Introduction

Abstract

The increased prevalence of coronary artery disease (CAD) among migrant Asian Indians and individuals in the subcontinent of India is partly attributed to elevated plasma levels of homocysteine (Hcy). Hcy, a sulfur-containing amino acid, is derived from the metabolic demethylation of dietary methionine (1,2,3). Four different forms of Hcy exist: 1% is present as free thiol; 70-80% circulates as a disulphide-bound to albumin; and the remaining 20-30% forms a dimer with itself or other thiols (1). The grouping of these four forms is referred to as total plasma Hcy (tHcy) and it is the elevation of this serum component that has been noted as an independent risk factor for CAD. Total plasma Hcy within the normal range is 5 to 15 μmol/L and hyperhomocysteinemia (HHC) is categorized as moderate (16-30 μmol/L), intermediate (31100 μmol/L), and severe (>100 μmol/L) HHC (4). The concentration of tHcy is determined by genetic and nutritional factors, such as levels of dietary folate and cobalamin. Since these nutrients are essential co-factors in the metabolic pathway of Hcy, deficiencies of folate and cobalamin result in elevated Hcy levels in the Asian Indian population (2,4,5,6,7,8).