The control of coronary heart disease (CHD) depends primarily on its prevention at an early stage. It is generally agreed that this depends upon the elimination or treatment of the known risk factors for CHD. Among these, hyperlipidaemia occupies a central position. The diagnosis and treatment of this condition is the subject of this statement. Before initiating therapy for primary hyperlipidaemia the common causes of secondary yperlipidaemia are sought and dealt with, including diabetes, hypothyroidism, over-use of alcohol, renal and liver diseases and certain drugs. Next, an assessment of all risk factors for CHD is carried out, i.e. family history of CHD, smoking, hypertension, high density lipoprotein (HDL) cholesterol measurement, diabetes tnellitus and overweight. More intensive therapy is called for in patients with multiple risk factors than in those with lone hyperlipidaemia, and also after successful bypass operation or after coronary angioplasty. Evaluation of hyperlipidaemia in the patient's family is often appropriate. The diagnosis and follow-up of the hyperlipidaemic patient depend on reliable and well-controlled laboratory support. The primary hyperlipidaemias include several distinct diseases that are characterized by elevated serum levels of cholesterol andj or triglyceride with or without abnormally low levels of HDL cholesterol. From these measurements, low-density lipoprotein (LDL) cholesterol levels are calculated [except when triglyceride levels are > 500 mg dl−1 (5·6 mmol l−1)]. Elevated LDL levels are causally important in atherosclerosis, and occur in three disorders: familial hypercholesterolaemia, familial combined hyperlipidaemia and common hypercholesterolaemia. The finding of elevated serum triglyceride without marked hypercholesterolaemia may occur in familial h vpertriglyceridaemia and sometimes in familial combined hyperlipidaemia. Elevation of serum cholesterol and triglyceride can have several genetic bases, including remnant (type III) hyperlipidaemia and familial combined hyperlipidaemia. The characteristic feature of remnant (type III) hyperlipidaemia (demonstrated by ultracentrifugation in a specialized laboratory) is the presence of cholesterol and triglyceride-rich very low density lipoproteins (VLDL), whereas combined (mixed) hyperlipidaemia is diagnosed when both VLDL (of normal composition) and LDL levels are elevated. In vestigation of other family members is necessary to make the diagnosis of familial combined hyperlipidaemia. It depends on the identification of different lipoprotein profiles in affected members of the same family. In two rare disorders, the chylomicronaemia syndrome and severe primary familial hypertriglyceridaemia, gross elevation of triglyceride is found to levels above 1000 mg dl−1(II mmol l−1). Such patients are at risk of pancreatitis and should be promptly and effectively treated. Therapy of hyperlipidaemia always starts with dietary counselling. The general principles of the lipid-lowering diet are: (I) weight reduction in overweight subjects [body mass index (weight/height2) > 27]; (2) a lipid-lowering diet providing 55% of calories from carbohydrates, 10–15% from protein andup to 30% from fat comprising 10% each of saturated, monounsaturated and polyunsaturated fatty acids, cholesterol −1 and 35 g day−1 of fibre derived largely from legumes and other vegetables, and fruit. Further reduction of fat consumption to 20–25% of total energy and of cholesterol to −1 (3·5 mmol l−1) is the aim in hypercholesterolaemic patients with multiple or severe risk factors and of 155 mg dl−1 (4 mmol l−1) in the absence of other risk factors. Some patients with hyperlipidaemia do not respond adequately to diet and correction of underlying causes; drug treatment is then additionally required, but careful attention to diet is continued. Five treatment groups are defined: Group A consists of subjects with mild hypercholesterolaemia [serum cholesterol 200–250 mg dl−1 (5·2–6·5 mmol l−1), serum triglyceride < 200 mg dl−1 (2·3 mmol l−1) J. Diet alone is effective and drug therapy is rarely necessary. Group B subjects have serum cholesterol levels in the range 250–300 mg dl−1 (6·5–7·8 mmol l−1). If the response to a thorough trial of diet is not satisfactory, drug therapy should be considered, e.g. bile acid sequestrants at low dosage. Group C comprises subjects with hypertriglyceridaemia [serum cholesterol < 200 mg dl−1 (5·2 mmol l−1), plasma triglyceride 200–500mg dl−1 (2·3–5·6mmol l−1)]. Many of these patients also have low HDL-cholesterol levels. Management is primarily by control of underlying causes, particularly overweight and excessive intake of alcohol. A lipid-lowering diet is prescribed. Drug therapy is usually withheld, but may be considered when persisting high triglyceride levels are due to familial combined hyperlipidaemia or other high-risk subgroups. Group D consists of patients with elevated serum levels of both cholesterol and triglyceride [serum cholesterol 200–300 mg dl−1 (5·2–7·8 mmol l−1) and serum triglyceride 200–500 mg dl−1 (2·3–5·6 mmol l−1)]. Such patients may have familial combined hyperlipidaemia, the diagnosis of which depends on a family study (see text). Although the lipid elevation is often mild, this disorder is associated with increased risk of CHD. Management is by control of underlying causes, weight reduction, if necessary, and a lipid-lowering diet. Drug treatment together with controlled diet is necessary in a minority of patients. A drug combination is sometimes necessary. Group E includes patients with severe hyperlipidaemia [serum cholesterolabove 300 mg dl−1 (7·8 mmol l−1) and/or serum triglyceride greater than 500 mg dl−1 (5·6 mmol l−1)]. Patients with serum cholesterol levels > 300 mg dl−1 (7·8 mmol l−1) and with normal triglyceride commonly have familial hypercholesterolaemia and are at especially high risk of CHD. Therapy usually comprises diet and one or two drugs, e.g. bile acid sequestrants often together with a fibrate, or cholesterol synthesis inhibitor, or nicotinic acid. For the chylomicronaemia syndrome there is no satisfactory drug therapy, and it is managed by a low fat diet.