Effect of Omega 3 on Inflammatory Diseases - Coursework Example

Effect of Omega 3 on Inflammatory Diseases Introduction Inflammation may be understood as the process by which the body responds to injury through pain, heat and swelling. It occurs as a result of the movement of large blood molecules from the capillaries into surrounding tissue. Cells such as granulocytes and monocytes appear at the inflamed site and initiate destruction of pathogens. It is normal and expected for the process to occur during injury or infection, as the immune system depends on it. However, when inflammation persists for a long time or when unnecessary, then host tissue may be damaged. Eventually this leads to manifestation of diseases such as rheumatoid arthritis, asthma, psoriasis as well as inflammatory bowel disease. How Omega 3 PUFA relates to inflammation Human beings require polyunsaturated fatty acids for survival. This may come in the form of Omega 3 or Omega 6. Omega 3 polyunsaturated fatty acid (PUFA) and Omega 6 fatty acids often compete with one another in the body even though Omega 3 has more beneficial health benefits than the latter. Most western diets contain more Omega 6 fatty acids than Omega 3. It is for this reason that when compared to their Eastern counterparts, Westerners have high incidences of inflammatory disorders. Eskimos have little to no reports of autoimmune and inflammation-related disorders owing to their omega 3- rich diet. The latter community consumes plenty of sea food, which is a reliable source of Omega 3. The western diet currently lacks stipulated levels of omega 3. Most of it is dominated by omega 6 in ratios of 15 to 1 instead of 1:1 (Simopoulos, 2006). Evolution necessitates a relatively high amount of omega 3 in the diet but commercial and cultural patterns contradict this pattern. Omega 3 works to reduce inflammation in the body through a series of actions. As a soon a person takes fish or eats fish, the EPA (Eicosapentaenoic acid- an Omega 3 PUFA) minimises the release of prostaglandin metabolites. It also reduces the level of strong platelet aggregators in the blood. This causes the minimisation of leukotreine, which induces inflammation in the body. Furthermore, the acid also works by increasing the level of weak platelet aggregators (Simopoulos, 2006). Once a person increases their consumption of fish oil, they tend to report decreased levels of cholesterol as well as low amounts of triglycerides. These confer anti-inflammatory benefits to the host. EPAs in the body work to replace omega 6 acid in all cells of the body. However, particular attention is given to liver cells, monocytes, erythrocytes, neutrophils and platelets. Cell membranes polyunsaturated fatty acids are determined by the kind of diet that one consumes. Eicosanoid products often emanate from Omega 6 fatty acids (Oh da et. al., 2010). In small quantities, they are quite fine for the body but when released in large number, they often lead to inflammation and allergies. Eicosanoids increase the number of cells proliferating into different tissues and lead to diseases associated with the behaviour. Conversely, Omega 3 works by doing the opposite. It counters the effect of these eicosanoid products and thus increases antithrombotic effects in the body (He et. al., 2009). Another way in which omega 3 works to cause anti-inflammation effects is through its interaction with interleukins (IL). The latter are proteins that are responsible for differentiation and growth in cells. When an infection occurs, a significant amount of interleukins are produced. However, when excessive levels of the proteins exist in the body, then inflammatory conditions may manifest. Such proteins are referred to as cytokines; tumour necrosis factor (TNF) is another form of cytokine. Omega 3 PUFA has the ability to minimise the production of interleukins in the body. Suppression of cytokines leads to minimised coagulant activity as well as adhesion of leukocytes in the body. Capillary endothelium permeability reduces thus leading to diminished inflammation. Overall, Omega 3 has a contraindicative effect on most inflammation mediators like cytokines as well as eicosanoids like thromboxanes and other derivates of oxygen. Omega 3 induces inhibition of collagen and platelet aggregation. It also decreases the rate at which the body produced Thromboxane As. Eventually, this leads to minimised viscosity of the blood and rising fluidity of eruthrocytes. Plasminogen activator will be increased while its inhibitor goes up. It also propagates the increase of PG1 2 (Prostacylcin) in order to increase vasodilatation and prevent aggregation of platelets. It reduces the platelet derived growth factor – PDGF - release into the endothelial cells (Dwyer et. al., 2004). The result of this minimisation is that smooth muscle cells will not be attracted into monocytes, platelets or other similar endothelial cells. All its workings are geared towards reduced migration of cells into unwanted areas as well as reduced aggregation of the same molecules. A number of anti-inflammatory drugs already exist in the market but these have toxic side effects. Therefore, some scientists have proposed the consideration of Omega 3 acids as complementary to these drugs. They have the potential to decrease their toxicity in the body. When ingested, these fatty acids quickly get incorporated into monocyte cells and this alters the way cells function. Rheumatoid arthritis and Omega 3 The disease is an inflammatory one in which joints swell, pain occurs and the body becomes stiff in the morning. It impairs movement and causes molecules to degenerate. Rheumatoid arthritis is chronic and can be severely dilapidating. A number of blood molecules like lymphocytes, and macrophages will find themselves in joint tissue, yet this is abnormal. When a lab analysis is done of the patient’s synovium fluid, it is likely to contain a high concentration of cytokines such as TNFα and IL6 (Berbert et. al., 2005). Cyclooxygenase, which is another inflammation mediator, is also found in high proportions in the cell. Therefore it is imperative to prescribe medications that work on these pathways. Omega 3 is quite beneficial to patents with the disease. It works by minimising the amount of IL-1 being generated by monocytes as well as other types of interleukins. The final result of such an intervention is minimised reports of symptoms of arthritis. For instance, patients are likely to experience less pain in their joints, less fatigue, and even reduced stiffness in the morning. The omega 3 enters as Eicosapentaenoic acid into the body. This makes it influential in the action on eicosanoids, which have a significant role to play in the manifestation of the ailment. Omega 3 competes with Omega 6 in determining which acid will enter the inflammatory cell membrane. Patients with arthritis ought to minimise their intake of Omega 6 while increasing their consumption of Omega 3 in order to minimise these complications. A study carried out by Adam et. al. (2004) compared patients who consumed fish oil and restricted their level of arachidonic acid with those who did not consume fish oil and took typical levels of arachidonic acid. They measured arthritis activity in the patients at the beginning of the trial and subsequently after a set period of time. It was found that the experimental group reported relatively lower concentrations of thromboxanes than their counterparts in the control group. It was also found that the urine of the group on anti-inflammation diets had more pro-inflammatory agents than the one not on this diet. This implies that their body had been able to get rid of the metabolites. Furthermore, they reported significant decreases in symptoms of the disease. There was less pain and swelling in the joints. Eventually, person in the experimental group minimised their intake of anti-inflammatory drugs. One should note that Omega 3 fatty acids tend to give continued health benefits to those who take it. Fish oil suppresses the production of LTB4. However, even if a patient discontinues the intake of the dietary supplement, suppression of the same will still continue. It is for this reason that cross over analysis ought not to be done on patients since effects may be carried over from previous analyses. Sometimes reduction in mediating proteins has been reported even ten weeks after discontinuation of the diet (Berbert et. al., 2005). Preventive benefits of rheumatoid arthritis may also manifest after consumption of Omega 3. Some individuals have family history of the disease. They thus possess alleles that may make them susceptible to the illness. This particular group can benefit from the suppression of cytokines which predispose them to the illness (Wright et. al., 2008). However, more research is needed in this area as only possible suggestions have been made between preventive effects and the diseases. A review of several other studies examining the link between rheumatoid arthritis and Omega 3 consumption indicates that the acid has a significant effect on the disease (Calder, 2006). Therefore, it ought to be made as part of the therapeutic remedy. It also minimises reliance on anti-inflammatory drugs. However, this does not imply that fish oil is a supplement for the drugs. It complements the latter and ensures that other agents which will minimise its strength are reasonably reduced. Asthma Asthma is a respiratory inflammatory disease that affects the lungs. This illness manifests as breathlessness in the patient when passages in the lungs are inflamed owing to allergic responses. Studies examining the link between Omega 3 and asthma have found that the dietary supplements counter primary mediators in manifestation of the illness. A number of eicosanoids like PGD2 are found in mast cells among asthmatic patients (Bochner and Busse, 2005). When the blood or urine of these individuals is examined, it is likely to possess high concentrations of the inflammation mediators (eicosanoids). Patients with asthma are discouraged from consumed Omega 6 because it increased the level of eicosanoids in the body and thus propagates inflammation. Conversely, if a patient takes Omega 3 PUFA, they are likely to experience reduced production of cytokines by their T-cells (Dangardt et. al., 2010). Aggregation in the respiratory system therefore reduces and so does inflammation. For inflammation to increase in the patient’s airway, prostaglandins and leukotrienes are usually involved in the process. Certain cells contribute to the onset of asthmatic conditions, and they include lymphocytes, mast cells and eosinophils. Leukotrienes induce spasms of the bronchi and also cause secretion of mucus. They also induce edema of the airway and propagate migration of inflamed cells (Bochner and Busse, 2005). Omega 3 can reduce respiratory stress among those that take the supplements. It also works by minimising loss in respiratory capacity by changing leukotriene excretion. Omega 3 works by opposing the latter agents. Schacter et. al. (2004) did a study on the health effects of Omega 3 fatty acids on asthma patients. They found that fish oil’s effect on asthmatic patients came about by reduction of leukotiene production. In a review carried out by Calder (2006), it was found that the results are relatively inconsistent for asthmatic patients. Some studies showed no association between patient well being and asthma while some found that there were improvements. Those that found associations realised that significant changes were made on the peak flow rate when asthma began. This group of individuals relied less on the asthma medication than those who did not consume Omega 3 (Bochner and Busse, 2005). However, positive reviews have mostly been reported among individuals who work with children. Therefore, Omega 3 is beneficial to certain categories of asthma patients. Conclusion Western diets appear to be missing the point in terms of quantities of Omega 3 fatty acids to be consumed in the diet. Omega 3 is critical in food because it confers an anti-inflammation benefit. It works by inhibiting the production of few inflammatory metabolites or derivatives. It thus suppresses immune responses that have spiralled out of control. Studies have shown associations between rheumatoid arthritis treatment and Omega 3 consumption as well as asthma treatment and anti-inflammatory dies. However, more evidence can be found for rheumatoid disease than asthma because the latter works in children. Regardless, omega 3 works by minimising cytokines in the body for either disease. It thus reduces symptoms and reliance on drugs. The nutrient is very promising as part of treatment therapy. References Adam, O., Beringer, and Kless, T., 2004. Anti-inflammatory effects of a low arachidonic acid diet and fish oil in patients with rheumatoid arthritis. Rheumatol International, 23, pp. 27-36. Berbert, A., Kondo, C., Almendra, C., Matsuo, T., Dichi, I., 2005. Supplementation of fish oil and olive oil in patients with rheumatoid arthritis. Nutrition 21, pp.131– 6. Bochner, B. and Busse, W., 2005. Allergy and asthma. J Allergy Clin Immunol , 115, pp. 953–9. Calder, P., 2006. n-3 polyunsaturated fatty acids, inflammation and inflammatory diseases. American Journal of Clinical Nutrition, 83, pp. 1505s-19s. Dangardt, F., Osika, W., Chen, Y., 2010. Omega-3 fatty acid supplementation improves vascular function and reduces inflammation in obeseadolescents. Atherosclerosis 212(2), pp.580–5. Dwyer, J., Allayee, H. Fan. J. and Mar, R., 2004. Arachidonate 5 lipoxygenase promoter genotype, dietary arachidonic acid and atherosclerosis. New England Journal of Medicine, 350, pp. 29-57 He, K., Liu, K., Daviglus, ML., 2009. Associations of dietary long-chain n23 polyunsaturated fatty acids and fish with biomarkers of inflammation and endothelial activation (from the Multi-Ethnic Study of Atherosclerosis [MESA]). Am J Cardiol, 103, pp. 1238–43. Oh da, Y., Talukdar, S. and Bae, E., 2010. GPR120 is an omega-3 fatty acidreceptor mediating potent anti-inflammatory and insulin-sensitizing effects. Cell, 142(5), pp. 687–98. Schachter, H., Reisman, J., and Tran, K., 2004. Health effects of omega 3 fastty acids on asthma. AHRQ, 04-E013, p.2. Simopoulos, A., 2006. Evolutionary aspects of diet, the omega 6-omega 3 ratio and genetic variation. Biomedicine and Pharmacotherapy, 60, pp. 502-507. Wright, S., O’Prey, F., McHenry, M., 2008. A randomised interventional trial of omega-3-polyunsaturated fatty acids on endothelial function and disease activity in systemiclupus erythematosus. Ann Rheum Dis, 67, pp. 841–8. Read More