Saturated fatty acids platelet aggregation

As indicated above, there are many possible oxidation products of the different polyenoic acids. It is probably naive to ascribe the effects of dietary intervention reported thus far to such metabolites. Carefully controlled clinical studies will be needed before these questions can be satisfactorily answered. However, subjects on diets containing highly saturated fatty acids clearly show increased platelet aggregation when compared with other study groups. Such diets (eg, in Finland and the USA) are associated with higher rates of myocardial infarction than are more polyunsaturated diets (eg, in Italy). 

Yamada N, Takita T, Wada M, Kannke Y, and Innami S. (1996). Effects of dietary n-3/n-6 and polyunsaturated fatty acid/saturated fatty acid ratios on platelet aggregation and lipid metiriwiism in rats. J. Nutri. Sci. Vitaminol. 42,423-434. 

Certain physiologic and dietary materials affect the platelet reactions. Catechol amines enhance platelet aggregation and promote thrombus formation. Fatty acids appear to enhance platelet aggregation, with saturated fatty acids being more effective than unsaturated fatty acids. Thrombosis is produced in the dog by single rapid infusion of long-chain saturated fatty acids but chronic slow infusions are nonthrombogenlc. Apparently the dog has sufficient thrombolytic power to handle the latter situation. 

Diets rich in saturated fatty acids have also been associated with a lower ratio of cholesterol to phospholipids in platelet membranes, which may affect receptor activity and platelet aggregation. Flowever, these mechanisms have been described from studies in vitro and on animals and have not adequately been confirmed in human studies. 

Saturated fatty acids as a group affect factors involved in cholesterol metabolism. Relative to the carbohydrate content of the diet, a decrease in saturated fat content induces a favorable decrease in serum total and LDL cholesterol concentrations but unfavorably reduces HDL cholesterol concentrations. Both increasing and decreasing effects of saturates on platelet aggregation have been observed, as well as the absence of effect, so results are inconsistent and difficult to interpret. Whether the beneficial effect of a diet low in saturated fat on the prethrombotic state of blood depends on the dietary fiber content is still unclear. 

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.

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