Subject: The role of antibiotics in the emergence of AIDS: Conclusion
From: Study group AIDS therapy email@example.com
To those affected,
their doctors and carers
To Media in developed and developping countries
Chemoantibiotics, a principal cause of AIDS defining illnesses in developed and developing countries
Dear Sir or Madam
Chemoantibiotics (such as Septrime, TMPSMX, Cotrimoxazole) which are administrated in veneral di-seases and other infections are a principal cause of AIDS defining illnesses and immune deficiencies in developing and developed coundtries.
Chemoantibiotics block the formation and the release of folic acid and of purine, which are needed for the formation of the DNA in Mitochondria and exhaust thereby the mitochondrial thiol pool. They bind to SH-groups of glutathione and cysteine and impair thereby the activity of mitochondria. (When admi-nistred without control they also cause the formation of multiresistant strains of bacteries.) They inhibit by oxydation the transport of oxygen into the cells (causing methhaemoglobinaemy) and ex-haust by oxydation the glutathion molecules in the cells, which are needed for the reduction of oxygen and the production of ATP in mitochondria. By this they cause damage to the CD-4 and CD-8 helpercells and induce thereby the emergence of opportunistic infections (e.g. PCP, toxoplasmosis, herpes, Cyto-megalie), that define the AIDS-syndrome. The lack of glutathion molecules in antigen-presenting cells then induces the formation of CD-4 cells with the Th-2 cytokine prophile, that activate the formation of antibodies against external antigens, whereas the formation of CD-4 helpercells with Th1 cytokine profile, that activate the dedection and destruction of cells containing viruses, myccobacteries and fungy, is con-tinuosly inhibited.
The immune deficiencies and the AIDS defining illnesses induced by this chemoantibiotics have been treated from 1987 on with nucleosid analog drugs, that have been created for the treatment of leukemia. Nucleoside analog drugs damage the DNA in mitochondria, effecting damages to cells in the brain, the muscles, the bone marrow and internal organs and lasting damage to the CD-4 and CD-8 helpercells and thereby the emergence of the opportunistic infections, that define the AIDS syndrome. (Children from mothers, that receive AZT in their pregnancy, show a far higher risk for a progredient course of AIDS defining infections than children from pregnant mothers who did not take AZT (Jour. of AIDS 2000).
In regard of this well documented interactions, that have been demonstrated in various studies and ani-mal tryals, the reduction of the administration of chemoantibiotics is the most important mesure to reduce the emergence of AIDS defining illnesses in developed and developping countries.
In various articles, that we have sent you earlier, it was demonstrated, how AIDS defining illnesses can be treated without a continuous administration of chemoantibiotics and without nucleoside anlog drugs and how a prevention of infections and immune deficiencies can be achieved.
If you have questions concerning this articles, don't hesitate to get back on us by E-mail.
Enclosure: Treatment recommendations
AIDS defining illnesses, their causes and treatment (Treatment recommendations based on the works of Dr. Heinrich Kremer, Hamburg, Prof. Alfred Häs-sig, Berne), Dr. Stefan Lanka (Suttgart) and Eleni Papadopulos-Eleopulos (Royal Hospital, Perth) available at www.virusmyth.com and www.continuummagazine.org and works of L. A. Herzenberg, J.D. Peterson and S.C. De Rosa (Stanford University)and of Furchgott and Ignarro avaiable at www.ncbi.nlm.nih.gov
The many and varied diseases that can define the AIDS syndrome: fungal infections of the lung, of the mucous membranes, the brain, and the gut, and the degenerative chan-ges in the endothelial cells of blood vessels and lymphatic vessels (Kaposi Sarcoma), occur because of an ongoing heightened production of gaseous nitricoxide and oxygen radicals in immune cells and other cells. Under these conditions CD4 helper cells ma-ture predominantly to cells with TH2 cytokine prophile, which migrate to the bone mar-row, where they activate defences against bacteria by producing antibodies, but only few mature to TH1 cells mesurable in plasma, which activate the dedection and destruc-tion of fungus and virus infected cells and of altered cells. If this situation per-sists, a higher quantity of proteins of the cytoskeleton and of mitochondria is relea-sed as en effect of heightened cell decay. Against these proteins a higher rate of the antibodies are formed. This antibodies and antibodies that occure in hepatitis and due to toxic pollution are detected by the HIV-antibody tests. Once a certain, arbitrary level is reached, the patient is declared "HIV positive".
A elevated level of nitricoxide and oxygen radicals comes about as a result of:
- ongoing contact with antigens (e.g. from repeated or chronic infections, injuries, operations and dirty water).
- repeated contact of foreign proteins to the plasma (from coagulation proteins in blood preparations and from semen liquid in unprotected anal intercourse)
- contact to toxic substances in food (e.g. aphlatoxines in wet cereals), medica-ments and from environment pollution, toxic decomposition products from modern chemicals (heavy metals (e.g. carrier substances in hepatitis B-vaccines, amalgan fillings)
- inhalation of nitrites ("poppers") which are stored in cells as NO2. They are re-leased through physical exertion on increased exposure to calcium ions. This af-fects the endothelial cells of blood vessels and lymphatic vessels with a small capillary diameter, and leads thereby to degenerative changes (swollen lymph nodes and finally to Kaposi Sarcoma).
- impairment of the mitochondria, the single cell energy suppliers, which synthesize the energy-carrying-molecule ATP, used for all functions of the organism
The causes of chronic mitochondrial damage are:
- damage of the mitochondrial DNA due to antibiotics (e.g. sulpha compounds such as Septrime, TMPSMX) which block the synthetisation of folic acid and purine, and lead thereby to the exhaustion of the mitochondrial thiol-pool. Likely effects are caused by heavy metals and by cytostatics like AZT. All this substances bind the SH-groups of glutathione and cysteine and impair thereby the activity of mitochon-dria.
- reduced glutathione produced resulting from liver damage, e.g. chronic hepatitis (occuring frequently in gay men, hemophiliacs and intravenuous drug consumers), excessive alcohol consumption, or through shortage of nutritional cysteine, esp. in developing countries. Glutathion molecules reduce oxygen- and nitricoxydemole-cules, so that ATP production in mitochondria is not disturbed. An ongoing shorta-ge of glutathione means that phagozyte poison themselves attacking fungi and virus containing cells by means of NO.
- reduced oxygen transport in cells because of oxidation (methhaemoglobinaemia) which exceeds the reductive capacity of glutathione. This comes about because of the strongly oxidising effect of nitrites (poppers), antibiotics (Septrime, TMPSMX) and insecticides (e.g. Lindan in moistures against crab louse), nucleoside analogues (e.g. AZT), heavy metals and chemicals.
- lack of plant antioxidants which bind to toxic degradation products (oxygen radi-cals) and thereby reduce inflammation and stressreactions.
On prolonged impairment of mitochondria, they dissolve their symbiosis with the host ("Warburg Phenomenon"). Cells then increasingly switch over to producing energy by anaerobic fermentation, which results in excess lactic acid production, and the growth of fungi and opportunists, and ultimately to wasting, at which point cells obtain es-sential nutrients directly from the myoproteine. By an heightened activity of reverse transcription the cellnucleus then saves its genotype.
Continuous activation of macro-phages leads in this situation to an ongoing release of messanger substances (Inteleu-kine 2) which trigger the release of stress-hormones in the adrenal gland. This hormo-nes induce the formation of TH2 CD-4 cells, that activate the formation of antibodies in the bone marrow, whereas cellular immune reactions induced by TH1 cells are conti-nuously suppressed.
By means of:
- A supply of sulphur compounds in sea salt, mineral water and algal products, and of cysteine and methionine containing protein mixtures, (Cysteine, N-acetyl-cysteine and arginin, (3-8 gramme daily)also in curd and whey) and folic acid (300 miligramme daily) can stimulate glutathione formation in the liver. Glutathione must be administered in the mean time intravenously (600 milligramme daily) untill its formation in the liver works sufficiently again.
- Plant antioxidants, e.g. PADMA 28 (2-3 times 2 tabletts daily) or artemisia annua in UWEMBA pastilles (available from www.nusag.com) which bind to toxic oxygen de-cay products, and natural protease inhibitors (heparine and heparinoids in agar, algae or cartilage preparations), which activate the body's own anti-proteases and bind to cations that attack the cell walls, slow down chronic inflammatory reacti-ons going allong with increased cell division.
- Co-enzyme Q10 and NADH and high doses of Vitamin C and E can improve electron transport in the respiratory chain of cells. Folic acid (300 milligramme daily), thiols L-carnitin and low doses of selenium, (e.g. brewers'yeast), and zinc can support the synthetisation of ATP in mitochondria and the repair of damage to mi-tochondrial DNA.
- Opportunistic infections (fungy, PCP and others can be treated by omega-3 fatty acids in fishoil (3 tablespoons daily) In dificult cases gamma globulin, selective cyclo-oxygenese-2 inhibitors and difluoromethylornithine as a polyamine inhibitor can be administrated.
The activity of killer cells and neutrophillia can be sup-ported by the administration of glutamine (40 grammes daily) and L-Arginin (20-30 grammes daily).
- DHEAS (200 milligrammes daily) can diminish ongoing stress reactions in the immune system (TH1-TH2-switch) caused by the release of stresshormones (cortisol) in the adrenal gland.
- Essential fatty acids in linseed oil, thistle oil, soya oil and omega-3 fatty acid in fish oil mixed with curd, which enhighten the uptake of oxygen in cells
- Carduus marianus or Aloe vera to support the liver and partly fermented beverages that can restore the gut flora
- Ethereal oils, rubbed on to the chest and in the armpits serve to stimulate the immune system through the ground substance (matrix)
- Extract of grape fruit kernels, gargling with honey/vinegar andsulphur containing moistures or Melaleucae Alternifolia oil as a local treatment against fungal in-fection.
- Targeted stress reduction techniques, e.g. autogenic training, stretching and mas-sages, and refraining from excesive physical exercise (using perfomance-enhancing drugs, e.g. coffee, alcohol, nicotine, amphetamines (X-tasy), cocaine, heroin and poppers.)
- avoiding inflammatory reactions and infections by avoiding injuries and the con-tact of foreing proteins to the plasma (e.g. by protection in anal intercourse).
- of a nourishment poor in sugar amd acid but rich in roughage and bases, with much high-value carbohydrates and potatoe, plant antioxidants, e.g. vegetables, fruit, herbal and green teas, cold-pressed oils, partly fermented dairyproducts, algae, soya beans, and fish but not iron-rich red meat............a flexible resistance in people with AIDS defining illnesses can be resto-red.
If limited administration of antibiotics is necessary, this basic therapy has to be continued. The treatment can be adapted to the individueal illnesses occuring. Pro-gress achieved by these measures to bolster the immune system can be monitored by mea-suring stress hormone profiles, the T4/T8 cell ratio, macrophage activation (neopteri-ne test) and cutaneous anergy, the glutathione level in plasma and in T-4 helper cells.
HIV, which is held to be responsible for causing 30 different AIDS-defining diseases, has never been shown to be transmissible nor self-reproducing; it has never been iso-lated, photographed or otherwise properly characterised, as required by the esta-blished rules of virology. The original experimental technique of Gallo and Montagnier in 1984 on which the HIV-antibody-tests were constructed, involved culturing cells from AIDS patients with leucaemic cells and embryonal cells, that show a high activity of reverse transcription. This effect of an artificially amplified reverse transcrip-tion was then interpreted as signifying the presence a new virus. A virus-specific en-zyme could not be aprooved according to the established rules. Synthetic protease in-hibitors, which are supposed to inhibit the formation of essential viral building blocks, over time, cause malaise, diabetes, kidney stones and liver failure in pati-ents given them. After PIs and nucleoside analogues are first given, an apparent de-cline in inflammatroy reactions and „virus production" may be observed, but it then rises again, which is attributed to resistance developping. Nucleoside analog drugs, that destroy for a limited time through cytostatic effects bacteries and fungy, are only ever 1% incorporated into the cell nucleus, where they should work as DNA termi-nators against HIV. As it has been demonstrated by animal trials since 1990 they cause irreversible damage to the mitochondrial DNA and thereby damage to the brain, the bone marrow, the muscles and internal organs and a lasting decrease of CD-4 and CD-8 cells causing opportunistic infections (cytomegalie, herpes simplex, PCP and hepatitis non-A-non-B) that define the AIDS-syndrome.