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Subscribe NowB-Vitamins and Heart Disease
James Meschino DC, MS, ROHP
In regards to the role of B-vitamins in the prevention of heart disease and stoke, in the mid to late 1960s several researchers first identified that high blood levels of homocysteine was associated with premature narrowing of arteries leading to heart attacks and related heart disease. Homocysteine is thought to increase the risk for heart disease through direct toxic effects to the cells that line our blood vessels. It increases the tendency for blood platelet cells to clump together in the bloodstream thus, obstructing blood flow. It also stimulates muscle fibers beneath the blood vessels to grow into the artery, further impairing the flow of blood. High blood levels of homocysteine is now considered to be a significant risk factor for stroke, heart attack, and reduced blood flow to fingers, toes and peripheral body parts.
Homocysteine is formed routinely by the cells of our body during the course of normal metabolism. Fortunately, our bodies can eliminate homocysteine by converting it into other important amino acids such as methionine, cystathionine, serine, and cysteine. However, in order to convert homocysteine into these desirable, non-toxic amino acids, our bodies require an adequate intake of the B vitamins – folic acid, B6 and B12. A number of recent studies have shown that individuals with high blood levels of homocysteine can reduce their levels by supplementing their diet with folic acid, vitamin B6 and/or vitamin B12.
Reporting in the Journal of the American Medical Association (Feb. 1988) E Rimm and fellow researcher. demonstrated that women who supplement their diet with a multiple vitamin had a 24% lower risk of non-fatal and fatal heart attacks.
During the 14-year follow-up they documented 658 incident cases of non-fatal heart attacks and 281 cases of fatal heart attacks among the 80,082 women from the Nurses’ Health Study. After controlling for well known risk factors for heart disease they showed that high intake levels of folic acid (696 mcg/day) was associated with a 31% lower risk for heart disease episodes, compared with lower folic acid intake levels (158 mcg./day). For vitamin B6 there was a 33% lower risk for heart disease episodes in subjects ingesting 4.6 mg/day compared with subjects ingesting 1.1 mg/day. For individuals with high intakes for both folic acid and vitamin B6, they experienced a 45% reduced risk for fatal and non-fatal heart attacks.
A major conclusion of this study suggests that intake of folic acid and vitamin B6 above the current recommended dietary allowance, may be required to prevent heart disease. This means that taking a multivitamin and mineral supplement each day with extra B-vitamin protection is associated with a significant reduction in risk of heart disease.
Findings from the Health Professional Follow-up Study among male health practitioners demonstrated that high folic acid intake was associated with a significant reduction in heart disease risk, as well. Thus, for both men and women high levels of folic acid intake are strongly linked to the prevention of heart disease.
In the Nurses’ Health Study each 100 mcg./day increase in folic acid was associated with a 5.8% lower risk of heart disease. It is estimated that 88-90% of the population has dietary intakes of folic acid below 400 mcg/day.
Presently, elevated blood levels of homocysteine is considered to be responsible for approximately 10% of all heart attacks each year in the United States.
The current recommended dietary allowance for folic acid is 180 mcg/day for non-pregnant women. The average dietary intake in the United States among women is approximately 225 mcg/day.
The overall evidence suggests that this level of intake is insufficient to minimize risk of neural tube defects (i.e. spina bifida), and possibly heart disease. As such, many experts are urging that the recommended dietary allowance (RDA) be reset to the earlier level of 400 mcg./day.
To obtain 400-700 mcg/day of folic acid is exceeding difficult to do without using a multiple vitamin supplement.
The potential for this one simple intervention (multivitamin and mineral supplement) to prevent life threatening problems is staggering when you weigh all the evidence.
B-Vitamins and CVD: References
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2. McCully KS. Vascular pathology of homocysteinemia; implications for pathogenesis of arteriosclerosis. Am J Pathol, 1969;56:111-128
3 Mudd SH, FinkelsteinJD, Irreverre F, Laster L. Homocysteinuria: an enzymatic defect. Science. 1964;143:1443-1445.
4. Brattstrom L, Israelsson B, Norrving B, et al. Impaired homocysteine metabolism in early-onset cerebral and peripheral occlusive arterial disease: effects of pyridoxine and folic acid treatment. Atherosclerosis. 1990;81:51-60
5. Morrison HI, Schaubel D, Desmeules M, Wigle DT. Serus folate and risk of fatal coronary heart disease. JAMA. 1996;275:1983-1896
6. Chasan-Taber L, Selhub J, Roseberg IH, et al. A prospective study of folate and vitamin B6 and risk of myocardial infarction in US physicians. J Coll Nutr. 1996;15:136-143
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10. Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Willett WC. Dietary folate, vitamin B6, and vitamin B12 intake and risk of CHD among a large population of men. Circulation. 1996;93:625. Abstract
11. Tsai JC, Perrella MA, Yoshizumi M, et al. Promotion of vascular smooth muscle cell growth by homocysteine: a link to atherosclerosis. Proc Natl Acad Sci USA. 1994;91:6369-6373
12. Stamler JS, Osborne JA, Jaraki O, et al. Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen. J Clin Invest. 1993;91:308-318
13. Tawakol A, Omland T, Gerhard M, Wu JT, Creager MA. Hyper homocysteinemia is associated with impaired endothelium-dependent vasodilation in humans. Circulation. 1997;95:1119-1121
14. Pancharuniti N, Lewis CA, Sauberlich HE, et al. Plasma homocysteine, folate, and vitamin B12 concentrations and risk for early-onset coronary artery disease. Am J Clin Nutr. 1994;59:940-948
15. Bendich A. Folic and prevention of neural tube birth defects: critical assessment of FDA proposals to increase folic acid intakes. J Nutr Educ. 1994; 26:294-299