In recent years, clinical and epidemiological studies have suggested that increased concentrations of total plasma homocysteine (tHcy) could be an additional independent risk factor for cardiovascular disease [1]. It has been established that a very high tHcy concentration due to inborn metabolic errors causing enzyme alterations in homocysteine metabolism can lead to serious thrombotic events at a young age [2]. Mild to moderate hyperhomocysteinemia is recognized as a potential risk factor for adult cardiovascular disease, and many observational studies, and case and placebo-controlled trials, are seeking to determine whether it is a cause or an effect of the disease [3]. Hyperhomocysteinemia can be caused by genetic and/ or acquired factors due to lifestyle (i.e., nutritional habits), renal insufficiency and age [3]. It is known that low levels or deficiency in our diet of some group B vitamins, in particular cobalamin and/or folate (required cofactors for further homocysteine metabolism through the remethylation pathway), result in moderate elevations in tHcy levels.