ABC of Nutrition-Reducing the risk of coronary heart disease
For some doctors in affluent countries the first question about prevention of coronary heart disease (CHD) nowadays is whether to write a prescription for one of the statins (simvastatin, pravastatin, fluvastatin, atorvastatin, etc) which inhibit an early step of cholesterol biosynthesis in the body. Tables are available to show whether the 5- or 10-year risk justifies the cost of long term statin medication, but the relation of diet and CHD is still of primary importance for the majority of people. What we eat is bound up with the aetiology of CHD. Many people do not know their current plasma cholesterol, many coronary deaths occur before medical help and most countries cannot afford these expensive drugs.
Coronary heart disease is the largest single cause of death in Britain and the disease that causes most premature deaths, but it is only one-seventh as common in industrial Japan and rare in the masses in most developing countries. Its incidence must be environmentally determined because immigrant groups soon take on the incidence rate of their new country and there have been large changes in mortality over time. Coronary heart disease was uncommon everywhere before 1925 and then increased steadily in Western countries until the 1970s, except for a dip during the Second World War. Age-standardised mortality rates from coronary heart disease in the United States of America and Australia started to decline from 1966 and have reduced by more than 70%. In Britain rates are higher in Scotland and Ireland than in England, and higher in the north of England than the south. They have been declining since 1979 and have fallen by about 25%. Most EU countries have shown similar recent modest reductions of coronary mortality, but in the countries of eastern Europe coronary mortalities have risen. They have, however, recently fallen in Poland and the Czech Republic.
Coronary heart disease is a multifactorial disease, but diet is probably the fundamental environmental factor. The pathological basis is atherosclerosis, which takes years to develop. Thrombosis superimposed on an atherosclerotic plaque, which takes hours, usually precipitates a clinical event. Then whether the patient dies suddenly, has a classic myocardial infarct, develops angina, or has asymptomatic electrocardiographic changes depends on the state of the myocardium. Each of these three processes is affected by somewhat different components in the diet.
The characteristic material that accumulates in atherosclerosis is cholesterol ester. This and other lipids in the plaque, such as yellow carotenoid pigments, come from the blood where they are carried on low density lipoprotein (LDL). In animals, including primates, atheroma can be produced by raising plasma cholesterol concentrations with high animal fat diets. Much of this cholesterol is present in modified macrophages that have the histological appearance of foam cells. Experimental pathology studies indicate that these cells only take up large amounts of LDL if it has been oxidised.2 This oxidation probably occurs within the artery wall.
People with genetically raised LDL-cholesterol (familial hypercholesterolaemia) tend to have premature coronary heart disease. This is accelerated even more in homozygotes who have plasma cholesterols four times normal and all develop clinical coronary heart disease before they are 20.
Thousands of papers have been written on diet and CHD. Since early in the century scientists have suggested links between a series of dietary components and CHD. Some of these were subsequently found to be unconnected or of little importance, for example sucrose, soft water, milk. The latest component to be associated is in the news, but this does not mean that the older components have been disproved—just that well-established facts are not newsworthy.