Background Interest in the antioxidant vitamin E as a possibleprotective nutrient against coronary disease has intensifiedwith the recognition that oxidized low-density lipoprotein maybe involved in atherogenesis.
Methods In 1980, 87,245 female nurses 34 to 59 years of agewho were free of diagnosed cardiovascular disease and cancercompleted dietary questionnaires that assessed their consumptionof a wide range of nutrients, including vitamin E. During follow-upof up to eight years (679,485 person-years) that was 97 percentcomplete, we documented 552 cases of major coronary disease(437 nonfatal myocardial infarctions and 115 deaths due to coronarydisease).
Results As compared with women in the lowest fifth of the cohortwith respect to vitamin E intake, those in the top fifth hada relative risk of major coronary disease of 0.66 (95 percentconfidence interval, 0.50 to 0.87) after adjustment for ageand smoking. Further adjustment for a variety of other coronaryrisk factors and nutrients, including other antioxidants, hadlittle effect on the results. Most of the variability in intakeand reduction in risk was attributable to vitamin E consumedas supplements. Women who took vitamin E supplements for shortperiods had little apparent benefit, but those who took themfor more than two years had a relative risk of major coronarydisease of 0.59 (95 percent confidence interval, 0.38 to 0.91)after adjustment for age, smoking status, risk factors for coronarydisease, and use of other antioxidant nutrients (including multivitamins).
Conclusions Although these prospective data do not prove a cause-and-effectrelation, they suggest that among middle-aged women the useof vitamin E supplements is associated with a reduced risk ofcoronary heart disease. Randomized trials of vitamin E in theprimary and secondary prevention of coronary disease are beingconducted; public policy recommendations about the widespreaduse of vitamin E should await the results of these trials.
Rapidly growing evidence suggests that oxidation of low-densitylipoprotein (LDL) plays an important part in atherosclerosis.As Steinberg et al. have found,1,2,3 oxidized LDL is taken upmore readily than native LDL by macrophages to create foam cells.Also, oxidized LDL is chemotactic for circulating monocytes,4and it inhibits the motility of tissue macrophages5. It mayalso be cytotoxic to endothelial cells6 and may increase vasoconstrictionin arteries7. Oxidized LDL has been identified in atheroscleroticlesions,8,9,10 and elevated titers of circulating autoantibodiesto epitopes of oxidized LDL are found in patients with atherosclerosis11.Lipid peroxide concentrations have been found to be higher inpatients with atherosclerosis12. In addition, the susceptibilityof LDL to oxidation was correlated with the severity of atherosclerosis13.
Vitamin E is a potent lipid-soluble antioxidant carried in LDL14,15.It inhibits the proliferation of smooth-muscle cells in vitro,16and when added to plasma, it increases the resistance of LDLto oxidation17. LDL from volunteers given alpha-tocopherol supplementsshowed increased resistance to oxidation18. Several small trialsof vitamin E in peripheral vascular disease have been reported,but the results have been inconclusive19,20,21,22,23. We thereforestudied the association between vitamin E intake and the incidenceof major coronary disease events in the Nurses' Health Study.
Methods
The Nurses' Health Study began in 1976, when 121,700 femaleregistered nurses living in 11 states completed mailed questionnairescontaining items about lifestyle and medical history24,25. Everytwo years, follow-up questionnaires are sent to update the informationand identify newly diagnosed conditions.
Ascertainment of Diet and Use of Vitamin E Supplements
In 1980, a dietary questionnaire was included in the mailingthat listed 61 food items, each with a specified portion size.The women reported the average frequency with which they hadconsumed each item during the previous year. We computed theaverage daily intake of nutrients by multiplying the frequencyof consumption of each item by the nutrient content, and totalingthe nutrient intake for all the food items. The reproducibilityand validity of this questionnaire have been described elsewhere26,27,28,29,30,31,32,33,34,35,36.The correlation between vitamin E intake as assessed by thequestionnaire and plasma alpha-tocopherol levels was 0.34 (P= 0.006) in one study26 and 0.42 (P = 0.03) in another31. Becausethe correlation between two plasma levels measured eight weeksapart is about 0.6,36 a higher correlation between a singleplasma determination and dietary intake cannot be expected.
We assessed the dietary intake of the participants in 1980,but information on vitamin E intake and use of multivitaminsupplements was also collected on each subsequent biennial questionnaire.Participants reported whether they regularly used multivitaminsupplements, and if so, the exact type and brand. We also inquiredabout specific supplements, including vitamins A, C, and E andbeta carotene.
Study Population
A total of 98,462 nurses returned the 1980 diet questionnaire.We excluded women who left 10 or more items blank (4 percent),whose reported food scores were implausible (2.7 percent), andwho had a history of cancer (except nonmelanoma skin cancer),angina, myocardial infarction, stroke, or other cardiovasculardisease. A total of 87,245 women remained. All the exclusionswere made before the analysis of the data.
Follow-up questionnaires were mailed to the participants in1982, 1984, 1986, and 1988. Women who reported diagnoses ofcardiovascular diseases were asked for permission to examinetheir medical records. We included women with cardiovascularconditions that occurred after the return of the 1980 questionnairebut before June 1, 1988. For each woman, only the first eventwas considered. On the basis of the responses to the questionnaire,follow-up for nonfatal outcomes was 97.1 percent of the totalpossible person-years.
A myocardial infarction was considered confirmed if it met theWorld Health Organization criteria37 of symptoms and eithertypical electrocardiographic changes or elevated cardiac enzymes.Infarctions of indeterminate age were excluded. We designatedas probable infarctions those that were reported by the nurse,required hospitalization, and were corroborated by additionalinformation (in a letter or telephone interview), but for whichrecords were unobtainable.
Most deaths were reported by relatives or postal authorities.We searched the National Death Index for the names of nonrespondentsand estimate that over 98 percent of deaths were identified38.When death from cardiovascular disease was suspected, we requestedpermission to review the medical records. A death was designatedas due to coronary heart disease if it involved a confirmedfatal myocardial infarction or if the woman was known to havehad coronary heart disease and coronary disease was listed asthe underlying cause on the death certificate without another,more plausible cause. In no case did we rely solely on the listingof a cause on the death certificate as confirmation of deathfrom coronary disease. Since sudden death in women can oftenoccur without coronary disease, we excluded 26 cases of suddendeath -- i.e., death within one hour of the onset of symptomsin an apparently healthy woman without other evidence of coronarydisease.
Although the primary a priori end point was major coronary disease(defined as nonfatal myocardial infarction or death due to coronarydisease), we also assessed other cardiovascular events. We consideredas one category coronary-artery surgery (bypass or angioplasty),on the basis of reports by the women.
Strokes were confirmed by medical records and classified, accordingto the criteria of the National Survey of Stroke, as ischemicstrokes (embolic or thrombotic), subarachnoid hemorrhages, intracerebralhemorrhages, or strokes of unknown cause39. We included strokesthat required hospitalization and were corroborated by informationin a letter or interview, and fatal strokes that could be confirmedby medical records, other reliable information, or a death certificate.
Statistical Analysis
The primary analysis was based on incidence rates. For all women,person-months were allocated according to the exposure variableson the most recent questionnaire until death or an end pointwas reached, or until May 31, 1988. We used information on theintake of vitamin E in 1980 from dietary sources only. Heightand parental history of myocardial infarction were both ascertainedin 1976; all other exposures apart from diet, including theconsumption of multivitamins and vitamin E supplements, wereupdated on each follow-up questionnaire.
To avoid a spurious finding due to the influence of diseaseon the use of vitamin supplements, women with a diagnosis ofany cardiovascular disease or cancer (except nonmelanoma skincancer) were excluded from further analysis. Because diet wasnot updated after 1980, the analyses of dietary vitamin E intakewere based on women who did not have those diagnoses in 1980.In the analyses of the use of vitamin E supplements, for whichdata were updated biennially, women with new diagnoses of cardiovasculardisease or cancer were excluded at the beginning of each two-yearfollow-up period. Thus, at the start of each such period, thebase population included no women who reported these diagnoses.
For the analyses of total vitamin E intake, we divided the cohortaccording to quintiles based on intake, both with and withoutadjustment for total energy intake28. The relative risk wasdefined as the incidence in women in various categories of vitaminE intake (the number of end points divided by the person-timeof follow-up in that category) divided by the correspondingrate for the women in the lowest category of intake. For theanalyses of the use of vitamin E supplements, we compared usersof such supplements with nonusers. Relative risks with 95 percentconfidence intervals were adjusted for age in five-year categories,and tests for trend across fifths of the group were performed40.Stratified analyses that adjusted for age and one other variableat the same time were performed to assess possible effect modificationand confounding. To adjust simultaneously for multiple riskfactors, proportional-hazards models41 were employed with vitaminE supplements used as a time-dependent variable. All P valueswere two-tailed.
Results
During 679,485 person-years of follow-up from 1980 to 1988,552 cases of major coronary disease were documented: 437 nonfatalmyocardial infarctions (360 confirmed and 77 probable) and 115confirmed deaths from coronary disease. Because there were nomaterial differences in any analyses between fatal and nonfataloutcomes or in the results when the probable cases were excluded,these have been combined into a single category. Analyses withor without adjustment for total energy intake yielded very similarresults; for simplicity, therefore, only the unadjusted resultsare shown. We observed a pronounced and statistically significantreduction in the risk of major coronary disease among womenwith a high intake of vitamin E, as compared with those witha low intake (Table 1). After adjustment for age and smokingstatus, the relative risk for those in the highest fifth ofintake was 0.66 (95 percent confidence interval, 0.50 to 0.87),as compared with those in the lowest fifth. The apparent benefitwas attributable mainly to the use of vitamin E from supplements,because high levels of intake from dietary sources were notassociated with significant reductions in risk. Even the highestlevels of dietary intake of vitamin E were far lower, however,than the intake among supplement users. Analyses adjusting forage and smoking status (Table 1) showed even more clearly thatthe lower risk of coronary disease was associated primarilywith the intake of vitamin E from supplements rather than fromthe diet. Subsequent analyses therefore focused on vitamin Esupplementation.
Table 1. Age-Adjusted Relative Risks of Major Coronary Heart Disease, According to Quintile Group for Total Vitamin E Intake and Intake of Vitamin E from Dietary Sources.
The amount of vitamin E in multivitamins is typically 30 IUor less, whereas specific vitamin E supplements usually contain100 IU or more. After adjustment for age and smoking statusin separate stratified analyses, both vitamin E supplementsand multivitamins were associated with a lower risk of majorcoronary disease. The relative risk for women who took multivitaminswas 0.78 (95 percent confidence interval, 0.64 to 0.96), andfor those who took vitamin E supplements it was 0.57 (95 percentconfidence interval, 0.41 to 0.78), as compared with the riskin those who took neither.
The women who took multivitamins or vitamin E supplements differedsomewhat from those who took neither. Table 2 shows the age-standardizedpercentages and means for various known or suspected coronaryrisk factors, according to the use of multivitamins or vitaminE. Among women who took supplements there was a higher proportionof postmenopausal hormone users, vigorous exercisers, and nonsmokers.The magnitude of the overall differences was modest, however.For example, the 5.2 percent difference in hormone use betweenwomen who took both multivitamins and vitamin E supplementsand those who took neither would account for a risk reductionof just 2.5 percent24.
Table 2. Exposure to Various Risk Factors for Coronary Heart Disease, According to Type of Vitamin Use in 1984, after Standardization for Age.
Table 3 summarizes the multivariate models that controlled simultaneouslyfor risk factors including age, body-mass index, smoking status,alcohol intake, menopausal status, postmenopausal hormone use,vigorous activity, regular use of aspirin, hypertension, highcholesterol level, diabetes, total energy intake, use of vitaminE supplements, and use of multivitamin supplements. The relativerisk associated with the use of specific vitamin E supplementswas 0.63 (95 percent confidence interval, 0.45 to 0.88). Thosewho took multivitamins were also at lower risk, although thisassociation was not statistically significant.
Table 3. Relative Risks of Major Coronary Heart Disease, According to the Use of Multivitamin and Vitamin E Supplements, with Adjustment for Age and Coronary Risk Factors.
Because users of both vitamin E and multivitamin supplementshad a somewhat higher intake of other antioxidant nutrients,we repeated the multivariate analyses and controlled for theintake of carotene and vitamin C (including that consumed assupplements). This adjustment slightly attenuated the apparentbenefit of vitamin E, but the association remained statisticallysignificant with a relative risk of 0.69 (95 percent confidenceinterval, 0.49 to 0.97).
The best evidence for a mechanism by which vitamin E could reducecoronary disease is of a reduction in atherosclerosis. We thereforereasoned that the short-term use of vitamin E supplements wouldbe associated with little reduction in risk. Users of vitaminE for less than two years had no significant reductions in risk,with a relative risk of 0.86 (95 percent confidence interval,0.52 to 1.43). Use of vitamin E for two or more years, however,was associated with a decrease in risk of 41 percent (62 to9 percent) even after adjustment for the intake of other antioxidants.We found no significant trend toward lower risk for periodsof more than two years, but because of the small numbers oflong-term users, we had little statistical power to detect sucha trend if one were present. Users of vitamin E for 15 or moreyears had a relative risk of 0.59 (95 percent confidence interval,0.14 to 2.39).
When we adjusted for coronary risk factors and excluded womenwho used vitamin E supplements for less than two years, we foundthat a dose of less than 100 IU per day was associated withlittle or no apparent benefit, but the confidence intervalswere broad; the relative risk was 0.93 (95 percent confidenceinterval, 0.23 to 3.75). There was no suggestion of a trendtoward a greater decrease in risk with higher daily doses; therelative risks were 0.56 (95 percent confidence interval, 0.21to 1.51) for doses of 100 to 250 IU per day, 0.56 (95 percentconfidence interval, 0.33 to 0.96) for doses of 300 to 500 IUper day, and 0.58 (95 percent confidence interval, 0.24 to 1.42)for doses of 600 or more IU per day. The results in models thatomitted both the lowest dose and the shortest duration of vitaminE use are shown in Table 3.
To distinguish further the effect of vitamin E supplements fromthat of multivitamins, we compared the risk among women whoused only vitamin E supplements, women who used only multivitamins,women who used both, and women who used neither (the referencegroup). After omitting women who used vitamin E supplementsin low doses and for short periods and adjusting for the factorsshown in Table 3, we found a relative risk of 0.41 (95 percentconfidence interval, 0.18 to 0.93) for users of vitamin E supplementsonly, 0.87 (95 percent confidence interval, 0.69 to 1.09) forusers of multivitamins only, and 0.50 (95 percent confidenceinterval, 0.31 to 0.83) for users of both. In separate multivariateanalyses, the relative risk for specific vitamin E use amongthe multivitamin users was 0.58 (95 percent confidence interval,0.35 to 0.97); among nonusers of multivitamins, it was 0.46(95 percent confidence interval, 0.22 to 0.98).
We observed no marked differences between subgroups with respectto the association of vitamin E supplements with lower risk.Some investigators have suggested that antioxidants might bemore important among cigarette smokers, but we found similarreductions in risk among vitamin E users who smoked (relativerisk, 0.55; 95 percent confidence interval, 0.30 to 1.02) andthose who did not (relative risk, 0.52; 95 percent confidenceinterval, 0.29 to 0.90). Adjustment for the intake of saturated,monounsaturated, or polyunsaturated fat and analyses of differentcategories of fat intake had no material effect. Because thediagnosis of diabetes or high cholesterol level could alterdiet, we performed analyses in which women with those conditionswere excluded; we also performed analyses in which there wasno exclusion for prevalent disease at the base line of eachtwo-year follow-up period. The findings from these alternateanalyses were virtually the same as those for the whole cohort.
In further analyses, we explored the effect of vitamin E supplementationon other cardiovascular outcomes and overall mortality (Table 4).For none of the categories, including overall mortality,was the association as pronounced as for major coronary disease,which was a priori the main hypothesis. However, there weresuggestive trends for all the outcomes.
Table 4. Relative Risks for Cardiovascular Outcomes, According to the Use of Multivitamins and Vitamin E Supplements, after Adjustment for Age and Coronary Risk Factors.
Discussion
In this large prospective study, we observed a risk of majorcoronary disease among women who took vitamin E supplementsthat was about 40 percent lower than the risk in women who didnot take these supplements; this association changed littleafter adjustment for coronary risk factors and the intake ofother dietary antioxidants. The prospective study design eliminatedthe potential for biased recall of vitamin E use, and becausethe follow-up rate was high, it is unlikely that differentialfollow-up could have affected the results materially.
Information on vitamin use and other potential risk factorswas reported by the women, but we believe it to be reliable.Reports of various conditions have been validated by reviewof the medical records and by direct measurement27,42. Also,the risk factors reported by the women were strong predictorsof subsequent cardiovascular disease,24,43,44,45 and all theparticipants were registered nurses with a demonstrated interestin medical research.
Perhaps healthier women select themselves for vitamin supplementation.Nurses who took vitamin E had a somewhat better risk profilethan those who did not, but the differences were not striking.Adjustment for a wide range of risk factors had only a modesteffect on the estimates of relative risk (from 0.61 to 0.63)(Table 3), suggesting only minor confounding by the risk factorsmeasured. Some unmeasured factor might be a confounding variable,but it would have to be both highly associated with use of vitaminE supplements and a very strong risk factor to explain theseresults.
Although we cannot rule out such self-selection as an explanation,other lines of evidence also support a cause-and-effect relation.If self-selection were the entire explanation, one would expectto have observed a similar apparent benefit among short-termusers of vitamin E and users of other vitamin supplements, suchas multivitamins and vitamin C. In multivariate analyses (Table 3),a significant risk reduction was observed for vitamin E,but not for multivitamin supplements. Also, further analysisindicated a lower risk among the women who took vitamin E, butnot among those who took vitamin C, even in the highest quintile,which included only users of specific vitamin C supplements.We had insufficient statistical power to test adequately fora trend toward increased protection with longer use. The lackof a dose-response association is not surprising, because bloodlevels do not rise in a linear fashion with increasing dosesof vitamin E36. The modest trends toward reduced risk amongusers of multivitamins may possibly be explained by an effectof folate and vitamin B6 to reduce otherwise elevated levelsof homocyst(e)ine in a subgroup46.
As with postmenopausal estrogens,24 we did not observe the samemagnitude of effect of vitamin E on cardiovascular outcomesother than major coronary disease. Although the findings werenot statistically significant, there were trends toward a reductionin the risk of mortality from cardiovascular causes, ischemicstroke, coronary-artery surgery, and overall mortality.
A benefit of vitamin E in reducing the risk of major coronaryheart disease is plausible because of the substantial evidenceindicating the importance of oxidation of LDL in atherosclerosis1,2,3,47,48.No association was observed between plasma levels of vitaminE and resistance to LDL oxidation among nonusers of supplements,but vitamin E supplementation markedly increased the resistance18.This finding is consistent with our results in suggesting thatsupplementation at levels far higher than those achievable bydiet alone may be needed to reduce LDL oxidation. In a randomizedtrial in monkeys fed an atherogenic diet, animals given vitaminE supplements had less arterial stenosis than those given placebo,49but the study was small and the results somewhat inconsistent.
Epidemiologic data on this research question are sparse. Geyet al. observed that in regions of Europe with high rates ofcoronary disease, the mean plasma levels of vitamin E were lowerthan in other regions,50 but this association could also bedue to other differences. Although Salonen et al. found no associationbetween plasma levels of vitamin E and coronary disease,51 therewere few users of vitamin E supplements in the population. Ina case-control study of angina, Riemersma et al.52 observeda statistically significant relative risk of 0.37 when the highestand the lowest quintiles for plasma vitamin E intake were compared;no significant associations were seen for plasma levels of vitaminC or carotene. In a small, four-month randomized trial of vitaminE among patients undergoing angioplasty, restenosis was reducedby 25 percent in the treatment group, but the result was notstatistically significant21.
Rimm et al.53 have reported findings in men that were very similarto those we observed, using a similar prospective design. Asin our study, those findings could not be explained by confoundingby other coronary risk factors or dietary variables.
Although we cannot exclude the possibility of residual confounding,the consistency of our findings, the biologic plausibility,and the similar results from another prospective cohort53 allsupport the possibility of a causal explanation and suggestthat vitamin E supplements may reduce the risk of coronary heartdisease. Randomized trials of adequate size in secondary andprimary prevention will be needed to test this question3. Becausevitamin E appears not to be toxic, even in high doses,54 suchtrials, notably the Women's Health Study,55 have been initiated.Public policy recommendations about the widespread use of vitaminE should await the results of these trials.
Supported by research grants (HL 24074, HL 34594, CA 40935,and CA 40356) from the National Institutes of Health.
We are indebted to the participants in the Nurses' Health Studyfor their continuing outstanding level of cooperation; to FrankE. Speizer, M.D., overall principal investigator for the study;and to Mark Shneyder, Stefanie Bechtel, Gary Chase, Karen Corsano,Kate Saunders, Lisa Dunn, Barbara Egan, Lori Ward, and MarionMcPhee for their unfailing help.
Source Information
From the Channing Laboratory and the Division of Preventive Medicine, Department of Medicine (M.J.S., C.H.H., J.E.M., G.A.C., B.R., W.C.W.), Harvard Medical School and Brigham and Women's Hospital; and the Departments of Epidemiology (M.J.S., G.A.C., W.C.W.), Biostatistics (B.R.), and Nutrition (W.C.W.), Harvard School of Public Health -- all in Boston.
Address reprint requests to Dr. Stampfer at the Channing Laboratory, 180 Longwood Ave., Boston, MA 02115.
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