Homocysteinemia, cardiovascular risk and long-term enteral nutrition

The problem of micronutrients and vitamin supplementation in artificial nutrition is widely debated as it involves a large number of clinically heterogeneous patients. Homocysteine is a sulfur-containing amino acid produced in the metabolism of the essential amino acid methionine. In the metabolic pathways involved in homocysteine turnover, folic acid (FA) and vitamins B6 and B12 are important regulators. Experimental and clinical evidence has long suggested a causal relationship between hyperhomocysteinemia and cardiovascular disease. Reducing plasma homocysteine by multivitamin therapy consisting of FA and vitamins B6 and B12 has been proposed in clinical practice as a strategy to prevent cardiovascular disease in high-risk patients. Recently, however, the results of clinical controlled trials failed to show a conclusive relationship between homocysteine and cardiovascular disease. Thus, while multivitamin supplementation is indicated to prevent malnutrition and the clinical consequences of vitamin deficiency, its potential implications for the prevention of atherosclerosis need to be reassessed