Læknaneminn - 01.04.1997, Blaðsíða 126

Peter Duesberg and David Rasnick
demonstrates that the authors are clearly aware that a
drug-free control group of HlV-positive AIDS patients
is necessary to refute the drug hypothesis of AIDS,
while at the same time supporting the orthodox view
that HIV causes AIDS. However, the drug-free group
reported by the authors proved to be an empty set, as
no drug-free AIDS patients were recorded in the
Nature commentary 11‘1’335. Our independent analysis
of the data base also failed to identify the missing group
of drug-free AIDS patients 115’221. Despite our chal-
lenge in The Lancet 223, Genetica '15, and Science 3,6, to
this date the authors have failed to come up with an
explanation as to the origin of r/;«Vdrug-free group 337.
2) The re-investigation of the database of the Nature
commentary further revealed that 45 drug-using, HIV-
free patients had been omitted from the paper,
although they had AIDS defining diseases "5. This
brazen manipulation of the facts was legitimised with
the CDC’s HIV antibody-based AIDS defmition 337
(see 2.).
3) The Nature commentary also omitted the fact that
73% of the HlV-positive AIDS patients were on AZT.
However, in response to our challenge the authors
acknowledged the AZT prescriptions 2 years later 303.
Thus the drug hypothesis was refuted by claiming
non-existing, drug-free AIDS patients, by hiding HIV-
free AIDS patients, and by omitting widespread AZT
use by AIDS patients.
Numerous other epidemiologists have also investi-
gated “HIV disease progression” 102 to AIDS in drug
users 87,88,91‘93'101-104'106'279 without offering drug-free
controls. Indeed, there is not a single epidemiological
study in the bulging AIDS literature that ever
described a group of HlV-positive people, without
confounding health risks like drug use or hemophilia,
progressing from HIV to AIDS n'225. This absence of
drug-free controls is the single most damaging flaw of
AIDS epidemiology.
For example, Alcabes et al. conclude from a study of
HlV-positive intravenous drug users from New York
that, “The results of this analysis provide evidence for
a mechanism by which the clinical factors that predict
more rapid progression to AIDS, such as bacterial
infection, might work, and why other factors, such as
drug injection, are unrelated to AIDS rislc” 87. But no
control is offered for drug-free AIDS.
Based on analyses of HlV-positive intravenous drug
users, “with 45% injecting at least once per day,”
Margolick et al. conclude “that progression of HIV-1
infecdon in IV drug users, as reflected in the decline of
CD4 cell counts, is no more rapid than that reported
for other risk groups” 91. In an effort to exclude the
role of drugs in AIDS, the authors pointed out that in
a particular 6 month survey interval there was no
“effect of active vs inactive drug use” on T cell loss.
However, there was no verification for “inactive” drug
use, and no informatiom as to whether “inactive” street
drug use was substituted by methadone, which is itself
immune suppressive 33S. Moreover there was no effort
to determine the cumulative lifetime drug dose of
active or “inactive” drug users that is essential to evalu-
ate drug pathogenicity. There was also no information
as to whether “other risk groups” included drug-free
controls.
It is also claimed that cohorts of HlV-positive male
homosexuals using batteries of recreational drugs
including, “alcohol, tobacco, cannabis, nitrites, cocaine
and amphetamines” in addition to AZT developed
AIDS from HIV infection alone without offering a
population of drug-free HlV-patients as a control. For
example, a “Tricontinental” study from San Francisco,
Vancouver, Amsterdam and Sydney that was sponsored
by the American NIAID concluded that, “None of the
presented hazards is significant.” Although the study
acknowledged that, “there were no appreciable differ-
ences in the use of alcohol, tobacco or nitrites,” it
insisted that, “Notably, nitrite use was not associated
with disease progression, and the use of tobacco
appears not to be related to progression to AIDS or P.
carinii pneuntonia (data for the latter not shown)” 102.
A remarkable “Tricontinental” conclusion!
Likewise, the NIAID-sponsored MAC study of male
homosexuals published that there is “No evidence for a
role of alcohol or other psychoactive drugs in accelerat-
ing immunodeficiency in HIV-1 positive individuals”
103 although it had never identified even one drug-free,
HlV-positive homosexual with AIDS in 10 years 109.
Indeed, a recent report from the MAC study, published
in the Journal of Substance Abuse seems to contradict
their earlier message: “Men who combined volatile
nitrite (popper) use with other recreational drugs were
at highest risk both behaviorally and in terms of
human immunodeficiency virus-1 (HIV) seroconver-
sion throughout the study.” All of the 500-800 homo-
LÆKNANEMINN
124 1 ■ tbl. 1997, 50. árg.