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five years or longer to give results."

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Detox and Chelation


Magnesium – Antioxidant Status – Glutathione
The involvement of free radicals in tissue injury induced by Mg deficiency[i] causes an accumulation of oxidative products in heart, liver, kidney, skeletal muscle tissues and in red blood cells.[ii] Magnesium is a crucial factor in the natural self-cleansing and detoxification responses of the body. It stimulates the sodium potassium pump on the cell wall and this initiates the cleansing process in part because the sodium-potassium-ATPase pump regulates intracellular and extracellular potassium levels. Cell membranes contain a sodium/potassium ATPase, a protein that uses the energy of ATP to pump sodium ions out of the cell, and potassium ions into the cell. The pump works all of the time, like a bilge pump in a leaky boat, pumping K+ and Na+ in and out, respectively.

Potassium regulation is of course crucial because potassium acts as a counter flow for sodium's role in nerve transmission. The body must put a high priority on regulating the potassium of the blood serum and this becomes difficult when magnesium levels become deficient.[iii] Because of these crucial relationships, when magnesium levels become dramatically deficient we see symptoms such as convulsions, gross muscular tremor, atheloid movements, muscular weakness, virtigo, auditory hyperacusis, aggressiveness, excessive irritability, hallucinations, confusion, and semicomma. A magnesium deficiency can cause the body to lose potassium and this our bodies cannot afford. Within the cell wall is a sodium pump to provide a high internal potassium and a low internal sodium. Magnesium and potassium inside the cell assist oxidation, and sodium and calcium outside the cell wall help transmit the energy produced. The healthy cell wall favors intake of nutrients and elimination of waste products.

Magnesium protects cells from aluminum, mercury, lead, cadmium, beryllium and nickel, which explains why re-mineralization is so essential for heavy metal detoxification and chelation. Magnesium protects the cell against oxyradical damage and assists in the absorption and metabolism of B vitamins, vitamin C and E, which are anti-oxidants important in cell protection. Recent evidence suggests that vitamin E enhances glutathione levels and may play a protective role in magnesium deficiency-induced cardiac lesions.[iv] Magnesium in general is essential for the survival of our cells but takes on further importance in the age of toxicity where our bodies are being bombarded on a daily basis with heavy metals. Magnesium thus protects the brain from toxic effects of chemicals. It is highly likely that low total body magnesium contributes to heavy metal toxicity in children and is a strong participant in the etiology of learning disorders.

Without sufficient magnesium, the body accumulates toxins and acid residues, degenerates rapidly, and ages prematurely. Recent research has pointed to low glutathione levels being responsible for children’s vulnerability to mercury poisoning from vaccines.[v] It seems more than reasonable to assume that low levels of magnesium would also render a child vulnerable. And in fact we find out that glutathione requires magnesium for its synthesis.[vi] Glutathione synthetase requires ?-glutamyl cysteine, glycine, ATP, and magnesium ions to form glutathione.[vii] In magnesium deficiency, the enzyme y-glutamyl transpeptidase is lowered.[viii] Data demonstrates a direct action of glutathione both in vivo and in vitro to enhance intracellular magnesium and a clinical linkage between cellular magnesium, GSH/GSSG ratios, and tissue glucose metabolism.[ix] Magnesium deficiency causes glutathione loss, which is not affordable because glutathione helps to defend the body against damage from cigarette smoking, exposure to radiation, cancer chemotherapy, and toxins such as alcohol and just about everything else.


[i] Magnesium deficiency (MgD) has been associated with production of reactive oxygen species, cytokines, and eicosanoids, as well as vascular compromise in vivo. Although MgD-induced inflammatory change occurs during "chronic" MgD in vivo, acute MgD may also affect the vasculature and consequently, predispose endothelial cells (EC) to perturbations associated with chronic MgD. As oxyradical production is a significant component of chronic MgD, we examined the effect of acute MgD on EC oxidant production in vitro. In addition we determined EC; pH, mitochondrial function, lysosomal integrity and general cellular antioxidant capacity. Decreasing Mg2+ (< or = 250microM) significantlyincreased EC oxidant production relative to control Mg2+ (1000microM). MgD-induced oxidant production, occurring within 30min, was attenuated by EC treatment with oxyradical scavengers and inhibitors of eicosanoid biosynthesis. Coincident with increased oxidant production were reductions in intracellular glutathione (GSH) and corresponding EC alkalinization. These data suggest that acute MgD is sufficient for induction of EC oxidant production, the extent of which may determine, at least in part, the extent of EC dysfunction/injury associated with chronic MgD. Effect of acute magnesium deficiency (MgD) on aortic endothelial cell (EC) oxidant production.Wiles ME, Wagner TL, Weglicki WB.The George Washington University Medical Center, Division of Experimental Medicine, Washington, D.C., USA. mwiles@nexstar.com Life Sci. 1997;60(3):221-36.

[ii] Martin, Hélène. Richert, Lysiane. Berthelot, Alain Magnesium Deficiency Induces Apoptosis in Primary Cultures of Rat Hepatocytes.* Laboratoire de Physiologie, et Laboratoire de Biologie Cellulaire, UFR des Sciences Médicales et Pharmaceutiques, Besançon, France. 2003 The American Society for Nutritional Sciences J. Nutr. 133:2505-2511, August 2003

[iii] A magnesium deficiency can cause the body to lose potassium [Peterson 1963][MacIntyre][Manitius], possibly because of a poorly understood effect of magnesium on the efficiency of energy supply to the sodium pump [Fischer].

[iv] Barbagallo, Mario et al. Effects of Vitamin E and Glutathione on Glucose Metabolism: Role of Magnesium; (Hypertension. 1999;34:1002-1006.)

[v] Enviroonmental Working Group. http://www.ewg.org/reports/autism/part1.php

[vi] Linus Pauling Institute

[vii] Virginia Minnich, M. B. Smith, M. J. Brauner, and Philip W. Majerus. Glutathione biosynthesis in human erythrocytes. Department of Internal Medicine, Washington University School of Medicine, J Clin Invest. 1971 March; 50(3): 507–513. Abstract: The two enzymes required for de novo glutathione synthesis, glutamyl cysteine synthetase and glutathione synthetase, have been demonstrated in hemolysates of human erythrocytes. Glutamyl cysteine synthetase requires glutamic acid, cysteine, adenosine triphosphate (ATP), and magnesium ions to form ?-glutamyl cysteine. The activity of this enzyme in hemolysates from 25 normal subjects was 0.43±0.04 µmole glutamyl cysteine formed per g hemoglobin per min. Glutathione synthetase requires ?-glutamyl cysteine, glycine, ATP, and magnesium ions to form glutathione. The activity of this enzyme in hemolysates from 25 normal subjects was 0.19±0.03 µmole glutathione formed per g hemoglobin per min. Glutathione synthetase also catalyzes an exchange reaction between glycine and glutathione, but this reaction is not significant under the conditions used for assay of hemolysates. The capacity for erythrocytes to synthesize glutathione exceeds the rate of glutathione turnover by 150-fold, indicating that there is considerable reserve capacity for glutathione synthesis. A patient with erythrocyte glutathione synthetase deficiency has been described. The inability of patients' extracts to synthesize glutathione is corrected by the addition of pure glutathione synthetase, indicating that there is no inhibitor in the patients' erythrocytes.

[viii] Braverman, E.R. (with Pfeiffer, C.C.)(1987). The healing nutrients within: Facts, findings and new research on amino acids. New Canaan: Keats Publishing.

[ix] Barbagallo, M. et al. Effects of glutathione on red blood cell intracellular magnesium: relation to glucose metabolism. Hypertension. 1999 Jul;34(1):76-82. Institute of Internal Medicine and Geriatrics, University of Palermo, Italy. mabar@unipa.it

IMVA - Article - by Mark Sircus, Ac., OMD, author of Transdermal Magnesium Therapy.


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