Folate is a vital nutrient with participation in one carbon reactions, purine synthesis, formation of methionine from homocysteine and DNA synthesis. Its deficiency has been linked with a spectrum of diseases like gastrointestinal disorders, glossitis, megaloblastic anemia, peripheral neuropathy and hyperhomocysteinemia. It is singularly eminent methyl donor in body for stability of the genome and orderly expression of genes. Over recent years, endothelial dysfunction is considered a key element of vascular pathology, including the coronary artery disease and hyperhomocysteinemia, is shown to worsen endothelial dysfunction. Folate deficiency is one etiological element for hyperhomocysteinemia and folate supplementation is tried with intent to reduce cardiovascular risk in patients. Inconsistency of beneficial outcomes, however, highlights complexities in occurrence of hyperhomocysteinemia , the determinants of endothelial dysfunction and consequent cardiovascular risk. Research has revealed new potentially beneficial action profiles of folic acid for improving endothelial dysfunction and cardiovascular risk independent of homocysteine reduction. Attempt is herein made to translate new knowledge to suit clinical exploitation. (J Clin Prev Cardiol 2013;2(2):91-4)

Keywords: Endothelial dysfunction, hyperhomocysteinemia, coronary disease risk, Folate, preventive nutrition.

Volume 2, Number 2, Pages: 91-4

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