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Vitamin C Supplementation May Reduces Risk of Heart Attack and Stroke

James Meschino DC, MS, ROHP

Reporting in the February, 1988 edition of the American Journal of Clinical Nutrition, D. Harats and fellow researchers compared cardiovascular risk factors in subjects consuming 50 mg of vitamin C with those who were later assigned a vitamin C supplement of 500 mg per day for a two-month period.

In the subjects receiving the vitamin C supplement, blood levels of vitamin C rose from 13.5 micromoles per liter to 51.7 micromoles per liter.

Previously F. Gey demonstrated in the large MONICA study (a study involving 10 countries) that vitamin C blood levels above 50 micromoles per litre was associated with more than a 50% reduction in heart disease mortality rates. This reduction was experienced in contrast to populations where blood vitamin C levels averaged between 15-27 micromoles per litre.

In the MONICA study, low blood levels of vitamin C and vitamin E (vitamin E below the range of 25-30 micromoles per litre) were stronger predictors of future heart disease mortality than blood cholesterol levels, smoking or high blood pressure, which are known cardinal risk factors.

In a 20-year follow-up study, analysis of mortality in patients in the United Kingdom who were older than 65 years of age showed that low vitamin C status (either dietary intake or blood levels) was strongly associated with increased subsequent risk of death from stroke. A Swiss study uncovered an identical finding and was reported in 1993 in The Journal of Clinical Investigation by F.Gey, H. Stahelin and associates.

In the most recent study by D. Harats, the group receiving 500 mg of vitamin C not only attained more optimal blood levels of vitamin C, but also demonstrated other favorable indicators related to a decreased risk for cardiovascular disease.

The subjects ingesting 500 mg per day of vitamin C also showed decreased free radical damage to cholesterol in laboratory studies. When blood cholesterol becomes damaged by free radicals, it has a greater tendency to stick to the walls of the artery causing narrowing and blockage.

A number of prior studies have demonstrated that vitamin E protects blood cholesterol from free radical attack. It appears that vitamin C may share this important role as a water-soluble antioxidant circulating in the bloodstream. In fact, higher doses of vitamin C (500-1,000 mg) have been shown to actually lower blood cholesterol in high cholesterol patients receiving supplementation.

Currently about 50% of all deaths result from heart attacks, strokes and related vascular problems. It appears that vitamin C supplementation can play a significant role in the prevention of these problems in addition to its other widely known health benefits.

The recommended daily allowance for vitamin C is listed at 60 mg. This nominal amount of vitamin C is insufficient to raise blood levels into a more protective range, discouraging free radical damage to blood cholesterol and helping to lower the total amount of cholesterol in the bloodstream.

Unbelievably, 20-30% of U.S. adults fail to even attain 60 mg of vitamin C each day from their diet.

In my opinion, vitamin C is just too critical a nutrient to leave to chance. Even if your diet is good, most people will still only obtain 200-250 mg of vitamin C per day. For this reason, I continue to recommend 1,000 mg of vitamin C from supplementation for healthy adults.

It’s becoming more widely accepted that a number of vitamins work together to help maximize protection against heart disease and stroke. Those vitamins include vitamins E, C, B6, B12, B1, and folic acid.


Harats, D. et al. Citrus fruit supplementation reduces lipoprotein oxidation in young men ingesting a diet high in saturated fat: presumptive evidence for an interaction between vitamin C and E in vivo.Am J Clin Nutr. Feb 1998; 67:240-245

Gey, K.F. et al. Inverse correlation between plasma Vitamin E and mortality from ischemic heart disease in cross-cultural epidemiology. Am J Clin Nutr. 1991; 53 (suppl):326s-34s.

Frei, B. Ascorbic acid protects lipids in human plasma and low-density lipoprotein against oxidative damage. Am J Clin Nutr. 1991;54 (suppl):1113s-8s.

Knekt, P. et al. Antioxidant vitamin intake and coronary mortality in a longitudinal population study. Am J Epidemiol 1994;139:1180-9

Ginter, E. et al. The effect of ascorbic acid on cholesterolemia in healthy subjects with seasonal deficit of vitamin C. Nutr Metab 1970;12:76-86

Paolisso, G. et al. Metabolic benefits deriving from chronic vitamin C supplementation in aged non-insulin dependent diabetics. J Am Coll.Nutr.1995;14:387-92.

Non Pharmacological Prevention of Cardiovascular Disease
by Dr. James Meschino, D.C., M.S.
Coronary artery disease (C.A.D.) continues to be the leading cause of mortality and morbidity in the United States, where more than 500,000 people die of C.A.D. sequelae each year. Almost 70% of the adult population is affected with the disease to some extent. The annual cost of C.A.D. related health care and losses in productivity has been estimated to be greater than $50 billion. 1

Studies have proven beyond doubt, that certain behaviors (smoking, inactivity) and conditions (hypertension, diabetes, obesity, hyperlipidemia) increase the risk of coronary artery disease. In any case, the risk can be reduced dramatically with non-pharmacological methods, but if needed, effective medications are available. 2

In regards to reducing risk of C.A.D. with lifestyle Intervention, the Lipid Research Clinics Coronary Primary Prevention Trial 3 concluded that a 1% decrease in total serum cholesterol corresponded with a 2-3% decrease in risk of C.A.D. The Helsinki Heart Study yielded similar results.4,5 The recommended desirable level of total cholesterol is less than 200 mg/dL. 2 As well, the HDL cholesterol level is inversely related to the incidence of atherosclerosis. 6,7 This data is supported by the Framingham Heart Study, the Lipids Research Clinics Primary Prevention Trial, the Lipid Research Clinics Primary Prevention Trial, the Lipid Research Clinics Prevalence Mortality Follow-up Study, and the Multiple Risk Factor Intervention Trial 8

In concert with the National Cholesterol Education Program, every effort should be made to lower cholesterol levels by non-pharmacological means (diet, exercise, weight loss) before drug therapy is considered. The American Heart Association and the National Cholesterol Education Program have recommended a Step-Wise approach to diet therapy. 1

In most people, an average reduction in total cholesterol of 10% or more through diet can be expected. Other non-pharmacological measures to reduce coronary risk include those that increase HDL cholesterol levels, such as exercise, weight loss, cessation of smoking, etc. With respect to lifestyle changes, patient education and individual counseling with adequate follow-up achieve the best compliance.

Primary Prevention of coronary artery disease is the most cost-effective way of reducing coronary morbidity and mortality. 2

A practical approach to achieve this end is to maintain a total dietary fat intake at or below 25% of total calories, focus upon complex carbohydrates to attain 55-65% of calories, with emphasis on those carbohydrates that also contain cholesterol lowering soluble fiber (oats, beans, fruits, vegetables).

Clinical trials using 3½ oz of oatbran per day or ½ cup of beans per day have demonstrated a 15-25 per cent lowering of blood cholesterol in hyperlipidemic patients, under controlled conditions. 9

Recently, the Harvard Alumni Study and others have demonstrated that a threshold level of physical activity is significantly associated with a reduction in risk of C.A.D. 10, 11, 12, 13, 14, 15

Exercise has many beneficial effects, which have been postulated as mechanism for reducing C.A.D. risk. Exercise decreases platelet aggregation, myocardial oxygen demand, hypertension, obesity, and glucose intolerance, and it increases fibrinolytic activity, myocardial oxygen supply, threshold for ventricular ectopy, and the HDL cholesterol level. General guidelines for reducing cardiovascular risk suggest 30 to 60 minutes of exercise at least three days a week, with aerobic activity being the most beneficial. 16

Finally, a number of cross cultural, epidemiological and longitudinal studies have demonstrated a strong association between higher serum levels of antioxidants – beta carotene, vitamin C, and vitamin E and reduction in cardiovascular disease. 17, 18,19

A number of mechanisms are now in place to explain the protective effects that these nutrients offer with respect to C.A.D. risk. It appears that attaining more optimal levels of intake for these nutrients, than is the U.S. average, would be an additional preventative strategy in the fight against C.A.D.

In conclusion, hypercholesterolemia continues to be a problem in the U.S. with more than 55 per cent of the population having blood cholesterol in the undesirable range. (2) Over-consumption of saturated fat, cholesterol, and calories is the major factor underlying hypercholesterolemia and excess coronary artery disease in our society Modest dietary changes can have a significant impact on serum lipid levels in many patients. On average, a 10% to 15% decrease in cholesterol level is anticipated for those who adhere to dietary suggestions proposed in the report by the National Heart, Lung and Blood Institute. This decrease would reduce the estimated risk of coronary artery disease 20% to 30%. (20). It would seem an opportune time to act as the American Heart Association has estimated that C.A.D. statistics will increase another 17% over the next 2 decades if prevention strategies are not put in place. In addition to lowering saturated fat and cholesterol intake, synergistic preventive strategies would also include adequate soluble fiber from complex carbohydrates, optimal levels of activity and exercise, and serum antioxidants – beta-carotene, vitamin C and vitamin E.

A program that included education, daily implementation strategies and follow up re-enforcement would likely be the only effective way of facilitating these changes among the general population.

There is now unquestioned evidence that much of coronary artery disease is preventable or postponable. (21), (22). Prevention strategies are known to be effective, cost-efficient and without side effects.

Copyright Dr. James Meschino D.C., M.S.


  1. Carleton R A . Dwyer J., Finberg I, et al. Report of the Expert Panel on Population Strategies for Blood Cholesterol Reduction: A statement from the National Cholesterol Education Program, National Heart, Lung and Blood Institute, National Institutes of Health Circulation 1991; 83(6)2154-232.
  2. Kingsley C M, Gupta, S C. How to Reduce the Risk of Coronary Artery Disease. Post Graduate Medicine Vol. 91, No.4, March 1992:147-160.
  3. Lipid Research Clinics Program. The Lipid Research Clinics Coronary Primary Prevention Trial Results. II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA 1984; 251(3):365-74,
  4. Frick M H, Elo 0, Haapa K, et al. Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes In risk factors, and incidence of coronary heart disease. N Engl J Med 1983;317(20):1237-45.
  5. Manninen V, Elo M O, Frick N H, et al. Lipid alterations and decline in the Incidence of coronary heart disease in the Helsinki Heart study. JANA 1988;260(5): 641-51.

6.Gordon D J., Probstfield J L., Rubenstein C , et al. Coronary risk factors and exercise test performance in asymptomatic hypercholesterolemic men; application of proportional hazards analysis. AM J Epidemiol 1984;120(2):21-24

7.Gofman J W ., Yound W., Tandy R. Ischemic heart disease, atherosclerosis and longevity. Circulation 1966; 34(4): 679-97

8.Castelli , W P Garrison, R J Wilson, P W et al. Incidence of coronary heart disease and lipoprotein cholesterol levels: the Framingham study. JAMA 1986; 256(20) 2835-8.

  1. Anderson J W , Gustafson N J Hypocholesterolemic effect of oat and bean products. AM J Clinical Nutrition l988; 48: 749-53.
  2. Paffenbarger, R S, Hyde R T , Wing A L, Hsieh, C. Physical activity, all-cause mortality and longevity of college alumni. N EngI J Med 314:605-613, 1986.
  3. Pekkanen J, Marti B, Nissinen A, Tuomilehto J, Punsar S, Karvonen M J, Reduction of premature mortality by high physical activity: a 20 year follow-up of middle-aged Finnish men. Lancet 1:1473-1477, 1987.
  4. Powell, K E, Thompson P D, Caspersen C J, Kendrick J S. Physical activity and the incidence of coronary heart disease. Annu Rev Public Health 8:253-287, 1987.
  5. Quinn, T.J., Sprague H A, Van Huss W D, Olson H W. Caloric expenditure, life status, and disease in former male athletes and non-athletes Med Sci Sports Exerc 22:742-750, 1990,
  6. Tsevat J, Weinstein M C, Williams L W, Tosteson, A N A, Goldman, L. Expected gains in life expectancy from various coronary heart disease risk factor modifications. Circulation 83:1194-1201, 1991.
  7. 15. Rotevatn S, Akseln L A, Bjelke, E. Lifestyle and mortality among Norwegian man. Prev Med 18:433-443, 1989.
  8. Butler R N, Goldberg, L. Exercise and prevention of coronary heart disease. Prim Care 1989;16(1):99-114.
  9. Enstrom J E, Kanin, L E, Klein, M A, 1992. Vitamin C intake and mortality among a sample of the U.S. Population. Epidemiology 2:194-202.
  10. Gey, K F, Brubacher G B and Stehelin, H B, 1987. Plasma levels of anti-oxidant vitamins in relation to ischemic heart disease and cancer. American Journal of Clinical Nutrition 45:1368-1377.
  11. Salonen J T, et al. 1987. Serum fatty acids, apolipoproteins, selenium and vitamins in relation to ischemic heart disease and cancer. American Journal of Clinical Nutrition 45:1368-1377.
  12. Lavie, C J, et al. High-density lipoprotein cholesterol. Post Graduate Medicine vol. 87 (7): 36-51, May, 1990.
  13. Castelli, W P, Griffin G C, 1988. Cutting back on saturated fat and cholesterol. Post Graduate medicine vol. 84 (3): 44-56.
  14. Keys A, Seven Countries: a multivariate analysis of death and coronary artery disease.. Cambridge, MA; Harvard University Press, 1980.

Prevention of Heart Disease in Women: Folic Acid and Homocysteine
by Dr. James Meschino D.C., M.S.
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 recycle homecysteine 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) Rimm et al. 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 subjected 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.

Presently, elevated levels of homocysteine are 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.

Because of evidence that this level of intake may be insufficient to minimize risk of neural tube defects (i.e. spina bifida), and possibly heart disease, some experts are urging that the recommended dietary allowance (RDA) be reset to the earlier level of 400 mcg./day.

Findings from the Health Professional Follow-up Study among male practitioners demonstrated that high folic acid intake was associated with a significant reduction in heart disease risk. 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.

To obtain 400-700 mcg./day of folic acid is exceeding difficult to do without using a multiple vitamin supplement. Most multiple vitamin supplements contain at least 400 mcg. of folic acid. The emerging evidence continues to support the use of a daily multiple vitamin and mineral product in the prevention of heart disease, neural tube defects, certain cancers, and other conditions.

In my view, otherwise healthy adults should incorporate a well designed multiple vitamin and mineral product into their dietary intake over and above consuming a healthy diet. The potential for this one simple intervention to prevent life threatening problems is staggering when you weigh all the evidence.

Copyright 1998 Dr. James Meschino D.C., M.S.


  1. Rimm E.B. et al. Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA 1998;279;5:359-64
  2. McCull 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.

  1. 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
  2. Morrison HI, Schaubel D, Desmeules M, Wigle DT. Serus folate and risk of fatal coronary heart disease. JAMA. 1996;275:1983-1896
  3. 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
  4. Giovannucci E, Stampfer MJ, Colditz GA, et al. Folate, methionine, and alcohol intake and risk of colorectal adenoma J Natl Cancer Inst. 1993;85:875-884
  5. Selhub J, Jacques PF, Wilson PWF, Rush D, Roseberg IH. Vitamin status and intake as primary determinanats of homocysteinemia in an elderly population. JAMA, 1993;270:2693-2698
  6. Nygard O, Nordrehaug JE, Refsum H, Ueland PM, Farstad M, Vollset SE. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med. 1997;337:230-236
  7. 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
  8. 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
  9. 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
  10. 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
  11. 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
  12. 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

The Three Primary Ways that Vitamin E Prevents Heart Attack and Stroke
by Dr. James Meschino D.C., M.S.
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.

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.

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.

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.

Copyright 1998 Dr. James Meschino D.C., M.S.


  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.

Vitamin E and Cardiovascular Disease: The Human Studies and Trials
by Dr. James Meschino D.C., M.S.
The evidence that Vitamin E supplementation is an important means to prevent heart attack and other vascular problems continues to be reported in human studies.

In 1987 Gey et all published the results of a large cross-sectional survey in Europe. The researchers collected blood samples from healthy men who lived in areas with high heart disease mortality (Southwest Finland, North Karelia, and Scotland), medium mortality (Northern Ireland) and low mortality (Switzerland and Southern Italy). The average blood vitamin E levels were found to be significantly higher in regions with low heart disease mortality compared with vitamin E blood levels in regions with higher rates. In a subsequent, more detailed study of 16 European population samples in the Monica Study, Gey et al reported a remarkably strong relationship between, higher blood vitamin E levels and lower rates of heart disease mortality, even among the 12 populations with similar heart disease mortality rates.

In patients with angina, Riemersma et al, in a case-control study, found lower vitamin E levels in newly documented angina patients (105 patients) compared with normal subjects (382 control subjects). Individuals with the lowest 20% blood levels of vitamin E had a 2.7 times greater risk of developing angina.

Kok et al followed 10,532 people in a Dutch nested case-control study. After 9 years, 68 cardiovascular deaths were documented (mostly heart disease). In this study subjects with the lowest 20% of vitamin E blood levels had a 1.5 times greater risk of cardiovascular disease mortality.

A similar finding was reported by Street et al in the Washington County MD Study. Individuals with the lowest 20% blood levels of vitamin E had a 1.4 times greater risk of heart disease.

In a 14 year study of 5,133 Finnish men and women aged 30-69, Knekt found that individuals consuming the most vitamin E (top 1/3 intake level) had the lowest rates of heart disease.

In another Finnish study Salonen found that low vitamin E status (from diet) was associated with increased risk of heart attack only if vitamin C status was also low. Because vitamin C is required to regenerate vitamin E, this finding could explain the lack of protective effect of vitamin E reported in a few studies, which go against the body of evidence. Hence, future studies should consider both vitamin E and vitamin C status as vitamin C helps to maintain optimal function of vitamin E. With lower vitamin C status, vitamin E is used up faster and can not be recycled back to an effective antioxidant state to provide continual protection against heart disease.

In the largest study to date Stampfer et al reported results from the Nurses’ Health Study. In this prospective cohort study, dietary data were collected in 1980 from 87,245 US female nurses aged 34-59 years old, who were free from diagnosed cardiovascular disease and cancer at the beginning of the study. After 8 years of follow up the study showed that nurses who consumed vitamin E supplements (greater than/or equal to 100 I.U.) for at least 2 years had a 41% reduction in risk of heart disease compared with other nurses. As with other studies this finding held true even after factoring in other heart disease risk factors.

In this same study, the risk of ischemic stroke was also reduced 29% in nurses using vitamin E supplementation at or above 100 I.U. per day.

Very similar findings were seen in men in the Health Professionals Follow-up Study as reported by Rimm et al. This study followed 39,910 men aged 40-75 years old in 1986 who were free of prevalent cardiovascular disease, diabetes, or high cholesterol at the beginning of the study. Once again the men using vitamin E supplementation showed the greatest reduction in risk of heart disease (46% reduction in risk) compared with non supplement users. This fact remained unchanged after factoring in other known risk factors such as age, smoking, high blood pressure etc. The protective vitamin E supplementation dosage was found to be 100-350 I.U. per day in this study. As in the Nurses’ health Study vitamin E supplementation below 100 I.U. per day did not provide significant protection against heart disease. Hence, regular multiple vitamins, which contain vitamin E at does of 12 I.U. to 30 I.U. are an insufficient means of attaining protective vitamin E intake levels. An antioxidant-enriched multiple vitamin, or a separate vitamin E supplement are required to achieve 100 I.U. or more of vitamin E from supplementation sources.

In a most remarkable study, Hodis et al assessed the progression of coronary artery narrowing by using serial, quantitative coronary angiographic methods. He found that in 162 nonsmoking men aged 40-59 years old, men who took vitamin E supplements had a significant reduction in the narrowing of coronary arteries compared with non supplement users. The apparent benefit was once again limited to those taking greater than 100 I.U. of vitamins E per day. In this study subjects receiving cholesterol-lowering medication and who also took vitamin E supplements showed regression (reversal) in coronary artery narrowing. No other group demonstrated this finding. The ability to reverse heart disease by this form of combination therapy is indeed, a remarkable finding, which has important implications for society.

Other intervention trials using vitamin E supplementation have also been effective. In a study of patients with severe claudication from atherosclerosis (narrowed arteries) in peripheral vessels, the improvement in symptom-free walking distance in the vitamin E group (n=24) was twice as great as the results achieved in the placebo group (n=9).

DeMaio conducted a study in 100 patients who underwent coronary angioplasty. They were given either a placebo (n=48) or vitamin E at 1,200 I.U. (n=52) for 4 months after the procedure. Among those given the placebo, 50% had significant restenosis (narrowing), whereas only 35% of those in the vitamin E group had significant restenosis.

Similar findings were observed by DuBroff et al in 440 patients with coronary angioplasty. The restenosis rate was only 15% in the vitamin E users versus 31% in those taking no supplements and 32% in those taking vitamin C supplements.

An attractive feature of vitamin E is that it has little toxicity, making it a very safe supplement to take. The preceding human studies discussed in this review suggest that vitamin E supplementation (greater than 100 I.U. per day) may represent a simple and extremely effective way to significantly reduce the risk of the number one killer in our society (heart disease). The magnitude of this effect may be in the order of a 40% reduction in risk for heart attack and other cardiovascular problems related to atherosclerosis (narrowing of arteries).

Unless otherwise indicated my view is that healthy adults should consider ingesting 300 – 400 I.U. of natural vitamin E succinate each day as an important prevention strategy.

Copyright 1998 Dr.James Meschino D.C., M.S.

Stampfer MJ and Rimm EB Epidemiologic evidence for vitamin E in prevention of cardiovascular disease. AM J Clin Nutr 1995;62(suppl):1365S-9S.

Gey KF, Brubacher GB, Stahelin HB. Plasma levels of antioxidant vitamins in relation to ischemic heart disease and cancer. AM J Clin Nutr 1987;45(suppl):1368-77.

Gey KF, Moser UK, Jordan P, Stahelin HB, Eichholzer M, Ludin E. Increased risk of cardiovascular disease at sub-optimal plasma concentrations of essential antioxidants: an epidemiological update with special attention to carotene and vitamin C. Am J Clin Nutr 1993;57(suppl):787S-97S.

Riemersma RA, Wood DA, Macintyre CCA, Elton RA, Gey KF, Oliver MF. Risk of angina pectoris and plasma concentrations of vitamins A, C and E and carotene. Lancet 1991;337:1-5.

Kok FJ, de Bruijn AM, Vermeeren R, et al. Serum selenium, vitamin antioxidants, and cardiovascular mortality: a 9 y follow-up study in the Netherlands. AM J Clin Nutr 1987;45:462-8.

Street DA, Comstock GW, Salkeld RM, Schuep W, Klag M. Serum antioxidants and myocardial infarction: are low levels of carotenoids and a-tocopherol risk factors for myocardial infarction? Circulation 1990;90:1154-61.

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