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.
There was a recent publication 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 paper 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
- 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).
- Mayer et al. The effects of folate supplementation on
some coagulation parameters and oxidative status surrogates. Eur J Clin
Pharmacol 58:1-5 (2002).