MODERATE HYPERHOMOCYSTEINEMIA AND ATHEROTHROMBOSIS

Elevated levels of plasma total homocysteine are now accepted as an in dependent risk factor for premature atherosclerosis. Nutritional, envi ronmental and genetic factors may contribute to increase the levels of homocysteine. The exact pathogenesis of vascular damage induced by ho mocysteine is still not completely understood. Various mechanisms have been proposed, including a significant prooxidative activity, a stimu lation of smooth muscle cells proliferation and an endothelial dysfunc tion. Folate, pyridoxine and cyanocobalamin are important cofactors fo r homocysteine metabolism. In most cases, elevated homocysteine can be reduced by administration of vitamin supplements. It has not yet been demonstrated that reduction in mortality and morbidity can be achieve d with these regimens. However, food supplementation with folic acid h as been recommended for treatment or prevention of homocysteine-relate d disorders in the North American population. Appropriate clinical tri als are needed to evaluate the effect of lowering moderate homocystein e levels on atherosclerosis.