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Peter Duesberg and David Rasnick
and of which most are now treated with AZT and
other toxic antiviral drugs, is compared to that of
untreated, HlV-free hemophiliacs (see 7.8.) 22-2,í-s».m_
Naturally, all excess mortality from immunosuppres-
sive transfusions, AZT and other anti-HIV/AIDS
drugs is credited to HIV. This practice obscures the
role of drugs and other non-contagious risk factors in
AIDS in favor ofHIV.
7.8. Hiding evidence that AZT accelerates death,
eleven examples. In an effort to hide the emerging
tragedy, the medical establishment either trivializes or
disclaims the evidence that AZT causes diseases and
accelerates death. An analysis of several of the above
cited examples of AZT-accelerated morbidity and mor-
tality (see 4.) documents this assertion:
1) The observation that among male homosexuals,
“HIV dementia among those reporting any antiretrovi-
ral use (AZT, ddl, ddC, or d4T) was 97% higher than
among those not using this antiretroviral therapy” is
interpreted by its authors with little concern for per-
centages: “This effect was not statistically significant”
117
2) The stunning results that HlV-positive hemophil-
iacs on AZT have 4.5-times more AIDS and have a
2.4-times higher mortality than untreated HIV-posi-
tive hemophiliacs, is excused by the NIH researcher
James Goedert, the former proponent of the nitrite-
AIDS hypothesis (see 3.), with the casual explanation,
"probably because zidovudine was administered first to
those whom clinicians considered to be at highest risk”
204. But, although AZT apparently increased the mor-
bidity and mortality of hemophiliacs significantly,
Goedert et al. did not question the appropriateness of
AZT therapy.
3) Darby et al. report in Nature in 1995 that the
mortality of HlV-positive British hemophiliacs
increased 10-fold since the introduction of AZT in
1987 l83. The authors acknowledge that “treatment, by
prophylaxis against Pneumocystis carinii pneumonia or
with zidovudine [AZT] has been widespread” in HIV-
positive hemophiliacs. But instead of even considering
that these drugs could play a role in accelerating the
deaths of hemophiliacs, they argued that “HlV-associ-
ated mortality has not been halted by these treatments”-
183. They failed to explain why HlV-associated mortal-
ity would have risen 10-fold only after the introducdon
ofAZT and other anti-AIDS therapies in 1987, rather
than in the two decades before 1985 when HIV was
unknowingly transfused into hemophiliacs together
with clotting factor 24.
4) Saah et al. explain their observation that male
homosexuals on AZT have a two- to four-fold higher
risk of Pneumocystis pneumonia than untreated con-
trols as follows: “Zidovudine was no longer significant
after T-helper lymphocyte count was considered, pri-
marily because nonusers had higher cell counts...” 201.
The fact that an inhibitor of DNA synthesis designed
to kill human cells would reduce lymphocyte counts
was not mentioned.
5) An evaluation of AIDS prophylaxis with AZT
produced in 1994 the following results: “the average
time with neither a progression of disease nor adverse
event was 15.7, 15.6, and 14.8 months for padents
receiving placebo, 500 mg zidovudine, and 1500 mg
zidovudine, respectively. ...After 18 months, the 500-
mg group gained an average of 0.5 month without dis-
ease progression, as compared with the placebo group,
but had severe adverse events 0.6 month sooner.” On
this basis the authors concluded that, “...a reduction in
the quality of life due to severe side effects of therapy
approximately equals the increase in the quality of life
associated with a delay in the progression of HIV dis-
ease” 202. It remains unclear, however, how one gains
0.5 months “without disease progression” while one
has “severe adverse effects” 0.6 months sooner.
In view of this one wonders why since 1994 at least
220,000 mostly healthy, HlV-positive people continue
to receive AZT, either by itself or combined with other
drugs like protease inhibitors, all of which have no
therapeutic value and cost the patient or tax payer over
$12,000 per year 26.
6) The blunt result that AZT prophylaxis reduced
survival from 3 to 2 years, and caused “wasting syn-
drome, cryptosporidiosis, and cytomegalovirus infec-
tion ... almost exclusively” in AZT-treated AIDS
patients, was interpreted like this: “The study of
patients who progress from primary HIV infection to
AIDS without receiving medical intervention gives
insights into the effects of medical intervention on pre-
sentation and survival after developing an AIDS defm-
ing illness”. But the nature of these “insights” was not
revealed by the authors 203.
7) The largest test of AIDS prophylaxis with AZT of
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