No abstract

SUMMARY Coagulation and platelet aggregation induced by thrombin, ADP, adrenaline, and collagen were studied in three contrasted groups, each of 20 to 22 middle-aged male farmers. Serum lipids were similar in the three groups. In the west of Scotland group, however, platelet reactivity was significantly greater than in the east of Scotland. This was associated with a dietary intake, evaluated by three different techniques, higher in saturated fat but also lower in polyunsaturated fat and alcohol. Platelet function in the southern England group also correlated with dietary fats and in addition inversely with calcium intake. On an individual basis in the 63 farmers, all the platelet function tests were significantly correlated with the intake of saturated fat regulated by that of calcium and alcohol.The dietary effects on platelets appear to be mediated by the fatty acid composition of plasma lipids and of platelet phospholipids. In that fraction, the fatty acids 20:3w9, 22:3w9 and 20:4 were the most closely related to the platelet function tests. The trienoic acid 20:3w9, identified with essential fatty acid deficiency, was also correlated with the intake of saturated fat and calcium. In this study, platelet functions were more dependent upon the dietary factors associated with coronary heart disease such as saturated fats, calcium, and alcohol than upon serum lipids.

Although the intake of saturated facts still appears to be the environmental factor most closely assosiated with coronary heart disease (CHD), this does not necessarily mean that CHD is caused essentially or solely by blood lipids, as suggested by several investigators. It seems that blood platelets rather than (or at least in addition to) blood lipids might be the intermediate link between certain environmental factors (saturated fats, hard water) and CHD, through an effect on both thrombosis and atherosclerosis. Our recent studies in French and Scottish farmers, have shown that blood platelet function is more drastically affected by saturated fats than blood lipids. In those studies, platelet function was the only blood parameter correlated on an individual basis with the intake of saturated fat and inversely related to calcium intake. Calcium is probably the cation responsible for the protective effect of hard water against CHD in various countries. The results obtained also indicate that platelet function can be improved by increasing the intake of polyunsaturated fats at the expense of saturated fats. Finally, only platelet function was different from one region of France to another and from one region of Scotland to another; this difference could be related to the reported incidence of CHD in these various regions.

Results in animals and in man indicate that in many circumstances, lipemia is not closely related to the severity of atherosclerosis nor to the incidence of coronary heart disease (CHD) or the intake of saturated fats as observed in paired studies between farmers from Moselle and Var in France and from West and East Scotland. In rabbits, an increased response of platelets to thrombin occurs before any deposition of cholesterol, as a result of a saturated fat feeding. Under these conditions, the addition of alcohol to the drinking water decreases significantly both the platelet response to thrombin and the severity of atherosclerotic lesions without much affecting plasma cholesterol. In farmers from Moselle and Var (as well as from Scotland), platelet functions, namely the aggregation to thrombin and their clotting activity, i.e. PF₃, are closely related to the intake of saturated fats, either as a result of the long-term feeding or of a 1 year change in the diet of Moselle farmers. Certain platelet functions appear to be the only blood parameter related to the incidence of CHD and significantly correlated on a group, as well as on an individual basis, with the intake of saturated fat, and inversely related with that of calcium. Saturated fats and calcium are known to be the two main dietary factors related to CHD. These results suggest that the intermediate link between dietary fats and CHD might be blood platelets rather than serum lipids, through an effect on both thrombosis and atherosclerosis.