Diet and aging: bearing on thrombosis and hemostasis

Abstract

Diet is one of the environmental factors that influences thrombosis and hemostasis. Macronutrients, micronutrients, and other bioactive food components alter the predisposition to thrombosis. The type and amount of dietary fat has been shown to alter thromboxane A2 production and platelet aggregation, bleeding time, factor VII, fibrinogen, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1). Both epidemiological studies and clinical trials indicate that the very long chain n-3 fatty acids lower thrombotic tendency and risk of heart disease. Other polyunsaturated fats and monounsaturated fat appear to have antithrombotic properties, but further studies are indicated. Hypercaloric diets and those with high glycemic loads are associated with elevations of PAI-1. Moderate consumption of alcohol is associated with decreased platelet aggregation. Low intakes of folate, vitamin B12, and vitamin B6 predispose to hyperhomocysteinemia, and the benefits of supplementation in decreasing vascular disease are under investigation. In a limited number of clinical and laboratory studies, vitamin E has been shown to decrease platelet aggregation and the concentration of PAI-1. Flavonoids and isoflavones appear to inhibit platelet aggregation at pharmacologic concentrations only. Nutritional status frequently declines with aging and may exacerbate the already increased risk for thrombosis. Diet presents an interesting area for research into thrombophilia, but additional work is indicated before specific recommendations are made.