Heart Health: Folic Acid Supplementation

Now here’s a question you don’t hear everyday: How effective are folic acid supplements for maintaining a healthy heart? Uh, I don’t know. I wonder what the experts are saying. Serena Gordon of HealthDay News reports some health researchers aren’t exactly impressed with folic acid supplementation:
"Consuming a supplement of folic acid is probably not going to mitigate your risk of cardiovascular disease," said the study's lead author, Dr. Lydia Bazzano, an assistant professor of epidemiology at Tulane University School of Public Health and Tropical Medicine, in New Orleans…


… According to Dr. Stephen Siegel, a cardiologist at New York University Medical Center in New York City: "The whole concept [of folic acid supplementation] began because we know there's an association between homocysteine levels and atherosclerotic disease, and we know that we can safely lower homocysteine with folic acid. But we don't know if there's a cause-and-effect relationship between homocysteine and cardiovascular disease, or simply an association. Many doctors jumped on the bandwagon, however, because folic acid didn't have the potential to do any harm, but it looked like it might help."
Okay, so far we’ve got two thumbs down. Let’s see what Dr. Fuhrman has to say about folic acid supplements for heart health. In Cholesterol Protection For Life it comes up during his analysis of high homocysteine levels:
Consider an abnormal homocysteine that may require treatment above 15, not above 10. Levels between 10 and 15 have not been consistently associated with worse outcomes.1

If one homocysteine is elevated above 15, make sure a blood level of B12, and MMA (methlymalonic acid) and a folate level is drawn.

Mild elevations of homocysteine between 10 and 15 do not appear to place people at higher risk. In most of these cases, the mild elevation is just a marker for a low nutrient diet in general and the correct treatment is the improvement of the entire diet, not just a supplement to lower homocysteine. Folate alone in these cases cannot compare with the value of actually eating a diet rich in folate and gaining all the other essential cardio-protective compounds that are found in natural plant foods. It is similar to taking a cholesterol-lowering drug instead of eating healthfully; a pill cannot take the place of the full symphony of dietary elements that contribute to heart and vascular health.

When the abnormality (elevated homocysteine) is due to B12 deficiency it is wise to take more B12. Whether you are consuming sufficient B12 or not is best ascertained by a normal MMA (methylmalonic acid) because a B12 level in the 200 to 400 range, which is considered in the normal range could still be abnormal. Paradoxically, MMA is actually a better marker for B12 deficiency than B12 itself. If the MMA is elevated a B12 deficiency exists, even if the B12 is in the normal range. When this is the case, extra B12 is the correct treatment for the elevated homocysteine.

If the folate level is excellent (15 – 25) and the B12 level is normal (as documented with a normal MMA) and the homocysteine is still significantly elevated,then the cause of the elevation is most likely a genetic defect in folate conversion. In this case, folate (or folic acid) supplementation may not be totally effective; because the patient is just taking more of the folate that they don’t convert effectively to begin with. They don’t need more folate, rather they need more of the biologically active form of folate that they don’t make well (called methyl tetrahydrofolate or formyl tetrahydrofolate.)

So if the B12 is normal and the folate is normal, and the homocysteine is still significantly elevated, it may make more sense to take a supplement containing additional tetrahydrofolate, and not just pile on huge doses of folate (folic acid) attempting to drive the homocysteine down with overwhelming high doses of folate.

In conclusion, it is wise to target therapy based on known deficiencies and not just blanket patients with high dose supplements that they do not need. Nevertheless, an attempt to uncover the cause of the homocysteine elevation and lower it accordingly may be an important intervention for patients with unique needs.
1. Sacco RL, Anand K, Lee HS, et al. Homocysteine and the risk of ischemic stroke in a triethnic cohort: the Northern Manhattan Study. Stroke 2004;35(10):2263-2269.
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