Dr. Kurt Oster of Germany had a theory, thirty years ago, that xanthine oxidase (XO) enzyme was partly the cause of atherogenesis. He believed that folic acid was a XO inhibitor, mistakenly, and used folic acid to treat circulatory problems. (It was later found that a contaminant in the folic acid actually caused the XO inhibition.)
Dr. Osler used 80 mg. of folate, with 80 mg. ascorbic acid (vitamin C), as a preservative. He had success in treating coronary artery disease, such as angina, and peripheral artery disease, such as intermittent claudication. In spite of the success, he did not do a double-blind study of the folic acid therapy.
Although the XO theory is no longer accepted, it is now believed that folic acid may work by restoring the function of nitric oxide synthase (eNOS) in cases of tetrahydrobiopterin (BH4) deficiency. BH4 is difficult to use as a supplement. But, 5-methyltetrahydrofolate substitutes for the loss of BH4 and improves vasodilatation in cases of endothelial dysfunction. Folate at 5-10 mg. per day increases nitric oxide function and improves coronary disease, hypercholesterolemia and type 2 diabetes mellitus.
High-dose arginine is helpful in eNOS deficiency and is of benefit in intermittent claudication. A double-blind trial of mega-dose folate therapy for arteriosclerosis is needed. A very-low-fat/exercise program, arginine (about 8 gm daily), taurine (about 6 gm daily), carnitine, policosanol, Ginkgo biloba extract and Co-Q 10 may be beneficial in coronary and peripheral vascular disease.
CONCLUSION: Oster’s mega-dose folate therapy for atherogenesis may be right for a reason other than the one he described. He thought that the folate was suppressing xanthine oxidase enzyme. It may have been really inhibiting eNOS-mediated superoxide production.
NOTE: Read about high homocysteine levels as a biomarker for low vitamin B levels and low folic acid (folate) in neurodegenerative disease.
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