Solving the Antioxidant Question in Aids
The immune deficiency seen in Aids is caused by excess cellular oxidation brought about by external factors and the cure is entirely within our means - simply supplying the antioxidant nutrients necessary to reverse the oxidative overload. That is the gist of Beldeu Singh's recent article which you can read in its entirety below.
Glutathione - key to reversing Aids
Vitamin C, a heavy antioxidant, together with some amino acids and a mineral, are the principal arms we need to defeat the syndrome. The cocktail of anti-retroviral drugs normally prescribed is not only useless - it makes things worse than they would be without. The "side effects" of those drugs are practically indistinguishable from the symptoms of the illness they are supposed to slow down.I only want to add one piece of pertinent infromation to what Beldeu Singh explains below. He mentions Fe2+ and Fe3+, two forms of iron in the blood. Iron is contained in hemoglobin, the red blood pigment. Normal hemoglobin contains Fe2+ and altered hemoglobin also called methemoglobin contains Fe3+. The most important function of hemoglobin is the transport of oxygen in the blood stream. But once it is turned into methemoglobin, it no longer is able to carry oxygen. Aids patients have a high percentage of methemoglobin, that is, their blood contains the oxidized form of iron that is Fe3+. Consequently their cells are starved of oxygen and they die ... unless the over-oxidation can be reversed, that is. And this is where anti-oxidants come into the picture.
It goes without saying that Aids patients are almost never given an analysis of their level of methemoglobin, and neither are they supplied with the simple nutrients that could reverse their condition.
Knowing this, does it make you as mad as it makes me, when we are treated to "scientific studies" such as the one published some time ago in the Journal of the American Medical Association, that say "stay away from antioxidants - they may be bad for you". Now who would have an interest in making nothing of a perfectly good cure for all those people suffering from Aids?
And coming to think of it - the solution has been right in front of our eyes for more than a decade: See Glutathione Helps Aids Survival and An Underlying Factor In AIDS Is Suggested.
Yes, you are right - there may be a very dirty war going on for your health, or rather for your very profitable sickness. Certainly the solution, which antioxidant nutrients offer us, isn't being advocated by those who say they are fighting the epidemic.
Here is a comment sent to Beldeu Singh today:
Practically, this mechanism [of hemoglobin/methemoglobin], together with the oxidation hypothesis, explains Aids way better than the virus hypothesis and what's more - it opens a door to a simple, effective cure by giving glutathione or its precursors. Selenium works because it is a catalyst for the production of glutathione in the body. Aminoacid supplements work because they provide necessary raw materials for glutathione production. Vitamin C works because it reverses oxidation.- - -
SOLVING THE ANTIOXIDANT QUESTION IN AIDS
Beldeu Singh
Dr. Rath cited a study by Harvard Medical School researchers that showed dietary supplements slow the progression of AIDS and resulted in a significant decline in viral count. [New England Journal of Medicine 351: 23-32, 2004] 'Harvard researchers responded by saying vitamin therapy is important but may not replace anti-viral drug therapy'.Dr. Rath is reported to recommend 4000 milligrams of daily vitamin C to patients. The amount of oral vitamin C that a patient can tolerate without diarrhea increases proportionately to the severity of their disease. [Med Hypotheses 18:61-77, 1985] AIDS patients often don't exhibit any diarrhea with extremely high-dose vitamin C therapy. Diarrhea may occur among healthy individuals following high-dose vitamin C therapy depending upon how much vitamin C is consumed at a single point in time. Divided doses taken throughout the day minimize this problem. However, the use of vitamin C in therapy may be curtailed by Codex if Codex establishes a 2000 mg upper limit for vitamin C as previously proposed by the National Academy of Sciences, or as low as 225 mg which was recently established by German health authorities. Hopefully that limit applies only to racemic mixtures that contain the L-form and D-form but not the dietary intake from fruits and vegetables.
This battle over vitamin supplements may be a foretaste of what will happen later this year when a worldwide body called Codex Alementarius will meet to establish upper limits on vitamin and mineral supplements. Fixing the upper limit is a fallacy because of the antioxidant nature of vitamin C and because:
1. Natural vitamin C or L-ascorbic acid is an antioxidant that can recharge alpha-lipoic acid, glutathione and other antioxidant molecules in the body's natural antioxidant network system,2. After it is spent as an antioxidant in free radical scavenging activity, the stable ascorbate radical can pass the blood-brain barrier and enter the iron-based antioxidant system in the brain where it recycles Fe2+ into Fe3+ that can scavenge the superoxide in the brain and protect the brain from oxidative stress,
3. The spent ascorbate may be converted into other molecules for the body's use such as in the formation of collagen.
Anyone can understand that simple fact that different people have different amounts of free radical and secondary radical populations in the disease states that depend on age, amount of fatty tissue, nutritional status and the extent of disease sites and free radical chain reactions occurring in the body, drugs being consumed etc., and require different amounts of L-ascorbic acid to quench the varying amounts of superoxide in various patients. It is not a question of dosage but amounts that are adequate for free radical scavenging activity and the actual amount required may be customized as in personalized medicine. In the brain, the ascorbate has a unique role and the "investment" during the course of mammalian evolution in a complex and thinking organ that also houses important regulatory mechanims was sabotaged by the loss of the glucoronic pathway in apes that forms L-ascorbic acid (natural vitamin C) from glucose.
Antioxidants, when they are in slight excess, they readily scavenge the superoxide and the hydrogen peroxide formed in the cells and tissues and when the function of the antioxidant network system declines as with age or during oxidative stress or under chronic malnutrition, there is a build up of the super oxide radical and there is insufficient glutathione and catalase to spontaneously convert hydrogen peroxide into water and oxygen. This is an "intelligent biochemical system" that converts toxic submolecular species and toxic hydrogen peroxide into useful molecules essential for life – water and oxygen but a decline in the functioning of this system allows the superoxide to build up along with the hydrogen peroxide.
Hydrogen peroxide is not very toxic but when the superoxide reacts (within micro seconds to nanoseconds) with hydrogen peroxide, the very highly reactive hydroxyl radicals are produced that can oxidatively damage cell membranes, destroy the cytochrome enzyme system, deplete coQ10 and subtract hydrogen atoms from fatty molecules and DNA molecules. In the mitochondria, there can be destruction of mDNA. It can precipitate fatigue, chronic fatigue and muscle wasting and other symptoms associated with cell wall integrity and ATP output and ATP utilization.
That free radical mechanism explains Dr. Peter Duesberg's assertion that it kills or inhibits all DNA synthesis. One of the symptoms observed in AIDS patients is muscle wasting, chronic tiredness and mDNA depletion. This means that the genetic material in mitochondria (the power house of the cell), is destroyed or depleted or its multiplication is inhibited and the energy output drops and the affected person feels muscle pains and fatigue. Over time, AZT came to be associated with interference with DNA synthesis in mitochondria just as in AIDS.
An article in the New England Journal of Medicine describes the muscle wasting caused by AZT and compares it to muscle wasting, called "myopathy", presumed to be caused by HIV. Their comments in the abstract are shocking: "We conclude that long-term therapy with Zidovudine can cause a toxic mitochondrial myopathy, which... is indistinguishable from the myopathy associated with primary HIV infection..." That finding is exactly what Glaxo Wellcome puts as a warning in large, bold-faced, capital letters at the start of the section in the 1998 Physician's Desk Reference that describes AZT (brand name Retrovir or Zidovudine):
"RETROVIR (ZIDOVUDINE) MAY BE ASSOCIATED WITH SEVERE HEMATOLOGIC TOXICITY INCLUDING GRANULOCYTOPENIA AND SEVERE ANEMIA PARTICULARLY IN PATIENTS WITH ADVANCED HIV DISEASE (SEE WARNINGS). PROLONGED USE OF RETROVIR HAS ALSO BEEN ASSOCIATED WITH SYMPTOMATIC MYOPATHY SIMILAR TO THAT PRODUCED BY HUMAN IMMUNODEFICIENCY VIRUS."A study on cardiovascular toxicology reports "AZT treatment increases superoxide (oxygen free radical) production" and "the effects of AZT on endothelium-dependent relaxation are eliminated by pretreatment with a free radical scavenger" (anti-oxidant) which proves that AZT toxicity is due to its free radical generating capacity. This study also provides the scientific inference that AIDS can be caused by excess superoxide free radicals and oxidative stress. In fact, AIDS is a free radical and oxidative stress induced condition that appears more easily in people with malnutrition associated with low organic selenium intake and in people exposed to chemical stressors.
The immunotoxicity of AZT has been solidly documented. Azidothymide (AZT) and AZT monophosphate (AZT-MP) in concentrations as low as 10 and 50 microM, respectively promote oxidation. This prescription drug for AIDS patients is a very toxic medication that promotes free radical generation in a cell free system and in the body.
It is not surprising that a British study found that AZT prophylaxis decreased survival and induced the wasting syndrome, cryptosporidiosis, and cytomegalovirus infection, and the American MAC study shows that AZT increases the risk of pneumonia, one of the AIDS defining diseases.
AZT has effects of toxicity in animals and humans. "It produces excruciating headaches; severe nausea; muscular pain; wasting of the muscles; damage to kidneys and nerves; excruciating pains in the legs; encephalitis; severe anemia requiring transfusions to stay alive; lymphoma (cancer); cancer in 49% of cases, versus 2% incidence in non AZT group; liver damage; nail dyschromia (fingernails turn black); insomnia; impotence; dementia; mania; ataxia (failure of muscular coordination); seizures; alopecia (hair falls out). It is a fairly well established fact that AZT was designed to kill the bone marrow. It causes neutropenia or leukopenia (loss of white blood cells) or bone marrow aplasia and bone marrow toxicity. White blood cells are the basis of the immune system. T cells, granulocytes, those are all parts of the immune system. You kill those with AZT and the immune system is gone," Harvey Bialy, Research editor Bio/Technology Science Journal.
Dr Peter Duesberg, Professor of molecular and cell biology, University of California at Berkeley says that it is not arrogant for him to say that AZT is AIDS by prescription because it is "the most toxic drug that has ever been licensed for long term consumption in the free world ... AZT is a prescription drug and according to the manufacturer itself it causes symptoms that are indistinguishable from AIDS".
SeleniumAIDS is prevalent in many parts of Africa but Senegal has the lowest number of AIDS patients which coincides with the fact that Senegal has soil that is relatively rich in selenium. Hence the fruits and other food that is grown in Senegal have a much higher concentration of selenium. Selenium from organic sources is essential for the production of antioxidant selenoproteins and glutathione. Other correlational evidence comes from the observation that adults and children dying of AIDS display both depressed CD4 T-lymphocyte counts and much depleted plasma selenium stores (Baum et al, "High risk of HIV-related mortality is associated with selenium deficiency", J Acquir Immune Defic Syndr Hum Retrovirol 1997; 15(5):370-374). HIV-seropositive individuals are deficient in glutathione peroxidase (Gil et al, "Contribution to characterization of oxidative stress in HIV/AIDS patients", Pharmacol Res 2003; 47(3):217-224) and depressed glutathione peroxidase levels in men with HIV/AIDS could be raised by supplementation with selenium and other antioxidants (Batterham et al, "A preliminary open label dose comparison using an antioxidant regimen to determine the effect on viral load and oxidative stress in men with HIV/AIDS", Eur J Clin Nutr 2001; 55(2):107-114). In fact glutathione levels in HIV-positive patients is a predictor of survival rates (Breitkreutz R., "Improvement of immune functions in HIV infection by sulfur supplementation: two randomized trials", J Mol Med 2000; 78(1):55-62.).
Chronic selenium deficiency therefore depresses free radical scavenging activity to extents that it impairs metabolic pathways such as formation of nicotinamide adenine dinucleotide and conversion of methionine to cysteine and AIDS patients have inadequate levels of both nicotinamide adenine dinucleotide (NAD) and cysteine (see:Bunk et al, "Evidence for an impairment in conversion of methionine to cysteine in the Se-deficient chicken", Proc Soc Ex Biol Med 1981; 167:87-93: Murray et al, "HIV infection decreases intracellular nicotinamide adenine dinucleotide (NAD)", Biochem Biophys Res Commun 1995; 212(1):126-131). In HIV+ patients and SIV-infected macaques, a decrease of the plasma cysteine level was found to coincide with the decrease of CD4+ T cells (Hack et al, FASEB J. 1997 Jan;11(1):84-92). Chronic selenium deficiency can also deplete antioxidant enzymes such as deiodinase required in the thyroxine pathway leading to a depressed CD4 T-lymphocyte counts.
The thyroxine pathway is critically important in immune function because it produces T4 cells (see: Foster, H.D., " AIDS and the 'selenium-CDR T cell tailspin': The geography of a pandemic", Townsend Letter for Doctors and Patients 2000; 209:94-99: Baum et al, "High risk of HIV-related mortality is associated with selenium deficiency", J Acquir Immune Defic Syndr Hum Retrovirol 1997; 15(5):370-374). Selenium deficiency weakens and later compromises immune function. Selenium deficiency is known to be associated with oral candidiasis and abnormal phagocytic function in animals and depressed helper T-cell numbers in humans (Dworkin et al, J Parenteral Enteral Nutr 1986; 10: 405) and may be associated with myopathy, cardiomyopathy and immune dysfunction and decreased CD4 T-cells (Dworkin BM, Chemico-Biological Interactions 1994; 91: 181-186).
Phagocytic function in the mammalian system can be severely impaired by low levels of antioxidant enzymes and low L-ascorbic acid intake. Research has proven that when the natural antioxidant enzyme levels in cells drop below 80% the cell dies and when the natural vitamin C level in white blood cells drops below 60% it cannot function properly in its cytotoxic role that kills pathogens. During phagocytosis, the white blood cell resorts to anaerobic respiration to rapidly produce hydrogen peroxide in order to generate a sudden burst of free radicals directed at the pathogen destroy their cell membrane integrity and inactivates the enzymes in the bacterial cell but it requires excess natural vitamin C to stop the anaerobic respiration initiated to produce free radicals that are cytotoxic to the bacterial cell. L-ascorbic acid is used in such a biochemical control mechanism together with glutathione. Phagocytic function and immune function are antioxidant dependant and can be compromised or impaired by declining levels of antioxidants in the body due to age or on account of depletion by free radicals generated by drugs and chemical stressors.
Glutathione (GSH), a cysteine-containing tripeptide, is essential for the viability and function of virtually all cells. In vitro studies showing that low GSH levels both promote HIV expression and impair T cell function suggested a link between GSH depletion and HIV disease progression (Herzenberg et al, Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1967-72).
"Apoptosis is the main cause of CD4+ T-lymphocyte depletion in acquired immune deficiency syndrome (AIDS). Various agents appear to be able to trigger apoptosis in CD4+ T cells... Since oxidative stress can also induce apoptosis, it can be hypothesized that such a mechanism could participate in CD4+ T-cell apoptosis observed in AIDS. This correlates strongly with the observation that AIDS patients present low levels of antioxidants (i.e. superoxide dismutase-Mn, vitamin E, selenium and glutathione) most likely due to ... drug consumption..." (Romero-Alvira and Roche, Med Hypotheses 1998 Aug;51(2):169-73).
Of special interest is a note on oxidative stress by Montagnier himself. A book published with Luc Montagnier as principal editor further confirms the involvement of oxidative stress in AIDS. "We have shown that GSH depletion is associated with impaired survival; the greater the depletion, the worse the prospects for survival...By replenishing GSH, NAC or other agents we may be able to modulate such adverse effects of GSH depletion... HIV-infected individuals would be better served if we could identify the mechanism that underlines the GSH depletion and intervene, if possible, to prevent its occurrence... The best advice they can give in this regard is: "it may be prudent for those individuals to avoid excessive exposure to UV irradiation and unnecessary use of drugs that can deplete GSH - e.g., alcohol and prescription or over-the-counter formulations containing acetominophen [paracetamol]" (Montagnier et al, New York: Marcel Dekker Inc, 1998). It should be obvious that AZT and the toxic retrovirals generate free radicals and through oxidative stress deplete GSH and destroy or weaken the body's antioxidant defense mechanism and impair the immune function through inhibition of white blood cell formation and impair T4 cell formation and consequently these are the drugs to avoid in AIDS patients who must consider antioxidant therapies using a broad range of antioxidants, including coconut oil.
"Due to its antiviral effects and its importance for all immunological functions, the administration of selenium is suggested as a supportive measure in early as well as in advanced stages of HIV-induced disease. Initial observations on the effects of selenium supplementation in HIV-infected patients indicate that selenium causes symptomatic improvements and possibly slows the course of the disease. As selenium inhibits reverse transcriptase activity in RNA-virus-infected animals, supplemental selenium could also prevent the replication of HIV and retard the development of AIDS in newly HIV-infected subjects. An adequate supply of selenium and of antioxidant vitamins is also proposed as a measure to reduce the probability of the placental transmission of HIV in pregnancy." (Schrauzer and Sacher, Chem Biol Inter., 1994, 91:199).
There is a wealth of evidence that correcting one or more of the deficiencies of selenium, cysteine, glutamine and tryptophan, which are characteristic of HIV/AIDS, has significant health benefits. Selenium, for example, is a key immunological enhancement agent that has a strong impact on lymphocyte proliferation. This relationship was confirmed by Peretz and co-workers, who monitored enhanced lymphocyte response in elderly subjects given a daily 100-microgram selenium supplement over a six-month clinical trial (Peretz et al, Am J Clin Nutr 1991; 53(5):1323-1328). Unfortunately medical focus has shifted away from the selenium deficiency problem and its antiviral effects and effects on biochemistry in the body and to reverse the effects of selenium deficiency by dietary means or through rapidly acting antioxidant sprays to raise the levels of cysteine, NAD and deiodinase to improve the healthy functioning of the immune system and thereby prevent opportunistic infections.
The focus of the medical industry is on administering AZT and other toxic drugs, sometimes in a cocktail, that eventually succeed in depressing the white blood cell counts especially the T4 cell counts through free radical mechanisms that over time systemically precipitate a host of free radical induced disease conditions through excess superoxide, formation of the hydroxyl radical, the peroxynitrite radical and other secondary radicals that oxidatively damage cell membranes and the body's enzyme systems. And there are many studies that show selenium supplementation improves the condition of the AIDS patient as well as survival rates.
It is pertinent to note that "the combination of abnormally low plasma cystine and glutamine levels, low natural killer (NK) cell activity, skeletal muscle wasting or muscle fatigue, and increased rates of urea production defines a complex of abnormalities that is tentatively called "low CG syndrome." These symptoms are found in patients with HIV infection, cancer, major injuries, sepsis, Crohn's disease, ulcerative colitis, chronic fatigue syndrome, and to some extent in overtrained athletes. The coincidence of these symptoms in diseases of different etiological origin suggests a causal relationship (Droge and Holm, FASEB J. 1997 Nov;11(13):1077-89, Review). There is certainly an underlying causal relationship – a biochemical one that is understood as the free radical mechanism of disease and can be countered only by antioxidants to improve free radical scavenging activity – something which seems to be the basic principle in ayurveda.
Natural vitamin C readily scavenges superoxide and improves white blood cell function and improves antibody production. Vitamin C also recycles alpha lipoic acid that can recycle glutathione and catalase. In other words, it improves the immune function at the cellular level as well as the functioning of the antioxidant system of the body at the biochemical level. This properly explains why depressed glutathione peroxidase levels in men with HIV/AIDS could be raised by supplementation with selenium and other antioxidants and why viral counts decline significantly in AIDS patients. Beta-carotene also scavenges superoxide and one would expect beta-carotene supplementation to improve GSH levels in AIDS patients. Indeed this is the case. Daily supplementation with selenium or beta-carotene for 1 year led to significant increases in glutathione peroxidase activity at 3 and 6 months among HIV-positive men and women in France (Delmas-Beauvieux MC et al, Am J Clin Nutr 1996; 64: 101-107).
It is about time that the UN policies on AIDS pursue a proper and biochemically logical response and practices that promote integration of nutrition into a comprehensive response to HIV/AIDS.
This is primarily because many AIDS patients do not have the virus, pointing clearly to oxidative stress in malnourished people as the actual cause factor of AIDS and even when the reactivated EBV is involved, in certain groups of people, in the destruction of parts of the immune system, it occurs in conditions of oxidative stress and more startling is the fact that when EBV viral parts 'hide' in cells of the immune system, they are reactivated by hydrogen peroxide which is a by-product of oxidative stress. So, however you look at the AIDS condition, oxidative stress is a critical factor. Logically, therefore nutritional intervention is the key and should form the basic thrust in responding to the AIDS problem. Resolution WHA57.14 which urged Member States, inter alia, to pursue policies and practices that promote integration of nutrition into a comprehensive response to HIV/AIDS is therefore considered urgent.
The recommendations of WHO's technical consultation on nutrition and HIV/AIDS in Africa (Durban, South Africa, 10-13 April 2005), which were based on the main findings of a detailed review of the latest scientific evidence on the macronutrient and micronutrient needs of HIV-infected people, including pregnant and lactating women and patients on antiretroviral therapy, make more sense now than before these recommendations were drafted. The need to consider antioxidant intake for health and in therapy comes from a study of Fenton Reactions that occur in the body and other deleterious Fenton Reactions that can establish in the body when antioxidant levels decline and excess free radicals begin to induce reactions that are harmful and lead to disease states while adequate antioxidants promote antioxidant-driven pathways that are healthy.
Vitamin C cannot function in the brain because it cannot pass the blood-brain barrier. After it donates its electron to a free radical it is spent and exists as an ascorbate radical, which is a stable radical. In this form it can enter the brain where it has a very unique function. The brain is rich in iron and uses the Fe2+/Fe3+ ion system to scavenge the superoxide formed in the brain. Consider the following Fenton reactions which show that Fe2+ can react with excess hydrogen peroxide to form the highly reactive hydroxyl radicals that, if not scavenged, will cause oxidative injury to molecules, mDNA and cell membranes and disrupt cell function and ATP output and ATP utilization, leading to fatigue or chronic fatigue and over time the process can lead to the formation of cancer cells.
Fe2+ + H2O2 ----> Fe3+ + .OH + OH-Excess Fe2+ will certainly react with oxygen and convert it into superoxide, as follows:-
Fe2+ + O2 ----> Fe3+ + O2. (superoxide)The problem of excess superoxide in the cytochrome system is that it will use up the proton (H+) formed in the protonation process to produce the ATP molecule as follows:-
2O2- + 2H+ ----> H2O2 + O2This Fenton Reaction that utilizes the proton (H+) will disrupt the electron transfer process required for ATP formation, the energy molecule for aerobic respiration and lower the amount of cellular energy available for use by cells, while forming hydrogen peroxide. Excess superoxide will react with the hydrogen peroxide to form hydroxyl radicals. This reaction produces hydrogen peroxide rapidly and it rapidly depletes the glutathione-catalase enzymes that work as a system to convert hydrogen peroxide into water and oxygen. In the muscles, this disruption in the energy pathway will cause muscular aches and pains. Chronic disruption, as in the case of chronic malnutrition or chronic oxidative stress in which hydroxyl radicals are also formed, there is mDNA depletion that leads to pain in the muscles and later on to muscle wasting.
Fe3+ from fruits and vegetables can change the course of biochemistry as it scavenges the superoxide to form oxygen through Fenton Reaction, as follows:-
Fe3+ + O2. ----> Fe2+ + O2And it is important to keep the reaction flowing in that direction for therapeutic results. One way is to have sufficient amounts of the ascorbate radical in the brain and the body to accept an electron from Fe2+ and convert it into Fe3+.
Fe3+ + O2. ----> Fe2+ + O2| || |
| |
<-- Spent L-Vit C <--
In Fenton Medicine, it is critical to drive reactions, just like managing antioxidant–driven reactions for maintaining healthy biochemical pathways, failing which free radical-induced pathways may establish, initiating disease states. Spent glutathione can also readily accept an electron from Fe2+ to form Fe3+. Hence, its importance in liver, brain and muscle biochemistry. Low antioxidant levels are associated with chronic malnutrition. Recreational drugs, cigarette smoke and alcohol lower glutathione and catalase levels and prolonged use will deplete them in the body to levels that weaken the antioxidant defense mechanism sufficiently to decline cell function or impair it or lead to cell death.Chronic oxidative stress associated with low levels of glutathione and L-ascorbic acid will allow a Fenton Reaction to establish that enables excess Fe2+ to take up electrons from protons in the cytochrome system that tends to deplete oxygen in the mitochondria, as follows:-
Fe2+ + H+ + O2 → Fe3+ + H2OWhen this reaction continues in the red blood cells, methemoglobin is formed and over time there is accumulation of methemoglobin that impairs the transport of oxygen in the body as observed in AIDS patients. When this reaction occurs in white blood cells, the older cells die off quickly for lack of oxygen and energy while such lack of energy leads to a decline in immune cell function or impair it, depending on the rate of this reaction in those cells. The low amounts of cellular energy can impair the "oxidative burst" mechanism of the immune cells that is used in the destruction of pathogens and opportunistic infections can take root. Such low amounts of cellular energy in the thymus can prevent the formation of T4 cells while the older ones die off, something very characteristic in AIDS patients. Similarly, low amounts of cellular energy results in lower rates of formation of new cells in the immune system that eventually fails to perform its function in the body and a host of symptoms appear beginning with fatigue, chronic fatigue, muscle wasting, decline in the immune cell counts and finally ends with impairment of the immune system that cannot prevent opportunistic infections while the biochemistry favors cancer cell formation and the NK cells lack the energy to seek out and destroy them.
These Fenton Reactions explain how the oxidative stress problem arises and leads to disease states and why natural antioxidant supplementation that also includes selenium helps to alleviate the symptoms in AIDS patients as noted in many studies.
This article forms a chapter in the book titled FENTON MEDICINE authored by Beldeu Singh which is not yet released.See also:
Beyond the 'HIV-Causes-AIDS' Model
AIDS disease is generally characterised by a decline in CD4+ T lymphocytes circulating in the blood, which are responsible for cell-mediated immunity. As a result, the patient becomes susceptible to opportunistic infections (those affecting weakened immune systems) such as tuberculosis, pneumonia, meningitis, and other diseases caused by parasites, bacteria and viruses that can enter and multiply in the cells of the body.But models that assume the human immunodeficiency virus (HIV) plays a central role in disease progression run into considerable difficulties. If the decline in CD4+ cells is due to HIV killing the cells, then there should be a correlation between the 'viral load', which estimates the amount of virus in the body, and the CD4+ cell count. But that is not the case. CD4+ cell count is not a reliable indicator of disease progression at all, nor for that matter is viral load (Chapter 2, Unraveling AIDS, ISIS Report), and they bear little relationship to each another. This has been confirmed in a recent study on untreated HIV+ individuals.
posted by Sepp Hasslberger on Monday March 26 2007
updated on Wednesday December 8 2010URL of this article:
http://www.newmediaexplorer.org/sepp/2007/03/26/solving_the_antioxidant_question_in_aids.htm
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