Homocyst(e)ine, vitamins and genetic interactions in vascular disease.
Blood homocyst(e)ine levels are an important, independent and frequent risk factor for clinical atherosclerosis and venous thrombosis. Folic acid, vitamins B6 and B12, renal and thyroid functions, certain medications and certain genotypes are known to modulate plasma homocyst(e)ine levels. Intake of B vitamins through diet, supplementation and fortified foods effectively reduces homocyst(e)ine concentration and thus may reduce the risk of cardiovascular disease. This is true even in individuals who are genetically predisposed to hyperhomocyst(e)inemia. Randomized clinical trials are needed to investigate these effects further.
Malinow
M R
MR
Oregon Health Sciences University, Portland, Oregon, USA. malinowr@ohsu.edu
D001161:Arteriosclerosis / Q000097:blood* / Q000235:genetics; D005260:Female; D005838:Genotype; D006710:Homocysteine / Q000097:blood* / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D011736:Pyridoxine / Q000008:administration & dosage* / Q000494:pharmacology; D012307:Risk Factors; D013924:Thrombophlebitis / Q000097:blood* / Q000235:genetics; D014805:Vitamin B 12 / Q000008:administration & dosage* / Q000494:pharmacology
D006710:Homocysteine; D011736:Pyridoxine; D014805:Vitamin B 12