Morbidity and mortality through coronary atherosclerosis are higher in Type 2 diabetic patients than in nondiabetic subjects, roughly by a factor of 2 in males and 3 in females. Methodological problems in attempting to weigh the relative effects of each factor make it difficult to accurately interpret the numerous epidemiological data already available. Three issues are discussed here:--Do diabetics have more "classic" risk factors than nondiabetics? The incidence of hypertension, lipid disorders, and even smoking is practically consistently higher in diabetics, with "diabetic" lipid disorders (decreased HDL cholesterol and hypertriglyceridemia) topping the list.--Do diabetics have specific risk factors which could explain the observed increase in coronary morbidity and mortality? The answer would appear to be yes, as patent microalbuminuria--between 30 and 300 mg/24 hours--is found, as well as retinopathy and an increase in fibrinogen and PAI1 plasminogen activator inhibitor. Recent genetic studies have highlighted the role of Lp (a), and particularly that of angiotensin converting-enzyme gene polymorphism (DD allele).--What are the respective roles of hyperglycalmia and elevated levels of circulating insulin? In contrast to the importance of insulin in nondiabetics as demonstrated in longitudinal studies, insulin appears to play a marginal or even nil role in diabetics once the disease is established. It is probably glycaemia itself which remains the fundamental factor, even though the mechanisms leading from hyperglycemia to macrovascular complications remain unknown.