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Omega 3 fatty acid hypothesis
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===Mechanism=== Puri theorizes that a persistent, low grade viral infection blocks the [[delta-6-desaturase enzyme]], which is required for generating the long chain [[omega 3 fatty acid|omega-3]] and [[omega 6 fatty acid|omega-6]] [[polyunsaturated fatty acids]] such as [[DGLA]], [[arachidonic acid]] and EPA. This in itself will cause a variety of symptoms including sleep disturbances and improper immune responses.<ref>http://www.positivehealth.com/article/cfs-me/clinical-impovements-in-cfs-me-the-role-of-fatty-acids</ref>{{citation needed|reason=blog not adequate scientific source}} Moreover, EPA, a long chain omega 3 acid, is both a precursor to [[interferon]]s and is directly antiviral.<ref>http://www.positivehealth.com/article/cfs-me/clinical-impovements-in-cfs-me-the-role-of-fatty-acids</ref> These fatty acids are also precursors to [[eicosanoids]], signaling molecules that regulate growth during and after physical activity, inflammation or immunity after the intake of toxic compounds and pathogens, and act as messengers in the [[central nervous system]].<ref>http://www.positivehealth.com/article/cfs-me/clinical-impovements-in-cfs-me-the-role-of-fatty-acids</ref> Finally, deficiencies in arachidonic acid and [[docosahexaenoic acid]] (DHA) have deleterious effects on cell membranes. They lose their normal flexibility and become more rigid, affecting the protein receptor molecules and disrupting cell signaling. This causes cognitive impairment.<ref>http://www.positivehealth.com/article/cfs-me/clinical-impovements-in-cfs-me-the-role-of-fatty-acids</ref> Puri points to several very small studies that found increased [[choline]] in specific areas of the brains of CFS patients, including the [[occipital cortex]] and [[basal ganglia]] as evidence of unspecified alterations in fatty acid metabolism.<ref>http://www.sciencedirect.com/science/article/pii/S0952327804000122</ref><ref>http://journals.lww.com/neuroreport/pages/articleviewer.aspx?year=2003&issue=02100&article=00013&type=abstract</ref><ref>http://onlinelibrary.wiley.com/doi/10.1034/j.1600-0447.2002.01300.x/abstract</ref> Grey, et al have a similar theory. However, they think the impairment is not in the production of long chain fatty acids but rather the cleaving of long chain fatty acids from cell membrane to produce eicosanoids. They think that the immunological dysfunction and [[exercise]] intolerance seen in ME/CFS can be explained by an increased ratio of two eicosanoids, namely [[Leukotriene]] B4/[[Prostaglandin]] E2. Moreover, the increased choline observed in studies of ME patients could be due to increased [[Phospholipase A2]] activity and the breakdown of [[cell membrane]]s.
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