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Dr. Bennett feels that oxidation is an iffy possible 'side effect' of AZT, while
acknowledging mitochondrial toxicities.
In research titled, 'Azidothymidine causes functional and structural
destruction of mitochondria, glutathione deficiency and HIV-1 promoter
sensitization', researchers from Japan said, 'Our results suggest that, in the
process of AIDS myopathy development, AZT or oxidative agents directly
impair the energy-producing system of mitochondria, causing dysfunction of
cellular redox control, which eventually leads to loss of the mitochondrial
Mitochondrial toxicity is LINKED to AZT induced oxidation.
Researchers from the University of Nagoya studied the mtDNA of mice given either 1mg/kg/day or 5mg/kg/day of AZT orally for 4 weeks. Their findings, published in 1991, 'suggest that the oxygen damage of mtDNA is the primary cause of mitochondrial myopathy with AZT therapy… oxidative damage of mtDNA can be accumulated during even short period of AZT administration'.
Other researchers, looking at whether a strong antioxidant panel would help
with neuropathy found a surprise. They found that antioxidants significantly
raised CD4 counts compared to placebo. They state, 'Dideoxynucleoside-
related neuropathy affects upwards of 20% of patients taking stavudine (d4T;
Zerit) or didanosine (ddI; Videx). A possible mechanism is mitochondrial
toxicity due to free oxygen species toxicity. Based on this hypothesis,
researchers tested a potent antioxidant formula designed to lessen the
systemic clinical effects of mitochondrial toxicity."
In 'Mechanisms of Antiretroviral Toxicities', By Ross Hewitt, MD, we read: "Nucleoside analogues (NAs) can also affect adipocyte tissue. Zidovudine (AZT) was able to decrease mitochondrial DNA in subcutaneous fat but not visceral fat, due to slower mitochondrial activity in visceral fat. There are other mechanisms besides mitochondrial toxicity, e.g., certain metabolites of AZT and stavudine (d4T) decrease body fat and increase fatty acid oxidation."
"NAs are involved in the pathogenesis of subcutaneous fat wasting. This is
thought to be due to decreased mitochondrial DNA (mtDNA) in adipocytes
and some studies have demonstrated decreases of 67% with AZT and up to
90% with d4T. Switching off these agents increases mtDNA over time, but fat
does not come back in the short term (6 months)."
'decreases (of adipocytes) of 67% with AZT and up to 90% with d4T' are not trivial 'side effects' and are indications of a strong oxidation taking place. That many people taking these 'therapies' experience toxicological complications is an indication that their bodies are being damaged, strong oxidation being one of the foremost pathways of this damage.
For instance, Fellay et al., reported ‘a high prevalence of toxic effects’ in a
cohort of 1160 patients on AZT and related drugs, more than two thirds of
whom suffered side effects severe enough to affect treatment adherence.
Fortyseven per cent reported clinical problems like vomiting, diarrhoea,
nausea, abnormal fat growth, mood swings, insomnia and fatigue. Blood tests
revealed ‘potentially serious’ abnormalities among twenty-seven per cent.
The researchers classed a ‘significant proportion’ of these adverse events as
‘serious or severe’. Kidney dysfunction and severe fatigue that were ‘probably
or definitely’ due to the drugs led to some patients winding up in
We know from the Concorde Trials extended follow-up that AZT increases a person's chances of dying. And we know AZT destroys bodily tissues like muscle, fat, bone marrow, and mitochondria. We know that AZT causes anemia which is a predictor of mortality. We know AZT increases oxidation and depletes glutathione, low-levels of which are a predictor of morbidity and mortality. We know AZT doesn't triphosphorylate terribly well and has at best dubious antiretroviral properties.
Peter Flegg wrote:
I find it incredulous that in the face of all the data regarding AZT's toxicities
and modes of action (bone marrow, muscle, fatty tissue destruction,
mitochondrial destruction, carcinogenesis, DNA destruction, glutathione
depletion), that the only conclusion Dr. Flegg would reach is that AZT is
Let's not forget what the Concorde Coordinating Committee had to say about
AZT, 'A total of 172 participants died [169 while taking AZT, 3 while on
placebo]...The results of Concorde do not encourage the early use of
zidovudine in symptom-free HIV-infected adults..."
It's just strange that the ad-hoc explanation for 'treatment failure' is always 'viral mutation'. This is the catch-all used to explain away problematic issues. If CD4 cells don't rise, it's 'viral resistence'; if CD4 cells drop, the virus has become resistent; if there's 'viralogic failure', it's because of 'viral mutation'; if more people die while on the drug, it's 'viral mutation'. This is not much different than the 'just have faith' exhortation used by religions when a person begins questioning dogmas. The real question is, where is this virus that is supposedly mutating and why can't even the likes of Hans Gelderblom find it in fresh, uncultured human blood?
Let me again quote from the De Souza research, 'RESULTS: HIV vertical transmission rates were significantly different (no ZDV versus ZDV: 22.3% versus 12.2%; p = .034). Among infected infants, the RPD rate was 29.4% in the no ZDV group compared with 70.6% in the ZDV group (p = .012), and prematurity was significantly associated with a higher risk of RPD (p = .027). CONCLUSIONS: The rate of RPD was significantly higher among perinatally infected infants born to HIV-infected mothers treated with ZDV than among infected infants born to untreated mothers…”
The least Dr. Flegg could do would be to acknowledge the obvious link between poorer outcomes in infants and AZT usage, WHATEVER, is causing it.
We've often spoken of the more overtly grotesque manifestations of AZT (and other AIDS drugs); vomiting, diarrhea, neuropathy, bone marrow suppression, etc.; but in the case of fetuses and infants, mitochondrial damage may not immediately manifest itself, but take on the more subtle, and difficult to link to, forms of neurobehavior problems. Just to name some research in treated rats;
• Learning disturbances in offsprings of zidovudine (AZT) treated rats in
Let's not forget our medical history. The alarm we 'dissidents' feel can best be illustrated by another agent pushed on pregnant women, and fervently claimed to be harmless and even beneficial. Diethylstilbestrol, a synthetic oestrogen-like hormone, was prescribed to pregnant women “for routine prophylaxis in ALL pregnancies... 96 per cent live delivery with desPLEX in one series of 1200 patients - bigger and stronger babies, too. No gastric or other side effects with desPLEX - in either high or low dosage.” This an advertisement from a 1957 medical journal. See a copy of this ad, 'http:// www.desaction.org/ad-info.htm'. We hear the claim, AZT doesn't cause any harm to infants, that it will 'protect' them from 'HIV' infection.
To quote Nora Cody speaking in Bethesda, US at the National DES Research Conference in July 1999, “30 years ago today DES was still being prescribed to pregnant women in this country and, indeed, around the world. By 1969 scientists had studied this scientific substance for over three decades. Over and over, they had found cancer in laboratory animals [like AZT]. In the famous Dieckmann study in 1953, they had discovered that DES was completely ineffective in preventing miscarriage and in fact more harmful than a placebo [like the Concorde Trials]. Yet for all of this scientific inquiry, there was a fundamental failure, and DES showed us the terrible potential for human tragedy from scientific discovery.”
Legal actions are now taking place 30 years after DES use was halted.
That the medical profession can be slow in realizing its hand in causing
diseases can best be seen in SMON, thought for some time to be caused by a
virus. It was instead iatrogenic, caused by pharmaceuticals. To quote Peter
Duesberg, 'Assistant Professor Shigeyuki Inoue at Kyoto University's Institute
for Virus Research claimed discovery of a virus in the spinal fluid and
excretions of SMON patients. He added the extracts to laboratory culture
dishes of hamster tumor cells and found that the new agent killed the cells.
With more experimentation, Inoue classified the microbe as a new herpes
virus. He was able to isolate this particular virus from nearly all SMON
patients he tested, more than forty in all, and found antibodies against the
virus in other victims.'
How soon we forget our history.
Competing interests: None declared