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764 PA R T V / Health Promotion and Disease Prevention
studies suggested that consumption offoods high in -carotene world, efforts directed toward translating prevention and risk-re-
might reduce CHD risk, 46,163 the results of randomized trials in ducing strategies to the “real world” are absolutely essential.
men 164 and men and women 165 show no benefit of -carotene
supplementation on CHD risk. Similarly, evidence that vitamin C R EFERENCES
reduces CHD risk is weak or lacking. 46,166,167 Recently the
Women’s Antioxidant Cardiovascular Study examined the effects 1. Last, J. M. (1988). A dictionary of epidemiology (2nd ed.). New York: Ox-
ford University Press.
of ascorbic acid (500 mg per day) and -carotene (50 mg every 2. Kelsey, J. L., Thompson, W. D., & Evans, A. S. (1986). Methods in ob-
other day) (as well as vitamin E) on the combined outcome of MI, servational epidemiology. New York: Oxford University Press.
stroke, coronary revascularization, or CVD death among 8,171 3. Rothman, K. J. (1986). Modern epidemiology. Boston: Little, Brown.
female health professionals aged 40 years and older. 168 All partic- 4. Rosamond, W., et al. (2008). Heart disease and stroke statistics—2008
ipants had a history of CVD or at least three riskfactors for CVD; update: A report from the American Heart Association Statistics Com-
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the participants were followedfor a mean duration of 9.4 years. mittee and Stroke Statistics Subcommittee. Circulation, 117(4),
e25–e146.
Results showed no overall effect of ascorbic acid, or -carotene on 5. Sempos, C., Cooper, R., Kovar, M. G., et al. (1988). Divergence of the
the primary combined outcome, or on any of the individual sec- recent trends in coronary mortality for the four major race–sex groups in
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ondary outcomes which included MI, stroke, coronary revascu- the United States. American Journal of Public Health, 78, 1422–1427.
larization, or CVD death rate. 6. Pell, S., & Fayerweather, W. E. (1985). Trends in the incidence of my-
ocardial infarction and associated mortality and morbidity in a large em-
There is some evidence of cardiovascular benefit associated ployed population, 1957–1983. New England Journal of Medicine, 312,
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with vitamin E for women, 167,169,170 men 169 and in the elderly 1005–1011.
population. 171 Although a randomized trial of 50 mg of vitamin 7. Ford, E. S., Ajani, U. A., Croft, J. B., et al. (2007). Explaining the de-
E in male smokers found only a 4% reduction in major coronary crease in U.S. deaths from coronary disease, 1980–2000. New England
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Journal of Medicine, 356, 2388–2398.
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events, 172 a trial of patients with angiographically proven CHD, 8. Kannel, W. B., Doyle, J. T., Ostfeld, A. M., et al. (1984). Report of In-
supplementation with 400 to 800 IU of vitamin E resulted in a ter-Society Commission for Heart Disease Resources: Optimal resources
75% reduction in nonfatal MI compared withplacebo. 173 These for primary prevention of atherosclerotic diseases. Circulation, 70, 181A.
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trials imply that supplementation at high doses may yield CHD 9. Stangl, V., Bauman, G., & Stangl, K. (2002). Coronary atherogenic risk
factors in women. European Heart Journal, 23(22), 1738–1752.
protection. However, as mentioned above, in addition to investi- 10. Palaniappan, L., Wang, Y., & Fortmann, S. P. (2004). Coronary heart
gating the effect of ascorbic acid and -carotene in CVD pre- disease mortality for six ethnic groups in California, 1990–2000. Annals
vention, the Women’s Antioxidant Cardiovascular Study trial also of Epidemiology, 14(7), 499–506.
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examined the use of vitamin E (600 IU every other day) and 11. Mensah, G. A., Mokdad, A. H., Ford, E. S., et al. (2005). State of dis-
found no effect on primary or secondary outcomes (RR, 0.94; parities in cardiovascular health in the United States. Circulation,
111(10), 1233–1241.
95% CI, 0.85 to 1.04 [p 0.23]). 168 12. Burke, G. L., Savage, P. J., Sprafka, J. M., et al. (1991). Relation of risk
[
Thus, while some evidence exists for the possible benefit of an- factor levels in young adulthood to parental history of disease. The CAR-
tioxidant supplementation in the prevention of CVD, the concept DIA study. Circulation, 84, 1176–1187.
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has not been proved and the results are somewhat inconsistent. In 13. Jousilahti, P., Puska, P., Vartiainen, E., et al. (1996). Parental history of
a recent review of the literature regarding antioxidant vitamin sup- premature coronary heart disease: An independent risk factor of myocar-
dial infarction. Journal of Clinical Epidemiology, 49, 497–503.
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plementation in cardiovascular diseases, the authors concluded 14. Nyboe, J., Jensen, G., Appleyard, M., et al. (1989). Risk factors for acute
that “although scientific rationale and observational studies are myocardial infarction in Copenhagen: I. Hereditary, educational and so-
convincing, randomized primary and secondary intervention tri- cioeconomic factors. Copenhagen City Heart Study. European Heart
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als have failed to show any consistent benefit from the use of an- Journal, 10, 910–916.
tioxidant supplements on CVD.” 174 The United States Preventive 15. Roncaglioni, M. C., Santoro, L., D’Avanzo, B., et al. (1992). Role of
family history in patient with myocardial infarction: An Italian case-
Services Task Force states that the evidence is insufficient to rec- control study. GISSI-EFRIM investigators. Circulation, 85, 2065–2072.
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ommendfor or against the use of supplements of vitamins A, C, 16. Yusuf, S., Hawken, S., Ounpuu, S., et al. Effect of potentially modifiable
or E; multivitamins withfolic acid; or antioxidant combinations risk factors associated with myocardial infarction in 52 countries (the IN-
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for the prevention of cancer or cardiovascular disease. The The TERHEART study): Case-control study. The Lancet, 364(9438),
937–952.
United States Preventive Services Task Force also recommends 17. Friedlander, Y., Arbogast, P., Schwwartz, S. M., et al. (2001). Family his-
against the use of -carotene supplements, either alone or in com- tory as a risk factor for early onset myocardial infarction in young
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bination, for the prevention of cancer or cardiovascular disease. 175 women. Atherosclerosis, 156, 2101–2207.
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18. Marenberg, M. E., Risch, N., Berkman, L. F., et al. (1994). Genetic sus-
ceptibility to death from coronary heart disease in a study of twins. New
England Journal of Medicine, 330, 1041–1046.
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CONCLUSIONS 19. Centers for Disease Control and Prevention. Smoking and tobacco use.
Retrieved from http://www.cdc.gov/tobacco/data_statistics/tables/adult/
table_2.htm
Outstanding progress has been made in our understanding of 20. MMWR (2006, July 7). Cigarette use among high school students—United
CHD risk factors and their management. The evidence against cig- States 1991–2005, 55(26), 724–726. Retrieved from http://www.
cdc.gov/mmwr/preview/mmwrhtml/mm5526a2.htm#tab1
arette smoking, elevated serum cholesterol, and high blood pres- 21. Glantz, S. A., & Parmleyn, W. W. (1991). Passive smoking and heart dis-
sure is strong, and sustained campaigns are underway to prevent
ease: Epidemiology, physiology and biochemistry. Circulation, 83, 1–12.
and appropriately manage them. The importance of adequate 22. Jensen, G., Nyboe, J., Appleyard, M., et al. (1991). Risk factors for acute
physical activity and weight control is also acknowledged. Research myocardial infarction in Copenhagen: II. Smoking, alcohol intake, phys-
continues on other emerging risk factors. The focus of future re- ical activity, obesity, oral contraception, diabetes, lipids, and blood pres-
sure. European Heart Journal, 12, 298–308.
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search will be on clarifying the roleof these factors, particularly for 23. Slone, D., Shapiro, S., Rosenberg, L., et al. (1978). Relation of cigarette
women and ethnic minorities. In addition, as the rates of diabetes smoking to myocardial infarction in young women. New England Jour-
and obesity continue to rise in the United States and around the nal of Medicine, 298, 1273–1276.
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