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The Three Primary Ways that Vitamin E Prevents Heart Attack and Stroke


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There is increasing evidence from well-designed studies that vitamin E helps prevent heart attacks and other cardiovascular diseases. Our present understanding suggests that vitamin E reduces risk of cardiovascular disease through 3 primary mechanisms: antioxidant effects, inhibition of the proliferation of smooth muscle, and reducing the stickiness of blood platelets.

Intercepts Free Radicals

As an antioxidant, vitamin E travels in the bloodstream bound to cholesterol (LDL). As part of this cholesterol complex, vitamin E serves to intercept free radicals, which may otherwise damage cholesterol and its related unsaturated fats. Cholesterol that gets damaged by free radicals is much more inclined to stick to the walls of the artery and cause narrowing, obstructing blood flow. Scientifically speaking, we would say that LDL cholesterol, modified by oxidation, creates a particle that is taken up with greater affinity by the macrophages incorporated into the areas of atheroma within the blood vessel wall. Regardless of how we state it, the point remains that vitamin E protects cholesterol from free radical damage resulting in a cholesterol particle that tends not to clog up arteries as easily.

Regulates Artery wall smooth muscle growth

Secondly, vitamin E regulates the rate at which smooth muscle, below the artery wall, will grow or proliferate. Narrowing of the arteries involves several events. As part of the progression of this process smooth muscle grows into the artery from above and below the artery wall. This event contributes to further narrowing of the blood vessel at the involved site. As the artery becomes more plugged up with smooth muscle fibers growing into the channel of the artery and damaged cholesterol accelerating the narrowing process, the risk of a heart attack or stroke is greatly increased. Vitamin E is important to prevent both of these events.

Reuduce Stickiness of blood platelets

The third protective action of vitamin E involves its ability to reduce the stickiness of blood platelets. Platelets are the blood cells that clump together and form a clot in the event you cut yourself. Their ability to form a clot when necessary prevents us from bleeding to death each time we nick ourselves with a sharp object or develop a nosebleed. Thus, platelets are supposed to clot under certain conditions.

However, several common lifestyle factors encourage platelets to be excessively sticky and to form abnormal clots or mini-plugs inside our arteries. Environmental factors such as obesity, high saturated fat diet, smoking and a sedentary lifestyle contribute to excessive platelet stickiness. The clumping together of platelets at the site of artery narrowing is frequently the final event that precedes a fatal or non-fatal heart attack or ischaemic stroke. The platelet plug completes the total obstruction to blood flow. Ideally, platelets should clump together to save your life, not to end it. Vitamin E functions to reduce platelet stickness, helping to discourage platelets from clumping together inside the artery wall. As a result, platelets are less inclined to contribute to blood flow obstruction even when other lifestyle factors are present that would otherwise encourage excessive platelet stickiness.

As demonstrated by a number of prominent researchers, to achieve blood levels of vitamin E necessary to materially reduce free radical attack of LDL-cholesterol, inhibit smooth muscle growth into the channel (lumen) of the artery and reduce platelet stickiness, vitamin E must be provided at doses obtainable only through supplementation.

From the available data, it appears that at least 100 I.U. of vitamin E per day is necessary to obtain a cardio-protective effect. Levels of up to 400 I.U. or more  may be even more desirable.

 

 

References:

1. Stamfer M.J., Rimm E.B., Epidemiologic evidence for vitamin E in prevention of cardiovascular disease. 1995. Am J Clin. Nut. 62 (suppl); 1365s-1369s.

2. Steinberg D. Antioxidants and artherosclerosis. A current assessment. Circulation 1991;84:1420-5 (editorial).

3. Puurunen M, Manttari M, Mannienen V, et al. Antibody against oxidized low-density lipoprotein predicting myocardial infraction. Arch Intern Med 1994; 154:2605-9.

4. Princen HMG, von Poppel G, Vogelezang C, Buytenhek R, Kok FJ. Supplementation with Vitamin E but not b-carotene in vivo protects low density lipoprotein from lipid peroxidation in vitro: effect of cigarette smoking. Arterioscler Thromb 1992;12:554-62.

5. Boscoboinik D, Szewczyk A, Hensey C, Azzi A. Inhibition of cell proliferation by a-tocopherol: role of protein kinase C. J Biol Chem 91;266;6188-94.

6. Steiner M, Glantz M, Lekos A. Randomized, double-blind study of vitamin D plus aspirin compared with aspirin alone for the prevention of recurrent strokes and transient ischemic attacks. Am J Clin Nutr 1995;62(suppl):1381S-4S.

7. Stampfer MJ, Rimm EB. A review of the epidemiology of dietary antioxidants and risk of coronary heart disease. Can J Cardiol 1993;9:14B-8B.

 

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