Postprandial lipids and lipoproteins have been associated with the presence of cardiovascular disease in a large number of case-control studies. Because the metabolic perturbations around the postprandial situation is a key driving force for cholesterol flux between lipoproteins and tissues, together with the augmented generation of potentially atherogenic cholesterol-rich remnant lipoproteins, several hypotheses have been formulated to link excessive lipoproteinaemic response to fat intake with cardiovascular disease. Recent information on the regulation of lipoprotein remnant formation and its relation to atherosclerosis will enable us to test a pertinent clinical question: is there a direct relationship between repeated elevations of postprandial lipoproteins and development of atherosclerosis?