Homocysteine is an amino acid in the blood. Epidemiological studies have shown that too much homocysteine in the blood (plasma) is related to a higher risk of coronary heart disease, stroke and peripheral vascular disease.
Other evidence suggests that homocysteine may have an effect on atherosclerosis by damaging the inner lining of arteries and promoting blood clots. However, a direct causal link hasn’t been established.
Plasma homocysteine levels are strongly influenced by diet, as well as by genetic factors. The dietary components with the greatest effects are folic acid and vitamins B6 and B12. Folic acid and other B vitamins help break down homocysteine in the body. Several studies have found that higher blood levels of B vitamins are related, at least partly, to lower concentrations of homocysteine. Other recent evidence shows that low blood levels of folic acid are linked with a higher risk of fatal coronary heart disease and stroke.
Several clinical trials are under way to test whether lowering homocysteine will reduce CHD risk. Recent data show that the institution of folate fortification of foods has reduced the average level of homocysteine in the U.S. population.
Recent findings suggest that laboratory testing for plasma homocysteine levels can improve the assessment of risk. It may be particularly useful in patients with a personal or family history of cardiovascular disease, but in whom the well-established risk factors (smoking, high blood cholesterol, high blood pressure) do not exist.
Although evidence for the benefit of lowering homocysteine levels is lacking, patients at high risk should be strongly advised to be sure to get enough folic acid and vitamins B6 and B12 in their diet. Foods high in folic acid include green, leafy vegetables and grain products fortified with folic acid. But this is just one risk factor. A physician taking any type of nutritional approach to reducing risk should consider a person's overall risk factor profile and total diet.
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