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Abstract
Almo st two decades of unp recedented effo rts in research costing US taxp ayers over $50 billion have
failed to d efeat Acq uir ed I mmune Deficiency Synd r o me ( AI DS) and have failed to exp lain the
chr o no lo gy and ep id emio lo gy o f AI DS in Amer ica and Eur o p e. T he failur e to cur e AI DS is so co mp lete
that the lar gest Amer ican AI DS fo und atio n is even exp lo iting it fo r fund r aising: 'Latest AI DS statistics
- 0,000,000 cured. Support a cure, support AMFAR.' T he scientific basis of all these unsuccessful
effo r ts has b een the hyp o thesis that AI DS is caused b y a sexually tr ansmitted vir us, ter med Human
immunodeficiency virus (HIV), and that this viral immunodeficiency manifests in 30 previously kno wn
microbial and no n-microbial AI DS diseases.
I n o r d er to d evelo p a hyp o thesis that exp lains AI DS we have co nsid er ed ten r elevant facts that
Amer ican and E ur o p ean AI DS p atients have, and d o no t have, in co mmo n: ( 1 ) AI DS is no t co ntagio us.
Fo r example, no t e ve n o ne he a lth c a r e wo rke r has c ontra c te d AI DS fr om ove r 800,000 AI DS patients in
Amer ica and Eur o p e. ( 2 ) AI DS is highly no n-r and o m with r egar d to sex ( 8 6 % male) ; sexual p er suasio n
( o ver 60% ho mo sexual) ; a nd a ge ( 8 5 % are 25-49 ye a rs old). (3) Fr om its be ginning in 1980, the AI D S
epidemic progressed no n-exponentially, j ust like lifestyle diseases. (4) T he epidemic is fr agmented
into distinct subepidemics with exclusive AI DS-d efining diseases. For example, only ho mo sexual
males have Kap o si's sar c o ma . ( 5 ) P a tients do no t have a ny one of 30 AI DS-de fining dise a ses, no r even
immunodeficiency, in commo n. For example, Kaposi's sarcoma, dementia, and weight loss may occur
without immunodeficiency. T hus, there is no AI DS-specific disease. (6) AI DS patients have antibody
against HI V in co mmo n o nly b y d efinitio n-no t b y natur al co incid ence. AI DS-d efining d iseases o f
HIV-fr ee patients are called by their old names. (7) Recreational drug use is a commo n deno minator
fo r o ver 9 5 % o f all Amer ican and Eur o p ean AI DS p atients, includ ing male ho mo sexuals. ( 8 ) Lifetime
prescriptions of inevitably toxic anti-HIV drugs, such as the DNA chain-terminator AZT , are another
commo n deno minator of AI DS patients. (9) HIV proves to be an ideal surrogate marker fo r recreational
and anti-HIV drug use. Since the virus is very rare (< 0.3%) in the US/European populatio n and very
hard to tr ansmit sexually, only those who inj ect street drugs or, have over 1,000 typically
d r ug-med iated sexual co ntacts ar e likely to b eco me p o sitive. ( 1 0 ) T he huge AI DS liter atur e canno t
offer even one statistically significant gr oup of drug-fr ee AI DS patients fr om America and Europe.
I n view of this, we p r o p o se tha t the lo ng-te rm c onsumptio n of re c re a tio nal drugs (such as cocaine,
her o in, nitr ite inhalants, and amp hetamines) and p r escr ip tio ns o f DNA chain-ter minating and o ther
anti-HIV drugs, cause all AI DS diseases in America and Europe that exceed their long-established,
national backgr ound s, i.e. >95%. Chemically distinct drugs cause distinct AI DS-defining diseases; fo r
example, nitrite inhalants cause Kaposi's sarcoma, cocaine causes weight loss, and AZT causes
immunodeficie nc y, lymp ho ma, muscle a trophy, a nd de mentia. T he drug hypothesis pre dicts that AI D S:
( 1 ) i s no n-conta gi o us; ( 2 ) i s no n-r a nd o m, be c a use 85% of AI DS c a using drugs a re use d by males,
particularly sexually active ho mo sexuals between 25 and 49 years of age, and (3) wo uld fo llow the
d r ug ep id emics chr o no lo gically. I nd eed , AI DS has incr eased fr o m negligib le numb er s in the ear ly
1 9 8 0 s to a b o ut 8 0 , 0 0 0 a nnual cases in the ear ly '9 0 s and has since d eclined to ab o ut 5 0 ,000 cases (U S
figur es) . I n the same p er io d , r ecr eatio nal d r ug user s have incr eased fr o m negligib le numb er s to
millions by the late 1980s, and have since decreased possibly twofold. However, AI DS has declined
less because since 1987 increasing numbers of mo stly healthy, HIV-positive people, currently about
2 0 0, 000, use a nti-HI V d r ugs tha t c a use AI DS a nd other dise a se s. At le a st 64 scientific stud ies,
go ver nment legislatio n, and no n-scientific r ep o r ts d o cument that r ecr eatio nal d r ugs cause AI DS and
o ther d iseases. Likewise, the AI DS liter atur e, the d r ug manufactur er s, and no n-scientific r ep o r ts
confirm that anti-HIV drugs cause AI DS and other diseases in humans and animals. In sum, the AI DS
d ilemma could b e so lve d b y b a nning a nti-HIV drugs, a nd by pointing out tha t drugs c a use AI D S -
modeled on the successful anti-smo king campaign.
An unflinching determination to take the whole evidence into account is the only method of preservation
against the fluctuating extremes of fashionable opinion.
Al f r e d N o r t h W h i t e h e a d ( 1 8 6 1 - 1 9 4 7 ) ( W h i t e h e a d , 1 9 6 7 ) .
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Introduction
In the US, the epidemic of the Acquired Immune Deficiency Syndrome (AIDS) has risen from
negligible numbers in the early 1980s to about 80,000 annual cases in the early 1990s and has
since declined to about 50,000 cases (Centers for Disease Control and Prevention, 1997). In
the same period, the European epidemic has reached about 20,000 annual cases in the ´90s,
and is now also declining slowly (World Health Organization, 1995b; AIDS-Zentrum im
Robert Koch-Institut, 1997). To date, the epidemic has generated 650,000 American and over
150,000 European AIDS patients (Figure 1A, C) (World Health Organization, 1995b;
AIDS-Zentrum im Robert Koch-Institut, 1997; Centers for Disease Control and Prevention,
1997; Fiala & Lingens, 1997).
Since 1984, all efforts in research, treatment and prevention of AIDS are based on the
hypothesis that AIDS is an infectious immunodeficiency caused by a sexually transmitted
virus, termed human immunodeficiency virus (HIV) or ´AIDS virus´ (Altman, 1984).
According to the Centers for Disease Control (CDC) in Atlanta, the viral immunodeficiency
manifests in 30 previously known microbial and non-microbial diseases (Centers for Disease
Control and Prevention, 1992). However, 15 years after the discovery of HIV (Barre-Sinoussi
et al., 1983), leading scientists and policy makers cannot demonstrate that their efforts against
the virus have saved a single life. Despite a cost of over 50 billion dollars to US taxpayers,
there is no vaccine and no effective anti-AIDS drug (Gutknecht, 1995; Duesberg, 1996d). The
failure to defeat AIDS is so complete that it is now even exploited by America´s largest
private AIDS research foundation for fundraising:
´Latest AIDS statistics - 0,000,000 cured. Support a cure, support AMFAR.
Call 1-800-39AMFAR.´
In reality, even the zero-cure admission is a massive understatement of the non-achievements
of the HIV hypothesis. Since HIV has become the official cause of AIDS, hundreds of
thousands of HIV antibodypositive Americans and Europeans with and without AIDS (!) have
been put on lifetime prescriptions of inevitably toxic DNA chain-terminators and protease
inhibitors prescribed as anti-HIV drugs (Duesberg, 1992a; Duesberg, 1996d; Hodgkinson,
1996) (see below). Moreover, in the name of the HIV-AIDS hypothesis, recreational drug use
is not only disregarded as a cause of AIDS, it is instead explicitly excused as a cause of any
disease (Kaslow et al., 1989; Ascher et al., 1993; Schechter et al., 1993c), and even promoted
with slogans like ´heroin is a blessedly untoxic drug´ (Cohen, 1994a). The heroin slogan was
published by Science in the same year, 1994, in which 3,522 Americans died and 64,013 were
hospitalized because of heroin toxicity (see below, Table 4). Proponents of the HIV hypothesis
blame the high morbidity and mortality of drug addicts only on HIV.
In contrast to AIDS, all infectious epidemics of the past, such as polio, cholera, tuberculosis,
small pox, and syphilis, have long been brought under control, or even eliminated, at a
fraction of the cost of AIDS, and with technology that was far less sophisticated than what is
available now. As a result of these scientific triumphs of the past, only less than one percent
of us now die from infectious diseases (Cairns, 1978). In view of this, the continued failures
of the war on AIDS call into question the hypothesis that AIDS is an infectious disease.
In the meantime, the multibillion dollar AIDS research effort also proved to be disappointing.
Despite unprecedented efforts by thousands of virologists and hundreds of thousands of
medical scientists, there are numerous unanswered questions about the AIDS epidemic in
America and Europe:
1. Why would antibodies against HIV (a positive HIV test), which are so effective that leading
AIDS researchers cannot detect HIV in most AIDS patients (Gallo, 1991; Weiss, 1991;
Cohen, 1993), not protect against AIDS?
2. Why have doctors and nurses never caught AIDS from over 800,000 American and European
AIDS cases - particularly in the absence of a HIV vaccine?
3. Why are 9 out of 10 AIDS patients males?
4. Why are about two-thirds male homosexuals?
5. Why are one-third intravenous drug users?
6. Why are most AIDS patients 25-49 years old, and why don´t teenagers get AIDS?
7. Why is AIDS new, although HIV is long-established in the US and Europe?
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8. Why would a new, sexually transmitted disease not have exploded in the millions of
heterosexually active Americans and Europeans - j ust as syphilis once did in medieval
Europe?
9. Why did HIV-positive American hemophiliacs live over twice as long in 1987 as they did in
the pre-AIDS era, and why has their mortality increased ten-fold after the introduction of
the anti-HIV drug AZT?
10. Why does AIDS manifest in totally unrelated diseases, for example, dementia, diarrhea, and
Kaposi's sarcoma?
11. Why do only male homosexuals get Kaposi's sarcoma?
12. Why are thousands of AIDS cases HIV-free (Duesberg, 1993e)?
…◆…HIV + cases × 10
-4
Figure 1
Each of these questions addresses a paradox of the HIV hypothesis. But there are no paradoxes
in nature, only flawed hypotheses.
To solve the AIDS dilemma, and to develop a hypothesis that answers all of these questions,
we have considered all available facts of the AIDS epidemic in America and Europe, following
the classic procedure described by Cairns: ´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 the sufferers have in common. This was true for the infectious diseases, the various
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dietary and vitamin deficiencies, the many kinds of "natural" and industrial poisonings and so
on´ (Cairns, 1978). The scope of our study is limited to American and European AIDS for
reasons that will become apparent in this article. African, Haitian, and Asian AIDS have been
covered elsewhere (Duesberg, 1992a; Duesberg, 1996d; Hodgkinson, 1996; Fiala & Lingens,
1997; Fiala, 1998; Shenton, 1998).
Goedert, 1996; O'Brien, 1997). However, until their AIDS diseases and their anti-AIDS
treatments are described they cannot even be considered anecdotal cases.
Further, the three million Americans who annually receive blood transfusions for
life-threatening diseases (Duesberg, 1992a) should have developed AIDS from blood donors if
AIDS were infectious. But there was no increase in AIDS-defining diseases (Table 1) among
transfusion recipients in the AIDS era (Ward et al., 1989), and no AIDS-defining Kaposi´s
sarcoma has ever been observed in millions of transfusion recipients (Haverkos et al., 1994;
Duesberg, 1995d; Duesberg, 1996c; Hodgkinson, 1996). Contrary to predictions of
transfusable AIDS, the life span of American hemophiliacs has increased more than two fold,
from 11 years in the early 1970s to 27 years in 1987 (the year AZT was introduced, see below)
because they were prophylactically treated with transfusions of factor V III (Duesberg, 1995c).
Numerous anecdotal cases of ´discordant couples´ confirm that AIDS is not contagious: The
tennis star Arthur Ashe lived for 10 years with his wife and had an 8-year-old daughter before
he died from AIDS and AZT in 1994, but his family is AIDS-free (Ashe & Rampersad, 1993;
Duesberg, 1996d). Also in 1994, the wife of Hollywood actor Paul Glaser died from AIDS and
AZT, but after a marriage of 13 years and two children Glaser is healthy to this date
(Duesberg, 1996d) (Sherry Thorup, personal communication 1998). Likewise, movie star Rock
Hudson died from AIDS wasting and Kaposi´s sarcoma in 1985, but Marc Christianson, his
last relationship of over two years which began during an era before safe sex, is healthy 13
years later (Hudson & Davidson, 1986; Duesberg, 1996d). Thus, the huge body of literature on
AIDS cannot offer convincing evidence that AIDS is contagious (Duesberg, 1992a; Stewart,
1996). Instead, all published data prove that AIDS is not.
AIDS progresses non-exponentially - unlike infectious disease, and unlike the HIV
epidemic
In America and Europe, AIDS has progressed slowly and non-exponentially over 10 years and
then declined slowly (Figure I A and C, see also page 105) (Centers for Disease Control and
Prevention, 1996; Centers for Disease Control and Prevention, 1997; Fiala & Lingens, 1997;
National Commission on AIDS, J uly 1991) - j ust like a lifestyle disease (Cairns, 1978). By
contrast, a new viral epidemic, such as, for example, a seasonal flu, spreads exponentially in a
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susceptible population within weeks or months (Fenner et al., 1974; Evans, 1982; Mims &
White, 1984). This characteristic of an infectious epidemic, pathogenic (like flu) or not (like
HIV), was first discovered in the early 19th century by the British scientist William Farr, and
has since been called Farr´s law (Bregman & Langmuir, 1990).
Subsequently, infectious epidemics, particularly viral epidemics, disappear again within weeks
or months as a result of anti-viral or microbial immunity and the selection of resistant
survivors (Stewart, 1968; Fenner et al., 1974; Mims & White, 1984). This generates the
conventional bell curve, a rapid rise of cases within weeks or months, followed by a decline as
immunity arises and susceptible hosts die out (Bregman & Langmuir, 1990). But there is no
evidence for the emergence of immunity as the AIDS epidemic continues to progress (Figure
1A and C). Thus, according to Farr´s law, American and European AIDS is incompatible with
infectious disease but consistent with non-contagious lifestyle diseases.
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T able 1 :
From the beginning, the AIDS diseases fell
AIDS- def ining dis eas es in the U.S. in 1995
1) into two categories that are totally unrelated
Immuno- (in %) Non-immuno- (in %) to each other: (1) the non-immunodeficiency
deficiencies deficiencies diseases including dementia, the cancers
pneumonia 33 wa s t i n g / we i g h t 15 Kaposi´s sarcoma and leukemia, and weight
loss
candidiasis 14 Kaposi´s sarcoma 6 loss, and (2) the immunodeficiency diseases,
2)
tuberculosis 10 dementia 3 including the viral and microbial
cytomegalovirus 7 lymphoma 2
t o xo p l a s m o s i s 4 pneumonias, the diarrheas, yeast, and other
herpesvirus 4 opportunistic infections (Table 1).
diarrhea 2
Despite the profound disparity in the AIDS
total 74 26
diseases, the CDC proposed in 1982 that
1)
2)
(Center for Disease Control and Prevention, 1995) immunodeficiency was their common
includes other mycobacterial infections
denominator (Centers for Disease Control,
1982). But since immunodeficiency was not considered to be infectious in 1982, AIDS was not
classified as an infectious epidemic. Moreover, immunodeficiency, no matter what its cause, is
not a known cause of cancer, dementia, and weight loss (Duesberg, 1992a; Duesberg, 1996c).
Accordingly, there is no immunodeficiency in many AIDS patients with Kaposi´s sarcoma
(Afrasiabi et al., 1986; Murray et al., 1988; Spornraft et al., 1988; Archer et al., 1989;
Friedman-Kien et al., 1990).
On April 23, 1984, the Secretary of Health & Human Services (HHS), the directors of the CDC
and NIH, and the NIH´s virus researcher Robert Gallo announced j ointly at an international
press conference in Washington that a previously unknown virus, since called HIV, was the
´probable cause of AIDS´ (Altman, 1984). The only evidence for this claim was the presence
of antibody against the ´AIDS virus´ in most, but not all, AIDS patients that Gallo and his
collaborators had analyzed (Gallo et al., 1984). Even to this date, AIDS researchers cannot
find HIV antibody in all (Duesberg, 1993e), nor infectious HIV in most, AIDS patients
(Duesberg, 1992a; Duesberg, 1996d; Duesberg, 1996c).
Despite the instant popularity of an immunodeficiency virus, the hypothesis had four serious
birth defects:
1. Oblivious of AIDS epidemiology, Gallo, other virus researchers, and the secretary of HHS
tacitly assumed that ´where there is a virus, or even j ust antibody against one, there must be
an infectious disease´ [according to the proverbial, "where there are hoofbeats, there must
be horses"] (Blattner et al., 1988; Weiss & J affe, 1990; Harden, 1992; O'Brien & Goedert,
1996; O´Brien, 1997). But the epidemiology of AIDS is incompatible with infectious
disease.
2. Gallo and other AIDS researchers apparently had overlooked that antibodies are hardly a
cause of disease. Instead, antibodies offer the only known protection against viral
pathogenesis - the operating principle of vaccination (Blattner et al., 1988; Weiss & Jaffe,
1990; O'Brien & Goedert, 1996; O´Brien, 1997).
3. Gallo and other AIDS researchers apparently also overlooked that their hypothesis failed
Koch's first postulate, according to which every case of a disease should contain the
suspected causative microbe (Merriam-Webster, 1965; Harden, 1992).
4. They also overlooked that over a third of all American AIDS patients in 1984 (Duesberg,
1991; Duesberg, 1992a), and 26% in 1996, do not even have immunodeficiency diseases
(Table 1).
Nevertheless, the ´AIDS virus´ was accepted without delay, and without review, even before it
was published in a scientific j ournal (Altman, 1984). Both the threat of a new infectious
epidemic and the endorsement by the US government immediately established the virus-AIDS
hypothesis as a national article of faith. In 1985, one year after Gallo's announcement, the
CDC officially redefined AIDS as an infectious disease. According to the CDC's 1985 AIDS
definition, HIV had become the one and only definitive diagnostic criterion of AIDS (Centers
for Disease Control, 1985). Moreover, HIV had become the first virus to cause 30 fatal
diseases, but no specific disease of its own - because each of the 30 diseases can result from
previously known causes. Thus, as of 1985, the following definition applied:
Any of 30 diseases + HIV = AIDS
Any of the same 30 diseases - HIV = any of the 30 diseases.
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This definition has made AIDS an ´HIV disease´ (Institute of Medicine & National Academy
of Sciences, 1986), although there was no proof in 1985 that HIV causes AIDS (Duesberg,
1987; Blattner et al., 1988; Duesberg, 1988). And there has been no proof since (Cohen, 1995;
Mullis, 1996; Balter, 1997). On the contrary, according to Nature Medicine, two papers in
1998 drove ´the final nail in the coffin´ of the hypothesis that HIV causes AIDS by killing
T-cells (Roederer, 1998).
The CDC´s HIV-based AIDS definition has relegated into a gray zone thousands of HIV-free
AIDS cases that had been diagnosed clinically and on the basis that the patient belonged to an
´AIDS risk group´ (Duesberg, 1993e). While the existence of HIV-free AIDS continued to be
acknowledged despite the 1985 AIDS definition (Centers for Disease Control, 1987; Centers
for Disease Control and Prevention, 1992), HIV-free cases could now be readily dismissed as
an argument against the HIV hypothesis by classifying them as non-AIDS cases under their old
names (see 6). By allowing AIDS diagnosis without HIV yet insisting on an HIV-based AIDS
definition, the CDC has created many unnecessary problems that have obscured AIDS research
to this date (see pages 102, 103) (Duesberg, 1993e; Duesberg, 1996d).
Moreover, from the beginning, the AIDS and HIV epidemics were not at all compatible.
Instead they have moved in different directions in the US and Europe since both can be tested
simultaneously - despite their linkage by the HIV hypothesis. In the US, the HIV epidemic has
been steady at about one million from 1985, with small downward adj ustments since 1996
(Figure 1A) (Curran et al., 1985; Duesberg, 1992a; Duesberg, 1996c; Krieger, 1996; World
Health Organisation, 1996; Centers for Disease Control and Prevention, 1997). New HIV
infections have even declined fivefold from 1985 until 1993, based on over 50 million blood
donations collected in that time (Figure 2A) (Centers for Disease Control, 1995). By contrast,
during the same time period AIDS has increased from a few dozen to over 50,000 cases
annually (Figure 1A).
In Europe, a steady 0.5 million individuals were positive between 1988 and 1995 (Figure 1C)
(Mann et al., 1988; Merson, 1993; World Health Organization, 1995a). In Germany, the
number of new infections declined about twofold during the same time period in which AIDS
rose from none to 2000 cases per year (Figure 2B) (AIDS-Zentrum im Robert Koch-Institut,
1997; Fiala & Lingens, 1997).
Since the American and European AIDS and HIV epidemics move in totally different
directions, the HIV hypothesis cannot explain AIDS. Moreover, the steady state of infection
proves that HIV is an old, long-established virus in the US and Europe (see Farr´s law above)
(Bregman & Langmuir, 1990; Duesberg, 1992a).
Thus, AIDS patients have neither an HIV- nor an AIDS-specific disease, nor any one of the 30
AIDS-defining diseases, nor even immunodeficiency, in common. However, by definition they
all share antibodies against HIV.
stated between 1981 and 1982: ´At this point our best clue to the cause of the disease was
poppers´ [nitrite inhalants]' (Fettner &Check, 1985). Curran's clue was gleaned from anecdotal
evidence including the first two Kaposi´s sarcoma patients seen by Alvin Friedman-Kien,
professor of dermatology at New York University. Both of these patients were male
homosexuals who ´had a multiplicity of sexual partners over an extended period of time as
well as using a variety of recreational drugs - cocaine, marij uana, LSD, THC, MDA, and amyl
nitrite.´ Friedman-Kien regularly called CDC officials to report his experience with AIDS:
´...as patients started coming in, it turned out that all of them, 100 percent, had been using
amyl nitrite´ (Fettner & Check, 1985).
(A) America
(B) Germany
Figure 2:
( A) New HIV inf ec tions in per c ent of over 50 m illion blood donor s , and AIDS
c as es per year in Am er ic a ( Center f or Dis eas e Contr ol, 1995) ;
( B) New HIV inf ec tions per year in G er m any ( AIDS Zentr um im Rober t Koc h
Ins titut, 1997)
Evidence continued to mount strongly supporting a connection between nitrite use, other
recreational drugs, and AIDS. This included articles by J ames Goedert and William Blattner
from the NIH, the CDC's sister institution (Goedert et al., 1982), by Harry Haverkos with the
CDC's Kaposi's Sarcoma Opportunistic Infection (KSOI) task force, and an abundance of other
studies on the immunotoxic and carcinogenic effects of nitrite inhalants (Newell et al., 1984;
Haverkos & Dougherty, 1988a; Haverkos & Dougherty, 1988b). An English team reported in
1984 that 86% of male homosexual AIDS patients from St Mary´s Hospital in London had
inhaled nitrites compared to 86.4% from clinics in New York, San Francisco, and Atlanta
(McManus et al., 1982). In 1983, two dozen of America´s leading AIDS investigators
including Friedman-Kien, Curran, and CDC worker Harold J affe, later director of the CDC's
HIV/AIDS Division, had conducted extensive epidemiological studies which revealed
overwhelming drug use, including nitrite inhalants, cocaine, and amphetamines by all
homosexual AIDS patients studied (Table 2) (J affe et al., 1983).
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nitrite inhalants 96% 82% 79% 71-100% 100% 98% 50% 80%
ethylchloride 35-50 18
cocaine 50-60 84 69 40-66 yes yes 12-34 40
amphetamines 50-70 64 55 26-46 yes yes 6-27 4 8 ( e c s t a s y)
57 (speed)
phenylcyclidine 40 22 23 yes
LSD 40-60 49 yes 48
metaqualone 40-60 51 44
barbiturates 25 41 30 yes
marijuana 90 85 88 41-68 76
heroin 10 20 3 yes 25
alcohol 46 95 90 95
cigarettes 33 yes 50 58
AZT most most 15-64
drug-free 0 0 0 0 0 0 0 0
N o t e : N o t o n e o f t h e s e s t u d i e s r e p o r t e d a d r u g - f r e e m a n wi t h A I D S o r a t r i s k f o r A I D S .
Drugs seemed to be the most plausible explanation for the restriction of AIDS to risk groups,
because drug consumption was the only health risk male homosexuals and intravenous drug
users had in common (Krieger & Caceres, 1985). This original drug-AIDS hypothesis was
euphemistically called the ´lifestyle hypothesis´ (Oppenheimer, 1992). Indeed, massive
supplies of illicit recreational drugs such as nitrite (poppers) and ethylchloride inhalants,
cocaine, heroin, amphetamines, phenylcyclidine, and LSD had reached America and Europe
since the Vietnam War and were the only statistically significant new health risks that had
affected these countries since World War II (see page 103).
Suddenly, after the announcement of the discovery of the ´AIDS virus´ by Gallo at the
international press conference in Washington on April 23, 1984 (see above), the lifestyle
hypothesis was dropped without notice - as if it never existed - in favor of the virus-AIDS
hypothesis. Since then, any revisionism was immediately regarded as obsolete, or in the words
of David Baltimore even as a ´pernicious and irresponsible´ obstacle (Booth, 1988) in the war
against the AIDS virus (Weiss & J affe, 1990; Cohen, 1994a; Duesberg, 1996d; O´Brien &
Goedert, 1996; O'Brien, 1997). Henceforth, recreational drugs were only studied, if at all, as
risk factors of HIV infection or as obstacles in anti-HIV medications.
An article in the gay interest magazine Genre captures the ´fashionable opinion´ (A. N.
Whitehead) of the HIV era: ´...the real danger of the drug lies in its crystalline high that
engenders dangerous behavior. One doctor recounts the story of a young patient of his who
´bumped´ (took crystal [amphetamine]) for four days at Rehoboth Beach - four days of parties
and sex and more parties and more sex. When he came down at last, he felt drained and
depressed. But that was nothing compared to how he felt when he discovered he had
contracted HIV.. The same doc also talks about an HIV patient who got ´methed up´ (with
methamphetamine) and went off his medication... The doc was angry, but he´s wise to the
ways of addicts´ (Bergling, 1997).
In a rare response to the situation, William Lerner, from the Division of General and
Preventive Medicine of the University of Alabama at Birmingham, writes in the Journal of
American Medicine: ´With few exceptions, the treatment of drug problems in the United States
occurs both figuratively and literally, a long distance from the maj or medical centers. ... the
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efforts expended stand in stark contrast to those rallied in the investigation of AIDS.... A
recent survey of medical centers from the United States revealed fewer than 30 current
fellowship programs in alcoholism and drug abuse in the entire country, with approximately 60
enrolled´ (Lerner, 1989).
Intravenous drug use is reported for a third of all AIDS patients in the HIV era
Although the lifestyle hypothesis has been discredited by proponents of the virus-AIDS
hypothesis, government statistics and independent publications continue to confirm to this
date that about one third of the American, and over one third of the European AIDS patients,
are intravenous users of cocaine, heroin, and other drugs (Duesberg, 1992a; World Health
Organization, 1995b; Centers for Disease Control and Prevention, 1996; Duesberg, 1996c;
Duesberg, 1996d; Hodgkinson, 1996; Duesberg & Rasnick, 1997; Fiala & Lingens, 1997).
Indeed, virtually all of the female and heterosexual male AIDS patients are intravenous drug
users.
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Swiss states, because amyl nitrites, but not other nitrites, are listed as poisons by the federal
public health office, BGA.
stimulant that keeps people up for hours on end, sometimes for 48 hour stints, dancing,
posing, and having sex. Some people snort their crystal in powder form, but more and more
men are inj ecting intravenously after liquefying it. ... a taxi driver tells me ... ´It was great
to work to, I mean I could work for two days straight through. And of course for sex.´
... outside the ballroom on the grounds of the pool, several men vomit on the lawn, others
pass out; at some point paramedics arrive and in the blur from the lights and the drugs, I
see someone taken out on a stretcher. He overdosed on something. ´Another circuit
casualty,´ someone says to me with a smile. Indeed another man tells me that there´s an OD
[overdose] at j ust every big party. ´That´s how you know it's a good party,´ he j okes, ´if you
can attract an ambulance or two.´
Later, however, when the partying momentarily stops and I go back to my room, I´m unable
to sleep ... I´ll need more drugs. ... The opposite choice, staying sober (not being
´medicated´ as one of my party chumps puts it)... seems not to offer the authentic circuit
experience, and the possibility of finding someone else in the same state is rather nil.
Staying sober seems a dismal prospect, as if someone has told a funny j oke and you are the
only one not ´getting it.´
Burnt out and sometimes hooked on coke (cocaine) and crystal (amphetamines) too, some of
these men see their careers and their relationships - not to mention their health, particularly
if they are HIV-infected - completely unravel (Signorile, 1997b).
The German gay interest magazine First confirms that ´Ecstasy [amphetamines], LSD, and
other amphetamines have become indispensable for ´House- and Technoclubs.´ The use of
´Partydrogen´ and their dangers are described by diverse informational brochures´. ... Some
take so much speed that they can´t sleep for 3 days. ´E´ (ecstasy) makes contact happy and
chummy, LSD develops secret desires, and cocaine makes you j ust horny. But who enj oys
pleasant chemical feelings ... does not care about damned condoms' (Holtermann, 1997).
Surprisingly the article recommends free ´drug checking´ by the German government -
supported AIDS Hilfe, to avoid the ´dangers of drug taking.´
Based on hundreds of interviews, the American gay interest magazine Out also analyzed why
male homosexuals take drugs: ´Once in the gay world, we often became obsessed with never
being excluded again by the popular crowd. For many young men today that obsession leads
them to ingest or inj ect themselves with powerful and dangerous steroids, a trend that appears
to have begun slowly in the 1980s and taken off in the past few years´ (Signorile, 1997a).
On J une 21, 1998, the San Francisco radio station KGO AM warned about combining nitrite
inhalants with Pfizer´s new erection enhancing drug Viagra (both drugs are vasodilators).
Several deaths had occurred among male homosexuals in Southern California who had used
these drugs in combination. The warning followed one issued by The Lancet on combining
orthodox nitrite prescriptions with Viagra: ´...Pfizer and the US FDA confirmed that [by May]
six deaths had occurred among the million or so men who have used Viagra since its approval
on March 27 [1998]´ (Bradbury, 1998).
Thus, male homosexuals with AIDS and at risk for AIDS have continued to use drugs in the
HIV era to this date, although drug use is no longer investigated as a possible cause of AIDS.
Remarkably, not one of the many, NIH-sponsored single- or multi-center cohort studies
recording drug use by homosexual men with AIDS or at risk for AIDS has ever identified, or
tried to identify, even one AIDS patient who was drug-free (Lauritsen, 1994; Lauritsen &
Young, 1997) (see page 101 and Table 2)!
1% of AIDS patients are babies who shared drugs with their mothers before birth
In the US, between 500 and 800 babies are listed annually as pediatric AIDS cases by the CDC
(Centers for Disease Control and Prevention, 1995; Centers for Disease Control and
Prevention, 1997). In Europe also, about 500 to 600 babies are annually recorded as AIDS
patients (World Health Organization, 1995b). Numerous reports confirm that the mothers of
about 80% of these babies were intravenous drug users during pregnancy (Mok et al., 1987;
Blanche et al., 1989; European Collaborative Study, 1991; Duesberg, 1992a; Centers for
Disease Control and Prevention, 1995; Drug Strategies, 1995; World Health Organization,
1995b; Moye et al., 1996; Rodriguez et al., 1996). The remaining 20% of AIDS babies from
non-drug using mothers probably represent the long-established background of infant
morbidity and mortality due to congenital diseases, malnutrition and poverty.
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A survey by the NIDA conducted in 1994 extends and confirms this scenario: ´More than 5
percent (221,000) of the 4 million women who give birth each year use illicit drugs during
their pregnancy´ (Drug Strategies, 1995). And the Office of the National Drug Control Policy
estimates that ´3.2% of the pregnant women (approximately 80,000)´ are drug users (White
House Office of National Drug Control Policy, 1998). Thus, many more infants have shared
drugs with their mothers as embryos than are showing up as AIDS babies.
Drugs - the common denominator of AIDS in America and Europe: (b) the
anti-HIV drugs and the 'polypharmacy' of anti-AIDS drugs
In the name of the hypothesis that HIV causes AIDS, several DNA chain-terminators and other
chemicals have been licensed since 1987 to cure and prevent AIDS by inhibiting HIV
replication. The first of these was the DNA chain-terminator AZT (Kolata, 1987; Nussbaum,
1990; Duesberg, 1996d).
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HIV is rare in the US and Europe, and extremely hard to transmit horizontally
HIV is very rare in the non-drug-using population of the US and Europe. Only one out of 260
Americans, and one out of 900 Europeans, are HIV-positive (Figure 1A, C). Moreover, HIV
does not readily spread from its established reservoir because it is very difficult to transmit
horizontally (as compared to perinatally). It takes, on average, over 1000 sexual contacts with
an HIV-positive individual (Peterman et al., 1988; J acquez et al., 1994; Padian et al., 1997),
or parenteral transmission via frequent inj ection of unsterile street drugs, or blood
transfusion, to acquire HIV (Duesberg, 1992a). The inefficiency of transmission reflects the
absence of infectious virus, and the very low percentage of even latently infected cells (about
I per 1000) in antibody-positive persons (Duesberg, 1989; Duesberg, 1992a; Duesberg &
Bialy, 1996).
Antibody against HIV and other rare microbes are markers for drug use
The more frequently a person inj ects unsterile drugs, and the more sexual partners a person
has, the more likely that individual is to become infected with a rare microbe (Durack, 1981;
Stewart, 1989; Mullis, 1995). Because recreational drugs are typically used to achieve the
average of 1000 sexual contacts that are necessary to transmit HIV sexually (Durack, 1981;
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Fiala & Lingens, 1997), antibody against HIV is a marker for drug use in the US and Europe,
where HIV is rare. In the words of a drug addiction counselor from Washington DC, ´addiction
to drugs, or at least heavy drug use, is the number one cause of HIV infection´ (Bergling,
1997).
Antibodies against other rare passenger viruses are also surrogate markers for recreational
drug use. These include Hepatitis B virus (Duesberg, 1992a), the human T-cell leukemia virus
that was once considered the cause of AIDS (Gallo et al., 1983), a recently discovered herpes
virus, termed HHV-8, which is currently considered a cause of Kaposi´s sarcoma (Cohen,
1994b; Ganem, 1997), cytornegalovirus, also once considered a cause of AIDS, and many
other rare viruses and microbes (Durack, 1981; Sonnabend et al., 1983; Stewart, 1989;
Duesberg, 1992a).
Thus, the high incidence of antibodies against HIV and other rare passenger viruses and
microbes in AIDS patients is direct confirmation of many parenteral and sexual contacts, and
is indirect confirmation of long-term recreational drug use. But before we can determine
whether drugs may cause AIDS, we must determine whether AIDS occurs without drugs.
Indeed, an independent analysis of the database of Ascher et al. confirmed that impression and
also revealed that Ascher et al. had omitted from their paper 45 HIV-free, but drug-using,
patients with AIDS-defining diseases (Ellison et al., 1996).
Despite the highly personalized style of the Nature commentary (Duesberg's name was
mentioned 13 times), Nature´s editor J ohn Maddox refused to publish Duesberg´s letter
inquiring about the confounding problem of the Ascher article in an editorial entitled ´Has
Duesberg a right of reply ?´ (Maddox, 1993). But after The Lancet and Science published
critical letters (Duesberg, 1993d; Duesberg, 1993a; Duesberg, 1995a), Ascher et al. replied
two years later in Science, ´The proposed AIDS-drug use association is a classic example of
confounding, that is, a suggestion of a correlation caused by the association of a spurious
factor (drug use) with a factor (HIV infection) causally related to the outcome (AIDS). The
standard statistical methods that we used to differentiate cause from confounding factors
showed, in this case, that HIV was the cause and that drug-use association was spurious´
(Ascher et al., 1995b). Thus, neither Nature nor The Lancet could find authors that were able
to dissociate AIDS from drugs.
With so much encouragement from editors of leading j ournals, the San Francisco and
Vancouver groups teamed up with Australian and Dutch colleagues to refute drugs as the cause
of homosexual AIDS once more (Veugelers et al., 1994). Again, all of 403 AIDS patients
studied reported extensive drug use, particularly nitrites, and many were also on AZT (see
Table 2). The ´relative [AIDS] hazard´ for nitrite use was 1.03 and for AZT use was 1.04. Yet
the authors concluded: ´No relation ... of alcohol, tobacco, and recreational drugs with rates
of disease progression could be demonstrated,´ and ´the observed relations between
zidovudine [AZT] and faster progression from seroconversion to death should not be
interpreted as causal´ -but they could be (see page 117)!
But the CDC, Ascher et al., Schechter et al. and their ´tricontinental´ alliance were not the
only AIDS epidemiologists who have failed to dissociate AIDS from drugs as the following
titles of their articles reveal:
1. AIDS and intravenous drug use: the real heterosexual epidemic (Moss, 1987).
2. A larger spectrum of severe HIV-I-related disease in intravenous drug users in New York
City (Stoneburner et al., 1988).
3. Cocaine abuse and acquired immunodeficiency syndrome: tale of two epidemics (Lerner,
1989).
4. The Twin Epidemics of Substance Use and HIV (National Commission on AIDS, J uly
1991).
5. AIDS, drugs of abuse and the immune system: a complex immunotoxicological network
(Pillai et al., 1991).
6. Entangled epidemics: cocaine use and HIV disease (Larrat & Zierler, 1993).
7. Recreational drugs and sexual behavior in the Chicago MACS/CCS cohort of
homosexually active men (Ostrow et al., 1993).
8. New picture of who will get AIDS is dominated by addicts (Kolata, 1995).
9. Clinical features of drug use and drug use related to HIV (Brettle, 1996).
10. Tuberculosis, AIDS, and death among substance abusers on Welfare in New York City
(Friedman et al., 1996).
11. The influence of drug use patterns on the rate of CD4+ lymphocyte decline among
HIV-1-infected inj ecting drug users (Lyles et al., 1997).
12. Immunodulation by nitrite inhalants may predispose abusers to AIDS and Kaposi's
sarcoma (Soderberg, 1998).
In searching for a drug-free, homosexual AIDS patient, the AIDS reporter J ohn Lauritsen
interviewed Michael Callen, a founder of the People With AIDS Coalition (Lauritsen &
Young, 1997). According to Lauritsen, ´possibly no one personally knew more persons with
AIDS than Michael Callen.´ Indeed, Callen reports in his book, Surviving AIDS, his over 3000
sexual contacts and extensive drug use before he adopted a monogamous lifestyle (Callen,
1990). Asked whether "he had ever encountered a gay male person with AIDS who did not fit
the profile of vene real diseases, antibiotics, drugs..., his answer was: ´No. Not in eleven
years. I have gone to a great deal of trouble to find these people. I found ten, who were saying
in public, ´I only had one or two contacts,´ ... [but] each one ended up telling me they had
been lying ... in the support group setting, they would regale us with tales of bathhouses and
promiscuity and lovers on the side and drug use" (Lauritsen & Young, 1997). Thus, neither
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individual investigators, nor the CDC, nor other government statistics have ever shown that, in
the HIV era, the incidence of AIDS-defining diseases among non-drug-users has exceeded
long-established, national backgrounds.
Nevertheless, a few American and European drugfree AIDS patients must exist based on the
CDC´s AIDS defintion (see page 90 and 91). They would represent the normal incidence of the
30 AIDS-defining diseases among HIV-positive Americans and Europeans under the new name
AIDS (World Health Organization, 1995b; Centers for Disease Control and Prevention, 1996).
Cocaine
The director of the NIDA wrote in 1985 that, ´Over the past 10 years, cocaine ... has evolved
from a relatively minor problem into a maj or public health threat´ (Schuster, 1985) with a
´negligible´ number of users in 1973 and 9,946 non-fatal and 580 fatal medical cases in 1985
(Kozel & Adams, 1986). The numbers of cocaine patients have since increased even more to
80,355 in 1990, and to a plateau of about 140,000 in the mid 1990s (Figure 1B and Table 4).
In 1996, the number of regular cocaine users had reached 3.6 million, with 28 million who had
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at least tried the drug once in their lifetime (Bureau of J ustice Statistics, 1992; Office of
National Drug Control Policy, 1996; McEvoy et al., 1998). Clearly, cocaine is the most
popular illegal drug in America, accounting for $38 billion of the $53.7 billion spent on
illegal drugs in 1995 (Associated Press, 1997; White House Office of National Drug Control
Policy, 1998). Another measure of the popularity of the drug is that by 1997, 78% of all
one-dollar bills in the US contained chemically detectable amounts of cocaine from using
these bills for drug inhalation (New York Times, 1997).
T able 4.
1)
Chr onology of dis eas es and death f r om illic it r ec r eational dr ug us e in the US
Drug e ve n t 1990 1991 1992 1993 1994 1995 1996
cocaine death - 2,938 3,285 3,633 3,687 - -
hospital 80,355 101,189 119,843 123,423 142,878 142,494 144,180
amphetamines death - 252 334 566 751 - -
hospital 8,800 7,363 10,615 15,630 17,665 17,547 16,787
heroin death - 2,260 2,782 3,558 3,522 - -
hospital 33,884 35,898 48,003 63,232 64,013 76,023 70,463
all drugs death - 6,246 6,870 7,602 8,541 9,216 -
hospital 371,208 393,968 433,493 460,910 518,521 531,827 487,564
1)
(U.S. Department of Health & Human Services, 1993; U.S. Department of Health & Human Services, 1994;
Drug Strategies, 1995; Office of National Drug Control Policy, 1996; US Department of Health & Human
Services & Public Health Service & Substance Abuse and Mental Health Services Administration (SAMHSA),
1996; W hite House Office of National Drug Control Policy, 1998).
T able 5.
1
Dr ugs c onf is c ated in the USA Eur opean Union, and G er m any bef or e and af ter the dr ug
2
ex plos ion ( 'Dr ogen- Ex plos ion')
Drug USA European Union Germany
before after before after
(kilograms)
cocaine 500(1980) 100,000 (1990-96) 29,000 (1994) 0.09(1963) 1,846 (1995)
heroin 1,500 (1990-95) 5,900 (1994) 1.8 (1968) 933 (1995)
amphetamines 1,900 (1994) 6.6 (1972) 138 (1995)
cannabis 733,400 (1994) 5.5 (1962) 14,245 (1995)
(doses)
amphetamines, 2 million (1981) 97 million (1989) 1.25 million (1994) 730 (1987) 700,000 (1996)
ecstasy
LSD 61,000 (1994) 10 (1967) 71,069 (1995)
1 (Flanagan & Maguire, 1989; Bureau of Justice Statistics, 1991; Duesberg, 1996b; Office of National Drug
Control Policy, 1996; W hite House Office of National Drug Control Policy, 1998);
2 (Deutsche Hauptstelle gegen die Suchtgefahren, 1996; Springer Verlag, 1996; Holtermann, 1997); and
Section 8.
From 1980 to 1990, imports of cocaine have increased two-hundredfold, from two tons to 400
tons, and have since been kept at this level (Figure 1B, Table 5) (Duesberg, 1992a; Clinton &
The White House, 1996; Office of National Drug Control Policy, 1996). These data are based
on cocaine seizures that increased from 500 kg in 1980 to 100 tons in 1990 and have since
remained at this level (Flanagan & Maguire, 1989; Bureau of J ustice Statistics, 1991; Office
of National Drug Control Policy, 1996; White House Office of National Drug Control Policy,
1998), and on estimates that no more than 10-20% of the imported cocaine is confiscated
(Anderson, 1987; Clinton & The White House, 1996; Associated Press, 1997). This
corresponds to about 110 g for each of the 3.6 million regular users per year, which is rather
close to the estimated daily consumption of 1g per day per addict (Schnoll et al., 1985;
Volkow et al., 1997).
Heroin
Between 1992 and 1995 about 1,500 kg of heroin were confiscated annually (Table 5) (Office
of National Drug Control Policy, 1996). In view of these statistics, the San Francisco
Chronicle warned in 1996 that 'a growing segment of the population [is] attracted by its
[heroin] deadly mystique and encouraged by its low prices ...´ (Evenson & Whiting, 1996).
According to the Drug Abuse Warning Network (DAWN) of the Department of Health and
Human Services (HHS), heroin deaths climbed from 2,260 in 1991 to 3,522 in 1994 (Table 4).
Heroin-related hospital emergencies increased over fivefold from 12,000 in 1978 to a plateau
of about 70,000 in the mid 1990s (Table 4 and Figure 1B). The heroin epidemic accounted for
$10 billion of the $53.7 billion spent on drugs in 1995 (Associated Press, 1997).
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Amphetamines
Based on US government statistics, the amounts of amphetamine confiscated have spiraled
fiftyfold in the 1980s, from 2 million doses in 1981 to 97 million doses in 1989 (Table 5)
(Flanagan & Maguire, 1989). According to the US Department of HHS, ´amphetamine-related
emergency room episodes... [presenting with] violent paranoid behavior as well as stroke,
seizure and death ... ´ (Drug Strategies, 1996) increased from 8,800 in 1990 to about 17,000 in
the mid 1990s (Table 4). In California, amphetamine or ´speed´ hospitalizations rose even
faster: from 1,466 in 1984 to 10, 167 in 1994 (Russell, 1996; Wallace, 1996).
It is apparent from the data shown in Figure I A, B that the chronology of the American drug
epidemic closely paralleled that of the American AIDS epidemic.
Both drug use and AIDS are non-random and spread non-exponentially
Sex and age of the AIDS epidemic match those of the drug epidemic
The National Drug Control Strategy: 1996 from the White House reports that 78% of the hard
recreational drug users are males (Clinton & The White House, 1996). Earlier studies have
reported similar non-random sex distributions, that is, that between 70 and 80% were males
(Table 6). As in America, 66% of the German drug users are males (Deutsche Hauptstelle
gegen die Suchtgefahren, 1996; Fietz, 1997). Thus, male drug users outnumber females
between two and fiftyfold (e.g. nitrites, page 95) depending on the drug used.
All American consumers of hard recreational drugs such as cocaine, heroin, and amphetamines
are over 18 and under 54 years of age (Table 6). The National Drug Control Strategy: 1996
reports that 74% of the drug users are 21-44 years old (Clinton & The WhiteHouse, 1996).
Almost all drug decedents are also over 18 and under 54 years of age, and most are over 25
(Office of National Drug Control Policy, 1996) (Table 6). Germans who have used illegal
drugs were also between 18 to 59 years old (Deutsche Hauptstelle gegen die Suchtgefahren,
1996). And 83% of the 15,000 first-time users in 1995 were over 21 years old (Springer
Verlag, 1996).
A breakdown according to sexual persuasion is offered by Kim Gilliam, the drug addiction
counselor from Washington, DC cited above: 'Addiction knows no boundaries, but in the gay
community you find addicts of all ages. It's j ust not like that in the heterosexual population,
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where the addicts are generally younger' (Bergling, 1997). Indeed, according to a continental
European investigation, the median age at death of mostly heterosexual, intravenous drug
users is 30 years (Lockemann et al., 1995). The average age of a small group of English drug
patients was 31 (McEvoy et al., 1998). Their American counterparts die between 25 and 44
years (Stoneburner et al., 1988; Hayes et al., 1994).
Thus, sex and age of those dying
from drugs matches that of those T able 6
Dr ug deaths and dis eas es in the USA by age and s ex
dying from AIDS. 1)
1990- 1994
The dynamics of the AIDS and drugs % male % 1 8 - 5 4 ye a r s
2)
cocaine users 70,82 99
drug epidemics coincide hospitals 67
The dynamics of the AIDS and drug deaths 80
2)
heroin users 69,83 99
epidemics also closely overlap as the hospitals 71
following two examples show: (1) In deaths 83
1997 the CDC reported that annual amphetamines users 80 97
hospitals 61
AIDS cases had continued to drop deaths 79
3)
since 1993, with a 19% drop from nitrites users 98 >98
hospitals
1996 (Centers for Disease Control deaths
and Prevention, 1997; Stolberg, all combined users
4)
75, 78 , 86
5)
>75
1997). The department gave the hospitals 71
deaths 77
credit for the decline to the new 1) (Bureau of Justice Statistics, 1992; U.S. Department of Health
anti-HIV drug cocktails (Centers for & Human Services, 1993; U.S. Department of Health & Human
Disease Control and Prevention, Services, 1994; Office of National Drug Control Policy, 1996)
2) (W esson & Smith, 1985)
1997; Stolberg, 1997; Russel, 1998). 3) (San Francisco Department of Public Health & Lesbian & Gay
Substance Abuse Planning Group, 1991; Ascher et al., 1993)
However, the CDC offered no 4) (Clinton & The W hite House, 1996)
evidence that dying AIDS patients 5) (Bureau of Justice Statistics, 1988).
were untreated and those on the new cocktails were the ones living and free of AIDS. On the
contrary, the New York Times reported that AIDS patients died 'despite new AIDS drugs'
(Stolberg, 1997), and the San Francisco Examiner reported that the cocktails had j ust begun to
fail up to 50% of those treated (Krieger, 1997) (see page 121). Indeed a national survey j ust
confirmed that all American AIDS patients are dying on anti-HIV treatments (Perlman, 1998).
Moreover, the CDC failed to explain that their own AIDS statistics had started to decline in
1994, whereas the new anti-HIV cocktails were only introduced in 1996. This discrepancy was
even pointed out by an AIDS correspondent from Science magazine (Cohen, 1997a). It follows
that anti-HIV drugs are not a plausible explanation for the recent decline in AIDS cases.
The CDC also failed to consider information from another federal agency. The White House's
National Drug Control Strategy: 1998 reported that hard recreational drug use had declined
from 25 million regular users in the 1980s to a low of 13 million in 1996, and spending for
drugs had declined from $91 billion in 1988 to $53.7 billion in 1995 (see page 103) (Los
Angeles Times, 1998; White House Office of National Drug Control Policy, 1998). Thus, the
less than twofold decline of AIDS cases appears to be a product of two competing factors: (1)
a drop in recreational drug use, and (2) a steady increase in the use of AIDS-causing anti-HIV
drugs (see below).
(2) In an effort to close the 9:1 gender gap of its AIDS statistics, the CDC has reported since
the early '90s that women had become the fastest-growing AIDS risk group (Centers for
Disease Control, 1994), sometimes even at the cost of the truth (Bennett & Sharpe, 1996),
suggesting each time that heterosexual 'transmission' was the cause. Again, the CDC failed to
reconcile its publications with the fact that 'women account for the fastest-growing population
in j ails and prisons, in large part because of drug offenses' (Drug Strategies, 1995).
Thus, the epidemiology and chronology of AIDS even mirrors the dynamics of the drug
epidemic exactly, confirming the view that the AIDS epidemic is a clinical subset of the drug
epidemic. To prove this we need to investigate whether drugs cause AIDS.
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to clarify that drugs differ from viruses as a cause of diseases in dose-dependence, and in
time-dependence.
Dose-dependence
It was 500 years ago that Paracelsus von Hohenheim first defined the primary criterium of
drug toxicity: the dose makes the poison. A pathogenic dose of recreational or medical drugs
is typically achieved cumulatively by long-term consumption over many years. But it can also
be achieved in a single application as an overdose.
By contrast, viruses and microbes are largely independent of the input concentration as causes
of diseases, because viruses and microbes are selfreplicating poisons. Once introduced into a
susceptible host, they grow exponentially to pathogenic titers within days or weeks, provided
they are not inhibited by antiviral immunity (Stewart, 1968; Fenner et al., 1974; Mims &
White, 1984; Duesberg, 1996d; Duesberg, 1996c). Thus, viruses and most microbes are
typically dose-independent pathogens.
Time-dependence
Because drug toxicity is dosage dependent, drugs typically take a long time to cause disease if
taken at recreational or medical doses. This ´latent´ or grace period is a function of the
chemical toxicity and the concentration of the drug, and the ability of the body to repair drug
damage over time. As a result, it takes decades of smoking before irreversible diseases such as
lung cancer, emphysema, and heart disease occur, and it takes decades of alcoholism before
the liver becomes cirrhotic. Likewise, it took months of clinoquinol (Enterovioform(E))
prescriptions against intestinal parasites before blindness, termed severe myelo-optic
neuropathy (SMON), occured in Japan in the 1960s (Duesberg, 1996d). The carcinogenic
effects of diethylstilbestrol prescriptions against premature delivery were also only discovered
years after the prescriptions were taken (Pitot, 1986). Thus, drugs taken at recreational and
medical doses are slow pathogens because their toxicity is dosage dependent, and microbes are
fast pathogens because their toxicity is dosage independent.
Therefore, one would expect only a small fraction of drug users to develop diseases at a given
time, namely those who have persisted in using drugs for the longest time. Statistics confirm
this point. There are currently 50 million smokers in the US (Associated Press, 1995), but only
200,000 per year develop lung cancer (Parker et al., 1996). Many smokers never develop lung
cancer because they discontinue to smoke, do not smoke enough, or die from other causes
before they reach a critical threshold of toxicity.
On the basis of their interactions with the body, the recreational and anti-HIV drugs of AIDS
patients fall into two categories, those that are (1) indirectly toxic by functioning
catalytically, and those that are (2) cytotoxic, mutagenic, and carcinogenic via chemical
reactions.
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illicit drugs. For example, an average cocaine habit of 1g per day costs $800 per week
(Schnoll et al., 1985).
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(Gottlieb et al., 19 8 1 a). The report even cites nitrites as the possible cause of their
diseases. HIV was not even a suspect because it was only discovered in 1983
(Baffe-Sinoussi et al., 1983).
2. In 1985, Haverkos et al. from the CDC analyzed the AIDS risks of 87 male homosexual
AIDS patients, 47 with Kaposi´s sarcoma, 20 with pneumonia, and 20 with Kaposi's
sarcoma plus pneumonia (Haverkos et al., 1985; Haverkos, 1988). All the men had used
several sexual stimulants; 98% had used nitrites. Those with Kaposi's sarcomas reported
two times more sexual partners and 4.4 times more receptive anal intercourse than those
with only pneumonia. The median number of sexual partners in the year prior to the illness
was 120 for those with Kaposi's and 22 for those with pneumonia only. The Kaposi´s cases
reported six-times more amyl nitrite and ethylchloride use, four times more barbiturate
use, and two times more methaqualone, lysergic acid and cocaine use than those with
pneumonia only. The authors concluded that the nitrites and other drugs had caused
Kaposi's sarcoma because no statistically significant differences were found for sexually
transmitted diseases among the patients.
3. A 4.5 year tracking study of 42 homosexual men with lymphadenopathy, but not AIDS,
reported that eight had developed AIDS within 2.5 years (Mathur-Wagh et al., 1984) and
12 within 4.5 years of observation (Mathur-Wagh et al., 1985). All of these men had used
nitrite inhalants and other recreational drugs, including amphetamines and cocaine, but
they were not tested for HIV The authors concluded that 'a history of heavy or moderate
use of nitrite inhalant before study entry was predictive of ultimate progression to AIDS'
(Mathur-Wagh et al., 1984).
4. Other studies also investigated the dose-response relationships between nitrites and AIDS:
(i) one compared 20 homosexual AIDS patients to 40 AIDS-free controls (Marmor et al.,
1982); (ii) another compared 31 patients to 29 controls (Newell et al., 1985b). Each study
reported that multiple ´street drugs' were used as sexual stimulants and concluded that
drugs were 94% to 100% consistent risk factors for AIDS (Newell et al., 1985b). Newell et
al. derived a direct ´dose-response gradient´: the higher the nitrite usage, the greater the
risk for AIDS. The Kaposi response was estimated to take a dose equivalent of 7 to 10
years of nitrite use (Newell et al., 1985a; Beral et al., 1990; Lifson et al., 1990; Duesberg,
1992a).
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T able 7
Dr ug dis eas es diagnos ed bef or e the AIDS er a, and in HIV- f r ee addic ts
Disease Drugs used* AIDS defining References
immunodeficiency C,H.N,A yes 1
Kaposi's sarcoma N yes 2
candidiasis C,H yes 3
pneumonia C,H,N yes 4
lymphadenopathy C,H yes 5
tuberculosis C,H yes 6
we i g h t l o s s C,H,A yes 7
dementia, encephalopathy C,H,A yes 8
diarrhea C,H yes 9
fever C,H yes 10
thrombocytopenia C,H yes 11
spontaneous abortion, C,H yes 12
premature birth,
congenital abnormalities
n i g h t s we a t s C,H 13
impotence C,H 14
severe atherosclerosis A 15
tooth loss, caries C,H 16
dermatitis C,H 17
hepatitis C,H 18
epileptic seizures C,H 19
endocarditis C,H 20
bronchitis C,H 21
4. An article entitled ´acute and chronic effects of cocaine on the immune system and the
possible link to AIDS´ points out in 1998 that 'human and animal studies document that
cocaine alters the function of ... T-cells, neutrophils and macrophages.' In view of this, the
authors propose a ´wide-ranging capacity for cocaine to suppress the immune system.´
Again, cocaine is proposed to be j ust a ´cofactor´ of HIV in the ´pathogenesis of AIDS´
without suggesting a control of the cofactor hypothesis by testing the effects of cocaine on
HIV-free addicts (Baldwin et al., 1998).
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5. Yet another review describes in 1998 the ´in vivo effects of cocaine on immune cell
function´ (Pellegrino & Bayer, 1998). The article carefully avoids a decision whether
cocaine is immunosuppressive on its own, but acknowledges that immune suppression in
animals is dose-dependent. It proposes animal studies to investigate ´decreased immune
responsiveness in cocaine addicts,´ which is thought to be responsible for an increased risk
of HIV infection. However, the risk of viral or microbial infection is independent of
immune function, but the possible consequences of an infection are not. Again, the question
whether the immunodeficiency diseases of cocaine addicts depend on HIV is not asked.
Despite their scientifically uncontrolled loyalty to HIV, each of the last three reviews confirm
that nitrites and cocaine are at least ´cofactors´ of immune deficiency in animals and man.
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of touch with reality], sleep disorders, and chronic fears ... These symptoms might not show
up for many years. ... well many of my colleagues are used to saying that all you need to do
to eat up T-cells quickly is do lots of crystal´ (Signorile, 1997b).
Regarding steroids, the report warns of ´danger ... on the brain,´ including ´aggression,
hypertension, the mythic ´roid rages,´ violent sex, [and] shrinking testicles,´ and complains
that ´long-term effects of cosmetic steroid use, even at small doses, are simply not known. ...
Studies have been inconclusive and few and far between´ (Signorile, 1997a; Signorile, 1997b).
One of the first observers to blame AIDS among male homosexuals on nitrites was Lauritsen
(see 6), author of Death rush, poppers and AIDS (Lauritsen & Wilson, 1986). In 1993,
Lauritsen says in The AIDS War:
Every Saturday night an estimated 2,000 gay men attend a dance club where drug
consumption is the main activity. According to London sources, virtually 100 percent of the
men are on drugs, from 3:00 in the morning, when the club opens, until it closes many hours
later. Especially popular is a variety of Ecstasy, whose ingredients are claimed to include
heroin. Poppers are sold legally in London [not since 1996]. No one seems to think they
even count as drugs, as gay physicians, writing in the gay press, have said that poppers are
harmless.
None of the maj or AIDS organizations have properly warned about the dangers of drugs. At
most, their risk-reduction literature has urged people to use alcohol and drugs in
moderation, so as not to affect the ´j udgment.´ Drugs are portrayed as risky only to the
extent that they might facilitate a lapse into 'unsafe sex.' Poppers - which cause genes to
mutate, which cause severe anemia, which can kill through heart attacks, which suppress the
immune system -are depicted as bad only if they cause someone to forget condoms
(Lauritsen, 1993).
Three years later, the British magazine Gay Times cites the concerns of a first aid officer from
a London gay club:
I see some faces in the same dire state every week for years and I personally think there's
gonna be an awful lot of very ill people in a few year's time.
Taking all these substances on such a regular basis cannot be good for you. Medically it
can't. Sooner or later, something's got to give (Gibbons, 1996).
And an article in the The Advocate with the title ´A deal with the devil´ asked philosophically
in 1996:
So why is it that in the gay world, where almost half the urban male population is dead or
sick from an epidemic closely associated with substance use, there is such ambivalence
about drugs that AIDS organizations profess to see nothing wrong with raising money from
events that glamorize drug use? Why, despite the bitter legacy of AIDS, do we continue
assuring ourselves that being gay means we have to be totally non-j udgmental about the
very things that have wiped us out (Rotello, 1996)?
In the summer of 1997, the San Francisco based gay-interest magazine Frontiers directly
addressed the long-term effects of methamphetamine addiction because they are only
´begrudgingly and rarely discussed´:
Crystal is, at face value, a great bargain. At an estimated cost of $40, it will create a ´high´
that can last the entire weekend. It makes its user incredibly sexual, energetic, euphoric and
confident. It is very easy to obtain (and equally easy to manufacture). In research studies
using low doses of the drug in animals, scientists were able to induce epilepticlike seizures
in the brain. Those frightening responses in animal studies have already occurred in
humans. Remember Robert, the young television executive? ´He was incredibly talented and
headed for a maj or career,´ says a Southern California therapist under the pseudonym Dr.
Clayton who treated dozens of crystal addicts during a 10-year period. 'Robert started doing
crystal at age 25, a few years after he'd begun his career ascent. He was handsome, worked
out Monday through Friday, was blue-eyed, blond and tanned.´ Positive and asymptomatic
for many years, Robert's addiction to crystal began affecting his life. Everything outside of
work revolved around the drug.
Dr. Clayton recalls one episode in which Robert missed his flight for the East Coast where
he was headed for a maj or circuit party on Fire Island. Robert was so desperate to be there
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that he chartered a private j et. On another party weekend, this one in Key West, he had his
first seizure and was hospitalized for three weeks. He began to go blind and ultimately died
at his parents´ home at the age of 32 last year. Doctors confirmed that crystal abuse caused
his death (Zachary, 1997).
According to the above cited (page 97) drug counselor from Washington DC: ´... there is a
distinct line that travels from the bar to the bedroom to the hospital´ (Bergling, 1997).
Drug-specific diseases
The drug-AIDS hypothesis predicts that chemically distinct drugs cause distinct diseases.
Indeed, the drug literature offers many examples, the most specific of these being the evidence
that nitrite inhalants cause Kaposi's sarcoma (Table 7).
after birth and after discontinuation of the maternal recreational drug supply, 61 had
recovered. Their T-cell levels had even gone up to normal, despite the continued presence
of HIV. Some of the 10 who did not recover were among the first to be treated with AZT.
2. A collaborative study from Europe reports that 60% of babies born to drug-addicted
mothers recovered from pneumonia, bacterial infections, candidiasis, and cryptosporidial
infection and were healthy at 6 years of age, despite the presence of HIV (The European
Collaborative Study, 1994). About 40% of the HIV-positive children died exactly the
percentage that was ´treated with zidovudine [AZT]´; 10% before 6 months of age and 40%
by 4 years.
Although this study of pediatric AIDS does not even mention maternal drug use (focusing
instead only on HIV), earlier reports from the European Collaborative Study group did.
One of these documented in 1987 that 'nearly all children were born to mothers who are
intravenous drug users' (Mok et al., 1987). In 1991, the European Collaborative Study
group reported that 80% of the children with pediatric AIDS were born to mothers who
were intravenous drug users (page 97, 98) (European Collaborative Study, 1991).
3. The risk of AIDS-defining diseases to HIV-positive intravenous drug users dropped
fourfold after giving up drug inj ection for treatment with synthetic methadone. Only 5%
(5/93) of those on methadone, compared to 19% (23/124) of those who continued illicit
drugs, developed such diseases over 16 months of observation (Weber et al., 1990). Since
methadone is immunosuppressive (Klimas et al., 1991), the difference could have been
even bigger if no drugs had been used.
4. The T-cell counts of HIV-positive intravenous drug users from New York had stabilized
after they had stopped inj ecting intravenous drugs. By contrast, that of controls, who
continued drug inj ection, dropped 35% over the 9 months of observation (Des Jarlais et
al., 1987).
5. The T-cells of 29% of 1,020 HIV-positive male homosexuals and intravenous drug users in
the placebo arm of an AZT trial increased over the span of two years, despite the
continued presence of HIV (Hughes et al., 1994). The probable reason is that those whose
T-cells increased had given up or reduced immunosuppressive recreational drug use under
the clinical surveillance of the drug trial.
Evidence from scientists, manufacturers, and the press show that anti-HIV
drugs cause AIDS-defining and other diseases
AZT and other DNA chain-terminators, prescribed as anti-HIV drugs, were first licensed in
1987 as reported by Science under the ominous title ´Imminent marketing of AZT raises
problems; marrow suppression hampers AZT use in AIDS victims´ (Kolata, 1987) . Indeed,
AZT was synthesized over 30 years ago for cancer chemotherapy, long before AIDS was
known (Horwitz et al., 1964). Because the operating principle of cancer chemotherapy is to
kill growing human cells by terminating cellular DNA synthesis at micromolar concentrations,
AZT was predictably pathogenic. To hide the emerging tragedy, HIV/AIDS doctors have tried
to trivialize or rationalize the fatal toxicity of their drugs.
affect the immune response to HIV antigens´ rather than function as an anti-HIV drug. Another
study points out that ´AZT [treatment] has a potent[ial] to transit into leukemias´ (Table 8)
(Inoue et al., 1997).
According to several studies, the pathogenic effects of short-term AZT treatment of several
weeks on adult animals are largely reversible (see references in Table 8). However, one also
reports on death from anti-HIV drugs. Combined treatment with ddC and AZT - as is now the
standard for cocktails including protease inhibitors - at 500 mg/kg each for 29 days killed 25
out of 30 mice (Thompson et al., 199 1). The survivors suffered severe 'nonregenarative'
anemia, lymphocytopenia, and thrombocytopenia (Table 8). On this basis, the authors warned,
´The overall similarities in hematopoietic effects between rodents and human beings,
especially for AZT, indicate that these studies can and do provide important information
relevant to the toxicity of these drugs.´
´Because of widespread proj ected use of AZT in human pregnancy,´ the effects of AZT on
animal embryos are also relevant (pages 99, 118, 120) (Olivero et al., 1997). These effects fall
into two groups: (1) Preimplantation embryos are killed by AZT at I um, which is only about
1/20 of the concentration of the daily dose of 500 mg prescribed to a pregnant mother in the
last two trimesters (Connor et al., 1994). (2) AZT treatment of postimplantation embryos
results in retarded development and cancer (Table 8).
Based on these results, Olivero et al. conclude that ´AZT is unequivocally a transplacental
genotoxin and carcinogen.... When given transplacentally to mice, benzo[a]pyrene produced
lung and liver tumor multiplicities similar to those observed [with AZT]´ (Olivero et al.,
1997). Therefore, the authors warn: ´our results suggest that the current practice of treating
HIV-1-positive women and their infants with high doses of AZT could increase cancer risk in
the drugexposed children when they reach young adulthood or middle age´ (Olivero et al.,
1997).
adult:
rat, mouse 1mg/ml H20 neutropenia anemia 1
7 wk s lymphopenia
thrombocytopenia
bone marrow depletion
we i g h t l o s s
mouse 0.5-1 mg/mI H20 thrombocytopenia anemia 2
7 wk s myelodysplasia leukemia
mouse 500 mg/kg T-cell depletion 3
7-14 days thymic atrophy
mouse 400 mg/kg l y m p h o t o xi c i t y anemia 4
17 days n e p h r o t o xi c i t y
mitochrondrial
necrosis
mouse, rat, 18-250 mg/kg cytostatic anemia 5
dog, monkey 2 - 5 2 wk s leukopenia
mouse, rat 500 mg/kg + lymphocytopenia, nonregenerative' 6
500mg/kg ddC thrombocytopenia, anemia
29 days marrow depletion,
death of 25/30 mice
e m b r yo :
mouse 12-25 mg/day cancer: 7
12-18 days of gestation lung
monkey 10mg/day liver
l a s t 1 0 wk s o f g e s t a t i o n vaginal
mouse 1µM preimplantation: 8
lethal
postimplantation:
retarded
development
1) (Cronkite & Bullis, 1990), 5) (Ayers et al., 1996),
2) (Inoue et al., 1997), 6) (Thompson et al., 1991),
3) (McKallip et al., 1995), 7) (Olivero et al., 1997),
4) (Omar et al., 1996), 8) (Toltzis et al., 1993)
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With regard to the protease inhibitors that were licensed in 1996, the Merck Company
published in 1997 that a coded 'HIV protease inhibitor' is 'rapidly' hepatotoxic in dogs and rats
30 min after administration. Histological examination revealed single cell necrosis (Grossman
et al., 1997).
to AIDS´ (Mathur-Wagh et al., 1984), and that the T-cells of intravenous drug users
dropped in proportion to drug use (Des Jarlais et al., 1987). Yet another anti-HIV
therapist, Michael Gottlieb, had reported in 1981 that all of five homosexual Pneumocystis
pneumonia patients, later described as the first AIDS patients ever diagnosed, had used
nitrite inhalants (Gottlieb et al., 1981 a).
2. In 1994, the British-French Concorde trial, the largest controlled study of its kind,
including 1749 subj ects compared the onset of AIDS and death in AZT-treated, healthy,
HIV-positive male homosexuals to untreated controls. It found that AZT is unable to
prevent AIDS and increases the mortality by 25% compared to the untreated controls. The
conclusion was: 'The results of Concorde do not encourage the early use of zidovudine
[AZT] in symptom-free HIV-infected adults' (Seligmann et al., 1994).
3. An independent British study found that AZT prophylaxis of mostly male homosexuals
reduced survival from three to two years and also observed AZT-specific AIDS diseases
such as 'wasting syndrome, cryptosporidiosis, and cytomegalovirus infection ... almost
exclusively' in AZT-treated AIDS patients (Poznansky et al., 1995). This result confirmed
Concorde's observation, in particular the 25% higher mortality of those on AZT. The
authors' interpretation: 'The study of patients who progress from primary HIV infection to
AIDS without receiving medical intervention gives insights into the effects of medical
intervention on presentation and survival after developing an AIDS-defining illness'
(Poznansky et al., 1995). But the nature of these 'insights' was not revealed.
4. An analysis of American homosexual men from the MAC study revealed that AZT
treatment increased the risk of pneumonia two to fourfold (Saah et al.,,1995). The AIDS
researchers explain their observation as follows: 'Zidovudine was no longer significant
after T-helper lymphocyte count was considered, primarily because non users had higher
cell counts...' (Saah et al., 1995). The fact that an inhibitor of DNA synthesis, designed to
kill human cells, would reduce lymphocyte counts was not considered.
5. According to HIV/AIDS researchers J ames Goedert et al. from the NIH, AIDS prophylaxis
by AZT also proved to be negative for American hemophiliacs. The AIDS risk of
hemophiliacs on AZT was 4.5 times higher and their mortality was 2.7 times higher than
that of untreated controls (Goedert et al., 1994). The authors' interpretation of the
increased morbidity and mortality was that this was 'probably because zidovudine was
administered first to those whom clinicians considered to be at highest risk' (Goedert et
al., 1994). In other words, 'clinicians' would be able to recognize hemophiliacs in which
HIV would strike first and prescribed AZT accordingly. AZT-specific mortality of
homosexual AIDS patients has been excused with the same argument (see 6) (Veugelers et
al., 1994).
6. Since the licensing of AZT in 1987, the mortality of British HIV-positive hemophiliacs has
increased tenfold (Darby et al., 1995) and that of American hemophiliacs has increased
sharply (Chorba et al., 1994). This has been blamed on HIV (Chorba et al., 1994; Darby et
al., 1995; Horton, 1995; Maddox, 1995).
However, the coincidence that the mortality of hemophiliacs started to increase in exactly
the same year they began taking AZT suggests that AZT was responsible (Duesberg, 1995c;
Duesberg, 1995d). In view of this, Darby et al. acknowledge that 'treatment, by
prophylaxis against Pneumocystis carinii pneumonia or with zidovudine [AZT] has been
widespread' in HIV-positive hemophiliacs, and that 'HIV-associated mortality has not been
halted by these treatments' (Darby et al., 1995). Challenged for an explanation by a
published commentary (Duesberg, 1996a), the British hemophilia researchers Sabin et al.
offered the same explanation as Goedert and Veuglers et al: 'Observational studies often
show that patients given zidovudine have a worse prognosis than untreated patients.
Patients receiving zidovudine are selectively treated because they are ill. The
interpretation of findings from these studies should not therefore be that zidovudine
increases the risk of AIDS' (Sabin et al., 1996). 'Should not,' but could.
7. An American study of intravenous drug users observed in 1993 that 'the rate of CD4
lymphocyte depletion did not appear to slow after the initiation of zidovudine therapy ...
[and] results suggested that zidovudine users in this sample may have experienced more
rapid CD4+ cell depletion' (Alcabes et al., 1993). The authors' interpretation was that 'The
results of this analysis provide evidence for a mechanism by which the clinical factors that
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predict more rapid progression to AIDS, such as bacterial infection, might work, and why
other factors, such as drug inj ection, are unrelated to AIDS risk' (Alcabes et al., 1993).
But no control is offered for drug-free AIDS.
8. In 1994, it was reported that among 104 pregnant women treated with AZT, eight aborted
spontaneously, eight were aborted 'therapeutically', and another eight delivered babies
with serious birth defects, including cavities in the chest, abnormal indentations at the
base of the spine, misplaced ears, triangular faces, heart defects, extra digits, and albinism
(Kumar et al., 1994). The conclusion of the authors was that their results were ´not
proving safety, thus lending tenuous support to the use of this drug´ (Kumar et al., 1994).
However, 'spontaneous' or therapeutic abortion as a result of AZT was not an unforseeable
accident. A review in The Lancet on 'non-surgical abortion' documents that
chemotherapeutic drugs, like methotrexate, have been used to abort normal and ectopic
pregnancies since 1952 (Potts, 1995). The article concedes 'early concerns over
teratogenicity,' but concludes: 'used correctly, the method could bring great benefits'
(Potts, 1995). Moreover, abortion of developing mouse embryos by AZT had been
published a year before HIVpositive, pregnant women were treated with AZT (see Table 8)
(Centers for Disease Control and Prevention, 1997).
9. In 1996, a study from the American National Institute of Child Health and Human
Development concluded that AIDS prophylaxis with AZT also harms children: 'In contrast
with anecdotal clinical observations and other studies indicating that zidovudine favorably
influences weightgrowth rates, our analysis suggests the opposite' (Moye et al.. 1996).
10. An American study on AIDS prophylaxis of 107 three-month to six-year-old HIV-positive
children with AZT reported depletion of 350 out of an average of 1044 T-cells per year,
and neutropenia of less than 400 cells per microliter in 20%. Since the study did not
include an untreated control, it is not directly obvious whether AZT or HIV was the cause
(Kline et al., 1998). However, because HIV is not known to infect neutrophils and the
children were free of neutropenia prior to AZT, the authors concluded that the neutropenia
was due to AZT. In view of this, they warned that 'neutropenia of the magnitude observed
in the present study (<400/[tL) can be an important limitation to the success of
antiretroviral therapy, requiring temporary or even permanent discontinuation of an
otherwise effective agent.'
By contrast, the authors blamed the dramatic loss of T-cells on natural, age-dependent
reduction: 'As expected in this population of young children, median absolute CD4+
lymphocyte counts decreased.....´ However, it is unlikely that children naturally lose 35%
of their T-cells per year. It is also unlikely that the hypothetical T-cell killer HIV was the
reason for the T-cell depletion because the study included up to six year-old children with
perinatally acquired HIV whose T-cell counts averaged 1044 per microliter before AZT
treatment. Thus, AZT remains the only plausible cause for the T-cell depletion in the
AZT-treated children.
11. The damage caused by AZT prescriptions is compounded by many of the concomitant
medicines taken by most, if not all, HIV-positive Americans with AIDS and at risk for
AIDS (Table 3). For example, some of the antiviral drugs such as ganciclovir and acyclovir
are also DNA chain terminators that are nearly as toxic as AZT (Douglas, 1990). As
expected, combination therapy of ganciclovir and AZT produces 'pancytopenia' (Jacobson
et al., 1988) by killing hernopoietic cells and has 'direct [toxic] effects on myeloid and
erythroid progenitor cells' (Fogelman et al., 1994; Retrovir, 1994). Thus, DNA
chain-terminators cause 'immunodeficiency.'
12. Anti-HIV/AIDS polypharmacies have 'nephrotoxic, cytotoxic, and myelosuppressive
[effects], such as amphotericin B, co-trimoxazole, dapsone, interferon, pentamidine,
vincristine, flucytosine, adriamycin, vinblastine, and others [which] could potentially
increase the risk of hematologic toxicities in patients being treated with ZDV [AZT]´
(Fogelman et al., 1994). In other words, these drugs are immunosuppressive because they
intoxicate and kill immune cells.
13. Three articles in The Lancet describe 'abnormal fat accumulation in patients with HIV- I
infection' (Lipsky, 1998) who were treated with HIV protease inhibitors. These
accumulations have been termed 'buffalo humps' and 'Crix belly' in various studies
(Lipsky, 1998; Lo, 1998; Miller et al., 1998). One of these studies showed a direct dose
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response relationship between the lengths of protease inhibition and fat accumulation
(Miller et al., 1998).
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6. After AZT treatment for about six months prior to birth and 1.5 months after birth because
of maternal HIV infection (pages 99, 118) (Connor et al., 1994), two HIV-free babies
developed AIDSdefining Pneumocystis pneumonia and high fever at the age of two months
(Heresi et al., 1997). Because both babies were HIV-free, there was no further AZT
treatment. Both babies fully recovered and remained healthy for the period of observation
of over a year. The authors entitled their report 'Pneumocystis pneumonia in infants...
exposed to HIV but ... not infected: an exception to the AIDS Surveillance case definition,'
but acknowledged in the text that 'it is unclear if ... zidovudine treatment set the stage for
PCP.' Had the babies had antibodies to HIV, they would have been AZT-treated to their
deaths.
The medical orthodoxy and the press, confirm that anti-HIV drugs cause
AIDS-defining and other diseases - but only informally
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and whether or not this is going to be an enduring marriage is unclear to me at this time, so,
I'm advising my patients if they still have time, to wait' (Tanaka, 1996).
Others echoed Abrams' concerns (Phillips & Smith, 1997, Karpas et al., 1997). For example,
J erome Groopman, from the Beth Israel Medical Center in Boston told Newsweek in December
1996 that 'some patients have been 'showing signs of the benefits wearing off' - an effect that
is termed 'crashing' (Leland, 1996). Doctors from the National Institutes of Child Health and
Development even published in a medical j ournal that 'zidovudine use is confounded by
progression of HIV disease' (Moye et al., 1996). And British researchers j ust wrote a letter to
Science: 'It is, unfortunately, quite possible that all of the current regimens are, to use Lange's
phrase, 'suboptimal' and the best strategy at present for asymptomatic individuals may be to
take none of the existing cocktails, but to wait for improved treatments' (Breckenridge et al.,
1997).
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The pressure did not j ust come from doctors, Callen told the Amsterdam meeting (Maddox,
1992; Hodgkinson, 1996), but from a certain segment of AIDS activism that seemed driven
by a 'drugs-into-bodies' mentality. J feel many AIDS activist friends who are in the
forefront of this frenzy are very misleading to people with AIDS, who are frightened and
desperate. They only seem to talk about two possible outcomes of taking experimental
drugs: one is that it works and one that it does not work. There is a third, apparently much
more common possibility, which is that you will be worse off than if you did nothing at all.
And nobody likes to talk about that because it is so unpleasant.' He had seen the devastation
wreaked by AZT, watching with horror as friends with AIDS 'turn the colour of boiled ham
from AZT poisoning, endure the melting away of their muscles, become transfusion
dependent, and experience drug-induced psychosis.' Yet, 'they would sell their grandmother
into slavery to get a slot in the latest drug-of-the-month clinical trial.' (Hodgkinson, 1996).
Callen was on a polypharmacy of 56 AIDS drugs composed by his friend Sonnabend (page
99), but not on AZT, when he died in December 1993 from pulmonary Kaposi's sarcoma
(Maddox, 1992; Lauritsen & Young, 1997). According to his biography, Callen had
achieved over 3000 sexual contacts using nitrites and other drugs before his AIDS diagnosis
(Callen, 1990; Farber, 1994).
In August 1997, about a year after the protease inhibitors had been introduced to the United
States as a ´miracle cure,´ The New York Times issued a first drug alert: 'Despite powerful new
AIDS drugs many are still losing the battle' (Stolberg, 1997). According to the Times,
'medications seem to be failing 25 percent to 30 percent of the 150,000 people who are using
them. For some the complex regimen of three drugs does not work from the onset, for reasons
doctors do not understand. Some people get sick from the combination therapy, which has side
effects ranging from diabetes to diarrhea. "There is an increasing percentage of people in
whom, after a period of time, the virus breaks through," said Dr. Anthony Fauci, director of
the National Institute of Allergy and Infectious Diseases in Bethesda.... The failure rate may
eventually run as high as 50%.'
Indeed, by September 1997, the 'failure rate' already did 'run as high as 50%.' At that time the
San Francisco General Hospital released cocktail treatment results from 'real world' patients,
'unlike the patients selected for well- controlled, industry- sponsored clinical trials.'
According to this trial, the new 'AIDS drug cocktails fail 53%. ... The 47 percent of patients
who obtained lasting benefit from the drugs ... were those who were more recently infected
and who had not been treated with earlier generations of anti-viral medicines' (Krieger, 1997).
In other words, healthy ´patients´ can tolerate the new cocktails longer than those already
rendered sick by AZT.
But even 'lasting benefit' seems not to last. According to a meeting report from Chicago in
February 1998, 'people taking advanced drug treatments for HIV infection...' now 'develop
hardened fat deposits in stomachs and on necks [termed] Buffalo hump [and] Protease Paunch'
(Garrett, 1998). One study reports that 11 % of drug takers have the 'abdominal fat problem.'
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Another reports that '60 percent of patients developed chemical changes akin to a pre-diabetes
state after 15 months on the drugs' (Garrett, 1998). The report even acknowledges that 'none of
the drugs [protease inhibitors] were originally tested on more than a handful of people for
more than a year, so the long-term effect is unknown.' Neither the press nor the medical
profession seem even to wonder anymore why there are no animal tests prior to the licensing
of the drug for humans- j ust human experiments.
But anti-HIV drugs are not the only medical drugs that take life prematurely. A recent study
from Canada has concluded that over two million Americans experience adverse reactions and
over 100,000 die prematurely from prescription drugs annually (Lazarou et al., 1998).
Acknow ledgments
W e t h a n k F r e d C l i n e ( S a n F r a n c i s c o ) , D r . H i l d e D u e s b e r g ( B e r l i n ) , E r n s t Gr a d l ( N u r e m b e r g ) , D r . H a r r y H a v e r k o s ( N ID A,
B a l t i m o r e ) , P r o f e s s o r P h i l J o h n s o n ( B e r k e l e y) , D r . C l a u s Ko e h n l e i n ( Ki e l ) , D r . Al wi n Kr a e m e r ( H e i d e l b e r g U n i v e r s i t y,
M a n n h e i m ) , P r o f e s s o r S e r g e La n g ( Y a l e U n i v e r s i t y, N e w H a v e n ) , J o h n La u r i t s e n ( P r o v i n c e t o wn ) , P r o f e s s o r D a v i d S h u g a r
( W a r s a w) f o r i n f o r m a t i o n a n d a d v i c e , D r . R u h o n g Li ( B e r k e l e y) f o r g r a p h i c s , a n d S i g g i D u e s b e r g f o r r e v i e w a n d h e l p wi t h
t h e p r e p a r a t i o n o f t h e m a n u s c r i p t . P . D . t h a n k s S i g g i a n d M a x D . f o r wa i t i n g . T h i s i n v e s t i g a t i o n wa s s u p p o r t e d i n p a r t b y
t h e Ab r a h a m Ka t z F o u n d a t i o n ( N e w Y o r k ) , a n d b y p r i v a t e d o n a t i o n s f r o m R o b e r t Le p p o ( S a n F r a n c i s c o ) , T o m B o u l g e r
( Lo s An g e l e s ) , C a r o l J . W i l h e l m y ( S a n M a t e o ) , R o b e r t A. T h r e l f a l l ( Al b u q u e r q u e ) , R o b b i n s R e s e a r c h In t e r n a t i o n a l ( S a n
D i e g o ) , a n d a f o u n d a t i o n t h a t p r e f e r s t o r e m a i n a n o n ym o u s .
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