Source of Support: None, Conflict of Interest: None
In recent years, a great deal of attentions has been focused on the role of homocysteine, a sulfur-containing amino acid, in the etiopathogenesis of atherothromobtic vascular disease. Multiple prospective and case-control studies have shown that a moderately elevated plasma homocysteine concentration is an independent risk factor for stroke. The exact molecular mechanism by which homocysteine or related metabolites promote atherothrombosis is unknown although several possible roles have been proposed. It is generally held that homocysteine promotes thrombosis by adversely affecting the functions of the vascular endothelium that maintain the blood's fluidity. Homocysteine concentrations are determined by genetic and nutritional factors including deficiencies of folate, vitaminB12 and B5 supplementation with the nutrient cofactors required for optimal functioning of the homocysteine metabolic pathways significantly impacts homocysteine levels, and offers a new integrated possibility for prevention of first and recurrent episodes stroke.