Background The oxidative modification of low-density lipoproteinsincreases their incorporation into the arterial intima, an essentialstep in atherogenesis. Although dietary antioxidants, such asvitamin C, carotene, and vitamin E, have been hypothesized toprevent coronary heart disease, prospective epidemiologic dataare sparse.
Methods In 1986, 39,910 U.S. male health professionals 40 to75 years of age who were free of diagnosed coronary heart disease,diabetes, and hypercholesterolemia completed detailed dietaryquestionnaires that assessed their usual intake of vitamin C,carotene, and vitamin E in addition to other nutrients. Duringfour years of follow-up, we documented 667 cases of coronarydisease.
Results After controlling for age and several coronary riskfactors, we observed a lower risk of coronary disease amongmen with higher intakes of vitamin E (P for trend = 0.003).For men consuming more than 60 IU per day of vitamin E, themultivariate relative risk was 0.64 (95 percent confidence interval,0.49 to 0.83) as compared with those consuming less than 7.5IU per day. As compared with men who did not take vitamin Esupplements, men who took at least 100 IU per day for at leasttwo years had a multivariate relative risk of coronary diseaseof 0.63 (95 percent confidence interval, 0.47 to 0.84). Caroteneintake was not associated with a lower risk of coronary diseaseamong those who had never smoked, but it was inversely associatedwith the risk among current smokers (relative risk, 0.30; 95percent confidence interval, 0.11 to 0.82) and former smokers(relative risk, 0.60; 95 percent confidence interval, 0.38 to0.94). In contrast, a high intake of vitamin C was not associatedwith a lower risk of coronary disease.
Conclusions These data do not prove a causal relation, but theyprovide evidence of an association between a high intake ofvitamin E and a lower risk of coronary heart disease in men.Public policy recommendations with regard to the use of vitaminE supplements should await the results of additional studies.
Antioxidants such as vitamin C, carotenoids, and vitamin E1,2are hypothesized to help prevent atherosclerosis by blockingthe oxidative modification of low-density lipoprotein (LDL),which may be selectively incorporated by monocytes in the arterialwall3,4. Oxidized LDL may also contribute to atherogenicityby reducing macrophage motility in the intima,5 increasing monocyteaccumulation,6 and increasing cytotoxicity7.
Accumulating laboratory data support a link between dietaryantioxidants and a reduced risk of atherosclerosis, but epidemiologicevidence is limited8,9,10. We therefore examined these relationsin men enrolled in the Health Professionals Follow-up Study.
Methods
The Health Professionals Follow-up Study is a prospective investigationof 51,529 male health professionals who were 40 to 75 yearsof age in 1986. The study population included 29,683 dentists,10,098 veterinarians, 4185 pharmacists, 3745 optometrists, 2218osteopathic physicians, and 1600 podiatrists. The study beganin 1986, when the participants completed a detailed questionnaireon diet and medical history. We mailed follow-up questionnairesin 1988 and 1990 to update information on exposure and to ascertainevents related to newly diagnosed coronary disease11,12.
We used a priori criteria to exclude from the study 1530 menwhose reported daily energy intake was outside the range of800 to 4200 kcal or who left blank 70 or more questions aboutfood on the dietary questionnaire. Because men with cardiovasculardisease or related conditions may alter their dietary patternsafter diagnosis, we excluded a further 10,089 men who reportedmyocardial infarction, angina, stroke, coronary-artery bypassgrafting or angioplasty, diabetes, or hypercholesterolemia onthe base-line 1986 questionnaire. The 39,910 remaining men wereeligible for follow-up.
After repeated mailings, we received questionnaires from orconfirmed the deaths of over 96 percent of eligible participantsin 1988 and 199013. The remaining nonresponding participantswere assumed to be alive if they were not listed in the NationalDeath Index.
Dietary Assessment
The 1986 dietary questionnaire inquired about the average frequencyof intake of 131 foods over the previous year. Ten additionalitems specifically addressed the current use of vitamin supplements,including the type, dose, and duration. Although we have noinformation on the specific forms of vitamin E supplements (naturalvs. synthetic), we did ask the participants to identify specificbrands of multivitamins, cooking oils, and cold cereals. Nutrientintakes were computed by multiplying the frequency with whicheach food item or supplement was consumed by its nutrient content,derived primarily from information from the Department of Agriculture,14for the portion size or dose listed15,16,17. We calculated nutrientscores for both dietary and supplementary intake, except inthe case of carotene, for which only the total intake was calculated,because only 2.2 percent of the men reported taking carotenesupplements. Carotene intake was calculated on the basis ofthe values for vitamin A in vegetables and fruits and the onethird of vitamin A from dairy products that is in the form ofcarotene14. We assigned a value of 10,000 IU for men who reportedtaking carotene supplements.
We assessed the validity of the food-frequency questionnairein a random sample of 127 men living in the Boston area. Wecompared nutrient intake as specified on the questionnaire withtwo one-week diet records spaced approximately six months apart16,17,18.Pearson correlation coefficients between the diet records andthe dietary questionnaire were adjusted for total energy intake19and for within-person variability in reported daily intake20.The adjusted correlation coefficients were 0.64 for carotene,0.92 for total vitamin C, and 0.92 for total vitamin E. Formen not taking supplements, the coefficients were lower: 0.77for vitamin C and 0.42 for vitamin E16.
Case Ascertainment
Fatal coronary disease, nonfatal myocardial infarction, coronary-arterybypass grafting, and percutaneous transluminal coronary angioplastyoccurring between 1986 and January 31, 1990, were consideredas end points. Participants who reported an incident myocardialinfarction on the 1988 or the 1990 questionnaire were sent aletter asking them to confirm the report and requesting permissionto review the medical records. Myocardial infarctions were confirmedwith use of the criteria of the World Health Organization21:compatible symptoms plus either typical electrocardiographicchanges or elevation of cardiac enzymes. We classified 3 percentof the fatal and 18 percent of the nonfatal myocardial infarctionsas "probable" because the medical records were unobtainablealthough the diagnosis was corroborated by supplementary information.Reports of bypass grafting or angioplasty were confirmed bymedical records for 98 of 102 participants (96 percent). Therefore,participants' own reports of these end points were consideredsufficient for confirmation.
Deaths were reported by next of kin, coworkers, postal authorities,or the National Death Index. Fatal infarctions were confirmedfrom medical records or autopsy reports. Fatal coronary diseasewas also considered confirmed if it was listed as the underlyingcause on the death certificate, and a diagnosis of incidentcoronary disease (after January 1, 1986) was confirmed on thebasis of records or interviews. The listing of a cause of deathon the death certificate was not accepted in itself as confirmingfatal coronary disease. Sudden death was defined as death withinone hour of the onset of symptoms in men who had no previousserious illness or plausible cause of death other than coronarydisease. Because in men sudden death is generally attributableto coronary disease, we included such deaths (for 33 men) asindicative of fatal coronary disease. When subjects had multipleend points, only the first was included in the analysis. Thephysicians reviewing the medical records were unaware of thereports of dietary intake.
Statistical Analysis
Each participant's follow-up time began with the date of returnof the 1986 questionnaire and continued until the diagnosisof an end point, death, or January 31, 1990, whichever camefirst. Relative risks were calculated by dividing the incidencerate of coronary disease among the men in each category of antioxidantintake by the rate for the men in the lowest category. Adjustedrelative risks for age (in five-year categories) were derivedby the Mantel-Haenszel method22. The Mantel extension test23was used to test for linear trends. To adjust for other riskfactors, we used multiple logistic regression to generate oddsratios as an estimate of relative risk. In multivariate logisticmodels, we tested for significant monotonic trends by assigningeach participant the median value for the category and modelingthis value as a continuous variable. All P values are two-sided.
Results
During 139,883 person-years of follow-up, we documented 667coronary end points: 360 bypass grafts or angioplasties, 201nonfatal myocardial infarctions, and 106 fatal coronary events.
The age-adjusted and multivariate relative risks of coronarydisease according to quintile group for the intake of vitaminE, carotene, and vitamin C (including supplements) are shownin Table 1. As compared with the men in the lowest quintilegroup for vitamin E intake, the men in the highest quintilegroup had an age-adjusted relative risk of coronary diseaseof 0.59 (95 percent confidence interval, 0.47 to 0.75; P fortrend = 0.001). The relative risks were similar after multivariateadjustment. For a high intake of carotene, the age-adjustedrelative risk of coronary disease was 0.71 (95 percent confidenceinterval, 0.55 to 0.92; P for trend = 0.02). The relative risksfor carotene were also not materially altered by multivariateadjustment. A high intake of vitamin C was initially suggestiveof a slight inverse association (age-adjusted relative risk,0.83; 95 percent confidence interval, 0.64 to 1.08) (Table 1).After further adjustment for risk factors and the use of otherantioxidants, however, the relative risk was 1.25 (95 percentconfidence interval, 0.91 to 1.71; P for trend = 0.98).
Table 1. Relative Risk of Coronary Heart Disease, According to Quintile Group for Carotene, Vitamin C, and Vitamin E Intake among 39,910 Male Health Professionals.
All the participants in the two highest quintile groups forvitamin E intake used multivitamins or specific vitamin E supplements.We suspected that these men might differ substantially fromthose who did not take supplements, and we therefore examinedthe distribution of risk factors according to quintile groupfor total vitamin E consumption (Table 2). The prevalence ofhypertension and the percentage of calories derived from fatwere similar. Differences in the intake of dietary fiber, cholesterol,and total fat were generally proportional to absolute differencesin caloric intake and were not due to differences in dietarycomposition. However, because patterns of smoking, fiber intake,aspirin use, and physical activity were different, we controlledfor these variables in all the multivariate analyses.
Table 2. Base-Line Characteristics, According to Quintile Group for Total Vitamin E Intake, among 39,910 Men Free of Heart Disease, Diabetes, and Hypercholesterolemia in 1986.
When the 5804 men with base-line hypercholesterolemia or diabeteswere included, the results were not appreciably different fromthose in Table 1. Also, there were no material differences betweenthe specific diagnostic categories. For fatal coronary diseaseor nonfatal myocardial infarction, the multivariate relativerisk between the highest and lowest quintile groups for vitaminE intake was 0.63 (95 percent confidence interval, 0.45 to 0.89),and for bypass grafting or angioplasty the relative risk was0.68 (95 percent confidence interval, 0.48 to 0.97). The correspondingresults for carotene and vitamin C were also similar to theresults in Table 1. Excluding probable cases of myocardial infarctiondid not alter these results appreciably.
To assess further the role of vitamin E supplements, we dividedtotal intake into dietary and supplemental sources. Quintilesof dietary vitamin E intake were calculated on the basis ofdietary intake without supplements, whereas the dose categoriesfor supplemental vitamin E were those specified in the base-linequestionnaire (Table 3). The two lowest categories of supplementuse represent men who reported using multiple vitamins or usingvitamin E supplements infrequently. Among men taking any supplementalvitamin E, we found only a modest inverse association betweenthe dose and the risk of coronary disease (P for trend = 0.22).The maximal reduction in risk was seen among men consuming 100to 249 IU per day, with no further decrease at higher doses.We found a suggestion of an inverse association between dietaryvitamin E and the risk of coronary disease among men who didnot take vitamin supplements, with a relative risk of 0.79 (95percent confidence interval, 0.54 to 1.15) for the highest ascompared with the lowest quintile group (P for trend = 0.11)(Table 3). The variation in dietary vitamin E intake was muchlower than the variation in intake from supplements; the medianof the highest quintile group for dietary intake (12.9 IU perday) fell within the lowest category of supplemental intake.We also examined the association between the duration of vitaminuse and the risk of coronary disease (Table 4). Using the categoriesfor the duration of vitamin use that appeared on the base-linequestionnaire (0 to 1, 2 to 4, 5 to 9, and 10 or more years),we found a suggestion of an inverse trend between the durationof vitamin E use and the risk of coronary disease. Men reportinguse of vitamin E supplements for 10 or more years had a relativerisk of 0.65 (95 percent confidence interval, 0.46 to 0.92)as compared with nonusers.
Table 4. Relative Risk of Coronary Heart Disease, According to the Duration of Current Supplement Use among Participants in the Study.
The multivariate relative risk of coronary disease among mentaking specific vitamin E supplements (i.e., not multivitamins)was 0.75 (95 percent confidence interval, 0.61 to 0.93) as comparedwith nonusers. Among men who took vitamin E supplements in dosesof at least 100 IU per day for two or more years, the relativerisk was 0.63 (95 percent confidence interval, 0.47 to 0.84)as compared with nonusers after we controlled for multivitaminuse.
The relative risk of coronary disease in men taking 100 or moreIU per day of vitamin E for two or more years, as compared withnonusers of supplements, ranged from 0.57 to 0.67 in multivariateanalyses after we controlled separately for quintile groupsfor the intake (from dietary sources and supplements combined)of retinol; vitamins B, B, B, B, C, and D; and calcium, folate,niacin, iron, magnesium, and zinc. Whereas the relative risksassociated with vitamin E remained significant in each model,those comparing the highest with the lowest quintile groupsfor the other nutrients were not statistically significant.
The reduction in the risk of coronary disease associated withthe highest quintile group for total vitamin E intake was somewhatless among current smokers (relative risk, 0.67; 95 percentconfidence interval, 0.34 to 1.31) than among those who hadnever smoked (relative risk, 0.52; 95 percent confidence interval,0.34 to 0.78). The inverse association was not appreciably modifiedby age, family history of myocardial infarction, or dietaryintake of alcohol, carotene, vitamin C, polyunsaturated fat,total fat, magnesium, or iron.
In our analysis of overall mortality (in 578 men), the relativerisk was 0.78 (95 percent confidence interval, 0.60 to 1.01;P for trend = 0.06) when we compared the highest and lowestquintile groups for vitamin E intake. Mortality during the firstfour years of follow-up of a healthy population is skewed towarddeath from sudden causes, such as trauma, and diseases witha delayed time to death are underrepresented.
The association between dietary carotene and the risk of coronarydisease differed significantly according to base-line smokingstatus (Table 5). Among men who had never smoked, no associationwas observed. We did, however, find a significant inverse associationbetween carotene intake and coronary disease among current andformer smokers. Among current smokers, the relative risk was0.30 (95 percent confidence interval, 0.11 to 0.82) when thehighest and lowest quintile groups for intake were compared;among former smokers, the risk was 0.60 (95 percent confidenceinterval, 0.38 to 0.94). The reduction in risk among currentsmokers was significant even in the third quintile group fordietary carotene intake (whose intake was equivalent to halfa carrot per day).
Table 5. Multivariate Relative Risk of Coronary Heart Disease, According to Quintile Group for Dietary Carotene Intake and Smoking Status.
Discussion
These data are compatible with the hypothesis that an increasedintake of antioxidants, primarily as vitamin E, but also asdietary carotene in former and current smokers, is associatedwith a reduced risk of coronary disease. Although we cannotexclude the possibility that an unknown variable associatedwith high antioxidant intake is responsible for the reductionin coronary disease, the lack of a significant association ofcoronary disease with other micronutrients (e.g., vitamin C)consumed as either diet or supplements suggests a causal interpretation.
The high rate of follow-up reduced potential bias due to lossto follow-up, and because dietary information was collectedprospectively, we eliminated recall bias. To reduce the possibilityof bias associated with recent dietary changes related to disease,we excluded men with coronary disease, diabetes, or high cholesterollevels at base line. The finding that the apparent benefit ofvitamin E supplements was stronger with longer-term use is furtherevidence of a specific effect rather than simply self-selection.
Men with a higher intake of vitamin E have somewhat healthierrisk profiles (Table 2). After we controlled for this health-consciousbehavior (Table 1), however, a strong protective associationwith vitamin E intake persisted. Any remaining residual confoundingwould need to be large to explain the relative risk we observed.Serum lipids were not measured in the total cohort and couldpotentially be confounding variables. In a subsample of participants,16however, vitamin E intake was not correlated with either totalor high-density lipoprotein cholesterol (r = -0.02 for both).In studies of vitamin E supplementation, vitamin E did not alterblood lipid levels24,25. Hence, confounding according to lipidlevel is an unlikely explanation of our results. If uncontrolledconfounding explains the inverse association for vitamin E,we would expect a similar effect for vitamin C, which was similarlyassociated with a healthier lifestyle (data not shown). Afteradjustment for vitamin E, however, vitamin C was not associatedwith a reduction in coronary disease (Table 1), a result thatsupported a specific effect of vitamin E.
Our findings for vitamin E are consistent with geographic correlationsbetween serum vitamin E levels and coronary mortality rates8and reduced serum levels of alpha-tocopherol (the principalcomponent of vitamin E) in patients with angina26. Most notably,the associations we found for vitamin E supplements were remarkablysimilar to those found among women in the Nurses' Health Study27.Vitamin E appeared to reduce atherosclerosis in a small experimentin monkeys28 and to decrease the rate of restenosis among patientsafter angioplasty29. Little difference in vitamin E levels wasseen, however, between persons with and persons without myocardialinfarction when measurements were made in previously collectedand stored serum samples30,31,32. These studies may have failedto find differences in serum alpha-tocopherol levels for severalreasons: because few participants used supplements, becausea single measurement cannot distinguish between short- and long-termsupplement use, and because the degradation of alpha-tocopherolin stored samples4 reduces the overall variation. Alternatively,intracellular antioxidant levels may be more important thanserum levels in inhibiting the cell-mediated oxidation of LDL33.
In addition to the strong association with vitamin E supplements,we found a moderate reduction in the risk of coronary diseasewith increasing intake of nonsupplemental dietary vitamin E.The primary sources of dietary vitamin E are vegetable oilsand to a lesser extent seeds, cereal grains, and nuts. Althoughwe incorporated information on specific brands of margarinesand cooking oils into the dietary intake scores, the vitaminE content of foods is dependent on cooking, processing, andstorage34. Limited variability in dietary vitamin E intake anderror in measurement due to the instability of vitamin E mayhave obscured a stronger inverse association. In a subsampleof 121 men in our study, we found only a weak partial correlation(r = 0.11) between dietary vitamin E and serum alpha-tocopherollevels, which was greatly enhanced (r = 0.51) after the inclusionof vitamin E from supplements1. The lack of a strong associationbetween dietary vitamin E alone and coronary disease is consistentwith experimental evidence in which the resistance of LDL tooxidation35,36,37,38 is increased only by supplemental vitaminE intake at levels 10 to 100 times the standard recommendeddietary allowance39. Supplementation at this level has beenshown to be nontoxic over a moderate follow-up period40.
With regard to carotene, in a cohort of 1299 elderly Massachusettsresidents followed for 4.75 years, Gaziano et al. found a relativerisk of 0.55 (95 percent confidence interval, 0.34 to 0.87)for death from cardiovascular causes when the highest and thelowest quartile groups for intake were compared10. In a preliminaryreport from the ongoing Physicians' Health Study trial, menwith angina who were randomly assigned to receive beta carotenehad fewer subsequent cardiovascular events than those assignedto placebo41.
We and others have reported lower levels of plasma carotene(but not alpha-tocopherol)1,2,26,35,42 among smokers. The increasedoxidative stress brought on by smoking may increase the susceptibilityof lipids to oxidation43,44,45,46 and increase the demand forplasma antioxidants to quench oxygen free radicals.
Vitamin C preserves the endogenous antioxidants47 and quenchesoxidants in hydrophilic environments48. Much of the oxidationof LDL particles, however, occurs in the subendothelial space,a hydrophobic environment that favors a protective effect offat-soluble vitamins (vitamin E or carotene) over water-solublevitamins (vitamin C)49.
Cross-cultural data suggest that men in countries with higherrates of mortality from coronary causes have, on average, plasmavitamin C levels that border on being deficient8. Because themedian of the lowest quintile group for dietary vitamin C intakewas 78 mg per day in our study (recommended daily allowance,60 mg),39 we could not test this hypothesis.
In the follow-up of the cohort in the first National Healthand Nutrition Examination Survey,9 men reporting an intake of50 mg or more of vitamin C per day (including supplements) hada standardized mortality ratio of 0.58 for all cardiovasculardisease. However, vitamin C from diet alone was not appreciablyrelated to cardiovascular disease. Hence, the effect appearsto be explained by the use of vitamin supplements, and perhapsnot specifically those of vitamin C, because the authors didnot account for vitamin E use.
We found an inverse association between vitamin E intake andcoronary disease that was weak at best when only dietary sourceswere taken into account. At the higher levels of intake reachedwith supplementation, the association became significant. Wecannot rule out the possibility that confounding may partlyaccount for our results; a cause-and-effect relation cannotbe established from these observational data. However, thesefindings, together with similar findings in women,27 supportthe hypothesis that supplemental vitamin E may reduce the riskof coronary disease. Public policy recommendations about theuse of vitamin E supplements should await the results of additionalstudies.
Supported by research grants (HL 35464 and CA 55075) from theNational Institutes of Health.
We are indebted to the participants of the Health ProfessionalsFollow-up Study for their continued cooperation and participation;to Al Wing, Karen Corsano, Mira Koyfman, and Steve Stuart forcomputer assistance; and to Mary Johnson, Betsy Frost-Hawes,Kerry Pillsworth, Mitzi Wolff, Jan Vomacka, and Cindy Dyer fortheir assistance in the compilation of the data and the preparationof the manuscript.
Source Information
From the Departments of Epidemiology (E.B.R., M.J.S., A.A., G.A.C., W.C.W.) and Nutrition (A.A., W.C.W.), Harvard School of Public Health; and the Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital (M.J.S., E.G., G.A.C., W.C.W.) -- all in Boston.
Address reprint requests to Dr. Rimm at the Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115.
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Vitamin E and the Risk of Coronary Disease
O'Keefe J. H., Lavie C. J., Steiner M., Powell L. H., Black H. R., Sullivan J. L., Stampfer M. J., Rimm E. B., Willett W. C., Steinberg D.
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N Engl J Med 1993;
329:1424-1426, Nov 4, 1993.
Correspondence
Beta Carotene, Vitamin E, and Lung Cancer
Marantz P. R., Kritchevsky D., Goldstein M. R., Pryor W. A., Leo M. A., Lieber C. S., Ballmer P. E., Stahelin H. B., Heinonen O. P., Huttunen J. K., Albanes D., Taylor P. R., The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group , Hennekens C. H., Buring J. E., Peto R.
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N Engl J Med 1994;
331:611-614, Sep 1, 1994.
Correspondence
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