HIV/AIDS Medicine Run Amok

HIV/AIDS Medicine Run Amok

Chapter IX from

Heinrich Kremer: The Silent Revolution in Cancer and AIDS-Medicine

2008 ©Heinrich Kremer, Barcelona (Spain)

Why Aids drugs cause cancer, degenerative changes in muscular and nervous cells, and even AIDS itself – the explanation of how ATZ, Bactrim/Septra, and their ilk actually work

The products of laboratory research initiated more than 50 years ago whose target was to plant analog transformed bases in the biosynthesis of the building blocks of nucleic acid of the DNA – the purine bases, adenine and guanosine as well as the pyrimidine bases thymine and cytosine - were supposed to inhibit the biosynthesis in microbe, immune and cancer cells. Hitchings’ laboratory team from Burroughs Wellcome synthesized three substance groups, which in their molecular composition contained nitro structure groups as a common characteristic. These substances produced both antimicrobial effects in microbe cells and immune suppressive and carcinogenic effects in immune and non-immune human cells on top of degenerative DNA damage.

-The first substance was Azathioprine, adopted as an immune suppressive drug for organ transplant patients since the 1960s (Chen 1987). Azathioprine triggered clinically opportunistic infections, Kaposi’s sarcoma and lymphomas (transplantation AIDS) (overview with Penn 1979, 1981).

-The second substance was Azidothymidine (AZT), from 1986 until today the most frequently prescribed drug for the prophylaxis of AIDS. AZT is supposed to inhibit the proliferation of the hypothetical “HIV retrovirus” in “HIV positive” and AIDS patients. AZT is highly toxic has antimicrobial, immune suppressive and carcinogenic effects and causes degenerative DNA damage in numerous human cell systems (overview with Duesberg 1996, Giraldo 1999, Brink 2000). ((248))

-The third substance was Trimethoprim (TMP). TMP as a combination preparation with sulfamethoxazole, a sulfonamide derivative, was authorized as Cotrimoxazole in 1969 in the USA and Europe as an antimicrobial drug (DTB 1969). Trimethoprim as sole medication or in combination with sulfamethoxazole (Cotrimoxazole) produced in addition to its antimicrobial mechanisms, immunosuppressive and carcinogenic effects and degenerative DNA damage in numerous human cell systems.

All three substances, Azathioprine, Azidothymidine (AZT) and Trimethoprim respectively Cotrimoxazole (T+S) possess the chemical attributes to realize the clinical research program postulated by the retrovirus cancer researchers at the historic conference in New York in March 1983 in “a series of human experiments, planned and executed in order to answer the sort of question which automatically raises itself: what would happen if you were to remove the putative defence mechanism of cellular immunity in human beings? Would this affect either the incidence or clinical course of cancer?” (Thomas 1984).

Background and manipulations behind the introduction of AZT for planned human experiments

The assumption that T-helper immune cells are destroyed by a hypothetical retrovirus was extremely helpful in leading to proof of whether the loss of the function of T-helper immune cells could cause the development of tumor cells. This hypothesis allowed for the deployment of a substance group that was known to have immunosuppressive effects and to cause the formation of tumor cells. Using the excuse of retrovirus inhibition in order allegedly to prolong the life of, according to medical opinion, the inevitably moribund AIDS patients it was possible to prescribe such experimental substances without ethical scruples to willing patients.

There was one such substance. It was first isolated in 1961 from herring sperm cells and in 1964 was synthesized as 3-azido 3-deoxythymidine by Horwitz from the Michigan Cancer Foundation (Horwitz 1964). Animal experiment trials in mice and rats with leukaemia showed the development of lymphomas (Yarchoan 1987, Adams 1989). As a result of its tumor-causing effects and the lack of inhibition of leukaemia cells this substance was not authorized for clinical human trials (Duesberg 1996). In 1985, shortly after the worldwide introduction on the market of the “anti HIV antibody tests”, developed according to the patented production procedures of Gallo at the National Cancer Institute in the USA, publications appeared from the same institute in which it was reported that Azidothymidine (AZT), a chemotherapeutic from nucleoside analog substances, inhibited the proliferation of “retrovirus HIV” in cell cultures (Mitsuya 1985).

Since 1984 it had been acknowledged that nucleoside analog substances not only cause lymphomas but also exercise massive immunosuppressive effects on the T-helper immune cells and provoke opportunistic infections.

“Each of the nucleoside analogs is associated with a profound lymphocytopenia [loss of T-helper immune cells], with a reversal of the CD4/CD8 [the ratio of T-helper immune cells to T8 lymph cells] and opportunistic infections” (Cheson 1997).

So nucleoside analog substances cause AIDS and cancer. AZT is consequently the suitable propagated substance for the “removal of cellular immunity” (Thomas 1984) and tumorigenesis.

After only a 17-week trial in a multi-center study in a number of US clinics in 1986/87 AZT was authorized in record time as a medication for AIDS patients. Clinical trials of a new medicament in the USA usually take on average 8 to 10 years. Burroughs Wellcome, the same US pharmaceutical firm that produced Azathioprine, undertook the marketing of AZT. The global British/American pharmaceutical giant Burroughs Wellcome, which in the 1990s merged to become the largest pharmaceutical company in the world – Glaxo Wellcome (now GlaxoSmithKline), had an unusual historical company policy, a large portion of the profits were directed to research foundations and donated to biochemical research institutes and clinical studies. As a result of this financial flow a close financial dependency developed between the researchers in laboratories and university clinics and the national health authorities and pharmaceutical companies. Burroughs Wellcome financed many experimental and clinical studies on chemotherapeutic treatment. The head of research there, Barry, had previously worked as a virologist for the American authority responsible for the admission and surveillance of food and drugs – the FDA. He was, conveniently, the right man at the right place at the right time to organize the mass human experiments of the cancer therapeutic, AZT on AIDS patients and to use the right channels of cooperation for the very rapid approval of AZT by the FDA. ((250)) The National Cancer Institute had conferred the data and technology for the synthesis of AZT to Burroughs Wellcome. In July 1985 Burroughs Wellcome was accorded “orphan drug status” for AZT by the FDA, even before the first scientific publications from researchers of the National Cancer Institutes on the “anti HIV effect” of AZT in October 1985. “Orphan drugs” are medications that are required by fewer than 200,000 patients annually in the USA so production by pharmaceutical companies is not financially lucrative. The respective US law provides for seven years of exclusive marketing rights and tax relief for the production of such “orphan drugs”. In the case of AZT, which is extremely expensive, the FDA did not assign a price limit for Burroughs Wellcome. In February 1986 Burroughs Wellcome transformed from a non-commercial organization into a corporation. In November 1986 Barry, together with his colleagues from the National Cancer Institute, published research data on “anti HIV inhibition” in T-helper immune cells of AIDS patients after AZT treatment causing a furor. Quotations for Burroughs Wellcome stocks almost quadrupled within a year (Adams 1989). The “invisible hand of the market” had ensured, as in the case of the patenting of Gallo’s “anti-HIV test” before the first publication of data that could be analyzed, that strategic decisions for the global marketing of “planned human experiments” for the “removal of cellular immunity” by medication with immunosuppressive and carcinogenic chemotherapeutic AZT had already taken place before the research data of the first experimental study (October 1985) as well as the second experimental and first clinical study (November 1986) were published. At the time of publication of the latter, clinical tests were already under way in a multi-center study in the USA. AZT was authorized by the FDA and was already being deployed for all AIDS patients in the early summer of 1987. Barry’s co-workers were, the then leader of the research and development department and later director of the National Cancer Institute (1989-95), Broder and the clinical retrovirologist Bolognesi from Duke University in North Carolina (Duesberg 1996). As authors they were responsible for the key publication in the proceedings of the National Academy of Science in 1986, in which it was claimed that AZT was 100 times more effective at inhibiting DNA synthesis in “HIV infected” cells than “non-HIV infected” cells in cell cultures. The same non-specific “molecular markers” were cited as proof of the presence of the “retrovirus HIV” that Gallo and Montagnier had deliberately misinterpreted as “evidence of the isolation and continuous production of cytopathic retroviruses” by virus-like particles (Popovic 1984). At the same time the allied experimental scientists from the pharmaceutical company Burroughs Wellcome, The National Cancer Institute and Duke University, claimed after intake of AZT in the first clinical studies on AIDS patients that the substance was 2,000 to 20,000 times more effective at inhibiting the replication of “HIV DNA” (measured by means of unspecific markers) than the nuclear DNA of “HIV infected” T-helper immune cells (Furman 1986). These claims have since been refuted in numerous experiments of orthodox HIV/AIDS researchers who had followed the same assumptions about the existence of “retrovirus HIV” on the basis of molecular markers and the workings of AZT (overview with Chui 1995). The supposition of a higher affinity for the integration of AZT in “retroviral DNA” in comparison to nuclear DNA of human cells has to this day not been corrected by the researchers of the producers, Burroughs Wellcome (now GlaxoSmithKline), the National Cancer Institute or Duke University. On the basis of this false assumption countless doctors all over the world have prescribed AZT to Aids patients since 1987 and to healthy, asymptomatic “HIV positive” patients since 1990 (Volberding 1990). Before the global marketing of AZT for “life-prolonging treatment of AIDS patients through inhibition of retroviral replication” in 1987 and the “preventative inhibition of HIV replication in T-helper immune cells of asymptomatic HIV patients” neither the researchers from the company producing AZT, nor the researchers from the NCI or any other researchers had tested the actual functioning mechanisms of AZT. Without exception all researchers and prescribed physicians, independent of the respective assumptions about the affinity of AZT to “retroviral DNA” or to nuclear DNA, took for granted, without checking, that AZT as a transformed molecular building block is integrated into the DNA chain in place of the natural building block, thymidine, either by the “HIV enzyme RT” or by the natural nuclear enzymes of the DNA polymerases.

In the long drawn-out chain of more than 100,000 human genes, spread out on 23 paired chromosomes, several billion building blocks are strung together. These nucleotides (from the Greek nucleos = core) are molecular, composed from a sugar, a base and three phosphate group atoms. Nucleotides contain one of four bases (adenosine, cytosine, guanosine or thymidine). These bases have an OH molecule group to which the respective proximate nucleotide is attached. The sequence of the bases in each case with three bonded sets of paired nucleotides form the coding pattern for the building instructions for the synthesis of proteins from amino acids in the cytoplasm. This DNA coding profile is transcribed, after redox dependent stimulation by transcription factors, to a messenger RNA and translated into the biosynthesis of proteins. This process is called expression and one talks of genes being expressed.

According to the dogmatic doctrine of HIV/AIDS medicine it is this process that the transformed building block AZT affects. In the thymidine base of this molecule the OH group is replaced by an azido group. Should the false building block AZT be integrated into a DNA copy of the “HIV RNA” via the RT enzyme of the supposed “retrovirus HIV”, then on this location of the short DNA string of “HIV” (termed provirus) no further nucleotides could align as the integrated AZT has the wrong pairing. The provirus genome of “HIV” would remain incomplete and could no longer be reproduced, with the aid of the cell division apparatus of the host cell, as new infectious “retrovirus HIV”.

That is the theory anyway by which the “invisible hand of the market” manipulated HIV/AIDS doctors suggest, to this day, to their asymptomatic “HIV positive” patients and AIDS patients that the intake of AZT for life, alone or in combination with other substances, will prolong their lives through the inhibition of the sooner or later “deadly retrovirus infection with HIV”. This doctrine spread by an immense propaganda input throughout all countries in the world has, however, nothing to do with the biological realities and those responsible know this full well.

The synthetic substance Azidothymidine is actually not a nucleotide. AZT is a synthetic nucleoside, the precursor of a nucleotide that merely docks one phosphate atom. In order to be integrated into DNA, regardless of whether it is “HIV provirus DNA” or nuclear DNA, the nucleoside AZT in the nucleus must have three phosphate atoms and could only then be incorporated at the growing end of the DNA as a then complex nucleotide by an “HIV RT” or the nuclear enzyme DNA polymerase. ((253)) In this case the synthetic nucleoside AZT would become the DNA nucleotide Azidothymidine triphosphate (AZT TP) that is capable of integration. Countless studies over the last decade, however, have clearly shown that only about 1 % of AZT is transformed to AZT TP, at prescribed AZT doses of between 500 and 1,500 mg per day, much too little to be able to cause any kind of inhibition of “HIV provirus DNA” or nuclear DNA as a “DNA terminator” as the claimed effects of AZT state (overview with Papadopulos-Eleopulos 1999).

When in 1961 Azidothymidine was isolated from the sperm cells of herrings and subsequently synthetically produced in 1964 (Adams 1989) the obvious question that nobody asked should have been: What was the natural function of Azidothymidine in the sperm cells of vertebrates? Two reasons are conceivable: the fertilization of the ova and the development of the embryo. Firstly, all eukaryotic organisms, which propagate sexually, inherit their mitochondria only through the maternal hereditary line (Wallace 1999). The mitochondria of the sperm cells have to be somehow inactivated before penetration of the egg cell, nobody has subsequently studied how this happens. Secondly, the sperm cells must not introduce intracellular agents to the egg shells as the embryonal cells, as a result of their Type-2 cytokine dominance, are not able to adequately eliminate intracellular agents (Coffman 1986, Mosmann 1996). Azidothymidine, as a nitrosative substance, serves both purposes. The azido groups of Azidothymidine inhibit the mitochondrial enzyme cytochrome oxidase (Tyler 1992). The biological logic is that the inhibition of cytochrome oxidase in sperm cells takes place shortly before they penetrate the egg cell, and the sperm cell mitochondria are inactivated by Azidothymidine. Azidothymidine is thought to have the same effect on cytochrome oxidase in microbes.

After the worldwide licensing of AZT as an AIDS drug for the supposed blockade of “retrovirus HIV” a number of research groups reported that the administration of AZT caused damage to DNA and mitochondria (overview with Lewis 1995). These findings did not concur with the claims of the HIV/AIDS researchers, neither with the claim that AZT is exclusively incorporated in the “HIV provirus DNA”, nor that the DNA chain terminated. In order to test the causes of AZT damage to mitochondria and to study whether the observed DNA damage was responsible for the subsequent growth inhibition of the cells after AZT treatment, researchers from the State University in New York carried out experiments of the effect of AZT on mitochondria. They allowed mitochondria to grow in a medium for five days with a pharmacotherapeutic AZT dose (5 micromoles for five days). Even after three hours after the addition of AZT the mitochondria showed signs of characteristic changes: reduced number of mitochondria, a reduction in the intake of oxygen, reduced ATP synthesis and an increased lactate synthesis. ((254)) As the new formation of DNA takes considerably longer than three hours the change in numbers, the energy production and the glycolytic formation of lactates could not be based on the primary inhibition of mitochondrial DNA (Hobbs 1995).

Research teams from a number of French research institutes studied the effects of AZT and two other AIDS drugs (the nucleoside analogs ddI and ddC) in human muscle cells. All three substances cause a dose-dependent reduction in the proliferation and differentiation of cells, a reduction in enzyme activity in the respiratory chain of mitochondria (cytochrome c-oxidase in complex IV and succinate dehydrogenase in complex II of mitochondria as well as an increase in glycolytic lactate synthesis). The researchers concluded that AZT, ddI and ddC exercise a cytotoxic effect on human muscle cells and cause functional changes through the blockade of mitochondrial respiratory enzymes.