Re: Re: Re: Neonatal HIV 8 October 2004
Previous Rapid Response Next Rapid Response Top
Christopher Tyler,

Send response to journal:
Re: Re: Re: Re: Neonatal HIV

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 DNA integrity.'

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." 030104_i.htm

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)." 072103e.html

'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 hospital.
'Prevalence of adverse events associated with potent antiretroviral treatment: Swiss HIV Cohort Study' published on 20 October 2001 in Lancet (358(9290): 1322-7)

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:
"Another explanation for more rapid progression in those on zidovudine is given by the authors of the Italian study – this is that transmission in the face of zidovudine is linked with high viral load, and by implication, with zidovudine resistance. Infants with high viral loads do worse, and if an infant has drug-resistant HIV, then zidovudine alone may not prevent infection, and the infant will respond less well to subsequent HIV treatment. The study authors are quite clear in their final conclusion:“Our findings should not be misinterpreted as a reason not to use ZDV prophylaxis, which is effective in preventing perinatal HIV-1 infection.” (2). Tyler is guilty of just this misinterpretation."

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 either,
a) inert, that is, having no effect on the clinical outcome of the child except in a putative positive way; or,
b) that in fact AZT is only involved negatively in relationship to causing viral mutation. That is, by causing 'mutant' virus to appear, which is then ascribed responsibily for the infants' poorer outcomes. Since we know from the Concorde trial that AZT is useless as an 'AIDS' drug, and, according to Dr. Flegg, 'zidovudine is linked with high viral load, and by implication, zidovudine caused resistance' and thus indirectly causes infants to do worse, why would anyone use this poison?

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..."
Concorde Coordinating Committee, Concorde: MRC/ANRS Randomised Double-blind Controlled Trial of Immediate and Deferred Zidovudine in Symptom-free HIV Infection, The Lancet, Vol 343, April 9, 1994

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 Neurobiology (5(1):83-5);
• Neurobehavioral and pregnancy effects of prenatal zidovudine exposure in Sprague-Dawley rats: preliminary findings in Neurotoxicology and Teratology (20(3):251-8);
• Long-term effects of prenatal 3'-azido-3'-deoxythymidine (AZT) exposure on intermale aggressive behaviour of mice in Psychopharmacology (145(3): 317-23);
• Prolonged perinatal exposure to AZT affects aggressive behaviour of adult CD-1 mice, reported in Psychopharmacology (150(4):404-11);
• Prenatal exposure to anti-HIV drugs: neurobehavioral effects of zidovudine (AZT) + lamivudine (3TC) treatment in mice, Teratology (63(1):26-37);
• Animal models of anti-HIV drugs exposure during pregnancy: effects on neurobehavioral development, Progressive Neuropsychopharmacology and Biological Psychiatry (26(4):74761)

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://'. 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