Marine n-3 Fatty Acids for Cardiovascular Risk Reduction and Disease Control in Rheumatoid Arthritis: “Kill Two Birds with One Stone”?

Victoria      G. Rontoyanni; Petros      P. Sfikakis; George      D. Kitas; Athanase      D. Protogerou

doi:10.2174/138161212799504722

Abstract

Rheumatoid arthritis (RA), the most common chronic systemic inflammatory disease leading to joint destruction and disability, is associated with increased cardiovascular mortality. Systemic inflammation and increased burden of traditional cardiovascular risk factors present in RA are currently considered responsible for the accelerated atherosclerosis in these patients. Herein, we highlight a potential double effect of dietary intake of the n-3 long-chain polyunsaturated fatty acids (LCP) eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3) on cardiovascular risk reduction and disease control in patients with RA. Large studies in non-RA populations provide strong evidence for the beneficial effect of n-3 LCP supplementation in primary and secondary cardiovascular prevention. Cardiovascular risk reduction is at least partly explained by n-3 LCP effects on blood pressure, dyslipidemia, thrombosis and inflammation, all important factors also in RA, whereas abnormalities in vascular function and in vascular morphology similar to those observed in RA patients may even be moderately reversed. On the other hand, there is evidence from 6 of 14 randomized controlled trials supporting a favorable effect of n-3 LCP supplementation in decreasing joint inflammation in RA. Although specific studies in RA patients are currently lacking, a double beneficial effect of n-3 LCP seems likely. The size of any such effect and how it compares with other interventions such as lifestyle changes, biologic therapies, and statin therapy, needs to be investigated prospectively in carefully designed studies.

Keywords: DHA, EPA, n-3 fatty acids, rheumatoid arthritis, cardiovascular risk, atherosclerosis, blood pressure, dyslipidemia, thrombosis, inflammation