Folic Acid Against Cardiovascular Disease

The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 5 No. 5 • October 2002

Folic Acid Against Cardiovascular Disease

It took a prolonged legal and political struggle to force the FDA to permit a health claim that folic acid reduces the risk of neural-tube-defect births. The two of us and coplaintiffs, represented by attorney Jonathan Emord, recently won a federal district court ruling that forces the FDA to permit a claim that folic acid, along with vitamins B12 and B6, may reduce the risk of cardiovascular disease. Nevertheless, there is considerable evidence that folic acid in adequate amounts may also reduce the risk of various cancers. It will no doubt take years of litigation* before this claim will be permitted. In the meantime, however, scientific data on the benefits of folic acid continue to be published.

*Make a blow against the empire by donating to our litigation fund. Even small amounts help. Send donations to: Pearson & Shaw Litigation Fund, c/o Emord & Associates, 5282 Lyngate Court, Burke, VA 22015. Thanks!

There was a recent publication1 of the results of a randomized, controlled trial of 553 patients who had had successful angioplasty of at least one significant coronary stenosis (equal to or greater than 50% reduction in lumen area) and who were then treated with either placebo or a combination of 1 mg/d of folic acid, 400 mcg/d of vitamin B12 (cyanocobalamin), and 10 mg/d of vitamin B6 (pyridoxine hydrochloride). The patients were evaluated at 6 months and 1 year for major adverse events (death, myocardial infarction, or need for repeated revascularization).

After a mean follow-up of 11 months, the risk of major adverse events was significantly lower in patients treated with the folic acid, B12, and B6 (15.4% vs. 22.8%), primarily owing to a reduced rate of target-lesion regrowth (9.9% vs. 16.0%). There was a nonsignificant trend toward fewer deaths and nonfatal myocardial infarctions with the vitamins.

Another recent paper2 suggests possible mechanisms that may be involved in the effects of folate supplementation. Fifty-seven volunteers (30 males, 27 females, mean age 61.2 years) with high risk of coronary events or established atherosclerotic disease and homocysteine concentration of at least 20 micromol/l participated in an open, prospective study. There was 1 month of placebo followed by 2 months of treatment with 10 mg daily of folate. Results showed that folate treatment caused a significant decrease of homocysteine and fibrinogen (a blood factor involved in clotting), while plasminogen (which, when activated by tissue plasminogen activator, dissolves clots) and antithrombin III were significantly increased. In addition, the antioxidant enzymes glutathione peroxidase and superoxide dismutase, as well as glutathione, significantly increased after folate treatment. Malonyldialdehyde (a breakdown product of peroxidized lipids) and von Willebrand factor decreased. Hence, the researchers reported, folate treatment resulted not only in homocysteine decrease, but also in an improvement in hypercoagulation, oxidative stress, and endothelial dysfunction.

  1. Schnyder et al. Effect of homocysteine-lowering therapy with folic acid, vitamin B12, and vitamin B6 on clinical outcome after percutaneous coronary intervention. JAMA 288(8):973-9 (2002).
  2. Mayer et al. The effects of folate supplementation on some coagulation parameters and oxidative status surrogates. Eur J Clin Pharmacol 58:1-5 (2002).

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