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| Homocysteine is a toxic end product of the metabolism (methylation) of methionine (an essential amino acid) and is now known to be a leading cause of heart and artery disease. TMG is a byproduct of sugar beet processing and is a known methyl donor. Betaine may influence neurological function indirectly via 5-adenosylmethionine synthesis. Methylation reactions and how they relate to the prevention of many diseases such as cancer, heart disease, liver disease and neurological disorders are a growing area of interest for researchers. When methylation is working properly, homocysteine is quickly converted back to methionine which is then converted to SAMe (S-adenosylmethionine), which protects the liver and is a natural antidepressant. [2][3] SAMe then acts as a methyl donor for DNA: when attached to DNA, methyl groups appear protective, preventing mutated genes from expressing themselves. Factors that decrease methylation include smoking, alcohol consumption, high fat diets and birth control pills. Multiple studies have demonstrated that medium to high levels of plasma homocysteine are associated with increased risk of heart disease, cerebrovascular disease and peripheral artery disease. In one study, daily treatment with TMG, folic acid and choline normalized homocysteine levels in 17 of 19 patients. [1] TMG lowers homocysteine levels with and without vitamins B12, B6 and folic acid. It aids the body in overcoming a number of adverse health conditions, and is an intricate part of human metabolism. In a broad sense, TMG protects the body from many forms of physical, metabolic and environmental stress. Folic acid appears to help neutralize this effect at one or two 800mcg tablets. Directions The usual TMG dose is 500 to 1,000mg per day - roughly equivalent to what a diet high in broccoli, spinach or beets would provide. Its occurrence, cofactor therapy and enzymology," Arteriosclerosis and Thrombosis 13(9): 1253-60, 1993 (2) Dudman, N. "Disordered methionine/homocysteine metabolism in premature vascular disease," Arteriosclerosis and Thrombosis 13(9): 1253-60, 1993 (3) Kishi, T. "Effect of betaine on s-adenosylmethionine levels in the cerebrospinal fluid in a patient with methylenetetrahydrofolate reductase deficiency and peripheral neuropathy" J Inherited Metabolic Disease 17(5): 560-5, 1994 (4) Cooney, C. "Are somatic cells inherently deficient in methylation metabolism?" Growth, Development & Aging 57(4): 261-73, 1993. |