Below is part of a publication by Dr Gordon on the effect of omega-3 on pain and inflammation. One of the studies he points to found 59% of arthritic patients were able to discontinue use of NSAIDS and substitute Omega-3 supplements for control of their arthritic pain. I am certainly one that would be in the 59% group. The pain relief does not just apply to arthritic patients. The bottom line–if you have pain– follow The Oil-Change Diet.
Omega-3 Fatty Acids and Neuropathic Pain
Case studies demonstrate that oral intake of omega-3
polyunsaturated fatty acids from pharmaceutical-grade fish oil
supplements results in pain reduction and functional improvement
in patients with neuropathic pain.
By Gordon D. Ko, MD, CCFP(EM), FRCPC, PhD, Leigh Arseneau, BSc, ND, Nathaniel Nowacki, BA and Serge Mrkoboda, BSc
PUFAs and Eicosanoid Metabolism
The n-3 and n-6 fatty acids are chemically and metabolically distinct and have contrasting physiological functions12 (see Figure 4). The eicosanoid metabolic products synthesized from AA, namely prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), hydroxy fatty acids and lipoxins are formed in larger quantities than those formed from n-3 PUFAs—such as EPA—because of the increased amounts of n-6 PUFAs in the Western diet.1 Eicosanoids derived from AA are biologically active in small quantities and, if they are formed in inordinate amounts, they contribute to the formation of atheromas and thrombi.1 In addition, they lead to the development of allergic and inflammatory disorders and to cell proliferation.
When humans increase their consumption of EPA and DHA, from oily fish or from fish oil supplements (liquids or capsules), an increased proportion of these fatty acids are found in the cell membranes of inflammatory cells in particular.14 EPA and DHA incorporation into these membranes occurs in a dose-response fashion and is partly at the expense of AA.15 Hence, since there is less AA available for eicosanoid biosynthesis by the cyclooxygenase (COX) and lipoxygenase (LOX) enzymes, fish oil supplementation of the diet results in a decreased production of the proinflammatory prostaglandin E2 (PGE2), thromboxane A2 (TXA2), TXB2, leukotriene B4 (LTB4), LTE4 and 5-hydroxyeicosatetraenoic acid, but not of prostacyclin I2 (PGI2).12,14
EPA can also act as a substrate for both COX and LOX enzymes and thereby compete with AA for prostaglandin and leukotriene synthesis.12 EPA gives rise to the 3-series PGs and TXs (such as TXA3, PGE3, PGI3) and to the 5-series LTs (LTB5, LTE5) and 5-hydroxyeicosapentaenoic acid.14 The eicosanoids formed from EPA are frequently less biologically potent than those formed from AA.15 For example, LTB5 is 10- to 100- fold less potent as a neutrophil chemotactic agent than LTB4 and PGE3 is a less potent inducer of COX-2 gene expression in fibroblasts than PGE2.15 Furthermore, TXA3 is a weaker platelet aggregator and vasoconstrictor than TXA2.12 Recent studies have shown that EPA and DHA also give rise to resolvins (from EPA and DHA) and docosanoids (from DHA) through pathways involving COX and LOX enzymes.16 In cell culture and animal-feeding studies, these novel mediators were demonstrated to be anti-inflammatory, inflammation resolving, and immu-nomodulatory.16
Some of the effects of n-3 PUFAs are elicited by eicosanoid-independent mechanisms. Studies have shown, for example, that the intake of dietary fish oil results in decreased leukocyte chemotaxis, decreased expression of adhesion molecules and decreased generation of reactive oxygen species.15 n-3 PUFAs have also been shown to inhibit the production of proinflammatory cytokines such as tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), IL-6 and IL-8, in both cell culture studies and in human trials.14,15 Additionally, n-3 PUFAs might exert their effects on inflammatory gene expression through direct action on intracellular signaling pathways which lead to activation of one or more transcription factors such as nuclear factor kappa B (NF-kb).14
Figures 4. Pathways to inflammation: omega-6 is pro-inflammatory and omega-3 is anti-inflammatory.
n-3 PUFAs and Chronic Disease
The benefits of n-3 PUFA supplementation are well documented in the literature for the prevention and management of a wide variety of health conditions including inflammatory and autoimmune diseases, cardiovascular disease, and depression. Less is known, however, about the use and efficacy of these fatty acids in the treatment of other disorders such as fibromyalgia syndrome and neuropathic pain.
n-3 PUFAs and Inflammatory/ Autoimmune Diseases
A number of clinical trials have been conducted assessing the benefits of dietary supplementation with n-3 PUFAs in inflammatory and autoimmune disease in humans, including RA, Crohn’s diseases, ulcerative colitis, psoriasis, lupus erythematosus, MS, and migraine headaches.12
A recent meta-analysis of 17 randomized controlled trials (RCTs) was conducted by Goldberg et al. to assess the pain relieving effects of n-3 PUFAs in patients with rheumatoid arthritis (RA) or joint pain secondary to inflammatory bowel disease and dysmenorrhea.17 Results from the analysis showed that supplementation with n-3 PUFAs for 3-4 months reduces patient-reported joint pain intensity, minutes of morning stiffness, number of painful and/or tender joints, and NSAID consumption.
Maroon et al. conducted a non-placebo controlled study to determine if patients could effectively substitute fish oil as an anti-inflammatory for NSAIDs.18 The study included 250 participants who had been seen by a neurosurgeon and were found to have chronic, nonsurgical, neck or back pain. After taking n-3 PUFAs for an average of 75 days, 59% discontinued their use of prescription NSAIDs and 60% stated that their overall pain was improved. Moreover, 88% stated they would continue to take the n-3 PUFAs. No significant adverse effects were reported. These results corroborate other controlled studies that compared ibuprofen and n-3 PUFAs demonstrating equivalent effects in reducing arthritic pain.18 Furthermore, such findings suggest that n-3 PUFAs may be a safe alternative to NSAIDs, particularly the COX-2 inhibitors which have been associated with extreme complications such as gastric ulcers, bleeding, blood pressure increase, myocardial infarction, and even death.19