Most epidemiologic studies and clinical trials using n-3 fatty acids in the form of fish or fish oil have been carried out in patients with coronary heart disease. However, studies have also been carried out on the effects of ALA in normal subjects and in patients with myocardial infarction.
The hypolipidemic effects of n-3 fatty acids are similar to those of n-6 fatty acids, provided that they replace saturated fats in the diet. n-3 fatty acids have the added benefit of not lowering high-density lipoprotein (HDL) and consistently lowering serum triacylglycerol concentrations, whereas the n-6 fatty acids do not and may even increase triglyceride levels.
Another important consideration is the finding that during chronic fish oil feeding postprandial triacylgly-cerol concentrations decrease. Furthermore, consumption of high amounts of fish oil blunted the expected rise in plasma cholesterol concentrations in humans. These findings are consistent with the low rate of coronary heart disease found in fish-eating populations. Studies in humans have shown that fish oils reduce the rate of hepatic secretion of very low-density lipoprotein (VLDL) triacylglycerol. In normolipidemic subjects, n-3 fatty acids prevent and rapidly reverse carbohydrate-induced hypertriglyceridemia. There is also evidence from kinetic studies that fish oil increases the fractional catabolic rate of VLDL (Table 7).
The effects of different doses of fish oil on thrombosis and bleeding time have been investigated. A dose of 1.8gEPAday-1 did not result in any prolongation in bleeding time, but 4 g day-1 increased bleeding time and decreased platelet count with no adverse effects. In human studies, there has never been a case of clinical bleeding, even in patients undergoing angioplasty, while the patients were taking fish oil supplements. Clinical investigations indicate that n-3 fatty acids prevent sudden death. A series of intervention trials have clearly shown that the addition of n-3 fatty acids in the form of fish oil (EPA and DHA) decrease the death rate in the secondary prevention of coronary heart disease by preventing ventricular arrhythmias that lead to sudden death.
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