Post-prandial lipaemia represents the state of absorption during which TG metabolic capacity is under challenge. Low TG metabolic capacity imparts the risk of development of atherosclerosis. TG-intolerance has been shown to be an independent risk factor for CAD and impaired TG metabolic capacity could underlie a common high risk lipoprotein constellation of low HDL cholesterol and small sized HDL and LDL. Magnitude and duration of post-prandial lipaemia determine how much cholesterol is diverted from LDL and HDL into TG-rich lipoproteins through which it causes atherosclerosis. Potential means of intervention are improvement of TG metabolic capacity by reducing obesity, prescription of aerobic exercise, reduction of oxidizability of post-prandial lipoproteins by antioxidants and TG-lowering drugs.