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(Circulation. 1996;94:2337-2340.)
© 1996 American Heart Association, Inc.
Articles |
From the Nutrition Committee of the American Heart Association
Key Words: AHA Medical/Scientific Statements lipids diet coronary disease fatty acids
| Introduction |
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| What Are Omega-3 Fatty Acids? |
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| Fish Intake and Risk Factors |
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A critical review by Harris2 has clarified the discrepancy among fish oil studies reporting effects on LDL cholesterol (LDL-C). He noted that in the majority of studies reporting reductions in LDL-C levels, the saturated fat intake was lowered when subjects switched from the control diet to the fish oil diet. When fish oil is consumed and saturated fat intake is constant, LDL-C levels either do not change or may increase.
Although fish oil is not recommended in the treatment of hypercholesterolemia, it does have a role in the treatment of lipoprotein disorders characterized by severe hypertriglyceridemia. It can be quite useful in those severely hypertriglyceridemic (triglyceride >1000 mg/dL) patients for whom attempts to correct secondary causes (through diet, exercise, and gemfibrozil) have proved inadequate.7 Although a negative aspect is the concomitant elevation in LDL-C that occurs when fish oils are given to these patients with lower plasma levels of triglyceride, this is usually not a problem for those with severe hypertriglyceridemia, because LDL-C values are usually quite low. It can be a problem for those with more modest elevations of triglycerides in whom the elevation of LDL-C will actually move the patient away from the desired LDL-C goal.
Fish oil supplementation does not appear to impair glucose tolerance in nondiabetic coronary bypass patients.8 Among diabetics, initial studies showed deterioration of glucose tolerance with fish oil consumption.9 Nonetheless, Connor and coworkers10 designed a longer term study in which body weights were unchanged between fish oil and olive oil groups and no deterioration in glucose homeostasis was demonstrated in those individuals with diabetes. Westerveld and colleagues11 conducted a randomized, blinded, placebo-controlled trial that also documented reduced platelet aggregation as well as triglyceride lowering in the fish oil group. In both trials the fall in triglyceride level was accompanied by a rise in LDL-C similar to that seen in studies of patients with combined hyperlipidemia.12 This rise in LDL-C level was not seen when a low dose of omega-3 fatty acids was given to 20 ambulatory subjects with noninsulin-dependent diabetes mellitus in a randomized, double-blind, prospective, controlled clinical trial.13 Although sample size may have been inadequate to show an LDL-C effect, fish oil significantly inhibited platelet aggregation and thromboxane A2 production, while it reduced triglyceride levels by 44 mg/dL and decreased upright systolic blood pressure by 8 mm Hg compared with safflower oil. Finally, a recent study looking at vascular reactivity suggested that fish oil ingestion in diabetics could favorably alter arterial wall compliance without affecting fasting blood sugar, cholesterol, or blood pressure.14 Clearly, further research on the use of n-3 PUFA in diabetics is required.
Effect of Omega-3 Fatty Acids on Hypertension
A meta-analysis of placebo-controlled studies showed that fish oil reduced blood pressure in a dose-response fashion in those with hypertension and hypercholesterolemia but not in those participants with normal blood pressures.15 The effects were small, and it is not clear whether this effect is sustained over the long term.
Effect of Omega-3 Fatty Acids on Coagulation Profiles
A concise review of studies on the prevention of thrombosis in laboratory animals and in humans emphasized the important role of n-3 PUFA, which affects cellular responses in platelets, monocytes, and endothelial cells.16 The reduced platelet aggregation and prolonged bleeding times of the Greenland Eskimos suggested an important mechanism by which n-3 PUFAs could affect CHD.17 When bleeding times are measured, the effects of fish oil are additive to those of aspirin.18 Studies in swine fed high cholesterol diets with and without cod liver oil showed that there was less coronary atherosclerosis in the cod liver oil group but that there was no relationship to lipid changes. The pigs fed cod liver oil had significant decreases in serum thromboxane B2 levels and increases in platelet fatty acid deposition of EPA.19 Fish oil supplements increased levels of tissue plasminogen activator (TPA) and decreased concentrations of plasminogen activator inhibitor, both enhancers of fibrinolysis.20 One study comparing fish oil with rapeseed oil noted that fish oil decreased lipoprotein(a) by 14%.21 This effect was not seen in all male subjects who were hospitalized with CHD but did correlate with a large reduction in TPA. The Atherosclerosis Risk in Communities study compiled data from four US communities (15 000 participants, both black and white) on six hemostatic factors: fibrinogen, factor VII, factor VIII, von Willebrand factor, protein C, and antithrombin III.22 These were communities not known for their high intake of fish. Dietary intake of n-3 PUFA showed negative associations with levels of fibrinogen, factor VIII, and von Willebrand factor and a positive association with protein C (whites only). These findings may help explain, in part, the reduced incidence of vein graft occlusion seen in patients after coronary artery bypass grafting who receive n-3 PUFA.23 In a randomized controlled trial of dietary supplementation with n-3 fatty acids in bypass patients who received usual anticoagulation with aspirin or warfarin, an inverse relation between relative change in serum phospholipid n-3 fatty acids and vein graft occlusions was observed. Thus, the prevention of thrombosis remains a promising area for n-3 PUFA research.
Effect of Omega-3 Fatty Acids on Immune Response
The potent anti-inflammatory effects of fish oils and their effects on the immune response are beyond the scope of this review. Worthy of mention are the detailed studies of Meydani et al24 on immune responses seen with dietary fish supplementation. They showed decreased cell-mediated immunity when the Step II National Cholesterol Education Program (or AHA) diet was supplemented with a high fish intake as compared with one low in fish intake (121 to 188 g of fish per day versus 33 g of fish per day). The clinical significance of this important finding needs further investigation.
| Fish Intake and CHD |
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Clinical Trials
There is no convincing role for fish oil supplements in the prevention of CHD. The strongest evidence indicating a beneficial effect of fish intake on CHD came from the Diet and Reinfarction Trial (DART), in which men who were instructed to eat fish after myocardial infarction (MI) had a 29% decline in all-cause mortality as compared with those in the placebo group.31 No significant lowering of cholesterol was seen, and very few men were taking aspirin. Yet the Health Professionals Follow-up Study,32 a large-scale prospective cohort study, reported no association between increasing fish intake and CHD. The authors concluded that increasing fish intake beyond one or two servings per week is not likely to improve the primary prevention of CHD.
A nested case-control study was conducted among the 14 916 participants in the Physicians' Health Study.33 Each participant with MI was matched by smoking status and age with a randomly chosen control participant who had not developed CHD. Fish oil intake was estimated by measuring plasma levels in cholesterol esters and phospholipids. No association was found between fish oil levels and the incidence of MI even when results were adjusted for major cardiovascular risk factors. Although early trials suggested that fish oil held some promise if ingested early before angioplasty, a clinical trial large enough to find a significant effect did not, despite a dose of 8 g/d of n-3 PUFA.34 This trial did document the safety of fish oil supplementation without any evidence of excess bleeding in the patients who all took aspirin. Moreover, a clinical trial with angiographic end points showed that among normocholesterolemic men with CHD, fish oil treatment (6 g n-3 PUFA for 2 years) did not produce significant changes in the diameter of the coronary arteries.35
Effects of Omega-3 Fatty Acids on Sudden Death
DART peaked interest in whether a diet rich in fish oil could reduce risk of sudden death because of the striking difference in sudden deaths seen early in the trial, suggesting a possible action on either thrombosis or arrhythmic death rather than on atherosclerosis.9 Support for the latter hypothesis came from the Lyon Trial,36 which compared a "Mediterranean-type" diet rich in LNA with the AHA Step I diet in patients with known MI. Although no improvement in lipids, lipoproteins, and body mass index was seen, there was a striking difference in mortality, with eight sudden deaths in the control group and none in the alpha LNArich diet group. The risk ratio of cardiac death was 0.19 (95% CI, 0.06 to 0.65), with P<.002. These findings were extended by the carefully done population-based case-control study from Seattle and King County, Washington.37 Among 334 patients with primary cardiac arrest, the intake of n-3 PUFA per month was significantly less than that seen in age- and sex-matched community controls. The data suggested that an intake of 5.5 g of n-3 PUFA per month (equivalent to one fatty fish meal per week) was associated with a 50% reduction in the risk of primary cardiac arrest after adjustment for potential confounding factors. Moreover, studies of red blood cell membrane n-3 PUFA in both patients and controls allowed calculation of risk based on this sensitive parameter of dietary n-3 PUFA intake. These findings were consistent with experimental evidence suggesting that the n-3 PUFAs have an important effect on vulnerability to ventricular fibrillation in the setting of myocardial ischemia.38 Of additional interest are recent data showing suppression of premature ventricular contractions (PVCs) in middle-aged patients with frequent PVCs randomly assigned to take either fish oil (as cod liver oil containing 2.4 g of n-3 PUFA) or sunflower seed oil.39 Clearly, further studies are needed to explore the potential of fish oil in the prevention of sudden cardiac death.
| Conclusions |
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| Footnotes |
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"Fish Consumption, Fish Oil, Lipids, and Coronary Heart Disease" was approved by the Science Advisory and Coordinating Committee of the American Heart Association in July 1996.
Single reprints are free: Call 1-800-242-8721 (US only) or write American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596.
| References |
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