Læknaneminn - 01.04.1997, Síða 109

The drug-AIDS hypothesis *
Human DNA is a string of 109 A, T, C and Gs linked
in a specific sequence
a) normal DNA synthesis
chain continues
b) DNA synthesis with the T-analog, AZT
chain terminates
Fig. 3.
’97. In addition, AZT is car-
cinogenic 26,19s. The long cata-
log of AZT diseases overlaps
extensively with the CDC’s
even longer catalog of AIDS-
defining diseases '7.
Considering the toxicity and
mode of action of the DNA
chain terminators, it is not sur-
prising that to date the profes-
sional literature has yet to offer
the first AIDS cure with AZT
or the other anti-HIV drugs n-
25. In 1993, the Bridsh-French
Concorde trial, the largest controlled study of its kind,
even buried the hope that AZT might prevent AIDS
199. Instead, the final report of the trial confirmed in
1994 that AZT is not only unable to prevent AIDS,
but even increases the mortality of recipients by 25%
compared to the untreated controls 16°.
Once the ice of absolute control on AZT by the
NIAID, NCI, and Glaxo/Burroughs Wellcome was
broken by the non-American Concorde trial, a series of
American and European studies confirmed and extend-
ed the predictable toxicity of AZT. Although in coded
language and with disclaimers that a specific detrimen-
tal outcome does not discredit the presumed merits of
AZT, these results show that AZT not only fails to pre-
vent AIDS, but actually causes AIDS diseases and
accelerates death (see 7.8):
1) 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 ... results suggested that zidovu-
dine users in this sample may have experienced more
rapid CD4+ cell depletion” 87.
2) An Indian-English collaboration reported in 1994
that among 104 babies of AZT-treated pregnant
women 8 aborted spontaneously, 8 were aborted “ther-
apeutically” and another 8 were born with serious birth
defects, including holes in the chest, abnormal inden-
tations at the base of the spine, misplaced ears, trian-
gular faces, heart defects, extra digits and albinism 20°.
Zidovudine users in this study may have experienced
more rapid CD4+ cell depletion.
3) The American MAC study of 5000 male homo-
sexual men observed that, “HIV dementia among
those reporting any antiretroviral use (AZT, ddl, ddC,
or d4T) was 97% higher than among those not using
this antiretroviral therapy” 117.
4) Another analysis of rhe of homosexual men from
the MAC study revealed that AZT treatment increased
the risk of pneumonia 2 to 4-fold 201.
5) And four years after introducing AZT prophylax-
is against AIDS '61, Paul Volberding et al. published in
1994 “the average time with neither a progression of
disease nor adverse event was 15.7, 15.6, and 14.8
months for patients receiving placebo, 500 mg zidovu-
dine, and 1500 mg zidovudine, respectively.” 202. Thus
even Volberding now confirms the Concorde study’s
conclusion that AZT does not prolong life or prevent
AIDS, but instead accelerates AIDS.
6) An independent British study even found that
AZT prophylaxis reduced survival from 3 to 2 years
and also observed AZT-specific AIDS diseases, “wast-
ing syndrome, cryptosporidiosis, and cytomegalovirus
infection ... almost exclusively” in AZT-treated AIDS
patients 203. This result confirmed Concorde’s observa-
tion, in pardcular the 25% higher mortality of those
on AZT.
7) The results of AIDS prophylaxis by AZT proved
even more devastating for American hemophiliacs: The
AIDS risk of hemophiliacs on AZT was 4.5 times high-
er and their mortality was 2.7 times higher than that of
untreated controls 204.
8) The mortality of British HlV-positive hemophili-
acs has increased even 10-fold since 1987, since most
are subjected to AZT and other anti-HIV/AIDS treat-
ments 22'H 3S’183.
9) In 1996 an American study from the National
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