FOLATE DEFICIENCIES AND CARDIOVASCULAR PATHOLOGIES

Although folates are widely distributed in foods, folate deficiencies may be more frequent than expected because their true availability may be impaired due to their lability under various food cooking and proc essing conditions. Folate deficiency is frequently observed in elderly people, smokers, alcoholics and oral contraceptive users. It is also associated with the mutation leading to the thermolabile variant of N- 5,N-10-methylenetetrahydrofolate reductase which is observed in about 10% of the population. In addition to the essential role of the intrac ellular pool of polyglutamates in de novo biosynthesis of deoxyribonuc leotides which allow cell growth and division, the reduced and methyla ted form of folate, N-5-methyltetrahydrofolate, is required for the re methylation of homocysteine to methionine. By inhibiting this remethyl ation pathway, folate deficiency induces homocysteine efflux into the circulation. Many studies have shown a negative correlation between pl asma folate, particularly N-5-methyltetrahydrofolate, and circulating homocysteine levels. In addition, folate deficiency is a major cause o f hyperhomocysteinemia which is fully recognised as an independent ris k factor for atherothrombosis. Epidemiological and recent experimental studies have demonstrated that folate deficiency might increase the r isk of cardiovascular disease by increasing circulating homocysteine l evels. Thus, the clinical efficiency of folate supplementation, especi ally N-5-methyltetrahydrofolate, in reducing homocysteine-dependent ca rdiovascular risk should be evaluated.