AIDS 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.