Dietary N-3 Fatty Acid Supplementation in Rheumatoid Arthritis-Mechanisms, Clinical Outcomes, Controversies, and Future Directions.

Völker, D; Garg, Manohar L.

doi:10.3164/jcbn.20.83

Cited by 34 publications

(14 citation statements)

References 45 publications

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“…Further studies are needed to investigate how n-3 PUFA control mRNA levels and activities of aggrecanases and inflammatory mediators in the bovine and human in vitro models of arthritis, and whether a common mechanism exists for the alteration of gene transcription by n-3 PUFA. These findings add further weight to the epidemiological and clinical studies that have reported the benefits of dietary supplementation of n-3 PUFA in reducing pain and inflammation in human arthritic diseases (Volker & Garg, 1996;Cleland & James, 2000;Calder, 2001;Calder & Zurier, 2001), and suggest molecular mechanisms as to how these benefits occur.…”

Section: Discussionmentioning

confidence: 53%

Effects ofn-3 fatty acids on cartilage metabolism

et al. 2002

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Although the clinical benefits of dietary supplementation withn-3 polyunsaturated fatty acids (PUFA) has been recognised for a number of years, the molecular mechanisms by which particular PUFA affect metabolism of cells within the synovial joint tissues are not understood. This study set out to investigate hown-3 PUFA and other classes of fatty acids affect both degradative and inflammatory aspects of metabolism of articular cartilage chondrocytes using anin vitromodel of cartilage degradation. Using well-established culture models, cartilage explants from normal bovine and human osteoarthritic cartilage were supplemented with eithern-3 orn-6 PUFA, and cultures were subsequently treated with interleukin 1 to initiate catabolic processes that mimic cartilage degradation in arthritis. Results show that supplementation specifically withn-3 PUFA, but notn-6 PUFA, causes a decrease in both degradative and inflammatory aspects of chondrocyte metabolism, whilst having no effect on the normal tissue homeostasis. Collectively, our data provide evidence supporting dietary supplementation ofn-3 PUFA, which in turn may have a beneficial effect of slowing and reducing inflammation in the pathogenesis of degenerative joint diseases in man.

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Section: Discussionmentioning

confidence: 53%

Effects ofn-3 fatty acids on cartilage metabolism

et al. 2002

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“…Each of these trials indicates benefits of fish oil which include reduced duration of morning stiffness, reduced number of tender or swollen joints, reduced joint pain, reduced time to fatigue, increased grip strength and decreased use of non-steroidal anti-inflammatory drugs. Details of these trials are reviewed elsewhere (Volker & Garg, 1996;James & Cleland, 1997;Geusens, 1998;Calder, 2001a,b;Calder & Zurier, 2001). In an editorial commentary discussing the use of fish oil in rheumatoid arthritis Cleland & James (2000) conclude that 'the findings of benefit from fish oil in rheumatoid arthritis are robust', that 'dietary fish oil supplements in rheumatoid arthritis have treatment efficacy', and that 'dietary fish oil supplements should now be regarded as part of the standard therapy for rheumatoid arthritis'.…”

Section: Rheumatoid Arthritis: a T-helper 1-type Disordermentioning

confidence: 99%

Dietary modification of inflammation with lipids

2002

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Then-3 polyunsaturated fatty acids (PUFA) eicosapentaenoic acid (EPA) and docosahexaenoicacid (DHA) are found in high proportions in oily fish and fish oils. Then-3 PUFA are structurally and functionally distinct from then-6 PUFA. Typically, human inflammatory cells contain high proportions of then-6 PUFA arachidonic acid and low proportions ofn-3 PUFA. The significance of this difference is that arachidonic acid is the precursor of 2-series prostaglandins and 4-series leukotrienes, which are highly-active mediators of inflammation. Feeding fish oil results in partial replacement of arachidonic acid in inflammatory cell membranes by EPA. This change leads to decreased production of arachidonic acid-derived mediators. This response alone is a potentially beneficial anti-inflammatory effect of n-3 PUFA. However,n-3 PUFA have a number of other effects which might occur downstream of altered eicosanoid production or might be independent of this activity. For example, animal and human studies have shown that dietary fish oil results in suppressed production of pro-inflammatory cytokines and can decrease adhesion molecule expression. These effects occur at the level of altered gene expression. This action might come about through antagonism of the effects of arachidonic acid-derived mediators or through more direct actions on the intracellular signalling pathways which lead to activation of transcription factors such as nuclear factor kappa B (NFêB). Recent studies have shown thatn-3 PUFA can down regulate the activity of the nuclear transcription factor NFêB. Fish oil feeding has been shown to ameliorate the symptoms in some animal models of chronic inflammatory disease and to protect against the effects of endotoxin and similar inflammatory challenges. Clinical studies have reported that oral fish oil supplementation has beneficial effects in rheumatoid arthritis and among some patients with asthma, supporting the idea that then-3 PUFA in fish oil are antiinflammatory. There are indications that inclusion ofn-3 PUFA in enteral and parenteral formulas might be beneficial to patients in intensive care or post-surgery.

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“…Such benefits include reduced duration of morning stiffness, reduced number of tender or swollen joints, reduced joint pain, reduced time to fatigue, increased grip strength and decreased use of non-steroidal anti-inflammatory drugs (Table 1). A number of reviews of these trials have been published (84)(85)(86)(87)(88)(89)(90) and each has concluded that there is benefit from fish oil. In an editorial commentary discussing the use of fish oil in RA it was concluded that 'the findings of benefit from fish oil in rheumatoid arthritis are robust', 'dietary fish oil supplements in rheumatoid arthritis have treatment efficacy' and 'dietary fish oil supplements should now be regarded as part of the standard therapy for rheumatoid arthritis' (91) .…”

Section: Trials Of N-3 Pufa In Rheumatoid Arthritismentioning

confidence: 99%

Session 3: Joint Nutrition Society and Irish Nutrition and Dietetic Institute Symposium on ‘Nutrition and autoimmune disease’ PUFA, inflammatory processes and rheumatoid arthritis

Calder

2008

Proc. Nutr. Soc.

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Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease manifested by swollen and painful joints, bone erosion and functional impairment. The joint lesions are characterised by infiltration of T lymphocytes, macrophages and B lymphocytes into the synovium and by synovial inflammation involving eicosanoids, cytokines and matrix metalloproteinases. In relation to inflammatory processes, the main fatty acids of interest are the n-6 PUFA arachidonic acid, which is the precursor of inflammatory eicosanoids such as PGE2 and leukotriene B4, and the n-3 PUFA EPA and DHA, which are found in oily fish and fish oils. Eicosanoids derived from the n-6 PUFA arachidonic acid play a role in RA, and the efficacy of non-steroidal anti-inflammatory drugs in RA indicates the importance of pro-inflammatory cyclooxygenase pathway products of arachidonic acid in the pathophysiology of the disease. EPA and DHA inhibit arachidonic acid metabolism to inflammatory eicosanoids. EPA also gives rise to eicosanoid mediators that are less inflammatory than those produced from arachidonic acid and both EPA and DHA give rise to resolvins that are anti-inflammatory and inflammation resolving. In addition to modifying the lipid mediator profile, n-3 PUFA exert effects on other aspects of immunity relevant to RA such as antigen presentation, T-cell reactivity and inflammatory cytokine production. Fish oil has been shown to slow the development of arthritis in an animal model and to reduce disease severity. Randomised clinical trials have demonstrated a range of clinical benefits in patients with RA that include reducing pain, duration of morning stiffness and use of non-steroidal anti-inflammatory drugs.

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Dietary N-3 Fatty Acid Supplementation in Rheumatoid Arthritis-Mechanisms, Clinical Outcomes, Controversies, and Future Directions.

Cited by 34 publications

References 45 publications

Effects ofn-3 fatty acids on cartilage metabolism

Effects ofn-3 fatty acids on cartilage metabolism

Dietary modification of inflammation with lipids

Session 3: Joint Nutrition Society and Irish Nutrition and Dietetic Institute Symposium on ‘Nutrition and autoimmune disease’ PUFA, inflammatory processes and rheumatoid arthritis

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