The Connection Between Omega-3 Fatty Acids and Inflammatory Illnesses - Essay Example

The effects of omega-3 PUFA on inflammation in general Omega-3 fatty acids are composed of a unit of polyunsaturated fatty acids (PUFA). The family of Omega-3 fatty acids has a comparable chemical arrangement. Three omega-3 fatty acids are known; these are essential components in the human diet. These include eicosapentaenoic acid (EPA), alpha-linolenic acid (ALA), as well as docosahexaenoic acid (DHA) (Fernandes 2004). According to Weber et al. (2006), the omega-3 polyunsaturated fatty acids (PUFA) obtained from fish oil, that is EAP and DHA possess the most potent immunomodulatory activities; hence it is more organically powerful than ALA. Interestingly, the human body cannot produce these acids, however, once in the body, they are transformed into more complex structures. These structures have been noted to perform numerous important biological functions. ALA is, in fact, a predecessor to EPA and DHA (Gura et al. 2008). This is because when ALA is taken by humans, it is transformed into EPA and DHA. This is because EPA and DHA are easily transformed into complex polyunsaturated fatty acids. The greatest suppliers of ALA originate from fish such as salmon herring, halibut, sardines and Chinook (Racco 2009). As a result, many people consume fish oil to acquire the omega-3 fatty acid, rather than taking itself, for several reasons. ALA, furthermore, can be obtained from foods such as seeds, oils, green leafy vegetables, nuts, and beans among many others. As said by Gura et al. (2008), dietary fish oil supplementation exists documented to enhance inflammatory illnesses, for example, irritable bowel, asthma as well as rheumatoid arthritis. Various impacts of omega-3 PUFA are as a result of modulation of the quantity depending on the types of eicosanoids that are produced. This is because other impacts are expressed by eicosanoid-independent means, which include the behavior following transcription factor activity, intracellular indicating routes as well as gene expression (Cheung et al. 2009). It is worth noting that animal experiments coupled with clinical intervention studies highlight the anti-inflammatory characteristics that omega-3 fatty acids pose. Therefore, these strengthen its worth in the running of inflammatory and autoimmune illnesses. Numerous clinical studies on the impact on different inflammatory diseases following the use of food supplements enriched with fish oils are coming up on a day-to-day basis. This is because of the increased knowledge in the causative agents of the diseases, which include rheumatoid arthritis, irritable bowel, and asthma. As a result of this, numerous place restricted tests on the effect of fish oil on chronic inflammatory illnesses reveal major benefits, including reduced disease action. This, as a result, has reduced the application of anti-inflammatory drugs (Price, Nelson & Clarke 2010; Simopoulos, Kifer & Martin 2004). The primary substantiation of the imperative function of the nutritional consumption of omega-3 PUFAs in inflammation exists as a result of epidemiological observations. These observations focused on inflammatory disorders such as asthma in a group of people of Greenland Eskimos when they were weighed against age and gender-matched population residing in Denmark (Kromann & Green 2010). It was noted that inflammation was mediated by how the pattern of eicosanoids differs, as well as the production of other lipid mediators. What is more, marine n-3 PUFAs were found to transform the production of inflammatory proteins, as well as growth factors, chemokines, cytokines, as well as matrix proteases. This outcome was as a result of the activation of principle transcription factors, which were noted to take part in the regulation of inflammatory gene expression (Wang et al. 2008). Notably, the two transcription factors that play an important function in inflammation include nuclear factor κ B (NFκB) and PPAR-γ. The main transcription factor in the upregulation of cyclooxygenase-2 genes, an inflammatory cytokine, and adhesion molecule is NFκB (Fortin et al 2005; Senkal et al 2007). Since NFκB is activated through signaling cascade, which is initiated by a stimulus situated at the extracellular space, it encompasses an inhibitory subunit called phosphorylation (IκB) of NFκB. This facilitates the movement of the lingering NFκB dimmer to the nucleus (Senkal et al 2007). PPAR-γ, the subsequent transcription factor, is considered to operate in an anti-inflammatory mode. This is because it disrupts the activation of NFκB while at the same time modifying inflammatory gene expression directly. This leads to the creation of interesting relations between the two transcriptions factors (Prickett, Robinson & Steinberg 2011). Notably, n-3 PUFAs is involved in the synchronization of NFκB and PPAR-γ. On another study, EPA and DHA repressed endotoxin-stimulated expression of IL-8 and of IL-6, which are end products of cultured human endothelial cells (Weber et al. 2006; Lewis, Lee & Austen 2006). In the study, APA or fish oil inhibited endotoxin stimulated TNF-α assembly through cultured monocytes (Jump & Clarke 2009; Price, Nelson & Clarke 2010). As a result, EPA (fish oil) reduced significantly NFκB’s endotoxin-induced activation, which is found in human monocytes. This was linked to decreased IκB phosphorylation (Prickett, Robinson & Steinberg 2011), which is possibly caused by diminished activation of mitogen-activated protein kinases (Caughey et al. 2007). Because of these observations, it is easy to understand the outcome of marine n-3 PUFAs, which operates on inflammatory gene expression through the restraining of activation of the transcription factor NFκB. The use of fish oil to test animal feeding exemplifies the behavior in the cell culture. This can be associated with the outcomes of marine n-3 PUFAs on NFκB formation as well as the production of inflammatory cytokine. Feeding on corn oil can be compared with fish oil reduced NFκB activation, which is typically found in endotoxin-activated murine spleen lymphocytes (Dinarello 2013). Some studies have found that feeding fish oil to mice relies on ex vivo production of TNF-α, IL-1β, and IL-6, which is a result of endotoxin-stimulated macrophages (Dinarello 2013; Cleland & James 2007). Several studies have researched the effect of healthy human supplementation of the diet with fish oil. They have found that there is a reduction in the production of TNF-α, IL-1β, IL-6 coupled with a variety of growth factors by endotoxin-stimulated monocytes (Dinarello 2013; Eaton, Eaton & Konner 2007). Rheumatoid Arthritis The treatment of rheumatoid arthritis using omega-3 fatty acids began to interest scientists in the mid-eighties. This was as a result of the demonstration in numerous autoimmune mice strains. This is because it demonstrated that omega-3 fatty acids condensed the spread of glomerulonephritis. Moreover, studies on dose-response confirmed that DHA functions better than EPA. As a result, foods with a combination of the two fatty acids proved to be more effective due to their combined energy (Eaton et al 2007; Cleland, Hill & James 2005). Kremer (2005) conducted a pilot study involving 17 patients diagnosed with rheumatoid arthritis who took 1.8 g EPA and 0.9 g DHA. It is worth noting that this study existed as a double-blind, restricted, randomized experiment of 12 weeks’ duration. A follow-up assessment one to two months after the foods were suspended was also conducted and documented. The outcome portrayed a momentous variation in morning stiffness among the two groups during the 12-week evaluation. It was noted that the control group worsened while the group that was enriched with fish oil remained unresponsive. In a succeeding experiment, Kremer (2005) calculated neutrophil 〖LTB〗_4 production. He noted that it stood at low levels in those people consuming fish oil. The extended inhibition of 〖LTB〗_4 past the time of fish oil supplementation was most probably attributed to the sustained clinical advantages experienced following discontinuation of fish oil. Moreover, drawn-out consequences on the immune system were consequently noted in ordinary volunteers consuming fish oil. In a differing study, Ross (2009) examined the possible mechanisms of EPA + DHA supplementation in a population diagnosed with rheumatoid arthritis. Daily for six weeks, twelve active-diseases victims ingested 3.6 g EPA and 2.4 g DHA daily for six weeks. Following 6 weeks of intake of fish oil, 〖LTB〗_4 diminished by 33 percent pegged with a 37 percent decline in the amount of platelet activation factor (PAF) (Friesecke et al. 2008). This is because the examination of the combination of neutrophil membranes in the fatty acid following the six weeks’ consumption of fish oils occasioned a 33 percent decline in AA coupled with an instantaneous twenty times increase in EPA composition from the period before the diet intake. It is worth noting that DHA was not identified. According to Ross (2005), IL-1β, IL-1α, and TNF were reduced by 42 percent at 6 weeks. However, a supplementary decline was noted 10 weeks following the discontinuation. It is, thus, evident that fish-oil stimulated repression of IL-1 gives rise to the restructuring of medical signs and symptoms of disease action in rheumatoid arthritis patients, which is greater than reticence of leukotriene metabolism. Inflammatory Bowel Disease Inflammatory bowel disease is linked but exist as diverse complex disorders with immunologic, genetic pegged with environmental components (Elson 2005). The modern move towards the management of ulcerative colitis has centered on soluble intermediaries of inflammation. The intermediaries that have been deliberated comprehensively are the AA metabolites, cytokines, prostaglandins, and leukotrienes. It is key to note that ulcerative colitis patients display a higher level of 〖LTB〗_4, the AA’s end-product, through the 5-lipoxygenase route. Heartening results have been documented by others (McCall et al. 2009; Salomon, Kornbluth & Janowitz 2010). Belluzzi et al. (2006) highlighted a condensed rate of degeneration Crohn’s patients through supplementation of fish oil concoction. Furthermore, Endres et al. (2009) assessed the proof of the therapeutic significance of omega-3 fatty acids in those suffering from inflammatory bowel illness. He concluded that several studies painted considerable progress in clinical achievement and a steroid-sparing outcome. On the contrary, others have shown simply a trend towards advancement. This difference in response may be as a result of the heterogeneity of inflammatory bowel disease (Blok, Katan & Van der Meer 2006). Asthma This is caused by intermediary inflammatory action in the lungs. It has been noted to be the most prevalent chronic disease during childhood. The prostaglandins and leukotrienes play a role in the inflammatory surge, which takes place in asthmatic airways. It is vital to state that evidence exists in regards to airway irritation even in recently established asthma patients in 2 to 12 months following their primary warning signs (Laitinen, Laitinen & Haahtela 2013). Lymphocytes, mast cells, eosinophils, and macrophages are some of the cells that play a part in asthma. Moreover, the inflammatory intermediaries include cytokines pegged with growth factors in addition to the eicosanoids. These are produced by AA metabolism, which plays key roles in the fundamental asthma inflammatory means (Adolf 2009). Prostaglandins and Leukotrienes have been found to play to the most significant role in the origin of asthma. As a result, the leukotrienes are essential causes of airway edema, bronchospasm, mucus discharge, as well as inflammatory cell movement (Broughton et al. 2007) - all of these components play significant roles in the asthmatic symptomatology. Elsewhere, Broughton et al. 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