Prevention of coronary heart disease by diet and lifestyle - Evidence from prospective cross-cultural, cohort, and intervention studies

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? 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 walls This hypothesis makes a role of diet and lifestyle in atherogenesis likely, because LDL can be oxidized by smoking, for example, and oxidation can be prevented by dietary antioxidants, eg, vitamins and polyphenols. There is overwhelming evidence that smoking, alcohol, and physical activity are important determinants of coronary heart disease. Prospective cohort studies showed a strong, graded relationship between cigarette smoking and coronary heart disease.(9) A moderate alcohol intake of 1 or 2 drinks per day is associated with a 30% to 40% lower risk of coronary heart disease.(10) Prospective cohort studies have also shown that the relative risk of coronary heart disease for inactive subjects compared with active persons is approximate to2 times higher.(11) Complex interactions between diet, lifestyle, and lipoprotein metabolism determine the development of atherosclerosis and its complications. This article reviews the evidence from major prospective cross-cultural, cohort and intervention studies and focuses on the effects of a healthy diet and lifestyle on heart health. Recently, the results of large prospective cohort studies became available that show that a healthy diet and lifestyle, along with low levels of serum cholesterol and blood pressure and not smoking, are associated with a low risk. of coronary heart disease.(12,13) The implications of these studies for primary and secondary prevention of coronary heart disease will be discussed.