Beyond the Mediterranean Diet: The Role of Omega-3 Fatty Acids in the Prevention of Coronary Heart Disease

Charles R. Harper, MD, Terry A. Jacobson, MD

Disclosures

Prev Cardiol. 2003;6(3) 

In This Article

Abstract and Introduction

Evidence from epidemiologic and clinical secondary prevention trials suggest that the omega-3 polyunsaturated fatty acids (n-3 PUFAs) may have a significant role in the prevention of coronary heart disease. Dietary sources of n-3 PUFAs include fish oils, rich in eicosapentaenoic acid and docosahexaenoic acid, along with plants rich in linolenic acid. Randomized secondary prevention clinical trials with fish oils (eicosapentaenoic acid, docosahexaenoic acid) and -linolenic acid have demonstrated reductions in risk that compare favorably to those seen in landmark secondary prevention trials with lipid-lowering drugs. Several mechanisms explaining the cardioprotective effect of the n-3 PUFA have been suggested including antiarrhythmic and antithrombotic roles. Although official US guidelines for the dietary intake of n-3 PUFA are not available, several international guidelines have been published. Fish is an important source of the n-3 PUFA in the US diet; however, vegetable sources including grains and oils offer an alternative source for those who are unable to regularly consume fish.

Scientific knowledge concerning the omega-3 polyunsaturated fatty acids (n-3 PUFAs) is rapidly expanding. Early work by Dyerberg et al.[1] with Greenlandic Inuits suggested the n-3 PUFAs may have a cardioprotective effect. Recent evidence from randomized trials in patients with coronary heart disease (CHD) suggests that n-3 fatty acids from marine (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) and plant sources (linolenic acid [ALA]) prevents cardiac death and nonfatal myocardial infarction (MI). The authors begin with a brief review of fatty acid structure and nomenclature, followed by a summary of the available epidemiologic evidence. Recent evidence from clinical trials with angiographic and hard clinical end points is reviewed. Finally a review of possible mechanisms of action is followed by a discussion of the implications for clinicians.

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