those
in the US and Europe (table 2). For example, the predominant and most
distinctive AIDS diseases in the US and Europe, Pneumocystis carinii
pneumonia and Kaposi's sarcoma, are almost never diagnosed in Africa
(Goodgame 1990; Abouya et al 1992).
According to the WHO the African epidemic has increased from 1984 until
the early 1990s, similar to the epidemics of the US and Europe, but has
since leveled off to generate about 75,000 cases annually (figure 1c),
(World Health Organization 2001b, and back issues). By 2001, Africa had
reportedly generated a cumulative total of 1,093,522 cases (World Health
Organization 2001b). However, there are three reasons for questioning these
numbers:
(i) During the African AIDS epidemic, the sub-Saharan African population
has grown, at an annual rate of about 2.6% per year - from 378 million in
1980 to 652 million in 2000 (US Bureau of the Census International Data Base
2001). Thus Africa had gained since 1980 274 million people, the equivalent
of the whole population of the US! Therefore, a possible, above-normal loss
of 1 million Africans over a period in which over 200 millions were gained
is statistically hard, if not impossible to verify - unless the African AIDS
diseases were highly distinctive.
(ii) However, the African AIDS-defining diseases are clinically
indistinguishable from conventional African morbidity and mortality (see
above).
(iii) Further the HIV-based definition of AIDS (see part 3) can not be
used in Africa to distinguish AIDS-defining from otherwise indistinguishable
diseases, because as of 1985 the WHO decided at a conference in Bangui,
Africa, to accept African AIDS diagnoses without HIV-tests (see part 3). This
was done because these tests are unaffordable in most African countries
(World Health Organization 1986; Fiala 1998; Fiala et al 2002). Thus without
the CDC's HIV standard (part 3), the diagnosis of African AIDS is arbitrary.
In view of the many epidemiological and clinical distinctions of African
AIDS from its US/European namesakes and the many uncertainties about the
diagnosis of African AIDS, both the novelty of African AIDS and its
relationship to the US/European AIDS epidemics have been called into
question (Hodgkinson 1996; Fiala 1998; Shenton 1998; Gellman 2000; Stewart
et al 2000; Malan 2001; Fiala et al 2002; Gisselquist et al 2002; Ross
2003). Indeed, all available data are compatible with an old African
epidemic of malnutrition and poverty-associated diseases under a new name
(Konotey-Ahulu 1987a, b; Oliver 2000; Stewart et al 2000).
In the following we will try to find the most probable causes for the
various AIDS epidemics based on epidemiological, clinical, microbial and
biochemical evidence.
Figures 1 and 2.
_________________________
2. 1981-1984: The "lifestyle"-AIDS hypothesis
Hardly anybody remembers now, that shortly after the origins of the AIDS
epidemics in the US and Europe scientists had already discovered that
illicit psychoactive and aphrodisiac drugs, consumed at massive doses, were
the common denominators and probable causes of the new AIDS patients. Drugs
such as cocaine, heroin, nitrite inhalants, amphetamines, steroids and
lysergic acid had become widely available and popular in the US and Europe
during and after the Vietnam war and the coincident era of "gay liberation"
(legal indemnity of homosexuality) (Duesberg and Rasnick 1998). The
phenomenon was dubbed the "drug explosion" in the US and Europe. Its
chronology is documented in figure 2 based on cocaine and heroin
hospital-emergencies and confiscations of cocaine. Figure 2 extends drug use
statistics described by us earlier until 2001 (Duesberg and Rasnick 1998),
and also compares the chronologies of the drug and AIDS epidemics in the US
(see also figure 1a and part 4).
The first series of publications linking homosexual AIDS with drugs,
particularly aphrodisiac nitrite inhalants (Gottlieb et al 1981), was
published in the New England Journal of Medicine in 1981 together with an
editorial by AIDS researcher David Durack suggesting that drugs are the
causes of AIDS (Durack 1981). Dozens of further drug-AIDS studies soon
followed from all prominent AIDS researchers of the time, including
Blattner, Bregman, Curran, Dougherty, Des Jarlais, Drotman, Friedman-Kien,
Goedert, Haverkos, Jaffe, Marmor, McManus, Mildvan, Moss, Newell,
Oppenheimer, Ortiz, Rivera, and Stoneburner (Goedert et al 1982; Marmor et
al 1982; McManus et al 1982; Jaffe et al 1983; Mathur-Wagh et al 1984;
Newell et al 1984; Haverkos et al 1985; Moss 1987; Haverkos and Dougherty
1988; Stoneburner et al 1988; Oppenheimer 1992).
Even the CDC, normally just a survey agency, conducted epidemiological
studies of their own, which confirmed that male homosexuals at risk for AIDS
and with AIDS were using batteries of recreational and aphrodisiac drugs
(table 3), (Jaffe et al 1983). Not even one male homosexual at behavioural
risk for AIDS or with AIDS was found to be drug-free by the CDC. However,
some CDC investigators suggested that nitrites depend on "infectious
cofactors" to cause AIDS diseases (Haverkos 1988).
Table 3. CDC 1983 : Drug use by American male homosexuals with AIDS and
at risk for AIDS. (Jaffe et al 1983).
Percentage of users among 50 AIDS cases
Drugs and 120 at risk for AIDS
______________________________________________
Nitrite inhalants 96
Ethylchloride 35-50
Cocaine 50-60
Amphetamines 50-70
Phenylcyclidine 40
LSD 40-60
Metaqualone 40-60
Barbiturates 25
Marijuana 90
Heroin 10
Drug-free None reported
The perfect correlations between recreational drug use and AIDS became
the basis for the hypothesis that drugs, or the drug use-"lifestyle" is the
cause of AIDS (Shilts 1987; Oppenheimer 1992). Moreover, the findings that
specific drugs, as for example nitrite inhalants, correlated with specific
AIDS diseases, such as immune suppression and Kaposi's sarcoma, directly
support the lifestyle hypothesis (Goedert et al 1982; Marmor et al 1982;
Haverkos and Dougherty 1988).
__________________________
By contrast, the African epidemic had been reduced right from its
presumed origin in 1984 to the consequences of malnutrition and lack of
drinkable water, alias poverty, consistent with its random distribution in
the population (Mims and White 1984; Seligmann et al 1984).
In sum all clinical and epidemiological data available on AIDS in 1984
made a coherent case for lifestyle- or chemical AIDS, caused by recreational
drugs or malnutrition.
3. 1984: The virus-AIDS hypothesis takes over
By 1983 AIDS had become big enough in the American and European press to
pique the interest of the influential infectious disease establishment,
particularly the cancer virus hunters. At that time the virus hunters had
been engaged for over a decade in president Nixon's War on Cancer with
unsuccessful attempts to find a human cancer virus (Duesberg 1996b; Fujimura
1996; de Harven 1999). Now they were looking for new diseases that could be
attributed to viruses (Duesberg 1987). Perhaps AIDS could at last yield
clinically relevant lymphoma-, Kaposi's sarcoma- or immunodeficiency-viruses
(Duesberg 1996b).
Indeed, virus hunters from the CDC were the first to alert the public
that AIDS may be "transmissible" (Francis et al 1983). A similar alert came
from a French virus team, which had discovered a retrovirus in a homosexual
man at risk for AIDS, which a year later became the accepted cause of AIDS
(Barre-Sinoussi et al 1983). News, that the cause of AIDS may be a virus,
and thus transmissible to the general population, immediately set off a
national panic that opened the doors for new surveillance programs by the
CDC and predictably set off a race among virus hunters for the AIDS virus
(Shilts 1987).
According to an international press conference called by the US Secretary
of Health and Human Services in Washington DC on 23 April 1984, that race
was won by government researchers from the NIH who had found in some AIDS
patients antibodies against a new retrovirus closely related to a
hypothetical human leukemia virus (Altman 1984). The virus was introduced as
fortunate fallout of the failed War on Cancer. The next day the new virus
was already termed, the "AIDS virus", by the New York Times (Altman 1984).
Overnight nearly all AIDS researchers dropped the lifestyle-AIDS hypothesis
to work on the new "AIDS virus", which was already endorsed by the US
government. The CDC's director of the Task Force on Kaposi's Sarcoma and
Opportunistic Infections, James Curran, was the only one who later announced
the reason for his conversion to the new "AIDS virus": "That's where the
money is" (Shilts 1987).
The National Academy, the Institute of Medicine and the CDC quickly
united the infectious disease establishment under the leadership of David
Baltimore, who had received a Nobel prize for his work on retroviruses, to
provide practical recommendations for the intimidated public. Their
recommendations were published in two consecutive monographs of Confronting
AIDS (Institute of Medicine and National Academy of Sciences 1986; Institute
of Medicine 1988), and initiated history's biggest and most expensive
anti-viral program ever, costing $ 93.3 billion by 2000 to the US taxpayer
alone (Johnson 2000). At the same time an international committee of
retrovirologists officially sealed the seemingly tight package of a new
"AIDS virus" and the CDC's assumption that immunodeficiency was the common
denominator of the 26 AIDS-defining diseases (table 1) by naming it, Human
Immunodeficiency Virus (HIV) (Coffin et al 1986).
__________________________
Even before the AIDS virus became the officially accepted cause of AIDS,
the CDC had already made antibodies against the virus the only definitive
criterion to diagnose any of the heterogeneous diseases as AIDS in 1985
(Centers for Disease Control 1985, 1987, 1992). Their unorthodox decision to
use antibodies against the virus (normally functioning as a vaccine),
instead of the virus, for the diagnosis of AIDS was based on the flawed
analogy with some bacterial pathogens. For example, syphilis bacteria can be
pathogenic despite the presence of antibodies, e.g. the Wassermann test for
syphilis (Brandt 1988). But viruses are typically unable to enter cells in
the presence of anti-viral antibodies - the basis for the effectiveness of
Jennerian vaccines. Because of the CDC's decision, AIDS is diagnosed
worldwide if antibody against (!) HIV, rather than HIV, is detectable in a
patient along with any of the CDC's 26 diseases. Since 1992 even low T-cell
counts are diagnosed as a condition, termed "HIV/AIDS", which is treatable
with anti-HIV drugs provided it occurs in the presence of antibodies against
HIV (Centers for Disease Control 1992), (see table 1, and part 4.2).
3.1 Discrepancies between the predictions of the virus-AIDS hypothesis
and the facts
Despite its spectacular birthday the HIV-AIDS hypothesis has remained
entirely unproductive to this date: There is as yet no anti-HIV-AIDS
vaccine, no effective prevention and not a single AIDS patient has ever been
cured - the hallmarks of a flawed hypothesis. Indeed the hypothesis was born
with several serious birth defects and has developed further defects since;
most of these should have given pause to HIV-AIDS researchers to rethink and
reconsider. However, in the race to claim a share of the new viral cause for
AIDS and of virus-based AIDS treatments, "The Trojan horse of emergency"
(Szasz 2001) was saddled so quickly that there was little time and no
interest to address these defects, not even the most fundamental ones (Weiss
and Jaffe 1990; Cohen 1994; O'Brien 1997).
An analysis of the defects of the HIV-AIDS hypothesis based on its
failure to predict AIDS facts is shown in table 4. Our analysis is based on
the most recent and most authoritative case made for the HIV-AIDS hypothesis
since 1984, namely the Durban Declaration that was published in Nature in
2000 and has been signed by "over 5,000 people, including Nobel
prizewinners" (The Durban Declaration 2000). It can be seen in table 4 that
the HIV-hypothesis fails to predict 17 specific facts of AIDS. The most
fundamental discrepancy between the HIV-AIDS hypothesis and the facts is the
paradox, that a latent, non-cytopathic and immunologically neutralized
retrovirus [a virus that is inherently not cytopathic (Duesberg 1987)], that
is only present in less than 1 out of 500 susceptible T-cells and rarely
expressed in a few of those, would cause a plethora of fatal diseases in
sexually active, young men and women. And, that the plethora of the diseases
attributed to this virus would not show up for 5-10 years after infection
(table 4). As a result of the many discrepancies between the HIV hypothesis
and the facts, we conclude that HIV is not sufficient for AIDS, and is most
compatible with being a passenger virus.
Surprisingly our conclusion is supported by a survey of AIDS researchers
conducted by the New York Times, shortly after the publication of the Durban
Declaration. At the 20th anniversary of AIDS, on 30 January 2001, the New
York Times interviewed a dozen leading AIDS researchers for an article that
turned into a list of questions, "The AIDS questions that linger" (Altman
2001a), similar to those asked by us in table 4:
__________________________
"In the 20 years since the first cases of AIDS were detected, scientists
say they have learned more about this viral disease than any other, and few
have disputed the claim. … Despite the gains … experts say reviewing
unanswered questions could prove useful as a measure of progress for AIDS
and other diseases. Such a list could fill a newspaper, and even then would
create debate. (E.g.): How does H.I.V. subvert the immune system? . . . Why
does AIDS predispose infected persons to certain types of cancer and
infections and not others? . . . Dr Anthony S Fauci, the director of the
National Institute of Allergy and Infectious Diseases, said, `It is the rare
person who gets up and strips himself of his personal agenda and articulates
what we really do not know because by saying that they would diminish the
impact of their own work, which is their agenda'. (Regarding anti-HIV
medications:) . . . the new drugs do not completely eliminate H.I.V. from
the body, so the medicines, which can have dangerous side effects, will have
to be taken for a lifetime and perhaps changed to combat resistance. The
treatments are now so complicated that it is difficult, expensive and
time-consuming to answer basic and practical questions. What combinations of
drugs should be started first and when? Why do side effects like unusual
accumulations of fat in the abdomen and neck develop? . . . Anti-H.I.V.
drugs suppress replication of the virus, which should give the functioning
parts of the immune system a chance to eliminate remaining virus. That does
not happen. `So something is bizarre about that, that we don't understand',
Dr Fauci said. Is a vaccine possible? . . . many unanswered questions exist
about whether and when one can be developed."
Thus HIV-AIDS researchers have not solved the discrepancies and paradoxes
of the HIV-AIDS hypothesis, but still do not follow the scientific method of
searching for alternative explanations (Costello 1995).
Since 19 years of HIV-AIDS research have failed to produce tangible
benefits for AIDS patients and risk groups, and since there are no paradoxes
in nature only flawed hypotheses, the scientific method calls for an
alternative, testable hypothesis. Here we offer one such hypothesis. Our
hypothesis extends the early, and now abandoned "lifestyle" hypothesis
(part 2)and subsequent drug-AIDS hypotheses from us and others (Duesberg
1992; Duesberg and Rasnick 1998).
4. Chemical AIDS
"Historically, the first step in determining the cause of any disease has
always been to find out if there is anything, apart from the disease itself,
that sufferers have in common" (Cairns 1978). However, the traditional
search for the cause is only completed, if something that sufferers have in
common can also be shown to cause the disease; in other words if Koch's
postulates can be fulfilled (Merriam-Webster 1965). This is true for viruses
just as much as for drugs. Following this tradition, we try here to provide
proof of principle for our drug and malnutrition hypothesis of AIDS - alias
chemical AIDS.
Table 4. The HIV-AIDS hypothesis: 17 predictions versus the facts.
All quotes are from The Durban Declaration, the most authoritative
edition of the HIV-AIDS hypothesis to date, which was signed "by over 5000
people, including Nobel prizewinners" and published in Nature in 2000 (The
Durban Declaration 2000).
__________________________
1. Since HIV is "the sole cause of AIDS", it must be abundant in AIDS
patients based on "exactly the same criteria as for other viral diseases."
But, only antibodies against HIV are found in most patients (1-7).
Therefore, "HIV infection is identified in blood by detecting antibodies,
gene sequences, or viral isolation." But, HIV can only be "isolated" from
rare, latently infected lymphocytes that have been cultured for weeks in
vitro - away from the antibodies of the human host (8). Thus HIV behaves
like a latent passenger virus.
2. Since HIV is "the sole cause of AIDS", there is no AIDS in HIV-free
people.
But, the AIDS literature has described at least 4621 HIV- free AIDS cases
according to one survey - irrespective of, or in agreement with allowances
made by the CDC for HIV-free AIDS cases (55).
3. The retrovirus HIV causes immunodeficiency by killing T-cells (1-3).
But, retroviruses do not kill cells because they depend on viable cells
for the replication of their RNA from viral DNA integrated into cellular DNA
(4, 25). Thus, T-cells infected in vitro thrive, and those patented to
mass-produce HIV for the detection of HIV antibodies and diagnosis of AIDS
are immortal (9-15)!
4. Following "exactly the same criteria as for other viral diseases", HIV
causes AIDS by killing more T-cells than the body can replace. Thus T-cells
or "CD4 lymphocytes . . . become depleted in people with AIDS".
But, even in patients dying from AIDS less than 1 in 500 of the T-cells
"that become depleted" are ever infected by HIV (16-20, 54). This rate of
infection is the hallmark of a latent passenger virus (21).
5. With an RNA of 9 kilobases, just like polio virus, HIV should be able
to cause one specific disease, or no disease if it is a passenger (22).
But, HIV is said to be "the sole cause of AIDS", or of 26 different
immunodeficiency and non-immunodeficiency diseases, all of which also occur
without HIV (table 2). Thus there is not one HIV-specific disease, which is
the definition of a passenger virus!
6. All viruses are most pathogenic prior to anti-viral immunity.
Therefore, preemptive immunization with Jennerian vaccines is used to
protect against all viral diseases since 1798.
But, AIDS is observed - by definition - only after anti-HIV immunity is
established, a positive HIV/AIDS test (23). Thus HIV cannot cause AIDS by
"the same criteria" as conventional viruses.
7. HIV needs "5-10 years" from establishing antiviral immunity to cause
AIDS.
But, HIV replicates in 1 day, generating over 100 new HIVs per cell (24,
25). Accordingly, HIV is immunogenic, i.e. biochemically most active, within
weeks after infection (26, 27). Thus, based on conventional criteria "for
other viral diseases", HIV should also cause AIDS within weeks - if it
could.
8. "Most people with HIV infection show signs of AIDS within 5-10 years"
- the justification for prophylaxis of AIDS with the DNA chain terminator
AZT (part 4).
But, of "34.3 million . . . with HIV worldwide" only 1.4% [= 471,457
(obtained by substracting the WHO's cumulative total of 1999 from that of
2000)] developed AIDS in 2000, and similarly low percentages prevailed in
all previous years (28). Likewise, in 1985, only 1.2% of the 1 million US
citizens with HIV developed AIDS (29, 30). Since an annual incidence of
1.2-1.4% of all 26 AIDS defining diseases combined is no more than the
normal mortality in the US and Europe (life expectancy of 75 years), HIV
must be a passenger virus.
__________________________
9. A vaccine against HIV should ("is hoped" to) prevent AIDS - the reason
why AIDS researchers have tried to develop an AIDS vaccine since 1984 (31).
But, despite enormous efforts there is no such vaccine to this day (31).
Moreover, since AIDS occurs by definition only in the presence of natural
antibodies against HIV (part 3), and since natural antibodies are so
effective that no HIV is detectable in AIDS patients (see No. 1), even the
hopes for a vaccine are irrational.
10. HIV, like other viruses, survives by transmission from host to host,
which is said to be mediated "through sexual contact".
But, only 1 in 1000 unprotected sexual contacts transmits HIV (32-34),
and only 1 of 275 US citizens is HIV-infected (29, 30), (figure 1b).
Therefore, an average uninfected US citizen needs 275,000 random "sexual
contacts" to get infected and spread HIV - an unlikely basis for an
epidemic! (Table 4. Cond.)
Table 4. No. Prediction
Fact
11. "AIDS spreads by infection" of HIV.
But, contrary to the spread of AIDS, there is no "spread" of HIV in the
US. In the US HIV infections have remained constant at 1 million from 1985
(29) until now (30), (see also The Durban Declaration and figure 1b). By
contrast, AIDS has increased from 1981 until 1992 and has declined ever
since (figure 1a).
12. Many of the 3 million people who annually receive blood transfusions
in the US for life-threatening diseases (51), should have developed AIDS
from HIV-infected blood donors prior to the elimination of HIV from the
blood supply in 1985.
But there was no increase in AIDS-defining diseases in HIV-positive
transfusion recipients in the AIDS era (52), and no AIDS-defining Kaposi's
sarcoma has ever been observed in millions of transfusion recipients (53).
13. Doctors are at high risk to contract AIDS from patients, HIV
researchers from virus preparations, wives of HIV-positive hemophiliacs from
husbands, and prostitutes from clients - particularly since there is no HIV
vaccine.
But, in the peer-reviewed literature there is not one doctor or nurse who
has ever contracted AIDS (not just HIV) from the over 816,000 AIDS patients
recorded in the US in 22 years (30). Not one of over ten thousand HIV
researchers has contracted AIDS. Wives of hemophiliacs do not get AIDS (35).
And there is no AIDS-epidemic in prostitutes (36-38). Thus AIDS is not
contagious (39, 40).
14. Viral AIDS - like all viral/microbial epidemics in the past (41-43) -
should spread randomly in a population.
But, in the US and Europe AIDS is restricted since 1981 to two main risk
groups, intravenous drug users and male homosexual drug users (part 1 and 4).
15. A viral AIDS epidemic should form a classical, bell-shaped
chronological curve (41-43), rising exponentially via virus spread and
declining exponentially via natural immunity, within months (see figure 3a).
But, AIDS has been increasing slowly since 1981 for 12 years and is now
declining since 1993 (figure 1a), just like a lifestyle epidemic, as for
example lung cancer from smoking (figure 3b).
16. AIDS should be a pediatric epidemic now, because HIV is transmitted
"from mother to infant" at rates of 25-50% (44- 49), and because "34.3
million people worldwide" were already infected in 2000. To reduce the high
maternal transmission rate HIV-antibody-positive pregnant mothers are
treated with AZT for up to 6 months prior to birth (part 4).
But, less than 1% of AIDS in the US and Europe is pediatric (30, 50).
Thus HIV must be a passenger virus in newborns.
__________________________
17. "HIV recognizes no social, political or geographic borders" - just
like all other viruses.
But, the presumably HIV-caused AIDS epidemics of Africa and of the US and
Europe differ both clinically and epidemiologically (part 1, table 2). The
US/European epidemic is highly nonrandom, 80% male and restricted to
abnormal risk groups, whereas the African epidemic is random among the poor.
Numbers in parentheses are for the following references: (1) (Marx 1984);
(2) (Gallo et al 1984); (3) (Altman 1984); (4) (Duesberg 1987); (5)
(Duesberg 1988); (6) (Duesberg 1994); (7) (Duesberg and Bialy 1996); (8)
(Levy et al 1984); (9) (Hoxie et al 1985); (10) (Anand et al 1987); (11)
(Langhoff et al 1989); (12) (Duesberg 1996b); (13) (Weiss 1991); (14) (Cohen
1993); (15) (McCune 2001); (16) (Harper et al 1986); (17) (Schnittman et al
1989); (18) (Hazenberg et al 2000); (19) (Duesberg 1988); (20) (Blattner et
al 1988); (21) (Enserink 2001); (22) (Fields 2001); (23) (Centers for
Disease Control 1992); (24) (Duesberg and Rasnick 1998); (25) (Duesberg
1992); (26) (Clark et al 1991); (27) (Daar et al 1991); (28) (World Health
Organization 2001b); (29) (Curran et al 1985); (30) (Centers for Disease
Control and Prevention 2001); (31) (Cohen 2003); (32) (Jacquez et al 1994);
(33) (Padian et al 1997); (34) (Gisselquist et al 2002); (35) (Duesberg
1995c; Hoots and Canty 1998); (36) (Mims and White 1984); (37) (Rosenberg
and Weiner 1988); (38) (Root-Bernstein 1993); (39) (Hearst and Hulley 1988);
(40) (Sande 1986); (41) (Bregman and Langmuir 1990); (42) (Anderson 1996);
(43) (Fenner et al 1974); (44) (Blattner et al 1988); (45) (Duesberg 1988);
(46) (Blanche et al 1989); (47) (Rogers et al 1989); (48) (European
Collaborative Study 1991); (49) (Connor et al 1994); (50) (World Health
Organization 2000); (51) (Duesberg 1992); (52) (Ward et al 1989); (53)
(Haverkos et al 1994); (54) (Simmonds et al 1990); (55) (Duesberg 1993d).
__________________________________________________________________________
4.1 The chemical-AIDS hypothesis and its predictions
The chemical-AIDS hypothesis proposes that the AIDS epidemics of the US
and Europe are caused by recreational drugs, alias lifestyle, and anti-HIV
drugs (Duesberg 1992, 1996b; Duesberg and Rasnick 1998), and by other
non-contagious risk factors such as immunosuppressive proteins associated
with transfusions of blood clotting factors (Duesberg 1995c; Hoots and Canty
1998). According to our hypothesis pediatric AIDS is due to prenatal
consumption of recreational and anti-HIV drugs by unborn babies together
with their pregnant mothers (Duesberg 1992; Duesberg and Rasnick 1998). The
chemical basis of African AIDS is proposed to be malnutrition and lack of
drinkable water (Duesberg 1992, 1996b; Duesberg and Rasnick 1998) - exactly
as proposed originally by the now leading HIV-AIDS researchers Fauci and
Seligmann: "The commonest cause of T-cell immunodeficiency worldwide is
protein-calorie malnutrition" (Seligmann et al 1984) and others (Mims and
White 1984), (see also part 1).
The chemical AIDS hypothesis makes the following testable predictions:
(i) Patients of the various epidemics have drug use, medications,
malnutrition or other chemical pathogens in common.
(ii) Distinct chemical pathogens cause distinct AIDS-defining diseases.
Since chemicals are not self-replicating, like viruses, pathogenicity is
dose- and thus also time-dependent (Duesberg and Rasnick 1998). Take for
example the average 20 years of smoking to cause cancer (figure 3b), (Cairns
1978).
(iii) Since there is no immunity against drugs or malnutrition, neither
drug diseases, nor malnutrition diseases, nor their corresponding epidemics
are self-limiting. In contrast to an infectious epidemic, the time curves of
chemical epidemics are not bell-shaped (see figure 3).
(iv) People who are not subject to drugs or malnutrition, or discontinue
drug use or malnutrition before irreversible damage has occurred, do not
develop AIDS, regardless of antibodies against HIV.
__________________________
Figures 3 and 4.
Here, we will focus on new and poorly known evidence confirming each of
these predictions, but also make references to prior supportive evidence by
others and us.
4.2 Prediction 1: AIDS coincides with recreational and anti-viral drugs
in the US and Europe and with malnutrition in Africa
4.2a Recreational drugs: Annually, the CDC and the WHO confirm that about
1/3 of all AIDS patients from the US and about 1/2 of those from Europe are
intravenous users of cocaine, heroin, amphetamines and other illicit,
psychoactive drugs, since the beginning of the AIDS epidemics (see part 1).
Most babies with AIDS in the US and Europe are also born to mothers who have
used recreational drugs (and antiviral drugs, see below) during pregnancy
according to the CDC, the WHO and independent publications reviewed below
and previously (Duesberg 1992; Duesberg and Rasnick 1998). In addition the
CDC and WHO confirm that about 2/3 of the AIDS patients in the US and 1/2 of
those in Europe are male homosexuals (part 1), but, after the lifestyle
hypothesis was abandoned in 1984, researchers no longer report subject drug
use.
However, rare independent investigations have confirmed continued use of
illicit recreational drugs by male homosexuals ever since the origins of the
epidemic (Lauritsen and Wilson 1986; Haverkos and Dougherty 1988; Rappoport
1988; Duesberg 1992; Lauritsen 1994; Duesberg and Rasnick 1998). Since there
is no general knowledge about the male-homosexual-AIDS-drug connection now,
we have summarized in table 5 rare, post-1984 studies which demonstrate that
male homosexuals with AIDS or at risk for AIDS have continued to use nitrite
inhalants, amphetamines, cocaine, heroin, steroids, and other recreational
drugs to this date, just as originally shown by the proponents of the
lifestyle hypothesis including the CDC (see part 2, table 3) (Duesberg and
Rasnick 1998).
As this article went to press, the San Francisco Chronicle published a
3-part front-page story on how "Crystal Meth (amphetamine) fuels HIV".
According to the article "the state's top AIDS and HIV prevention officials
came up with the smoking gun of all statistics: Gay men in California who
use speed are twice as likely to be HIV-positive . . ." (Heredia 2003a). But
the question whether meth "fuels" AIDS without HIV was not asked, even
though the featured case of a gay meth-addict had AIDS-defining dementia and
opportunistic infections (Heredia 2003a, b). Further, we confirm and extend,
in tables 6 and 7, the correlations between maternal drug use and baby-AIDS
documented previously (Novick and Rubinstein 1987; Duesberg 1992;
Root-Bernstein 1993; Duesberg and Rasnick 1998; Farber 1998). The
continuation of drug use in the HIV era is not surprising in the absence of
any advice from the medical establishment, that nitrite inhalants and other
drugs may cause AIDS (Lerner 1989).
4.2b Anti-viral DNA chain terminators and protease inhibitors: It is also
little known that since 1987 thousands of US citizens and Europeans with
AIDS (Kolata 1987), and (since 1990) even larger numbers of healthy HIV
antibody-positives, are on lifetime prescriptions of inevitably toxic DNA
chain-terminators, such as azi-dothymidine (AZT), and protease inhibitors, as
anti-HIV drugs (Volberding et al 1990). The original doses of these
prescriptions were 1.5 g per day of AZT or other DNA chain-terminator for
clinically ill patients (Fischl et al 1987) and 0.5 g per day for
asymptomatic, HIV-positives with low T-cell counts (Volberding et al 1990).
As of 1996 the DNA chain-terminators were mixed with HIV-protease inhibitors
to generate so-called "drug cocktails" (Ho 1995; Stolberg 2001). By 1996
200,000 US citizens (Hall 1996), and by 2001/2002 over 450,000 (France 2001;
Altman 2002), were taking prescriptions of such drugs to prevent or cure
AIDS (Stolberg 2001).
__________________________
Due to the CDC's 1993-definition of AIDS, well over half of these 450,000
treated subjects were clinically healthy at the time they started taking the
anti-HIV drugs (table 1) and are thus not patients (Centers for Disease
Control 1992; Centers for Disease Control and Prevention 1997). The
asymptomatic HIV-positives are treated according to the slogan, "Time to hit
HIV, early and hard", that was introduced by the New England Journal of
Medicine in 1995 (Ho 1995). Thus recreational and anti-HIV drugs are the
common denominator of AIDS in the US, and also in Europe (see below).
4.2c African AIDS coincides with malnutrition: The case for malnutrition
and lack of drinkable water as the common denominator and probable cause of
African AIDS in the HIV-era has been made by scientific (Mims and White
1984; Seligmann et al 1984; Konotey-Ahulu 1987a, b, 1989; Fiala 1998; Oliver
2000; Stewart et al 2000; Ross 2003) and non-scientific observers
(Hodgkinson 1996; Shenton 1998; Malan 2001). The non-scientific observers
even include the United Nations (Namango and World Food Program of the
United Nations 2001) and president Mbeki of South Africa (Cherry 2000;
Gellman 2000).
4.3 Prediction 2: Drugs cause AIDS and other diseases
4.3a Literature confirms that illicit recreational drugs cause AIDS
defining and other drug-specific diseases: We have recently summarized the
evidence from over 60 publications, beginning in 1909 (Achard et al 1909),
which prove that regular consumption of illicit recreational drugs causes
all AIDS defining and additional drug-specific diseases at time and
dose-dependent rates (Duesberg 1996b; Duesberg and Rasnick 1998). At
recreational doses, addictions ranging from years to over a decade are
typically required to reach pathogenic thresholds. Thus the literature
confirms the original "lifestyle"- or drug AIDS hypothesis.
Table 5. Studies describing illicit recreational (IR) and antiviral (AV)
drug use by male homosexuals with AIDS and at risk for AIDS in
the HIV era, since 1984.
Drugs Reference and Year
____ _____________________________________________
IR (Haverkos et al 1985; Newell et al 1985)
IR (Lauritsen and Wilson 1986)
IR (Darrow et al 1987)
IR (Haverkos and Dougherty 1988; Rappoport 1988)
IR (Adams 1989; Archer et al 1989; Kaslow et al 1989)
IR (Lifson et al 1990; Ostrow et al 1990)
IR (Eggers and Weyer 1991)
IR (Archibald et al 1992)
IR + AV (Ascher et al 1993b; Ostrow et al 1993; Schechter et al 1993)
IR + AV (Lauritsen 1994; Sadownick 1994; Veugelers et al 1994)
IR (Haverkos and Drotman 1995)
IR (Gibbons 1996; Haverkos 1996; Haverkos and Drotman 1996)
IR (McNall and Remafedi 1999)
IR (Craib et al 2000; Dukers et al 2000; Pauk et al 2000)
IR (Colfax et al 2001; Diamond et al 2001; Mansergh et al 2001;
Mattison et al 2001; Woody et al 2001)
IR + AV (Botnick et al 2002; Bull et al 2002)
IR, Illicit recreational drugs such as nitrite and other inhalants,
amphetamines, cocaine, heroin, steroids; AV, antiviral drugs such as DNA
chain terminators, protease inhibitors and others.
_____________________________________________________________________
__________________________
Table 6. Diseases and mortality of HIV antibody-positive people on anti-HIV
drugs that do not occur in, or exceed the rates of untreated controls.
AIDS-defining Other diseases References
________________ ___________________ ___________________________________
Immunodeficiency Anemia, Neutropenia (Gill et al 1987; Kolata 1987;Richman
Leukopenia et al 1988; Mir and Costello 1988;
Alcabes et al 1993; Poznansky et al
1995; Kline et al 1998; Levy 1998;
Anonymous 1999; Blanche et al 1999;
Mocroft et al 1999)
Fever Nausea (Richman et al 1987; Volberding et al
1990; Smothers 1991;Race et al 1998;
Fellay et al 2001)
Dementia (Hitchcock 1991; Smothers 1991;
Bacellar et al 1994)
Weight loss (Poznansky et al 1995; Moye et al
1996; Anonymous 1999)
Lymphoma (Pluda et al 1990)
Diarrhea Lipodystrophy, (Duesberg and Rasnick 1998;Levy 1998;
"protease paunch" Brinkman et al 1999;Carr et al 2000;
Fellay et al 2001)
Muscle atrophy (Richman et al 1987; Dalakas et al
1990; Till and MacDonnell 1990;
Hitchcock 1991; Blanche et al 1999)
Mitochondrial (Dalakas et al 1990; Blanche et al
dysfunction 1999; Carr et al 2001)
Hepatitis (Braeu et al 1997; Saves et al 1999;
Carr et al 2000, 2001; France 2001)
Birth defects (Kumar et al 1994; Newschafter et al
1999)
Nephritis (Fogelman et al 1994)
Lactic acidosis (Scalfaro et al 1998)
Heart infarct (Levy 1998; Altman 2001a; Carr et al
2001)
Death Death (Dournon et al 1988; Goedert et al
1994; Seligmann et al 1994;Veugelers
et al 1994; Fischl et al 1989, 1995;
Duesberg 1995c, 1996a; Sabin et al
1996; Anonymous 1999; Mocroft et al
1999; de Souza et al 2000;Kuhn et al
2000)
___________________________________________________________________________
Table 7. Diseases and mortality in HIV-free human babies, and in HIV-free
animals treated with anti-HIV drugs before and after birth (BB, AB).
Species AIDS-defining Other disease References
__________ ___________ _____________ ________________________________
Human Fever, Anemia, (Blanche et al 1999), (Heresi et
Babies (AB) Pneumonia Mitochondrial al 1997)
dysfunction
Animals (AB) Lymphopenia, Anemia, (Ayers 1988; Cronkite and Bullis
Mice, rats, Weight loss, neutropenia, 1990; Thompson et al 1991;
dogs, monkeys Leukemia, Thrombocytopenia, McKallip et al 1995;Omar et al
T-cell Bone marrow 1996; Grossman et al 1997;Inoue
depletion, depletion, et al 1997; Gerschenson et al
Thymic atrophy, Lymphotoxicity, 2000)
Death of 25/30 Myelodysplasia,
mice Muscle atrophy,
Nephrotoxicity
Hepatotoxicity
__________________________
Animals (BB) Death Lung, liver, (Toltzis et al 1993; Olivero et
vaginal cancer al 1997)
Retarded
development,
Abortion
___________________________________________________________________________
4.3b Epidemiological drug dose-AIDS-response curves: In figure 2 (part 2)
we have already shown that the chronology of the epidemic of illicit drug-use
in the US during the 1980s and 1990s closely paralleled the US AIDS
epidemics, see also Duesberg and Rasnick (1998). A report from the White
House, underwritten by president Clinton, provides additional data: It
states in 1996 that the number of regular users of illicit recreational
drugs in the US soared from a negligible background in the early 1960s to a
high of 25 million, or about 10% of the US population, in the late 1980s
(Clinton and The White House 1996; Duesberg and Rasnick 1998). Since its
peak in the late 1980s-early 1990s, the US drug epidemic has declined to an
estimated 13 million regular users in 1996 (Los Angeles Times 1998; White
House Office of National Drug Control Policy 1998), again roughly
paralleling the course of the AIDS epidemic (figure 2).
In addition, a fast-rising epidemic of volatile nitrite inhalants,
primarily among male homosexuals, was identified in the US by Newell et al,
Lauritsen and Wilson, and the National Institute on Drug Abuse (Lauritsen
and Wilson 1986; Haverkos and Dougherty 1988; Newell et al 1988). It started
in the late 1970s - immediately preceding the male homosexual AIDS
sub-epidemics of Kaposi's sarcomas and pneumonias (part 1). Newell et al
(1988) documented that recreational nitrite inhalant - alias "popper" - use
had increased from negligible numbers in the 1960s to 5 million users of one
ounce per week (!) in 1979 in the US. They even recorded the first
nitrite-linked Kaposi-cases, 3 years before the first description of AIDS.
The following surveys lend further support to the many synchronies between
the drug and AIDS epidemics: Duesberg (1988), Haverkos and Dougherty (1988),
Rappoport (1988), Duesberg (1992), Oppenheimer (1992), Lauritsen (1994),
Haverkos (1996), and Duesberg and Rasnick (1998).
We think that the chronological overlaps between the epidemics of
drug-use and drug-specific AIDS diseases are epidemiological dose-response
curves, and thus correlative proof of principle that drugs cause AIDS.
4.3c HIV-AIDS researchers confirm that recreational drugs cause AIDS and
other diseases - despite efforts to suppress this information: In their
efforts to promote the view that "HIV is the sole cause of AIDS" (The Durban
Declaration 2000), the proponents of the HIV hypothesis try to exclude all
non-HIV causes, particularly the illicit drugs that are the basis of the
competing "lifestyle"-AIDS hypothesis.
For example, the Lancet published in 1993 a Canadian epidemiological
study, "HIV and the etiology of AIDS", which found that 88% of AIDS cases in
a cohort of male homosexuals at risk for AIDS had used nitrite inhalants and
that 75-80% of the same cohort had also used "cocaine, heroin, amphetamines,
lysergic acid dimethyl amide, or methylenedioxy amphetamine" (Schechter et
al 1993). One of the subjects even passed away on an "overdose" of
recreational drugs during the study. In addition an undisclosed percentage
(but in 1993 certainly a high percentage, see above) was also prescribed the
DNA chain-terminator AZT as anti-HIV drug (Duesberg 1993a, c). Thus not a
single drug-free AIDS patient was identified. But, the study concluded,
"drugs and sexual activity is rejected by these data" as causes of AIDS.
Nevertheless, the authors acknowledged that their study "does not rule out a
role for cofactors . . .".
__________________________
Publishing in a high-profile commentary in Nature, a Californian HIV-AIDS
team also investigated the question, "Does drug use cause AIDS?" (Ascher et
al 1993a). The authors studied 215 HIV-positive homosexual AIDS patients of
which all were either "heavy" or "light" users of nitrites, of which unnamed
percentages had also consumed amphetamines, cocaine and marijuana, and of
which an unnamed percentage was also prescribed the DNA chain-terminator AZT
as anti-HIV drug (Ascher et al 1993a; Duesberg 1993a, c, 1995a). Thus again,
not a single drug-free patient was identified (Duesberg 1993a, c; Ascher et
al 1995; Ellison et al 1996; Duesberg and Rasnick 1998).
The authors did not inform the reader that their unpublished databank
included 45 patients which had used drugs and had AIDS-defining diseases, but
were HIV-free. Their conclusion states that, "when controlled for HIV
serostatus, there is no overall effect of drug use on AIDS", so that data had
to be left out (Ellison et al 1996). In a demonstration of their potentially
unreliable bias, the authors did remark to the reader that, "The energies of
Duesberg and his followers could better be applied to unraveling the
enigmatic mechanism of the HIV pathogenesis of AIDS". Despite numerous other
ad hominems, and the fact that Duesberg was named 13 times, the editor of
Nature vetoed a response, and even published his veto in an article, "Has
Duesberg a right of reply?", suggesting that discussing the chemical theory
of AIDS in a public forum is socially irresponsible (Maddox 1993).
Science Magazine also quoted a toxicologist ready to blame all
consequences of heroin addiction on HIV, because "heroin is a blessedly
untoxic drug" (Cohen 1994).
In an anonymous response to our hypothesis that drugs cause AIDS
(Duesberg 1995b; Duesberg and Rasnick 1998), the National Institutes of
Health (NIH) acknowledge drug-AIDS correlations on their website, The
evidence that HIV causes AIDS, but reject causation: "Because many
HIV-infected mothers abuse recreational drugs, some (unnamed researchers)
have argued that maternal drug use itself causes pediatric AIDS. However,
studies (unreferenced) have consistently shown that babies who are not
HIV-infected do not develop AIDS (per HIV-AIDS definition), regardless of
their mothers' drug use." Despite, "similar rates of alcohol, tobacco,
cocaine, heroin and methadone use …" none of "248 uninfected children" would
develop AIDS (National Institute of Allergy and Infectious Diseases and
National Institutes of Health 2001). However, the NIH does not mention even
one study that has ever described an AIDS-baby born to an HIV-positive, but
drug-free mother, to prove their website's claim that "HIV causes AIDS". The
NIH also does not mention the AIDS-defining and other birth defects of
HIV-free "crack" (cocaine) babies born to HIV-free drug-addicted mothers
that are described in the literature (Toufexis 1991; Duesberg 1992; Duesberg
and Rasnick 1998).
In contrast to the studies selected and promoted by the NIH, our study has
determined that nearly all AIDS-babies from the US and Europe were born to
mothers who had used either recreational or anti-HIV drugs or both during
pregnancy (Duesberg and Rasnick 1998), (part 4.2a and 4.3d, e, table 7).
4.3d Anti-HIV drugs cause AIDS defining and other drug specific diseases
- regardless of the presence of antibodies to HIV: The fundamental problem
of any chemical anti-virus "therapy" is that the cell carries out all viral
biochemical functions. Thus all anti-viral treatments are inevitably
anti-cell treatments. In the case of HIV, this problem is compounded by the
notorious biochemical inertia of HIV in antibody-positive people, and by the
extremely low multiplicity of infection of only 1 in 500 T-cells (table 4).
Thus in antibody-positive people there are no HIV functions that could be
targeted by DNA chain-terminators. As a result all treatments designed to
inhibit nucleic acid and protein synthesis of HIV with DNA chain-terminators
only inhibit cellular nucleic acid and protein synthesis. Since elimination
of the few cells that are latently infected is clinically not detectable,
"therapeutic" results are typically reported in terms of various lab
markers, primarily the "viral load", rather than in restored health (Ho et
al 1995; Wei et al 1995; Palella et al 1998; Hogg et al 2001).
__________________________
Even the term "viral load" is deceptive, because it suggests that there
is a high virus titer, although infectious virus is typically not detectable.
Instead this term describes the amount of viral DNA fragments that can be
generated in vitro by the polymerase chain reaction from RNA of rare, antibody
neutralized virus or of DNA of rare, latently infected cells isolated from
the patient (table 4), (Duesberg 1993b; Duesberg and Bialy 1996).
Nevertheless, the anti-HIV drugs have the unintended benefits of functioning
as true "anti-biotics", because of their general toxicity to all living
things. As such they will also reduce the load of opportunistic microbial
diseases that affect most AIDS patients (table 1), (Cohen 1987; Palella et
al 1998). In the following we briefly review the primary effects of the DNA
chain-terminators and protease inhibitors on the biochemistry of the cell.
(i) DNA chain-terminators: Currently nearly all anti-HIV prescriptions
include DNA chain-terminators, that were originally developed 40 years ago,
long before AIDS, to kill growing human cells as cancer therapy by
terminating DNA synthesis (Horwitz et al 1964). Considering their mechanism
of action, the DNA chain-terminators are inevitably cytotoxic, and thus
immunotoxic like most other chemotherapies (Stedman's Medical Dictionary
1982; Oliver 2000). DNA chain-terminators were first licensed as anti-HIV
drugs in 1987, although their immunotoxicity or bone "marrow suppression"
was immediately recognized (Kolata 1987; Richman et al 1987), see also
(Nussbaum 1990; Duesberg 1996b). The inevitable immunotoxicity and lethality
of AZT was confirmed in AIDS patients within less than a year after its
licensing as anti-HIV-AIDS drugs (Kolata 1987; Richman et al 1987; Dournon
et al 1988; Mir and Costello 1988). The label of a 100 mg-sample from the
Sigma Chemical Co, a non-medical supplier, even advertises the inevitable
toxicity of the DNA chain-terminator AZT with a scull and cross bones
(figure 4a).
Yet, the DNA chain-terminators are currently prescribed at doses of about
500 mg per day (part 4.2, and below). For example, a typical prescription flask
with 100 capsules of 100 mg Retrovir (AZT) from the medical supplier
Burroughs Wellcome instructs its late user (see below), "Take 1 capsule 5
times daily", but does not mention cellular or human toxicity (see figure
4b). Even HIV-positive pregnant mothers are prescribed 500 mg of AZT per day
during the second and third trimester of pregnancy to reduce the probability
of transmission of HIV to their babies by 17% (from 25% to 8%) - at the cost
of having to treat 100% of the pregnant mothers and babies with AZT (Connor
et al 1994), (see table 6 and particularly table 7 below for consequences).
(ii) HIV protease inhibitors: The HIV protease inhibitors were designed
to inhibit specifically auto-proteolytic processing of HIV proteins, which
is necessary for HIV assembly (Fields 2001). But since no therapeutic
effects were observed at the low doses at which these inhibitors "block HIV
replication in the test tube" (The Durban Declaration 2000), the
"anti-viral" doses were increased 4-5 orders of magnitude above what is
needed to render HIV noninfectious in vitro, or to 1 to 2 g of inhibitor per
day (Rasnick 1997). The high doses of protease inhibitors currently
administered to patients are at minimum 50 times that needed to completely
inhibit the cellular, intestinal aspartyl protease cathepsin D (calculation
based on the Roche inhibitor Saquinavir; the Abbott inhibitor Ritonivar is
1000 times more potent against cathepsin D than Saquinavir), (Deeks et al
1997).
Mice in which cathepsin D is deleted develop anorexia, their "Thymus and
spleen undergo massive destruction with fulminant loss of T and B cells",
and die about 26 days after birth (Saftig et al 1995). Thus protease
inhibitors can cause at least three AIDS defining diseases, anorexia (weight
loss), T-cell deficiency and death (see part 4e). In addition, diarrhea -
which is also an AIDS defining disease (Centers for Disease Control 1985,
1986, 1987) - is a common problem with all the protease inhibitors (table 6).
__________________________
(iii) Drug cocktails: AZT and other DNA chain-terminators are now
typically supplemented by inhibitors of proteases to form drug "cocktails"
(Ho 1995; Palella et al 1998; Day 2000; Stolberg 2001). A daily dose of
these includes about 1 g of one or more DNA chain-terminators per clinically
ill person and 0.5 g per asymptomatic HIV-positive per day (Stolberg 2001)
(see also part 4.2b), which is the equivalent of 1.5-3 . 10 6 molecules of
DNA chain-terminators per body cell!
Severe Hemophilia Moderate or Mild Hemophilia
100|- |
| |
| -^- All |
Deaths 80| -- HIV- ß | ß
per | -ß- HIV+ / | /
1,000 | / | /
60| ß | ß
| / | |
| / | |
40| ß | |
| / | /
| | - ß
20| ß | ß
| |
|_^_-_^_-_^_-_^____-__-__-_ | ^_-_^_-_^_-_^____-__-__-_
78 80 82 84 86 88 90 92 78 80 82 84 86 88 90 92
Figure 5. Mortality of HIV antibody-positive (+) and negative (-) British
hemophiliacs after the introduction of the DNA chain-terminator AZT, alias
zidovudine, in 1987 as anti-HIV therapy. The data are from a study by Darby
et al (1995) that considered HIV to be the cause of the sudden increase of
hemophilia mortality after 1985. Instead of HIV, which has been diagnosed in
hemophiliacs since 1984, the experimental introduction of AZT as anti-HIV
drug explains the sudden rise in mortality in 1985, and also the increase in
mortality irrespective of the degree of hemophilia (see part 4.3d).
___________________________________________________________________
Here, we present evidence that anti-HIV drugs cause AIDS defining
diseases, other diseases and death, both (i) in the presence and (ii) in the
absence of HIV.
(i) Diseases and death in HIV-positives treated with anti-HIV drugs: A
sudden 10-fold increase in the mortality of HIV-positive British
hemophiliacs, beginning right before the introduction of AZT in 1987, made
scientific headlines in 1995, because the increased mortality was attributed
to HIV by the authors of the study, i.e. Darby et al (1995), as well as by
the editor of Nature, "More conviction on HIV and AIDS" (Maddox 1995). Even
the editor of the Lancet wrote an editorial asking, "Will Duesberg now
concede defeat" (Horton 1995)? Darby et al based their conclusion on the
sudden 10-fold increase of the hemophiliacs' mortality around 1987, shown in
figure 5, on the facts that the increased mortality was restricted to
HIV-positive hemophiliacs and that the increase was independent of the degree
of hemophilia (which is inversely proportional to the life expectancy of the
patient). But, by 1987 transfusions of blood and factor VIII had already
infected most hemophiliacs for a long time. Most of them were already
infected well before 1984 (about 75% in the US), because all blood supplies
with HIV antibodies were banned after the introduction of the HIV-antibody
test in 1984 (Duesberg 1995c, 1996a). Moreover, the mortality of hemophiliacs
was steadily decreasing since the 1970s until 1985 - despite the presence of
HIV (Duesberg 1995c)!
__________________________
Thus the only new risk of mortality, beginning in 1985, was not HIV, but
AZT. Darby et al even acknowledged "treatment, by prophylaxis against P.
carinii pneumonia or with zidovudine (AZT), has been widespread for HIV
infected haemophiliacs since about 1989 (more accurately since 1987)". The
editor of Nature also pointed out that, "Darby et al failed to provide full
details of the drug regimen followed" (Maddox 1995). The AZT-mortality
hypothesis would of course also explain why the new hemophilia mortality was
independent of the severity of the hemophilia, as Darby et al observed.
Nevertheless Nature, did not accept an alternative interpretation,
specifically not from "Those who have made the running in the long controversy
over HIV in AIDS, Dr Peter Duesberg of Berkeley, California, in particular
. . ." (Maddox 1995). But, the Lancet accepted a response, which proposed
that AZT treatments were the probable cause of the sudden increase in
mortality of hemophiliacs (Duesberg 1995d).
According to researchers from the NIH, AZT also increased the mortality
of US hemophiliacs 2.7 times and their AIDS risk 4.5 times compared to
untreated controls (Goedert et al 1994; Duesberg 1995c). The medical
literature describes many more examples of AIDS defining, other diseases and
deaths that developed in HIV-positive asymptomatic people or in AIDS
patients treated with anti-HIV drugs, which were not observed in untreated
controls; some of these are summarized in table 6.
The case of Cesar Schmitz, married to an HIV-free wife and father of an
HIV-free healthy child in Miami, FL, is an example of AZT-mediated mortality
that did not appear in the medical literature (Duesberg 1996b). But his wife
Teresa has recorded his case in sufficient detail for inclusion in this
article. In March 1992, an asymptomatic Schmitz was found to be HIV-positive
at a medical check-up and pressured by his doctor to start AIDS prophylaxis
by AZT (figure 4b). Immediately after initiation of AZT treatment, Schmitz
developed "nausea, diarrhea and weight loss". In 1994 he decided, "against
his doctors will," to discontinue AZT medication, and "All of a sudden, like
magic, no more symptoms" (Duesberg 1996b). But, in 1998 Schmitz developed
lymphoma, which is a typical, late "side effect" that appears in 46% of
patients 36 months after initiation of AZT therapy (Pluda et al 1990). In
view of this and pressure from his doctors Schmitz started AZT therapy
again. Within months he was "paralyzed", suffered from "unbearable cramps"
and became incontinent (probably from mitochondrial dysfunction, see table
6), which his doctor explained as "side effects of one of the drugs he was
taking". And in October 1998 Schmitz passed away (T Schmitz, personal
communication).
(ii) Diseases and death in HIV-free humans and animals treated with
anti-HIV drugs: Table 7 lists rare studies reporting AIDS-defining and other
diseases in HIV-free humans and animals treated with anti-HIV drugs. Since
all HIV-positive, pregnant mothers are now treated with AZT during the last
6 months of their pregnancy to reduce the natural transmission of HIV to 25
to 50% of their babies, there are now over 50% HIV-free babies born to these
mothers who have all been treated with AZT (Connor et al 1994; The Durban
Declaration 2000). Table 7 lists two rare publications that describe the
diseases of these HIV-free, AZT-treated babies, such as fevers, pneumonia,
anemia, and mitochondrial dysfunction. In addition the table lists studies,
which have observed numerous diseases and deaths in HIV-free animals treated
with anti-HIV drugs. All of these animal studies were published after the
drugs had been licensed for humans (perhaps because licenses once issued are
almost impossible to withdraw) and only in specialty journals. Therefore,
these results are not known and not discussed in the popular and medical
AIDS literature.
The anti-HIV treatment-specific diseases and death summarized in tables 6
and 7 directly support the hypothesis that anti-HIV drugs are at least
necessary in the presence of HIV, and are sufficient in its absence to cause
most AIDS defining-diseases, other drug-specific diseases, and death. Since
about 450,000 US citizens are currently on DNA chain-terminators and
protease inhibitors as prophylaxis against, or therapy of AIDS (see above),
these drugs alone could have been sufficient to generate all of the 43,158
new AIDS patients reported in the US in 2001 (Centers for Disease Control
and Prevention 2001).
__________________________
4.3e The AIDS treatment dilemma: Do anti-HIV drugs, that cause AIDS
defining and other diseases, delay progression to AIDS and reduce
mortality?: Despite the inevitable toxicity of anti-HIV drugs, the over 5000
signatories of the Durban Declaration assert that, "drugs that block HIV
replication in the test tube also" (i) "delay progression to AIDS", and (ii)
"have reduced AIDS mortality by more than 80%". However, the authors of the
Declaration have not provided a reference for controlled studies in support
of their assertion. But, they do acknowledge "That it is crucial to develop
new antiviral drugs that . . . have fewer side effects" (The Durban
Declaration 2000). Since many doctors share the views of the Declaration, we
investigate here the evidence for these claims.
(i) Controlled studies investigating the ability of anti-HIV drugs to
"reduce mortality" and "delay progression to AIDS": The licensing study of
AZT, performed in 1987 by the NIH in collaboration with the drug's
manufacturer Burroughs Wellcome in the US, is the primary placebo-controlled
study set-up to test the ability of AZT to reduce the mortality of AIDS
(Fischl et al 1987; Richman et al 1987). The study showed that, after 4
months on AZT, 1 out of 145 AIDS patients died, whereas 19 out of 139 died
in the placebo group. The study interpreted this result as evidence for
reduced mortality by AZT. However, this interpretation failed to consider
that among the 4-month survivors of AZT, 30 could only be kept alive with
multiple blood transfusions because their red cells had been depleted by AZT
below survivable levels (Fischl et al 1987; Duesberg 1992). Thus, without
life-saving transfusions 30 more AZT-recipients would have died from anemia.
In addition many AZT recipients had developed life-threatening bone marrow
suppression, neutropenia, macrocytosis, headaches, insomnia and myalgia,
that augured poorly for their future survival (Richman et al 1987). Indeed,
the low mortality of 1/145 reported for the first 4 months on AZT, could not
be maintained in a follow-up study, which found the "survival benefits" of
AZT rapidly declining after the original 4 months period. By 21 months, 42%
of the original AZT group had died and 35% of the control group, which by
then had also received AZT for 12 months on a "compassionate" basis (Fischl
et al 1989). Thus the placebo-controlled, licensing study did not prove that
AZT "reduces AIDS mortality by more than 80%" compared to the untreated
control.
The ability of AZT to "delay the progression to AIDS" was investigated in
1994 by the largest, placebo-controlled study of its kind, the
British-French Concorde study (Seligmann et al 1994). This study
investigated 1749 HIV-positive, mostly male homosexual subjects divided into
untreated and AZT-treated subgroups for the onset of AIDS and death. The
Concorde study found in 1994 that AZT is unable to prevent AIDS and
increases the mortality of recipients by 25%. In view of this it concluded,
"The results of Concorde do not encourage the early use of zidovudine (AZT)
in symptom-free HIV-infected adults." (Seligmann et al 1994). Thus there is
no controlled evidence that anti-HIV drugs "reduce the mortality of "or
"delay progression to AIDS".
(ii) Uncontrolled studies investigating the mortality of HIV-positives on
HIV drugs: Despite the discouraging results of these controlled studies,
AIDS researchers now credit the more recently developed anti-HIV drug
cocktails for a "declining morbidity and AIDS (Palella et al. 1998).
However, the evidence for "declining morbidity and mortality" is only based
on uncontrolled survey studies that investigated how long HIV-positive,
clinically healthy subjects, but mostly from AIDS risk groups, survived on
various anti-HIV drugs. The largest and most influential of these surveys
was conducted by Palella et al (1998) who investigated in 1998 1255 anti-HIV
drug-treated "patients, each of which had at least one CD4+ count below 100"
from nine clinics in the US. However, all of these "patients" were
"nonhospitalized", AIDS-free subjects. "Patients with a diagnosis of
cytomegalovirus retinitis or M. aviarum complex disease before study entry
or during the first 30 days of follow-up and patients with active P. carinii
pneumonia at the beginning of follow-up were excluded."
__________________________
A similar survey investigated in 2001 1219 anti-HIV drug-treated Canadian
HIV-positives with less than 200 CD4+ cells, of which 87% were AIDS-free
(Hogg et al 2001). Neither of these studies mentions drug-free controls. On
this basis the Palella study found that the mortality of initially
asymptomatic, HIV-positive people, which are treated with new anti-HIV drug
cocktails, is 8.8% ("8.8 per 100 person-years") and the Hogg-study found it
is 6.7%.
But, in the absence of untreated control groups, the effects of the new
anti-HIV drugs on the morbidity and mortality of HIV-positive recipients can
not be determined scientifically from the results of these surveys. However,
the average annual AIDS mortality of all HIV-positives on this planet
[including the minority that is on anti-HIV drugs (The Durban Declaration
2000)] can be estimated for 2000, the year that falls in between the two
surveys, based on data provided by the WHO and the Durban Declaration: The
WHO and the Declaration report in 2000 34.3 million "living with HIV", and
the WHO reports 471,451 AIDS cases for 2000 (World Health Organization
2001b) (obtained by subtracting the WHO's cumulative total of 1999 from that
of 2000, see also table 4). Thus, even if we assume that all AIDS cases were
fatal in 2000, the resulting global mortality rate of HIV-positives would
only be 1.4% - and thus 4 to 6 times lower than the 6.7-8.8% mortality rate
of HIV-positives treated with anti-HIV drugs in the US and Canada.
Therefore, the claims that anti-HIV drugs reduce the mortality of, and delay
progression to AIDS are at odds with the AIDS facts reported by the Durban
Declaration and the WHO. Contrary to these claims, the controlled trials and
uncontrolled surveys listed above prove that anti-HIV drugs (possibly in
conjunction with recreational drugs) increase the mortality of HIV positives
4- to 6-fold. It would appear that anti-HIV drugs are prescriptions for,
rather than treatments of AIDS.
(iii) Skepticism about anti-HIV drugs in the medical establishment: Even
in the absence of scientifically controlled studies proving the toxicity of
the new anti-HIV drugs, many AIDS doctors and researchers have warned of the
numerous toxic effects of these drugs - even the Durban Declaration calls
for drugs wich "have fewer side effects". For example, HIV co-discoverer Jay
Levy wrote in the Lancet, "Caution: should we be treating HIV infection
early? . . . No cancer patient takes three or four chemotherapeutic drugs
for a lifetime. What is overlooked . . . is that these drugs can be toxic
and can be directly detrimental to a natural immune response to HIV." (Levy
1998). And retrovirus researcher Etienne De Harven describes the treatment
of AIDS with DNA chain-terminators as a "so-called therapy worse than the
disease itself!" (de Harven 1999).
Because of such concerns about the toxicity of anti-HIV drugs AIDS
doctors have recently introduced "structured treatment interruption" (Lori
et al 2000) or "drug holidays" (Christensen 2000), to allow the patients to
recover from the toxic effects of the DNA chain-terminators, such as AZT,
ddI, and d4T, and of the protease inhibitors prescribed to kill HIV. In the
words of Kendall Smith from the New York Hospital-Cornell Medical Center,
"Right now, the disease is life-threatening (he did not say HIV), on one
hand, and the drugs that we have so far have life-threatening toxicities, on
the other hand. It puts us between a rock and a hard place." (Christensen
2000).
In view of this the US government has appointed a panel of AIDS
scientists to review the toxic effects of antiviral medications and issued
recommendations to restrict prescriptions of anti-HIV drugs that were
published by the New York Times (Altman 2001b):
__________________________
"Altering a long-held policy, federal health officials are now
recommending that treatment for the AIDS virus be delayed as long as
possible for people without symptoms because of increased concerns over
toxic effects of the therapies. . . . More recently, concern has grown over
nerve damage, weakened bones, unusual accumulations of fat in the neck and
abdomen, diabetes and a number of other serious side effects of therapy.
Many people have developed dangerously high levels of cholesterol and other
lipids in the blood, raising concern that H.I.V.-infected people might face
another epidemic-of heart disease. . . . Dr Fauci, who is co-chairman of the
panel, said in an interview, "We are adopting a significantly more
conservative recommendation profile'". (According to the panel), "Much
remains to be learned about how best to treat H.I.V.-infected individuals".
However, it is hard to understand, why it should have taken AIDS
researchers 14 years since the introduction of DNA chain-terminators as
anti-HIV drugs (Kolata 1987) to make these observations and issue warnings
about the "side effects" of these drugs.
In April 2001, the FDA followed up on these concerns by "ordering drug
makers to tone down their upbeat ads for AIDS medications, calling them
`misleading' . . . because they imply greater efficacy than demonstrated by
substantial evidence, or minimize the risks associated with HIV drugs"
(Russell 2001) - again 14 years after approving these drugs for currently
450,000 American recipients.
Many other independent observers have since commented on the "U-turn" of
AIDS researchers (Day 2000) from "Hit HIV early and hard" in 1995 (Ho 1995)
to reducing, skipping and delaying treatments, and even recalling some
anti-HIV drugs (Altman 2001c; Associated Press 2001). Even conservative,
nonscientific media such as Mothering magazine now warn expecting mothers
not to use anti-viral drugs during pregnancy with heart-breaking accounts of
the clinical consequences for the babies, and of the bewildering pressures
by the medical and even legal authorities on mothers to enforce compliance
with prescriptions of DNA chain-terminators for their babies (Farber 1998;
Gerhard 2001; Hodgkinson 2001).
But despite a preponderance of evidence against anti-HIV drugs, these
drugs have not been restricted or banned by any country except South Africa
(Cherry 2000).
4.4 Prediction 3: AIDS diseases and epidemics
are not self-limiting via immunity
The drug hypothesis predicts that AIDS is not self-limiting via immunity.
Indeed twenty years into the AIDS epidemics, there is no evidence of
individual immunity against AIDS, nor is there any evidence that any of the
AIDS epidemics is self-limiting (World Health Organization 1999; The Durban
Declaration 2000; Centers for Disease Control and Prevention 2001), (see
figure 1a, c). According to the Durban Declaration, "there is no end in
sight". Indeed the chronologies of the current AIDS epidemics conform
exactly to the time courses of epidemics of chemical diseases that are not
self-limiting, such as the American drug epidemic shown in figure 2, and the
epidemics of smoking and of subsequent lung cancers in England, shown in
figure 3b.
4.5 Prediction 4: No AIDS in the absence of anti-viral and recreational
drugs, despite HIV
To test this prediction, HIV antibody-positive people, who are not using
drugs, must be identified who survive the average hypothetical latent period
from HIV to AIDS of 5-10 years (part 3, table 4). The following examples meet
this prediction.
__________________________
In 2002 the San Francisco Chronicle described a small group of drug-free
and AIDS-free long-term survivors of HIV. Among them is a healthy artist who
is HIV-positive for 23 years (based on frozen blood samples) and was
"chastised by his doctors when he refused to start taking medication"
(Hendrix 2002). Further, a 1-year old HIV-positive, AZT-treated baby girl
with severe muscle pain, insomnia, nausea and failure to grow was taken off
AZT treatments in 1992 based on our hypothesis; as a result the baby
immediately recovered (Duesberg 1996b). Now, at the age of 11, she is a
completely normal, healthy kid, and a leading player in her school's soccer
team (Sheryl and Steve Nagel, personal communication). In addition, People
magazine just described a healthy woman who is HIV-positive for an estimated
15 years, and "needs no medication". The woman has since founded a support
group, termed Center for Positive Connections, for HIV-positive
heterosexuals in Miami (Cheakalos and Rosza 2002). In Los Angeles, Christine
Maggiore is HIV-positive since 1992, has given birth to two very healthy
children, ages 1 and 5, and has never taken anti-HIV drugs. Maggiore, a
former HIV-AIDS counselor, has since also founded a support group, Alive &
Well, and has written a book, What if everything you thought you knew about
AIDS was wrong?, to instruct HIV-positives not to use anti-HIV drugs
(Maggiore 2000). An appendix of the book features letters from 34
Maggiore-graduates, all living over 10 years with HIV but without anti-HIV
drugs, or after having discontinued such drugs.
Even HIV-AIDS researchers have inadvertently confirmed our prediction of
no AIDS in drug-free HIV-positives. For example, David Ho, signatory of the
Durban Declaration, points out that in a group of "long-term survivors" of
HIV studied in his lab, "none had received antiretroviral therapy" (Cao et
al 1995). In a parallel publication, Pantaleo et al studying a group of
long-term "non-progressors" of HIV have made the same observation (Pantaleo
et al 1995). Ho et al recently attributed long-term survival to some special
human proteins, termed "defensins" (Zhang et al 2002), but acknowledged
personally that all long-term survivors had again abstained from anti-HIV
therapies (David Ho, personal communication). One wonders why any humans
would ever get sick from HIV, if the human genome encodes HIV defensins!
Munoz reported that none of the long-term survivors of the largest,
federally funded study of AIDS risk factors of homosexual men, the MACS
study, had used AZT (Munoz 1995). Fahey et al observed that among
HIV-positive male homosexuals with less than 200 T-cells per ml, "45% of the
group who were AIDS-free > or = 3 years after CD4+ cells fell below 200
10 6 /l had not used these (anti-HIV) treatments." (Hoover et al 1995).
According to a university magazine, AIDS researchers Abrams and Levy from
the University of California at San Francisco have lectured in 1998 on
drug-free long-term survivors of HIV to their medical students (Tanaka 1996;
Duesberg and Rasnick 1998). Levy also published in 1998 in the Lancet, that
"effective antiviral immune response is characteristic of long-term
survivors who have been infected for over 20 years, have no symptoms, and
have not been on any therapy" (Levy 1998). In 1999, Pitcher et al also
described a group of 9 "long-term non-progressors (with) untreated HIV-1
infection for 7-15 years", compared to controls with a "decline of (T cells)
with antiretroviral therapy" (Pitcher et al 1999). An Australian research
team described a group of untreated HIV-positives who were infected by blood
transfusions but did not develop AIDS 10 years later (Learmont et al 1992).
Further, Migueles et al (2000) reported that none of 13 long-term survivors
had received "antiretroviral therapy". Carr et al (2001) observed even
recovery from fatal hypertension, liver failure and mitochondrial
dysfunction after discontinuation of antiviral drugs that had been
prescribed to a previously healthy HIV-positive man. Thus HIV-AIDS
researchers confirm our prediction that HIV-positives, who do not use drugs,
do not develop AIDS or may even recover from it.
__________________________
In an effort to obtain independent proof that abstaining from anti-HIV
drugs and recreational drugs is sufficient to survive HIV-infection or even
to recover from AIDS, one of us, CK, in 1985 initiated a study of AIDS
patients from Kiel, Germany, who have volunteered to abstain from anti-HIV
treatments. Remarkably, only 8% (3 of 36) of the patients not treated with
anti-HIV drugs have died since their HIV antibodies were first detected, two
of them 16 years and one 10 years after their first diagnosis of antibodies
against HIV (table 8). Most have recovered from their initial AIDS-indicator
symptoms. By contrast, 63% of all German AIDS patients (11,700 out of
18,700) of which most were treated since 1987 with anti-HIV drugs have died
(Robert Koch Institut 2000). Thus our relatively small sample supports the
hypothesis that without anti-HIV drugs and/or recreational drugs HIV fails
to cause AIDS. Indeed without drugs AIDS patients recover, despite the
presence of HIV.
Table 8. Long-term HIV survivors not treated with antiviral drugs and
abstaining from illicit, psychoactive drugs from the Kiel-Koehnlein
study begun in 1985.
Date Illicit Cause of
Case HIV+ Age Sex Medical issues CD4 drugs Treatment Death
____ ____ __ _____ ______________ ___ ______ _________ ______
1 1985 52 m-homo Herpes zoster 256 ? None
2 1985 45 f Asymptomatic None
3 1985-2001 43 m PCP, TB 4 iv Antibiotics Heart fail
4 1985-2001 42 m-homo Kaposi, PCP Nitrites None Kaposi
5 1985 35 m Psoriasis None
6 1985 38 f Salmonella sepsis 28 Antibiotics
7 1985 31 m Hemophilia, low
lymphadenopathy
8 1985 30 m Hemophilia 325 None
9 1986 17 f(black) Asymptomatic 450 None
10 1986 31 m Asymptomatic
11 1988 32 f Asymptomatic None
12 1989 49 f Candida, TB 28 iv Antibiotics
13 1990 34 m-homo Coli-Meningitis, 85 Nitrites Shunt
Hydrocephalus
14 1991 6 m Pneumonia Antibiotics
15 1991 31 f Asymptomatic None
16 1991-2001 36 f Toxoplasmosis 1993-94 AZT, Toxoplas-
antibiotics mosis
17 1992 33 f Asymptomatic 460 None
18 1993 7 f Asymptomatic None
19 1996 52 m-homo Facial paresis 540 Nitrites None
20 1996 39 m-homo Asymptomatic 485 Nitrites None
21 1996 38 m Pneumonia, 53 Antibiotics
Sinusitis
22 1997 44 m-homo Colitis Nitrites None
23 1997 37 m-homo Asymptomatic 223 Nitrites None
24 1997 37 m-homo Thrombocytopenia 700 Nitrites Cortisone
25 1997 34 m-homo Asymptomatic 220 Nitrites None
26 1997 33 m-homo Lymphadenopathy None
27 1997 31 m-homo Thrombocytopenia 357 Nitrites Cortisone
28 1997 3 m Pneumonia Antibiotics
29 1998 31 m-homo Diarrhea Nitrites None
30 1998 40 m-homo Condyloma, 107 Nitrites None
Candida
31 1998 39 m-homo Diarrhea 187 Nitrites None
32 1998 27 m-homo TB of the bowel 18 Antibiotics
33 2000 35 m-homo Asymptomatic None
34 2000 31 m-homo Lymphadenopathy, None
EBV
35 2000 30 m-homo Asymptomatic 428 None
36 2000 27 f Lymphadenopathy, 107 None
EBV
__________________________
m, Male; f, female; PCP, Pneumocystis carinii pneumonia; EBV, Epstein-Barr
virus; AZT, azidothymidine; TB, tuberculosis. Evidence for illicit drug
use is self reported; iv, intravenous drug use.
__________________________________________________________________________
4.6 In sum, the chemical AIDS-hypothesis explains the AIDS facts, and
resolves all paradoxes of the HIV-AIDS hypothesis
Our review shows that the chemical-AIDS hypothesis explains all AIDS
facts: the non-random distribution of drug-AIDS in the US and Europe, the
risk-group-specific AIDS diseases in the US and Europe as consequences of
risk-group-specific drugs, the random distribution of malnutrition-AIDS in
impoverished parts of Africa, the non-contagiousness of chemical AIDS, the
absence of natural immunity against chemical AIDS, the lifestyle-dependent
onset of AIDS diseases - unrelated to, but typically long after infection by
HIV, and the time courses of the AIDS epidemics of the US and Europe as
consequences of the drug epidemics.
In addition chemical AIDS proves that HIV is not necessary for even one
AIDS-defining disease, because (i) drugs and malnutrition cause drug and
malnutrition specific AIDS diseases regardless of the presence of HIV,
because (ii) in HIV antibody-positives and negatives the risk of developing
AIDS is proportional to the degree or lifetime dosage of drug use, and (iii)
because all AIDS diseases have been diagnosed in HIV-free AIDS risk groups
by AIDS researchers (Duesberg 1993d) and also long before the AIDS era
(Stedman's Medical Dictionary 1982). Thus HIV meets all criteria of a
harmless passenger virus, laid out in table 4 and described previously
(Duesberg 1994; Duesberg and Rasnick 1998). In this way our proposal
resolves the fundamental paradox of the HIV-AIDS hypothesis: the paradox
that a latent, non-cytopathic and immunologically neutralized retrovirus,
that is only present in less than 1 out of 500 susceptible T-cells and
rarely expressed in a few of those, would cause a plethora of fatal diseases
in sexually active, young men and women. And, that the plethora of diseases
attributed to this virus would not show up for 5-10 years after infection.
The chemical AIDS hypothesis could be readily refuted by any of the
following experiments:
(i) Demonstrate that in two matched groups, differing only with regard to
HIV infection, HIV-positives develop AIDS but HIV-negatives do not (above
the low, long-established risk of AIDS defining diseases in the general
population). HIV antibody-positive and negative recruits from the US Army,
which tests routinely for HIV, would be ideal for this experiment since
their health, lifestyles and age are closely matched.
(ii) Demonstrate that in two matched groups of intravenous drug users,
differing only in the presence of HIV, only the HIV-positives develop AIDS
diseases.
(iii) Demonstrate that in two matched groups of HIV-positive humans,
differing only in the addiction to recreational drugs, both groups have the
same incidence of AIDS-defining diseases.
(iv) Demonstrate that in two matched groups of HIV-free humans or
animals, differing only with regard to the addiction to or treatment with
recreational drugs, neither group would develop AIDS defining diseases over
time.
(v) Demonstrate that in two matched groups of HIV-positives, differing
only in the treatment with anti-HIV drugs, the untreated group develops AIDS
long before the treated group.
(vi) Demonstrate that in two matched groups of pregnant, HIV-positive
mothers, differing only in the now standard treatment with AZT during the
last two trimesters, those treated with AZT are free of abortions and
deliver healthy babies, but those who are not treated either abort
spontaneously or deliver babies with AIDS.
(vii) Demonstrate that in two groups of HIV-positive hemophiliacs matched
for age and lifetime dosage of factor VIII, differing only in anti-HIV
treatments, those who are untreated have a higher mortality and a higher
AIDS risk than treated controls.
__________________________
Although the controlled studies proposed here follow classical,
scientific standards, they are not available in the huge AIDS literature.
This is surprising in view of the many AIDS advocacy groups or "activists"
reviewing AIDS research for flaws and for new clues. The lack of adequately
controlled studies of the long-term effects of recreational drugs and
anti-HIV drugs in animals is particularly surprising, because all of these
drugs and research funds for AIDS are abundant. Yet despite the scientific
intolerance of current AIDS science for alternative hypotheses (Weiss and
Jaffe 1990; Cohen 1994; O'Brien and Goedert 1996), the pathogenicity of most
of the chemicals proposed here to cause AIDS - illicit drugs, antiviral
drugs, and malnutrition - has de facto already been proved - even by
HIV-AIDS researchers, despite their efforts to the contrary [see above,
tables 6 and 7 and Duesberg and Rasnick (1998)].
Suppose the chemical-AIDS hypothesis were confirmed and accepted: AIDS
would be entirely preventable by banning anti-HIV drugs, by publicizing that
recreational drugs cause AIDS and by adequate nutrition. More-over, many
AIDS patients could still be saved from fatal damage by drug intoxication,
if their AIDS-defining diseases were treated with time-proven,
disease-specific medications. Such testable predictions are the hallmarks of
a good hypothesis.
So, why do current AIDS researchers not investigate and not even consider
the role of chemicals in AIDS or study other non-HIV-AIDS theories to solve
the AIDS dilemma? The following is an attempt to answer this question.
5. Epilogue
5.1 Why is AIDS research not free to investigate non-HIV hypotheses?
The probable answer to the question, of why HIV-AIDS researchers do not
study or fund non-HIV-AIDS theories, lies in the structure of the large,
government-sponsored research programs that have dominated academic research
since World War II (Duesberg 1996b). Such programs favour individual
investigators who contribute, to the common body of knowledge, a maximum of
data and a minimum of controversy. However, if individual researchers move
into new directions, that threaten the scientific and commercial investments
of the general body of established researchers, those affected can impose
various sanctions via the "peer review system". The most powerful of these
are denial of funding and of publication.
The peer review system derives its power from the little known practice
of governments to deputize their authority to distribute funds for research
to committees of "experts". These experts are academic researchers
distinguished by outstanding contributions to the current recognized body of
knowledge. They alone review the merits of research applications from their
peers, and they have the right to elect each other to review committees.
Outwardly, this "peer review system" appears to the unsuspecting
government and taxpayer as the equivalent of a jury system - free of all
conflicts of interest. But, in view of the many professional and commercial
investments involved in medical research, and financial rewards from
universities and institutions for the corresponding overheads and
partnerships - all legal in the US since president Reagan - "peer reviewers"
do in fact have severe conflicts of interest and do not fund applications
that challenge those interests (Duesberg 1996b; Lang 1998; Zuger 2001).
Since "peer review" is protected by anonymity, and does not allow the
applicant personal representation or an independent representative, nor a say
or even a veto in the selection of the "jury", and does not allow an appeal,
its powers to defend the orthodoxy are unlimited. The corporate equivalent of
academia's peer review system" would be to give General Motors and Ford the
authority to review and veto all innovations by less established carmakers
competing for the consumer.
__________________________
Even the professional journals and the science writers of the public
media comply with the interests of government-funded majorities because they
depend on their monthly "scientific breakthroughs", the lucrative
advertisements from their companies, and the opinion of their subscribers.
For example, an early precursor of this article was written in response to
an open invitation from a pharmacology-journal over 3 years ago. But, after
considerable pressure on the journal from anonymous "AIDS experts", the
editor requested a reduced article, which was neither accepted nor rejected.
Instead, the editor simply dropped all further correspondence. Subsequently,
the editor of a prestigious German-based science journal invited another
precursor of this article 2 years ago, which received two favourable reviews
in short order. But before the manuscript could be revised, the editor
informed us that the publisher was concerned about losing subscribers if our
paper were published and ceased all further correspondence. It is this
passive resistance that can grind down even the most determined truth
seeker.
Acknowledgements
We gratefully acknowledge critical and challenging information from the
presidential AIDS advisory panel of South African president Thabo Mbeki,
especially those who joined us in publishing a rebuttal to the Durban
declaration (Stewart et al 2000). Harry Haverkos (CDC/ FDA, Rockville, MD),
Phil Johnson (UC Berkeley), Roland Scholz (Institut fuer Physiologische
Chemie, University of Muenchen, Germany), David Steele (Attorney, San
Francisco), and Rudi Werner (University of Miami, School of Medicine) are
acknowledged for providing critical comments and specific information. We
also appreciate expert technical assistance in preparing the manuscript from
Sigrid Duesberg, and the figures from Ruhong Li (UC Berkeley). We thank
philanthropists Michael S Kennedy (Panama City, FL), Christopher Morrill
(San Anselmo, CA), Robert Leppo (San Francisco, CA), an American foundation
that prefers to be anonymous, the Abraham J and Phyllis Katz Foundation (New
York), and other private sources for support.
__________________________
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