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Omega 3 fatty acid hypothesis
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Professor [[Basant Puri]] of [[Imperial College London]] has theorized that some of the symptoms of [[ME/CFS]] are caused by abnormal [[:Category:Fatty acids |fatty acid]] [[metabolism]] and can be ameliorated by supplementation with high dose [[eicosapentaenoic acid]] (EPA) and [[evening primrose oil]], a source of [[gamma-Linolenic acid]] (GLA). Gray, et al posit a similar hypothesis whereby the core features of ME/CFS β including reduced [[natural killer cell]] (NKC) function and [[exercise intolerance|exercise]] intolerance βΒ may be due to abnormal production of [[eicosanoid]]s, [[signaling molecules]] involved in [[inflammation]] that are produced from [[:Category:Fatty acids|fatty acids]] found in [[Cell membrane|cell membranes]].<ref>www.sciencedirect.com/science/article/pii/0306987794900469</ref> ==Theory== [[File:480px-EFA_to_Eicosanoids.svg.png|right|insert caption]] ===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. ===Treatment=== Puri recommends treatment with evening primrose oil, a source of GLA, and high dose EPA without DHA, such as [http://www.amazon.co.uk/Igennus-Vegepa-E-EPA-70-high-EPA/dp/B007W1JIQ2 VegEPA]. Both EPA and GLA block the conversion of AA to inflammatory [[leukotriene]]s [[eicosanoid|through various mechanisms]]. Similarly, Grey, et al, citing studies in [[rheumatoid arthritis]] point out increasing dietary Omega 3's decreases the amount of AA and [[linoleic acid]] (LA) (omega 6's that are substrates for LTB4) in the cell membrane, thus reducing LTB4 production. They note that dietary changes can take 12-18 weeks to manifest in clinical improvement.<ref>www.sciencedirect.com/science/article/pii/0306987794900469</ref> They do not distinguish between EPA and DHA supplementation. ==Evidence== There is little direct evidence to support Puri's hypothesis and no large scale clinical trials evaluating his proposed treatment have been conducted. Further research is warranted. ===EPA/AA ratios in CFS patients=== A study of twenty-two patients (defined using the CDC criteria) and twelve controls found that [[chronic fatigue syndrome|CFS]] patients have significantly lower EPA/AA and Omega3/Omega 6 (Ο3/Ο6) ratios owing to substantially increased levels of Omega 6 fatty acids (but not lower Omega 3s). These ratios correlated with some of the items on the [[FibroFatigue scale]] such as pain, fatigue, and memory deficits. The study also found significant correlations between the Ο3/Ο6 ratio and lowered serum [[zinc]] levels and lowered mitogen-stimulated [[CD69]] expression on CD3+, CD3+CD4+, and CD3+CD8+ [[T cell]]s.<ref>http://nel.edu/26-2005_6_pdf/NEL260605A22_Maes.pdf</ref> However, since patients have normal levels of EPA, it may not be that delta-6-desaturase is being blocked by viral activity as Puri hypothesizes but rather that AA is increased because it is being hydrolyzed by [[Phospholipase A2]] (PLA2) to produce eicosanoids. Increased PLA2 activity is observed in many neurological conditions<ref>http://pharmrev.aspetjournals.org/content/58/3/591.full</ref> and in inflammatory disorders such as [[fibromyalgia]].<ref>http://www.ncbi.nlm.nih.gov/pubmed/26585319</ref> EPA competes directly with AA for the [[phospholipase A2]] enzyme (PLA2) and thus inhibits the production of inflammatory eicosanoids. Over time, it reduces the amount of AA available in cell membranes. This suggests a possible role for EPA in the treatment of diseases where increased PLA2 activity is observed. ===Effects of fatty acid treatment=== The evidence for fatty acid treatment is mixed, owing in part to varying research criteria and incomparable treatments. A double-blind, placebo-controlled study of 63 patients with [[postviral fatigue syndrome]] found the 85% of patients found improvement at three months on Efamol Marine, a high Omega-6 formulation of evening primrose oil and fish oil (linoleic acid: 58%, GLA: 7.2%, EPA: 3.6%, and DHA: 2.4%) .<ref>onlinelibrary.wiley.com/doi/10.1111/j.1600-0404.1990.tb04490.x/abstract</ref> An attempt to replicate the study using Efamol Marine and the Oxford Criteria found no effect.<ref>http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0404.1999.tb00667.x/abstract</ref> In a small case study of four patients diagnosed by the [[Fukuda criteria]], Puri found that high dose EPA was associated with significant improvement after 12 weeks of treatment.<ref>http://www.sciencedirect.com/science/article/pii/S0952327804000122</ref> ===Fatty acids and viruses=== In vitro studies have found polyunsaturated fatty acids kill [[Epstein-Barr virus]].{{citation needed}} and [[herpes simplex virus]].<ref>http://aac.asm.org/content/15/1/67</ref> Long chain polyunsaturated fatty acids inactivate lipid-enveloped viruses<ref>http://onlinelibrary.wiley.com/doi/10.1111/j.1423-0410.1988.tb01606.x/abstract;jsessionid=DF7B92F709B1CA63B3F45AC77BF30BD3.f01t03</ref> ==Alternative hypotheses== [[Patricia Kane protocol|Patricia Kane]] thinks that diseases she classes as those of neurotoxicity (e.g., [[multiple sclerosis]], [[Parkinson's disease]], [[Chronic Fatigue Syndrome]]) often involve deficiencies of omega 6 and arachidonic acid in cell membranes due in part to the over-expression of [[very long chain fatty acid]]s. She believes that adding omega 3s before omega 6s are properly supplemented can be deleterious to health. (Patricia Kane does not have a doctorate from an accredited university.<ref>{{Cite web|url=https://www.chicagotribune.com/lifestyles/health/chi-autism-science-nov23-story.html|title=Autism treatment: Science hijacked to support alternative therapies|website=Chicago Tribune|access-date=2023-04-17}}</ref>. Ms. Kane has a history of making unsubstantiated claims, such as disputing the ALS diagnosis of a patient who later died of ALS and was later dismissed from Haverford Wellness Clinic partly in response to investigations of this case.<ref>{{Cite web|url=https://web.archive.org/web/20090307114535/http://cbs3.com/investigations/i.team.investigation.2.814584.html|title=I-Team Follow-Up: False Hope - cbs3.com|date=2009-03-07|website=web.archive.org|access-date=2023-04-17}}</ref>) ==See also== *[[Omega 3 fatty acid]] *[[Patricia Kane protocol]] ==References== <references /> [[Category:Medical hypotheses]]
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