"And for your info, there are trials being conducted now that are testing the effects of a new drug seen as an alternative to AZT. So you see, the medical establishment as you see it does see the limitations of AZT....and all of our meds for that matter. But we, unlike you can also see the very evident benefits of our meds for those living with HIV."
Bear this comment in mind as you read the following:
Evidence exists which shows that AZT is rapidly reduced by compounds containing sulphydryl (-SH) in other words AZT oxidises SH groups (1). Ample evidence also exists showing that oxidation in general (and of SH levels in particular) and decreased levels of ATP (due to mitochondrial damage) can lead to many clinical abnormalities including wasting, muscular atrophy, damage to the liver and kidney, cancer and immunodeficiency (2, 3). Since patients who are at risk of AIDS are exposed to many oxidising agents and are known to have low SH levels (4, 5) one would expect AZT to have particularly toxic effects in these individuals and the sicker the patient the more toxic the drug. AIDS Inc. acknowledged this way back in 1988:
"Azidothymidine, however, is associated with toxicities that can limit its use.These toxicities are particularly troublesome in patients with established AIDS; the use of azidothymidine is often limited in this population" (6).
Considering the SH oxidising activity of the 3'azido group in AZT (1) substituting a SH group for the azido group would eliminate part of the toxicity of AZT. This safer AZT derivative was produced and according to researchers it was found to be an effective inhibitor of "HIV RT"(7). Note that this was done way back in 1992 (11 years ago!) but rather than implement the production and administration of this derivative, AIDS Inc. chose instead to maximise toxicity and death with AZT, knowing that everyone was credulous enough to just blame the "deadly virus" HIV anyway. For those few who still retain their critical faculties regarding HIV/AIDS, this is a small indication of the extent to which AIDS Inc. has the health of HIV-positives at heart.
I will end by quoting from "AZT: An AIDS Defining Drug" by Martin Walker:
"In 1990, when AZT had been licenced for 3 years, Wellcome got market analysts BdZ (Barclays de Zoete Wedd) to report on the prospects and risks to the marketing and production of AZT.
BdZ defined the factors which might destabilise the market position of AZT as:
These points speak volumes about the political economy of medicine in developed countries. To recoup its initial capital investment and secure a long market life for AZT on the basis of the BdZ report, Wellcome had to hope that no cure for AIDS was discovered; there was no criticism of AZT; there was no fast track approval of any other drug; reports of the (heterosexual) spread of AIDS continued. In the world of big business only the scent of scandal separates marketing theory from marketing practice. Wellcome, or agents on their behalf, carried out all five of these strategies between 1988 and 1993 during which time AZT remained unchallenged."
1. Haldon and Oppenheimer 1988. Thiol reduction of 3'-azidothymidine to 3'-aminothymidine: kinetics and biomedical implications. Pharm. Res. 5:297-299
2. Papadopulos-Eleopulos 1988. Reappraisal of AIDS: Is oxidation caused by the risk factors the primary cause? Med. Hypotheses, 25:151-162
3. Papadopulos-Eleopulos 1982. A Mitotic Theory, J. Theor. Biol. 96:741-758
4. Buhl et al 1989. Systemic glutathione deficiency in symptom-free HIV-seropositive individuals. Lancet 2:1294-1298.
5. Eck et al. 1989. Low concentrations of acid-soluble thiol (cysteine) in the blood plasma of HIV-1-infected patients. Biol. Chem. Hoppe-Sayler, 370:101-108
6. Surbone et al 1988. Treatment of the aquired immune deficiency syndrome (AIDS) and AIDS-related complex with a regimen of 3'azido-2',3'dideoxythymidine (azidothymidine or zidovudine) and acyclovir. A pilot study. Ann. Int. Med. 108:534-540
7. Yuzhakov et al 1992. 3'-mercapto-2',3'dideoxynucleotides are high effective terminators of DNA synthesis catalyzed by HIV reverse transcriptase. FEMS 306:185-188