Omega-3 Fatty Acids
Omega-3 Fatty Acids
Authors: DeFilippis, A.P. Blaha, M.J. Jacobson, T.A.
Publication Name: Current Treatment Options in Cardiovascular Medicine
Publication Details: Volume 12; Pages 365 – 380.
This paper provides an excellent review of omega 3 fatty acids, a class of bioactives that first gained attention with the observation that Greenland Eskimos have a low incidence of cardiovascular disease (CVD) in the setting of a diet rich in fatty fish. Over the past three decades, epidemiologic and experimental data have provided evidence for a beneficial effect of omega 3 fatty acids in preventing CVD. New data support previous studies on the beneficial modulation of platelet activity and the reduction in vascular inflammation. Major dietary sources of omega 3s are fish containing
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), as well as nuts, seeds, and vegetable oils containing alpha linolenic acid (ALA). ALA can be converted to EPA and then DHA by the same desaturase enzyme that converts linoleic acid to arachidonic acid. The conversion of ALA to EPA + DHA is influenced by multiple factors, including competitive inhibition of desaturase by linoleic acid, negative feedback inhibition of desaturase by EPA + DHA and gender differences; therefore, the conversion of ALA to EPA + DHA varies widely among different studies. There is a paucity of epidemiologic and clinical trial data on the impact of ALA on CVD outcomes as compared with EPA + DHA. However, in the Health Professional Follow-up Study cohort, the CVD protective properties of ALA were inversely related to baseline EPA + DHA intake. Omega 3s have been shown to have a favorable impact on multiple factors related to CVD: inflammation, platelet function/thrombosis, arrhythmias, telomere shortening, hypertriglyceridemia, adhesion molecule expression in plaque, nitric oxide induced endothelial relaxation, and elevated blood pressure. Clinical trial evidence suggests consistent reductions in proinflammatory cytokines such as IL6 and tumor necrosis factor alpha, with less consistent reductions in CRP, with ALA and EPA + DHA. Individuals with higher membrane omega 3 content (thus high omega 3 intake) will produce less thrombosis (blood clotting) promoting thromboxane A2 than individuals with lower membrane omega 3 levels. Data indicate antiarrhythmic effects of omega 3s in both basic and clinical studies in both reducing ventricular arrhythmias as well as atrial fibrillation. In 2004, FDA reviewed omega 3 fatty acid studies reporting on adverse events in more than 20,000 subjects. The agency concluded that adverse events related to consumption of fish oil or ALA supplements appear to be minor. The FDA has concluded that up to 3 g/d of EPA + DHA is safe, although most data are limited to less than 6 months. It is recommended that patients with known CHD consume one serving (200 to 400 g) of fatty fish or a fish oil supplement containing 900 mg of EPA + DHA every day and maintain a healthy diet rich in ALA. Patents with a CHD risk equivalent (eg, diabetes, peripheral vascular disease) also should consume a single serving of fatty fish several times a week or a daily fish oil supplement containing 900 mg of EPA + DHA. For patients without known CHD, a single serving of fatty fish approximately once or twice per week and a diet rich in ALA should be encouraged. It is prudent to avoid fish containing high levels of methyl mercury, as defined by the FDA. For patients with hypertriglyceridemia, 4 g/d of prescription omega-3 is a recommended therapy to reduce triglycerides and nonHDL cholesterol in both statin treated and statin na�ve patients. At this time, the authors indicate that there is insufficient evidence to recommend omega 3 therapy to reduce cardiac arrhythmias. (Editors comments)