LillyBritches wrote:Speaking of Golden - Gilgamesh! Nice to see you 'round here. So does this mean your non-academic sabbatical is no more?
Betaine can improve both risk factors, and in humans with cardiovascular disease, there is a significant inverse relation between plasma betaine and homocysteine concentrations in fasting (199) and postmethionine (200) states. A betaine-rich diet might lower cardiovascular disease risk in healthy humans (201)...
Prevention or treatment, such as activation of defective (mutant) enzyme activity with the relevant cofactor or its precursor (eg, folic acid or vitamins B-12 or B-6), is based on the cause and severity of the defect. If homocysteinemia does not respond to this treatment, pharmacologic doses of betaine or folic acid have been used to enhance the alternative pathway of homocysteine turnover (203, 204).
Mild homocysteinemia can be reduced immediately and in the long term by ingesting a combination of vitamin B-6, folic acid, and betaine (244, 245) or betaine (1.5-6 g/d) alone (57, 189, 198, 201, 246). Betaine, but not folic acid, is effective at preventing an increase in postmethionine homocysteine concentrations (198, 201, 244, 247, 248). Betaine-dependent remethylation occurs mainly in the liver and kidney, whereas folate-dependent remethylation occurs in most cells. Serum homocysteine concentrations may be represented by the extrahepatic supply to the liver via folate remethylation and by the hepatic output via betaine remethylation (198). Therefore, combined ingestion of folic acid and betaine may be the most effective method of lowering homocysteine.
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