AIDS defining Illnesses, their Causes and Treatment - Letters to the Editors

Townsend Letter for Doctors and Patients, April, 2002

Editor:

(Treatment recommendations based on the works of Dr. Heinrich Kremer, Hamburg, Prof. Alfred Hassig, Berne and Eleni Papadopulos-Eleopulos, Royal Hospital, Perth available at www.virusmyth.com whistleblowers) and works of Leonore A. Herzenberg (Stanford University) and Jeffrey D. Peterson (Northwestern University, Chicago)) available at www.ncbi.nlm.nith.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 changes 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 mature predominantly to cells with Th-2 cytokine profile, which migrate to the bone marrow, where they activate defenses against bacteria by producing antibodies, but only a few mature to Th-1 cells measurable in plasma, which activate the detection and destruction of fungus and virus infected cells. If this situation persists, a higher quantity of proteins of the cytoskeleton and of mitochondria is released as an effect of heightened cell decay. Against these proteins a higher rate of the antibodies are formed. These antibodies and antibodies that occur 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 persistently 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).

* contact with toxic substances in food, medicaments and from environmental pollution, toxic decomposition products from modem chemicals (heavy metals, carrier substances in vaccines, amalgam fillings).

* inhalation of nitrites ("poppers") which are stored in cells as N02. They are released through physical exertion on increased exposure to calcium ions. This affects the endothelial cells of blood vessels and lymphatic vessels with a small capillary diameter, and leads 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 to the mitochondrial DNA due to antibiotics (e.g. sulpha compounds such as Septrime, TMPSMX) which block the synthetization 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 these substances bind the SH-groups of glutathione and cysteine and inhibit the activity of mitochondria.

* reduced glutathione produced resulting from liver damage, e.g. chronic hepatitis (occurring frequently in gay men, hemophiliacs and intravenous drug users), excessive alcohol consumption, or through shortage of nutritional cysteine, especially in developing countries. Glutathione molecules reduce oxygen- and nitricoxide molecules, so that ATP production in mitochondria is not disturbed. An ongoing shortage of glutathione means that phagocytes 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 oxidizing effect of nitrites (poppers), antibiotics (Septrime, TMPSMX) and insecticides (e.g. Lindan in ointment against crab louse), nucleoside analogues, heavy metals and chemicals.

* lack of plant antioxidants which bind to toxic degradation products (oxygen radicals) and thereby reduce inflammation and stress reactions.

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 essential nutrients directly from the myoproteine. By a heightened activity of reverse transcription the cell nucleus then saves its genotype. The continuous activation of macrophages leads in this situation to an ongoing release of stress-hormones. The continuous activation of phagocytes then triggers the continuous release of messenger substances that mislead various reactions in the immune system.

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 arginine, (3-8 grams daily)also in curd and whey) and folic acid (300 mg daily, can stimulate glutathione formation in the liver. Glutathione must be administered in the meantime intravenously (600 mg daily) until its formation in the liver works sufficiently again.