THE FAUCI FILES, 3( 83): Nuremberg Code Vetoed for AZT HIV-Negative Baby Experiments
August 27, 2000
The AZT Model of Post-Partum Abortion and AIDS
Causation also appears to apply to the HIV-negative
children, not just the handful out of 100
who are "saved" from HIV infection:
"...that the current practice of treating
HIV-1-positive women and their infants with
high doses of AZT could increase cancer risk
in the drug-exposed children when they reach
young adulthood or middle age,"
While the proof that AZT is a cause of AIDS
in HIV+ babies born to AZT-poisoned mothers has
been establised in reproducible experiments, the silent
and not-so-silent defenders of baby killing continue
to assert The God Defense as they point to more
babies "saved" from HIV infection than are killed
by AZT "treatment".
But how do these God impersonators know if the
HIV-negative babies born to HIV-positive mothers
are really better off when only a handful out of
each 100 treated mothers are purportedly "saved"
from HIV infection by AZT? How dare they overlook
the risk of AZT long-term damage to those who would
have had healthy lives if AZT was never used on them?
Who gave these people the right to veto the
Nuremberg Code when it comes to the AZT neonate
studies in the November 1997 Journal of the
National Cancer Institute?
"The toxicities explored here suggest that
the mechanisms of AZT induced cytotoxicity
in bone marrow of the patients chronically
exposed to the drug in vivo may involve
both chromosomal and mitochondrial DNA damage."
-- Agarwal & Olivero
And which of these God knock-offs can claim that ALL
the AZT-exposed HIV-negative babies -- not just the
handful "saved" from HIV infection -- are truly
better off when one considers the horrifying
outcomes of 100% deaths in the rodent genotoxicity
studies by the National Cancer Institute, which
may extend the trajectory for AZT Post-Partum
abortions into the human-equivalent range of
early adulthood, at best:
"In utero-exposed mice "...exhibited statistically
significant, dose-dependent increases in tumor
incidence and tumor multiplicity in the lungs,
liver, and female reproductive organs..." at 1 year.
The same results were not seen in AZT-exposed
infant monkeys,but incorporation of the drug
"...into nuclear and mitochondrial DNA was
detected in multiple organs..." of these monkeys,
as well as in exposed mice, indicating genotoxicity.
As I recall, the AZT pregnancy studies only plan
to follow the HIV negative children for a few years,
certainly not long enough to determine the
scope of any harm done to these kids.
When their mother is gone and (if) they grow up, who
is there to tell them that their multiple cancers
of all kinds were the result of God Fauci's
antiviral hoax and political opportunism?
Who vetoed the Nuremberg Code?
W. Fred Shaw, Editor
THE FAUCI FILES
In Utero Exposure To AZT Causes Tumors In Mice
WESTPORT, Nov 05 (Reuters) - Although AZT is effective in
reducing the incidence of maternal-fetal HIV transmission,
evidence from animal experiments reported today suggests
that it may increase the risk of tumors in exposed infants.
Since the studies were conducted in mice, Dr. Ofelia A.
Olivero of the National Cancer Institute in Bethesda,
Maryland, and a multicenter team caution in the November
5th issue of the Journal of the National Cancer Institute
(JNCI) that the relevance "...to human exposure must be
considered in the context of dose-equivalency."
In utero-exposed mice "...exhibited statistically
significant, dose-dependent increases in tumor incidence
and tumor multiplicity in the lungs, liver, and female
reproductive organs..." at 1 year. The same results were
not seen in AZT-exposed infant monkeys, but incorporation
of the drug "...into nuclear and mitochondrial DNA was
detected in multiple organs..." of these monkeys, as well
as in exposed mice, indicating genotoxicity.
The findings indicate "...that the current practice of
treating HIV-1-positive women and their infants with high
doses of AZT could increase cancer risk in the drug-exposed
children when they reach young adulthood or middle age,"
according to the scientists. However, "The remarkable
effectiveness of AZT in preventing fetal HIV infection
indicates that the immediate need for treatment of a
potentially fatal disease should outweigh the potential
cancer risk." At this point, Dr. Olivero and colleagues
recommend that pregnant women should be notified of these
risks, and the appropriate informed consent to AZT
prophylaxis should be documented.
Last January, the National Institutes of Health convened a
panel of researchers to review this and other evidence of
the transplacental carcinogenic effects of AZT, according
to Dr. Atieno A. Reggy and others at the Centers for
Disease Control and Prevention in Atlanta, Georgia. They
write in JNCI: "In its summary of the studies, the panel
concluded that the known benefits of AZT in preventing
perinatal transmission far outweigh the theoretical risk of
carcinogenesis and that, in and of themselves, the data do
not suggest the need for changes in treatment
However, in light of the evidence, the "...Pediatric AIDS
Clinical Trials Group is currently conducting a long-term
follow-up study of children exposed to antiretroviral
therapy in clinical trials."
J Natl Cancer Inst 1997;89:1566-1567,1602-1608.
Agarwal RP, Olivero OA. Genotoxicity and mitochondrial
damage in human lymphocytic cells chronically exposed to
3'-azido-2',3'- dideoxythymidine. Mutat Res 1997 May
Medical Oncology, University of Miami School of Medicine, FL
Abstract: AZT (3'-azido-2',3'-dideoxythymidine), the first
nucleoside analog approved for the treatment of AIDS
(acquired immunodeficiency syndrome), induces significant
toxic effects in humans exposed to therapeutic doses. As an
inhibitor of the HIV-1 (human immunodeficiency virus 1)
reverse transcriptase, AZT blocks the incorporation of
nucleotides into the host's newly synthesized DNA.
Incorporation of AZT into mammalian DNA as well as specific
localization of the drug into telomeric DNA, has been
previously documented by immunohistochemistry. As with
other nucleoside analogs, AZT has affinity for
polymerase-gamma, the enzyme responsible for the
replication of mitochondrial DNA. In order to examine the
mechanisms of toxic events induced by long-term AZT
exposure, human T-lymphocytic H9 cells were cultured with 25
microM AZT for 7 months. In the resulting H9-AZT cells,
incorporation of AZT into DNA was demonstrated by
radioimmunoassay and immunohistochemistry, chromosomal
aberrations and micronuclei were scored and intracellular
lipid distribution was determined. Two pmol of AZT per
microgram of DNA were detected by radioimmunoassay in
H9-AZT cells. Control cells showed negative values in the
radioimmunoassay. Cytogenetic observations on H9-AZT cells
showed an increase in chromosomal aberrations and nuclear
fragmentation when compared with unexposed H9 cells.
Electron microscopy revealed mitochondrial damage and an
elevated accumulation of neutral intracellular lipid
deposits probably as a consequence of a distortion in the
beta-oxidation of fatty acids normally carried out by this
organelle. The toxicities explored here suggest that the
mechanisms of AZT induced cytotoxicity in bone marrow of
the patients chronically exposed to the drug in vivo may
involve both chromosomal and mitochondrial DNA damage.