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What people say makes us excited::
January 05, 2005
Selenium is an important micronutrient found in Brazil Nuts which have very high selenium levels and a variety of other foods such as grains, garlic, mushrooms, lobster, shrimp, oysters, barley, eggs, dried salted cod, sunflower seeds and certain types of yeast. Selenium functions as an antioxidant. It works in conjunction with vitamin E. It is an important component in the synthesis of natural antioxidant enzymes in the body. The antioxidant properties of selenoproteins help prevent cellular damage to heart cells and cells in the thyroid gland from free radicals.
Selenium (Se) is a part of the enzyme glutathione peroxidase, which metabolizes hydroperoxides formed from polyunsaturated fatty acids. It is also a part of enzymes that deiodinate thyroid hormones. A recent study of patients with a history of basal or squamous cell skin cancer reveals that selenium intake of 200 µg/day reduces mortality from all cancers and reduces the incidence of lung, colorectal and prostate cancers.
Plant foods are the major dietary sources of selenium in most countries throughout the world. Soils in some parts of China and Russia have very low amounts of selenium. Selenium deficiency has been reported in those regions because most food in those areas is grown and eaten locally. Selenium deficiency is not common but in China, where selenium intake averages 10 to 15 µg/day, selenium deficiency occurs in association with Keshan disease, an endemic viral cardiomyopathy affecting children and young women in that country. It is interesting to note the connection with a virus. Researchers believe that selenium-deficient people infected with a specific virus are most likely to develop Keshan disease. It is interesting to also note that this cardiomyopathy can be prevented but not cured by selenite supplement intake of 50 µg/day.
Patients receiving long-term total parenteral nutrition (TPN) also develop selenium deficiency with muscle pain and tenderness that was responsive to a selenomethionine supplement. TPN is a method of feeding nutrients through an intravenous (IV) line to people whose digestive systems are not functioning properly due to inflammations of the intestines or gastrointestinal disorders. In such cases, the reduced absorption of selenium through the intestines results in selenium depletion in the body and it suffers from selenium deficiency. This shows the importance of providing selenium in the organic form to the human body for its assimilation and utilization to produce selenium based antioxidant enzymes that target their free radical scavenging activity in heart cells and thyroid cells. Selenium occurs in staple foods such as corn, wheat and soybean as selenomethionine which is considered to be the best absorbed and utilized form of selenium in the human body and in primates.
Studies in which it was observed that death from cancer, including lung, colorectal and prostate cancers, is lower among people with higher blood levels or intake of selenium may be due to the active free radical scavenging activity of selenium ions on free radicals produced by cancer cells and prevent the formation of cancer cells or tumors in the body but it may not slow down metabolic activity in tumors.
The population surveys that clearly suggest an association between lower antioxidant intake and a greater incidence of heart disease must be seen together with the evidence that also suggests the ability of selenium ions and selenoproteins to remove oxidative stress from free radicals on the thymus. It may more likely to be a case of direct removal of oxidative stress in heart cells by selenium ions and prevent or reverse arrhythmia and prevent sudden heart failure. Antioxidants that have such a direct free radical scavenging activity on heart cells also benefit the health of the heart as a whole by preventing cardiovascular disease. Further evidence of its free radical scavenging activity may be found in individuals with rheumatoid arthritis. Arthritis is a chronic disease and arthritic patients have reduced selenium levels in their blood while some individuals with arthritis have a low selenium intake. Selenium, as an antioxidant, may help to relieve symptoms of arthritis by controlling levels of free radicals directly as well as removing or preventing oxidative stress to the endothelium of major blood vessels.
An oxidant burden established by hydrogen peroxide overload may elicit postischemic myocardial damage as shown in experiments using neonatal rat cardiomyocyte exposure to 50 uM-1.0 mM hydrogen peroxide. Cell exposure to hydrogen peroxide also depleted cardiomyocyte pyridine nucleotides as a consequence of enhanced utilization. The oxidative stress activated one major route of pyridine nucleotide catabolism (i.e., protein ADP-ribosylation) without acute inhibitory effect upon the other (cleavage by NAD glycohydrolase). The limited NAD sparing by metal chelators and inhibitors of ADP-ribosylation reflected pyridine nucleotide utilization for repair of single-strand DNA breaks caused by hydroxyl-like radicals formed intracellularly through iron-dependent hydrogen peroxide reduction. Cardiomyocyte NAD depletion during hydrogen peroxide induced oxidative stress was independent of cell integrity and lipid peroxidation. The NAD lost after a discrete hydrogen peroxide pulse was only partly replenished over a 24 hr postinjury period. Cardiomyocyte pyridine nucleotide metabolism is a nonperoxidative injury target that is chronically affected by hydrogen peroxide overload.
The effect of the oxidant hydrogen peroxide on the vulnerability of the myocardium to reperfusion induced arrhythmias following global ischemia has also been investigated. All hearts exposed to 200 uM hydrogen peroxide developed ventricular dysrhythmias during the reperfusion period. Coronary flow increased after 5 min of exposure to 200 uM hydrogen peroxide and remained elevated during reperfusion. Toxic oxygen derivedproducts are capable of increasing the susceptibility of the myocardium to reperfusion induced arrhythmias.
Of great interest is the relationship between selenium and HIV/AIDS, including the effect of selenium levels on disease progression and mortality in persons with AIDS or HIV infection. One study of 125 HIV-positive men and women linked selenium deficiency with a higher rate of death from HIV while another small study of 24 children with HIV who were observed for five years, those with low selenium levels died at a younger age. These studies support the notion that when the antioxidant defense mechanism is weak, many diseases progress at a faster rate.
Oxidative stress by free radicals to cells in the immune system contributes to suppression of the immune system. Oxidative damage to these cells impairs the immune system and opens it for opportunistic infections. AIDS is a deficiency in the body’s defense mechanism caused by suppression or weakening of the body's autoimmune system. This can be caused by heavy metal toxicity, including lead toxicity and other toxic or free radical generating chemicals such as benzene, talc and silicone lubricants in condoms, free radical generating sexual lubricants, drug and alcohol abuse and prolonged use of toxic or free radical generating medication such as AZT, medication for haemophiliacs, Cox-2 drugs, TCDD, DDT, PCBs, Remicade, Enbrel, drugs used in chemotherapy etc in which cases if the body's production of antioxidant enzymes is low and suffers from low levels of other antioxidants in the blood, its free radical scavenging activity drops and the immune system is open for suppression through oxidative stress and free radical damage and becomes open to opportunistic infections. When free radicals damage the cell walls of cells, in particular the cell walls of T4 cells, viruses including the "HIV-virus" enters these cells and destroys them. Otherwise the so called "HIV-virus" is practically harmless or non-pathogenic and is not proven to directly cause any immunosuppressive effect.
Environmental chemicals or drugs may affect diverse aspects of the immune system, leading to immunosuppression. Industrial compounds and environmental pollutants have been reported to decrease immunological responsiveness and to increase susceptibility to infection. Workers exposed to PCDFs in connection with PCB-fires have, besides classical acute PCB-related effects, shown effects on the cell-mediated immune system and the peripheral nervous system. Pesticides and insecticides, metals, halogenated polyaromatic hydrocarbons, ozone (10028156), tobacco smoke and ionizing radiation were noted as causative agents of immunodeficiency or immunosuppression.
So, Professor Harold D. Foster’s suggestion that lack of the trace element selenium plays a role in causing AIDS is interesting and requires proper examination. It should not be dismissed but rather it ought to attract some study. Foster provides evidence that low selenium levels predict the occurrence of AIDS in Africa better than sexual practices. In criticizing the theory that sexual transmission explains HIV infections and AIDS in Africa, he is echoing the criticisms of Gisselquist and others who have noted many anomalies in the association between heterosexual intercourse and AIDS in Africa, such as a lack of a strong association between the number of sexual partners and the disease, and the greater likelihood that a woman in a sexual partnership in Africa will be HIV+ than the man, even though men are more promiscuous. Naturally, if immune deficiencies can be acquired through many immunosuppressant and toxicants or free radical generating chemicals and if the “HIV-virus” is non- pathogenic then sexual practices will not adequately explain AIDS or HIV transmissions but high risk groups exposed to causative agents of immunodeficiency or immunosuppression can be identified and the antioxidant interference in the progression of AIDS and HIV infection can be studied.
Foster asserts that Hepatitis B and C, Coxsackie B and HIV-1 and HIV-2 viruses rely on a selenium-containing enzyme (selenoenzyme glutathione peroxidase) to function. Quite naturally one would think that a shortage of selenium would therefore suppress replication of these viruses, but this is countered by Foster in theorizing that they can out-compete the rest of the body for this element, exacerbating the damage that low selenium levels do to the human tissues. That is the core of his theory; that HIV and a shortage of selenium are co-factors that jointly cause AIDS.
In animals, immune competence is provided and maintained by two cellular systems which involve lymphocytes. Lymphocytes are cells produced by the body's primary (bone marrow and thymus) and secondary (lymph nodes and spleen) lymphatic organs. They are descendants of the bone marrow's pool of stem cells, and produce a circulating or humoral immune system derived from B-cells (bursa-dependent or bone marrow derived), and a cellular or cell-mediated immune system that derives from T-cells (thymus dependent). T-cell or cell-mediated immunity is the cellular mechanism whereby T-cells act as coordinators and effectors of the immune system. Cell-mediated immunity involves the lymph nodes, thymus, spleen, intestine (gut-associated lymphoid tissue), tonsils, and a mucosal secretory immunity conveyed by IgA. The major classes of T-cells are designated as helper, cytotoxic, and suppressor cells. The helper cells "help" coordinate the immune response whereas the cytotoxic cells comprise the effector network that participates in removing virus-infected cells from the body. The third class of suppressor T-cells is important in dampening the immune response when it becomes overactive or out of regulatory control. Finally, cooperation between the various T-cell classes and between T- and B-cells is an important component of the normal humoral and cellular immune response. Hyperactive cellular immune responses produce autoimmune and other immune-mediated diseases while hypoactive cell-mediated immunity causes immune suppression and immune incompetence.
Numerous studies have demonstrated that TCDD/induced thymic atropy in adult animals does not affect immunological response but prenatal and neonatal TCDD exposure induces thymic atropy and impairs the immune system. Several studies of host resistance showed that TCDD exposure increased susceptibility to bacterial, viral, parasitic, and neoplastic disease. Many chemicals or their metabolites have a direct effect on cells involved in immune function or on lymphoid tissues. PCBs interfere with many biological functions, including the immune system, the nervous system and several endocrine systems and the fetus appears to be particularly vulnerable to these actions.
The thymus gland lies just beneath the breast bone. It is large in infants and children and atrophies as we grow older. The thymus seeds the body with immature T-cells, the white blood cells responsible for "cell-mediated immunity". This gland secretes special chemicals called cytokines (ie.- interferon, interleukins) that influence the specialization and migration of T- lymphocytes throughout the body. The thymus also releases hormones that regulate immune function. These thymic hormones help immune cells to mature, "programming" them to recognize tissues as either self or invader. Recognizing the enemy is the first and likely most important step in the immune response.
The thymus shrinks as its role shifts from immune cell production to regulation of the immune response. Lower thymic hormone levels in the blood are associated with depressed immunity, and are typical of the elderly, individuals with chronic infections, autoimmune disorders, cancer and AIDS patients. The thymus is extremely susceptible to free radical and oxidative damage caused by chemicals, stress, and radiation and poor diet. People who have undergone radiation, chemotherapy or other immune-suppressing treatments also typically have low thymus function. Low thymus function induced by free radicals or oxidative stress diminishes its role in immune function.
Oxidative stress on the cardiovascular system can be removed by selenium ions derived from an organic source, whereas oxidative stress on the thyroid or thymus is removed by selenium antioxidants produced by the body that are synthesized from selenium ions from organic sources. Inflammations of the intestines and gastrointestinal disorders reduce the absorption of selenium ions which helps to aggravate oxidative stress in the cardiovascular system, thyroid and thymus in particular as the oxidative stress in the cardiovascular system may be alleviated by other antioxidants. Aggravation of oxidative stress promotes the progression of disease.
Recent research on antioxidants, vitamins including vitamin C, E, Beta Carotene and minerals such as selenium, copper, zinc and manganese have been strongly linked to the prevention and possible reversal of numerous chronic diseases and free radical generated disease conditions from heart diseases and cancers to cataracts and arthritis as well as to the regulation of the immune system and the prevention of premature aging.
Selenium has important antioxidant effects that derive from the ability of selenium ions to reduce hydrogen peroxide and phospholipid hydroperoxides and thereby stop the production of free radicals and reactive forms of oxygen. It also reduces hydroperoxide intermediates thus lowering the production of inflammatory prostaglandings and leucotrienes. These effects are potentiated in the presence of vitamin E. Selenium also antagonizes the effects of a number of toxic metals such as cadmium and arsenic.
Selenium-containing proteins (selenoproteins) have enzymatic functions. Selenium is best known for its role in the glutathione peroxidase (GPx) enzyme system. The GPx system is one of the major antioxidant defense systems in the body. Glutathione peroxidase and catalase remove hydroxyl radicals from tissues but glutathione peroxidase is considered more active due to its activity to remove radicals in cytoplasm and mitochondria. Glutathione is an important water-phase antioxidant and essential cofactor for antioxidant enzymes; through its significant reducing power, GSH also makes major contributions to the recycling of other antioxidants that have become oxidized. This could be the basis by which GSH helps to conserve lipid-phase anti-oxidants such as alpha-tocopherol (vitamin E) and possibly beta-carotene and how it provides protection also for the mitochondria against endogenous oxygen radicals. Its high electron-donating capacity endows GSH with great reducing power. It has been documented in many degenerative conditions that GSH depletion leads to cell death.
The consequences of sustained GSH depletion can be lethal. As cellular GSH is depleted, individual cells die in those areas with greatest oxidative stress. Then localized areas of tissue damage begin to appear; those tissues with the highest content of polyunsaturated lipids and/or the most meager antioxidant defenses are generally the most vulnerable. Localized free-radical damage spreads across the tissue in a self-propagating wave. This spreading wave of tissue degeneration can be halted by augmenting the antioxidant defenses. Investigators also found that dietary ascorbate can protect against the tissue damage that typically results from depletion of GSH.
Putting all this information together does not support the theory that viruses rely on selenoproteins or selenium antioxidant enzymes and can out-compete human cells to get selenium as an element to manufacture these complex organic bio-molecules or to direct their manufacture in the infected cells and consequently HIV and a shortage of selenium are the joint causative factors of AIDS. It is the suppression of the immune system or its impairment by free radical generated toxicity that causes AIDS and opens the body to opportunistic infections. Viruses proliferate more easily in persons whose immune systems are weakened by immunosuppressants or impaired by toxicity or free radicals. Viruses enter cells including T4 cells whose cell walls have suffered oxidative damage and destroy them, further weakening the body and the immune system and by generating toxins. These toxins produce oxidative stress and oxidative damage at the cellular level.
Viruses and frozen cancer cells do not produce toxins or free radicals but viral activity in infected cells and metabolic activity of cancer cells generate toxins and free radicals. There is experimental evidence that when cells become infected with rhinoviruses there is generation of hydrogen peroxide and free radical injury to cell walls of uninfected cells. Hydrogen peroxide dismutates readily when exposed to other bio-molecules formimg water and releasing an oxygen atom. In nature, oxygen consists of two atoms - a very stable combination but a single atom of oxygen, however, is very reactive and is referred to as a free radical that can produce oxidative stress on cell walls. Oxidative damage to oxidizable amino acids in the cell wall membrane increases susceptibility to other viruses and subsequent viral replication in these cells generates oxygen radicals. Selenium ions actively scavenge these free radicals and in consequence there may be insufficient selenium ions left in the body for the production of selenoproteins to scavenge free radicals that cause oxidative stress to the thyroid or thymus or the liver producing oxidative stress in the thymus and thyroid results in a mayhem involving cytokines and disturbance in the release of hormones that regulate immune function which impairs the immune system or results in immune incompetence. Chronic viral infections are known to trigger GSH depletion in circulating immune cells or GSH/GSSG imbalance. That may explain the increased rate of progression of disease in HIV/AIDS patients while it also explains why cancer patients given 200 µg/day of selenium reduces mortality from all cancers and reduces the incidence of lung, colorectal and prostate cancers and why cardiomyopathy in Keshan Disease can be prevented but not cured by selenite supplement intake of 50 µg/day. Some tumors have been shown by gas chromatography studies to exude minute amounts of formaldehyde, alkanes and benzene derivatives not found in healthy tissues, which means that cancer cells produce free radical generating compounds whose reactions deplete antioxidants in the body and can produce oxidative stress in affected tissues. That means proper doses of both selenium ions obtained from higher colloids and selenomethionine from food sources together with other antioxidants would prove beneficial to cancer and AIDS patients and improve quality of life or even reverse the disease and help the body’s immune system to fight virus infections or suppress cancer formation in the body.
Toxic substances, whose mechanisms of action involve free radical generation, e.g. toxic poisons such as snake bites, bee stings and spider bites, certain drugs, such as barbiturates, chemotherapeutic agents, narcotics, and powerful oxidizing pollutant chemicals, might be neutralized by antioxidants. Tumors invading the body or holding off the immune system by way of free radical toxicity might be naturally expected to respond to a regime of antioxidants to varying degrees. If oxidative damage contributes significantly to disease pathology then actions that decrease it should be therapeutically beneficial but such antioxidant interventions must include organic selenium to prevent GSH depletion and also include zinc and manganese. If the oxidative damage is involved in the origin of a disease, then successful antioxidant treatment should delay or prevent the onset of that disease. One of the common complaints in AIDS patients is chronic fatigue or tiredness. Free-radical damage reactions in cells produce toxic chemicals, destroy enzymes and kill cells. They also start chain reactions that are harmful to health and long term exposure to free-radicals can lead to chronic illness, chronic fatigue, cancers or early symptoms of aging. The free radical chain reactions produce other highly secondary products such as alkanes, alcohols, acids and carbonyls which react with proteins, amino-acids, amines and DNA leading to mutagenesis, cancers and promote aging. Chronic fatigue is a symptom that can also manifest in persons suffering from heavy metal toxicity or afflatoxins poisoning. Afflatoxins may belong to the category of toxic substances that rapidly generate free radicals in the body and deplete mDNA. Depletion of antioxidants, especially selenium ions and GSH by prolonged or chronic oxidative stress leads first to suppression followed by impairment of the cytokine and hormones that regulate immune function. Subsequently, chronic oxidative stress begins to compromise mitochondrial function and ATP production followed by mDNA depletion and opportunistic infections. This precipitates “AIDS defining illness.” “HIV-virus infected persons may not manifest them.
Chronic or long term exposure to immunotoxic molds, immunotoxic pollutants or immunotoxic medication or chemicals that generate excessive free radicals in the body that impair the immune system or deplete mDNA or severely disrupt the neurotransmission process in the immune system or low levels of organic selenium in the diet coupled with low antioxidant intake will lead to symptoms of AIDS without an “HIV-virus” infection.
It is not difficult to understand the destructive role of excess free radical activity in immune incompetence or immune deficiencies and mDNA depletion when one recognizes that complex role of antioxidants in healthy cellular function. Vitamin C (an antioxidant) is needed for the synthesis of carnitine which is required for long-fatty chain acids to enter mitochondria where they are used for energy production. Then, another antioxidant that prevents radical damage within the cell, called coenzyme10 is necessary for the synthesis of adenosine triphosphate (ATP). Interference with the production of ATP can cause significant damage to the cell because ATP is needed for important cellular processes such as membrane transport, lipogenesis and protein synthesis. Alpha lipoic acid, also known as lipoic acid is a powerful antioxidant that efficiently increases or maintain levels of other antioxidants including COQ 10, vitamin C, vitamin E and glutathione, which may decline with age. Alpha lipoic acid helps the cells use glucose for energy in a process that utilizes oxygen. Vitamin E is lipid soluble and almost exclusively resides in the cell walls prevents oxidative damage to the cell wall while vitamin C prevents oxidation of cholesterol and promotes production of antioxidant GSH but both of these vitamins need alpha lipoic acid to regenerate after they are oxidized. This “antioxidant network” can be effectively compromised or destroyed by chronic oxidative stress. Heavy metal poisoning also depletes alpha lopic acid in cells as it binds with heavy metals and reduce their harmful effects.
The body routinely converts some alpha-lipoic acid to dihydrolipoic acid, which appears to be an even more powerful antioxidant. Both forms of lipoic acid quench peroxynitrite radicals, an especially dangerous type consisting of both oxygen and nitrogen, according to a recent paper in FEBS Letters (Whiteman M, et al., FEBS Letters, 1996; 379:74-6). Peroxynitrite radicals play a role in the development of atherosclerosis, lung disease, chronic inflammation, and neurological disorders but the depletion of alpha lipoic acid by excess free radicals can be detrimental to the normal functioning of cellular enzymes.
Generally three biological components most commonly looked at in assessing oxidative stress: lipid peroxidation, protein oxidation and DNA oxidation. While excellent means for assessing lipid peroxidation and DNA oxidation exist, assessment of protein oxidation has been problematic. Recent research shows that decreased aconitase enzyme activity is a sensitive and specific indicator of oxidative damage during aging, Parkinson's and other disease progression. The function of aconitase is to isomerize citrate to isocitrate a key intermediate of the citric acid cycle. The enzyme function role of aconitase in cellular energy production sets it up as an important marker of decline in cellular function or biological decline of tissue function. Inactivation of aconitase appears to occur via direct interaction of hydrogen peroxide with the enzyme and it is perhaps inactivated by the hydroxyl ions.
Interaction of hydrogen peroxide with metal ions, such as Fe2+, can result in the formation of metal-centered oxygen radicals and hydroxyl radical (OH•). These species are highly reactive and can produce oxidative damage to protein, lipids, and DNA. Mitochondria maintain the delicate balance between production and removal of oxygen radicals through a vast array of antioxidant enzymes and low molecular weight scavengers.
During normal cellular metabolism, mitochondrial electron transport results in the formation of superoxide anion (O 2) and subsequently hydrogen peroxide (H2O2). Hydrogen peroxide increases in concentration under certain physiologic and pathophysiologic conditions such as viral invasion of cells or excessive exogenous free radicals and it can modify cellular components through oxidation reactions in the cells. It is critical to understand the response of mitochondria to hydrogen peroxide and excess free radicals especially when nutrition does not afford sufficient antioxidants.
In one study, treatment of isolated rat heart mitochondria with hydrogen peroxide resulted in a decline and subsequent recovery of state 3 NADH-linked respiration. Alterations in NADH levels induced by hydrogen peroxide closely paralleled changes in the rate of state 3 respiration. Assessment of electron transport chain complexes and Krebs cycle enzymes revealed that - ketoglutarate dehydrogenase (KGDH), succinate dehydrogenase (SDH), and aconitase were susceptible to hydrogen peroxide inactivation. Of particular importance, KGDH and SDH activity returned to control levels, concurrent with the recovery of state 3 respiration. Inactivation was not because of direct interaction of hydrogen peroxide with KGDH and SDH because removal of hydrogen peroxide alone is not sufficient for reactivation. It is important to note that enzyme activity does not recover unless mitochondria remain intact which means that free radical and radical damage to mitochondria is a critical factor in the progression of chronic fatigue syndrome and wasting.
With damaged mitochondria, depleted mDNA and weak respiratory activity and inability to use oxygen to generate energy from glucose, the cell reverts to the more primitive system of anaerobic respiration that is characteristic of cancer cells or when the compromised antioxidant defense system is not able to prevent chemical toxins from causing damage to DNA and any repair of this damage in a weak antioxidant environment in the cell may incorporate viral genetic information into the host cell’s chromosomes resulting in cell transformation and cancer. Whatever the hypothesis in cancer formation in the human body, the process involves a key role of oxidants and antioxidants. Life at the cellular level appears to be modeled on the roles of oxidants and antioxidants.
Apart from aconitase, other enzymes in the Kreb’s cycle may also suffer inactivation through oxidative stress. It is therefore useful to gain insight into potential mechanisms of enzyme inactivation and reactivation which can then be incorporated into processes to regain cellular function and arrest or slow down or reverse disease progression and in nutrition science maintain optimal health and prevent the onset of AIDS.
Over 75 years ago, Otto Warburg was awarded two Nobel prizes for his theories that cancer is caused by weakened cell respiration due to lack of oxygen at the cellular level. A normal healthy cell burns oxygen and glucose (blood sugar) for energy and releases carbon dioxide and water. The normal and healthy cell functions aerobically - in the presence of sufficient oxygen. Anaerobic diseases (cancer, Epstein Barr, herpes, mono, genital warts, etc.) cannot naturally flourish in this oxygen rich environment in the cell.
An unhealthy or diseased cell lacks sufficient oxygen but will continue to produce energy by using mainly glucose in a different process. This energy burning process (sugar fermentation) releases mainly lactic acid and carbon monoxide instead of carbon- dioxide. Under anaerobic growth conditions, pyruvate is primarily reduced to lactic acid, while it is oxidized to acetate and CO2 under aerobic growth conditions. This is a very inefficient pathway and a severe drain on the body. The cancer cell functions anaerobically – without any oxygen present and without using any oxygen. Cancers and viral diseases easily flourish in this type of anaerobic environment - little or no oxygen and low PH.
Anaerobic respiration to produce energy in cells is much less efficient compared to aerobic respiration. Cells that use anaerobic respiration must work harder than aerobic cells to produce energy from the glucose they metabolize. Anaerobic respiration in cells burns much more glucose to produce the same amount of energy as aerobic cells. Cancer cells exhibit this anaerobic mode of metabolism - lack of oxygen, high glucose consumption, carbon monoxide and high lactic acid production. Cancer cells thrive in this high sugar-low oxygen environment but cannot exist in the opposite condition of high oxygen-low sugar mode of healthy cells. Since, alpha lipoic acid helps the cells use glucose for energy in a process that utilizes oxygen, its depletion by excess free radicals is seen as a factor that promotes metabolic pathways found in cancer cells.
Since free radical depletion of antioxidants essential in healthy mitochondrial function in normal cells and subsequent damage to mitochondria and depletion of mDNA, whether by lead toxicity or benzene and its derivatives or AZT or other toxic chemicals can cause the “chronic fatigue” and weight loss symptoms diagnosed in early AIDS patients, and open up their bodies to opportunistic infections and cancers, models based on free radical exposure in relation to blood and daily intake of antioxidants will better predict the etiology and occurrence of AIDS whereas transmission of the “HIV-virus” will only show a weak correlation in the non- gay population or the expected anomalies in the association between heterosexual intercourse and “HIV-virus” transmission.
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