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. 2006;8(1):202.
doi: 10.1186/ar1876.

Fish oil: what the prescriber needs to know

Leslie G Cleland  1 , Michael J James, Susanna M Proudman
Affiliations

Fish oil: what the prescriber needs to know

Leslie G Cleland et al. Arthritis Res Ther. 2006.

Erratum in

  • Arthritis Res Ther. 2006;8(4):402

Abstract

There is a general belief among doctors, in part grounded in experience, that patients with arthritis need nonsteroidal anti-inflammatory drugs (NSAIDs). Implicit in this view is that these patients require the symptomatic relief provided by inhibiting synthesis of nociceptive prostaglandin E2, a downstream product of the enzyme cyclo-oxygenase (COX), which is inhibited by NSAIDs. However, the concept of 'safe' NSAIDs has collapsed following a multiplicity of observations establishing increased risk for cardiovascular events associated with NSAID use, especially but not uniquely with the new COX-2-selective NSAIDs. This mandates greater parsimony in the use of these agents. Fish oils contain a natural inhibitor of COX, reduce reliance on NSAIDs, and reduce cardiovascular risk through multiple mechanisms. Fish oil thus warrants consideration as a component of therapy for arthritis, especially rheumatoid arthritis, in which its symptomatic benefits are well established. A major barrier to the therapeutic use of fish oil in inflammatory diseases is ignorance of its mechanism, range of beneficial effects, safety profile, availability of suitable products, effective dose, latency of effects and instructions for administration. This review provides an evidence-based resource for doctors and patients who may choose to prescribe or take fish oil.

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Figures

Figure 1
Figure 1
20-Carbon fatty acid homologues.
Figure 2
Figure 2
Metabolism of AA or EPA by COX. -, inhibition; AA, arachidonic acid; COX, cyclo-oxygenase; EPA, eicosapentaenoic acid; NSAID, nonsteroidal anti-inflammatory drug; PG, prostaglandin; TX, thromboxane.
Figure 3
Figure 3
Effect of EPA on the production of eicosanoids and inflammatory cytokines. *Three different synthases (PGE, PGI, and TX synthase), each with different enzyme kinetic characteristics. -, inhibition; AA, arachidonic acid; COX, cyclo-oxygenase; EPA, eicosapentaenoic acid; IL, interleukin; LT, leukotriene; NSAID, nonsteroidal anti-inflammatory drug; PG, prostaglandin; TNF, tumour necrosis factor; TX, thromboxane.
See this image and copyright information in PMC

References

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    1. James MJ, Ursin VM, Cleland LG. Metabolism of stearidonic acid in human subjects: comparison with the metabolism of other n-3 fatty acids. Am J Clin Nutr. 2003;77:1140–1145. - PubMed

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