Homocysteine--an independent risk factor of premature vascular disease
Mansoor, M.A.; Vefring, H.; Kristensen, O.
Tidsskrift for den Norske Laegeforening Tidsskrift for Praktisk Medicin Ny Raekke 116(14): 1663-1667
1996
ISSN/ISBN: 0029-2001 PMID: 8658431 Document Number: 456065
Discovery of severe hyperhomocysteinemia and its relation to premature vascular disease among patients with homocystinuria was the basis for the development of the homocysteine theory of arteriosclerosis. The validity of this theory has been strengthened by several clinical investigations which suggest a positive relationship between moderate to intermediate hyperhomocysteinemia and premature vascular disease. Homocysteine levels in plasma are regulated by the activity of intracellular enzymes, methionine synthase, cystathionine beta-synthase, methylenetetrahydrofolate reductase and betaine-homocysteine methyltransferase and concentrations of vitamin B-12, vitamin B-6 and folate. Decreased activity of enzymes or deficiency of vitamins will increase total plasma homocysteine. Risk of thromboembolic events in subjects with various forms of homocystinuria is reduced after homocysteine-lowering therapy. Thus, it is possible that higher intake of folic acid and vitamin B-6 could reduce onset of vascular disease.