Meta-analysis justifies the use of folic acid to reduce heart disease and strokes
The November 25, 2006 issue of the British Medical Journal published the conclusion of researchers at The London Queen Mary's School of Medicine and Dentistry that there is enough scientific evidence to warrant the use of the B vitamin folic acid as an inexpensive and simple method of reducing heart disease and stroke. A greater intake of folic acid is associated with lower levels of homocysteine, an amino acid linked with the development of cardiovascular disease.
Dr David S. Wald and colleagues evaluated 27 cohort studies which examined the association between homocysteine levels and the risk of heart attack and stroke in large numbers of people, 80 studies which evaluated the effect of a genetic variant that increases homocysteine levels on heart disease and 30 that examined its effect on stroke, and 11 randomized controlled trials that examined the effect of lowering homocysteine on heart attack and stroke.
The cohort studies analyzed together confirmed a significant positive association between elevated homocysteine levels and heart attack and sudden cardiac death, and stroke. A reduction of 3 micromoles per liter serum homocysteine, which is achievable with 800 micrograms per day of folic acid, was associated with a 15 percent lower risk of heart attack and a 24 percent reduction in stroke. Analysis of the genetic studies provided similar results. Although the randomized trials were too small to provide conclusive results, their findings were consistent with small decreases in ischemic heart disease and stroke associated with homocysteine reduction.
"Since folic acid reduces homocysteine concentrations, to an extent dependent on background folate levels, it follows that increasing folic acid consumption will reduce the risk of heart attack and stroke by an amount related to the homocysteine reduction achieved," the authors conclude. "We therefore take the view that the evidence is now sufficient to justify action on lowering homocysteine concentrations, although the position should be reviewed as evidence from ongoing clinical trials emerges.
The following studies have shown a rapid and dramatic decrease in homocysteine levels caused by folic acid and some B vitamins:
In 1996, the Food and Drug Administration (FDA) mandated that cereal-grain flour products be fortified with folic acid. Modest but significant decreases in homocysteine levels followed (Jacques PF et al 1999; Anderson JL et al 2004).
One set of patients with a history of myocardial infarction or unstable angina was given 2000 mcg of folic acid daily. Another group of patients with the same conditions received only 200 mcg. The higher dosage significantly reduced total homocysteine levels (Neal B et al 2002).
Daily supplementation with 350 mcg of folic acid for 17 weeks reduced serum homocysteine levels by nearly 20 percent, enough to reduce the risk of vascular disease (Venn BJ et al 2002).
Folic acid and vitamins B6 and B12 reduced homocysteine levels, restored endothelial function, and reduced arterial plaque (Spence JD et al 2001).
Middle-aged to elderly men and women with initially modest to significantly elevated homocysteine levels (>8 µmol/L) who took a multivitamin and mineral supplement for 56 days had significantly higher vitamin B and lower homocysteine levels when retested. Plasma folic acid and vitamin B12 concentrations rose by 42 percent and 14 percent, respectively, while homocysteine concentrations fell 10 percent (McKay DL et al 2000).
Another B vitamin, vitamin B2, is also involved in remethylation pathways in the body (Devlin TM 2001).
A deficiency of folate can result in impaired cell division and protein synthesis. With diminished replacement of healthy red blood cells and intestinal cells, anemia and a decline in GI tract function ensue. The systemic need for folate increases in certain disease states in which increased cell multiplication is needed. Chronic use of medications such as aspirin and antacids can interfere with the natural synthesis of folate.
Source Naturals Metafolin® is a new coenzymated form of folic acid. Upon absorption, folate is converted into L-methylfolate, which is the predominant form of folate in circulation and is the only type of folate that can cross the blood-brain barrier. Metafolin does not require enzymatic conversion that folic acid does which is difficult for some people. Preliminary research suggests that it is more bioavailable than folic acid.
Homocysteine is an amino acid that, even at levels previously regarded as normal, exaggerates the adverse effects of other atherosclerotic risk factors and may heighten long-term risk for heart attack, stroke, osteoporosis, depression, blood clot formation, and even cancer.
Fortunately, the nutritional management of elevated homocysteine levels is a relatively straightforward proposition. Despite the government’s well-intended mandate to add folic acid to grain products, most of us are still marginally and sometimes substantially deficient of folic acid. Folic acid supplementation, along with other nutritional strategies to lower homocysteine—using vitamins B6 and B12, choline, and trimethylglycine (TMG)—can provide powerful protection against homocysteine’s ill effects on your life and health.