HOMOCYSTEINE and HEART DISEASE

Homocysteine is an amino acid(protein) which is found in the human body. It is normally broken down into cysteine or methionine by two enzymes which only work efficiently if there is a plentiful supply of  the nutrients folic acid, vitamin B6 and vitamin B12. If there is a lack of any of these nutrients the levels of homocysteine in the blood rise and become elevated.

It has been  demonstrated that serum Homocysteine can be lowered by the use of Folic Acid supplements. A decrease in serum homocysteine of 3 µmol/l  can be achieved by daily intake of aprox 800 micrograms of folic acid per day, which lowers the risk of heart attack by 15%.  In order for folic acid to be effective, however, levels of vitamin B 12 (cobalamin) must be normal.

Vitamin B6 (pyridoxine) also works to lower homocysteine like vitamin B12 and folic acid. Pyridoxine is necessary for homocysteine to convert to cysteine through the transsulfuration pathway. A 1996 study concluded that patients deficient in vitamin B6 can not convert homocysteine to cysteine causing levels to escalate. Therefore, vitamin B6 deficiency is an independent risk factor associated with vascular disease. (Ubbink, 1996)

A more recent treatment has been  trimethylglycine (TMG), also called Betaine . TMG is considered a "methylation enhancing compound" which helps homocysteine convert to methionine. In a 1993 study on patients with elevated homocysteine, the therapy with TMG in addition to Vitamin B6, folic acid and Vitamin B12 supplementation significantly reduced homocysteine plasma levels with no side effects during the two years in which treatment was monitored. Interestingly, on the cases where combined folate, pyridoxine and B12  did not dramatically lower homocysteine, adding TMG had significant effects. (Monatero et al., 1993

5. A Poduri,J Kaur, J S Thakur,S Kumari, S Jain and M Khullar Effect of ACE inhibitors and -blockers on homocysteine levels in essential hypertension