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Omega-3 Supplements and Pain


James JM, et al.Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr 2000;71(suppl):343S-8S.

Inflammation is characterized symptomatically by Pain, Redness, and Swelling.Disordered or excessive inflammation also entails loss of function. This clinical pathology results from the release of inflammatory mediators, predominantly from activated leukocytes that migrate into the target area. Among the key inflammatory mediators are the n-6 eicosanoids, Prostaglandin E2 (PGE2) and Leukotriene B4 (LTB4), which are derived from the n-6 polyunsaturated fatty acid (PUFA) Arachidonic Acid (AA; 20:4n26). Also important are the cytokines, Interleukin 1b (IL-1b) and Tumor Necrosis Factor-a (TNF-a), and there is strong evidence for the involvement of TNF-a in the joint pathology of rheumatoid arthritis.

Many anti-inflammatory pharmaceutical products inhibit the production of certain eicosanoids and cytokines and it is here that possibilities exist for therapies that incorporate n-3 and n-9 dietary fatty acids. The pro-inflammatory eicosanoids mentioned above are derived from the n-6 fatty acid Arachidonic Acid (AA), which is maintained at high cellular concentrations by the high n-6 and low n-3 polyunsaturated fatty acid content of the modern Western diet.

Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA) can act as competitive inhibitors of AA conversion to PGE2 and LTB4, and decreased synthesis of one or both of these eicosanoids has been observed after inclusion of flaxseed oil or fish oil in the diet. Analogous to the effect of n-3 fatty acids, inclusion of n-9 fatty acid Eicosatrienoic acid in the diet also results in decreased synthesis of LTB4.

Regarding the pro-inflammatory cytokines, Tumor Necrosis Factor-a (TNF-a) and Interleukin 1b, studies of healthy volunteers and rheumatoid arthritis patients have shown 90% inhibition of cytokine production after dietary supplementation with fish oil.

Use of flaxseed oil in domestic food preparation also reduced production of these cytokines.

Many anti-inflammatory pharmacotherapies are directed at inhibiting the production of these inflammatory mediators and thus possibilities exist for therapies that incorporate n-3 and n-9 dietary fatty acids.

Pain & Inflammation


James JM, et al.Dietary polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr 2000;71(suppl):343S-8S.

Inflammation is characterized symptomatically by Pain, Redness, and Swelling.Disordered or excessive inflammation also entails loss of function. This clinical pathology results from the release of inflammatory mediators, predominantly from activated leukocytes that migrate into the target area. Among the key inflammatory mediators are the n-6 eicosanoids, Prostaglandin E2 (PGE2) and Leukotriene B4 (LTB4), which are derived from the n-6 polyunsaturated fatty acid (PUFA) Arachidonic Acid (AA; 20:4n26). Also important are the cytokines, Interleukin 1b (IL-1b) and Tumor Necrosis Factor-a (TNF-a), and there is strong evidence for the involvement of TNF-a in the joint pathology of rheumatoid arthritis.

Many anti-inflammatory pharmaceutical products inhibit the production of certain eicosanoids and cytokines and it is here that possibilities exist for therapies that incorporate n-3 and n-9 dietary fatty acids. The pro-inflammatory eicosanoids mentioned above are derived from the n-6 fatty acid Arachidonic Acid (AA), which is maintained at high cellular concentrations by the high n-6 and low n-3 polyunsaturated fatty acid content of the modern Western diet.

Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA) can act as competitive inhibitors of AA conversion to PGE2 and LTB4, and decreased synthesis of one or both of these eicosanoids has been observed after inclusion of flaxseed oil or fish oil in the diet. Analogous to the effect of n-3 fatty acids, inclusion of n-9 fatty acid Eicosatrienoic acid in the diet also results in decreased synthesis of LTB4.

Regarding the pro-inflammatory cytokines, Tumor Necrosis Factor-a (TNF-a) and Interleukin 1b, studies of healthy volunteers and rheumatoid arthritis patients have shown 90% inhibition of cytokine production after dietary supplementation with fish oil.

Use of flaxseed oil in domestic food preparation also reduced production of these cytokines.

Many anti-inflammatory pharmacotherapies are directed at inhibiting the production of these inflammatory mediators and thus possibilities exist for therapies that incorporate n-3 and n-9 dietary fatty acids.

Bang HO, Dyerberg J.The composition of food consumed by Greenlandic Eskimos. Acta medica scandinavica 1973; 200:69-73.

"The unique properties of these fatty acids [Omega-3] in coronary heart disease first became apparent in the investigations of the health status of Greenland Eskimos who consumed diets very high in fat from seals, whales, and fish and yet had a low rate of coronary heart disease events."


Dyerberg J, Bang HO.Haemostatic function and platelet polyunsaturated fatty acids in Eskimos. Lancet 1979;2:433-5.

"The fat the Eskimos consumed contained large quantities of ... EPA / DHA which are abundant in fish, shellfish, and sea mammals and are scarce or absent in land animals and plants."


Connor WE.N-3 Fatty acids and heart disease. In: Kritchevsky D, Carroll KK, eds. Nutrition and disease update: heart disease. Champaign,IL: American Oil Chemists' Society, 1994:7-42.

"Effects of Omega-3 fatty acids on coronary heart disease have been shown in hundreds of experiments in animals, humans, tissue culture studies, and even clinical trials."


Siscovick DS, et al.Dietary intake and cell membrane levels of long-chain n23 polyunsaturated fatty acids and the risk of primary cardiac arrest. Journal of the American Medical Association 1995; 274:1363-7.

Men who consumed salmon > 1 time/week had a 70% less likelihood of cardiac arrest.


Burr ML, et al.Effects of changes in fat, fish, and fiber intakes on death and myocardial reinfarction: Diet and Reinfarction Trial (DART). Lancet 1989; 2:756-61.

Overall mortality was decreased by 29% in men with overt cardiovascular disease who consumed Omega-3 fatty acids from fish or fish oil.


de Lorgeril M, et al.Mediterranean alphalinolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet 1994;343:1454-9.

Coronary deaths were prevented by a diet high in ALA [Omega-3 fatty acid].


Albert CM, Hennekens CH, O'Donnell CJ, Ajani UA, Carey VJ.Fish consumption and risk of sudden cardiac death. Journal of the American Medical Association 1998;279:23-7.

Consumption of > 1 fish meal/week was associated with a 52% lower risk of sudden cardiac death compared with consumption of less than 1 fish meal/month.


Weiner BH, et al.Inhibition of atherosclerosis by cod liver oil in a hyperlipidemic swine model. Circulation 1986;315:841-6.

Davis HR, Bridenstine et al.Fish oil inhibits development of atherosclerosis in rhesus monkeys. Arteriosclerosis 1987;7:441-9.

EPA and DHA [Omega-3] contained in fish oil fed to experimental animals actually inhibited development of atherosclerosis [hardening of the arteries].


Phillipson BE, et al.Reduction of plasma lipids, lipoproteins, and apoproteins by dietary fish oils in patients with hypertriglyceridemia. New England Journal of Medicine 1985;312:1210-6.

Harris WS, et al.Effect of fish oil on VLDL triglyceride kinetics in man. Journal of Lipid Research 1990;31:1549-58.

Fish oil was shown to lower plasma cholesterol and triacylglycerol concentrations.

 

Vitamin D - Low Back Pain

Faraj SA, Mutairi KA.Vitamin D Deficiency and Chronic Low Back Pain in Saudi Arabia. Spine 2003; 28:177-179.

The purpose of this study was to investigate the contribution of vitamin D deficiency as a cause for idiopathic chronic low back pain, to find a simple and sensitive test for screening patients with low back pain for vitamin D deficiency, and to determine the correlation between the vitamin deficiency and pain.

The study included 360 patients (90% women and 10% men) attending spinal and internal medicine clinics over a 6-year period who had experienced low back pain that had no obvious cause for more than 6 months. The patients ranged in age from 15 to 52 years.

A biochemical assay of serum calcium, phosphate, alkaline phosphatase, and 25-hydroxy vitamin D level was performed before and after treatment with vitamin D supplements.

Results:
Findings showed that 83% of the study patients (n - 299) had an abnormally low level of vitamin D before treatment with vitamin D supplements. After treatment, clinical improvement in symptoms was seen in all the groups that had a low level of vitamin D, and in 95% of all the patients (n - 341).

Conclusions:
Vitamin D deficiency is a major contributor to chronic low back pain in areas where vitamin D deficiency is endemic. Screening for vitamin D deficiency and treatment with supplements should be mandatory in this setting. Measurement of serum 25-OH cholecalciferol is sensitive and specific for detection of vitamin D deficiency.

 

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