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(Circulation. 2002;105:893.)
© 2002 American Heart Association, Inc.

Current Perspective

Prevention of Coronary Heart Disease by Diet and Lifestyle

Evidence From Prospective Cross-Cultural, Cohort, and Intervention Studies

Daan Kromhout, PhD, MPH; Alessandro Menotti, MD, PhD; Hugo Kesteloot, MD, PhD; Susana Sans, MD, PhD

From the Division of Public Health Research (D.K.), National Institute of Public Health and the Environment, Bilthoven, the Netherlands; Association for Cardiac Research (A.M.), Rome, Italy; University of Leuven (H.K.), Department of Epidemiology, Faculty of Medicine, Leuven, Belgium; and Programa Cronicat (S.S.), Institute of Health Studies, Hospital de Sant Pau, Barcelona, Spain.

Correspondence to Daan Kromhout, Division of Public Health Research, National Institute of Public Health and the Environment, PO Box 1, 3720 BA Bilthoven, Anthony van Leeuwenhoeklaan 9, 3721 MA Bilthoven, The Netherlands. E-mail daan.kromhout@rivm.nl

Key Words: coronary disease • diet • lifestyle • prevention

	Introduction

 
Research on the cause of coronary heart disease has been ongoing for approximately a century.¹ From the beginning, diet played a prominent role in research on the origin of coronary heart disease. The original diet-heart hypothesis was very simple. Cholesterol is a constituent of the atherosclerotic plaque. Therefore, it was thought that there was a direct relation between cholesterol in the diet (ie, eggs), cholesterol in the blood, cholesterol in the plaque, and its clinical complications, such as myocardial infarction.

In the second part of the past century, it became clear that dietary cholesterol played a minor role in regulating serum cholesterol levels. It was also shown that dietary fatty acids are the major determinants of serum cholesterol.² The study of lipoprotein metabolism showed that the cholesterol-rich LDL fraction, not total cholesterol, was most strongly related to the development of atherosclerosis and its sequelae.³ Experimental research was essential to understand the mechanisms by which genes, hormones, and diet interact to regulate the serum cholesterol level.⁴ LDL cholesterol levels can be increased by saturated fatty acids, especially those with 12 to 16 carbon atoms, and by trans fatty acids.⁵

Several hypotheses have been proposed to explain the initiating events in atherogenesis, eg, the response-to-injury, response-to-retention, and oxidation hypotheses.^6–8 These hypotheses are not mutually exclusive and may even be compatible with each other. The oxidation hypothesis emphasizes the importance of oxidative modification in the atherosclerotic process, because compared with native LDL, oxidized LDL is preferentially taken up in the arterial wall.⁸ This . . . [Full Text of this Article]

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