Results from animal studies have shown an elevation in platelet activation and hence greater risk of thrombosis as a result of feeding saturated fat. Platelet aggregation thresholds, however, decrease when total fat intake is decreased or when dairy and animal fats are partially replaced with vegetable oils rich in PUFA. These studies failed, however, to keep the intakes of SFA and total fat constant. More recent work has shown that, in fact, diets high in PUFA significantly increase platelet aggregation in animals, compared with MUFA-rich diets. The changes in fatty-acid composition may affect blood clotting because the increase in PUFA allows for oxidation of LDL. As previously mentioned, OxLDL is cyto-toxic, and this can cause endothelial damage leading to the activation of platelets, generation of factor VII, and hence thrombus formation. Increased dietary intakes of MUFA may also increase the rate of fibrinolysis by lowering levels of LDL cholesterol and reducing the susceptibility of LDL to oxidation, thereby affecting both PAI-1 secretion and apo(a) activity.
It must be noted that both atherosclerosis and thrombosis are triggered by inflammation, and evidence suggests that several hemostatic factors other than the glycoprotein fibrinogen not only have an important role in thrombotic events but are also recognized as potentially important CHD risk factors.
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