-Arachidonic acid- “The Good & the Bad”

GOODArachidonic acid is not one of the essential fatty acids. However it does become essential if there is a deficiency in linoleic acid or if there is an inability to convert linoleic acid to arachidonic acid which is required by most mammals.

BAD – Scientists believe omega-6s are pro-inflammatory, while omega-3s are anti-inflammatory ( 1 ). Of course, inflammation is essential for your survival. It helps protect your body from infection and injury, but it can also cause severe damage and contribute to disease when it’s chronic or excessive. Pro-inflammatory eicosanoids are important chemicals in the immune system. However, when too many of them are produced, they can increase inflammation and inflammatory disease ( 36 ). Although omega6 fats are essential, the modern Western diet contains far more omega6 fatty acids than necessary

Arachidonic Acid: The Good and Bad

Arachidonic acid is an essential fatty acid, which is consumed in small amounts in our regular diets.  It is considered an “essential” fatty acid because it is an absolute requirement for the proper functioning for the human body.  Essential fatty acids (EFA’s) are polyunsaturated fatty acids that the body cannot synthesize and therefore must obtain from the diet.  There are two families of EFAs:  omega-6 and omega-3.  The most important omega-6 fatty acids are linoleic Acid (LA), gamma-linolenic acid (GLA), dihomogamma-linolenic acid (DGLA), and Arachidonic acid (AA).  The most important omega-3 fatty acids are alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA).  Omega-3 fatty acids can be found in fish and certain plant oils.  Linoleic acid, an omega-6 fatty acid, can be found primarily in seeds, nuts, grains and legumes.  Linoleic acid can be converted into arachidonic acid.  Arachidonic acid can be found mainly in the fatty parts of meats and fish (largely red meat), so vegetarians usually have lower levels of arachidonic acid in the body than those with omnivorous diets.   
There is a great deal of controversy about arachidonic acid.  Some information says that arachidonic acid can cause health problems and other sources say it is needed to aid in muscle growth.  Arachidonic acid is vital to the operation of the prostaglandin system.  Prostaglandins are part of a class of substances called eicosanoids.  Eicosanoids influence numerous metabolic activities including platelet aggregation (blood clotting), inflammation, hemorrhages, vasoconstriction and vasodilation, blood pressure, and immune function.  The eicosanoids contain twenty carbons and include the prostaglandins (PG), prostacyclins (PGI2), thromboxanes (TX), leukotrienes (LT), and hydroxy acids.  There are bad (pro-inflammatory) and good eicosanoids (anti-inflammatory) and they compete with each other.  Two prostaglandins arachidonic acid is the substrate to are PGE2 and PGF2a.  The first one is generally thought to be bad while the second is thought to be good.  Studies point to PGF2a, specifically, as being the prostaglandin most closely tied to increase skeletal muscle protein synthesis.  Skeletal muscle tissue has no capacity to actually store prostaglandins, so the only local source for PGF2a is the arachidonic acid that is retained in the outer phospholipids layer of each cell.  It is the stretching of muscle fibers during intense physical exercise that causes arachidonic acid to be released and metabolized to active prostaglandins.  Arachidonic acid is actually the chemical messenger first released by your muscles during intense weight training, controlling the core physiological response to exercise and regulating the intensity of all growth signals to follow.  Also, anytime you have tissue injury, inflammation is involved in healing the wound.  Some prostaglandins have pro-inflammatory affects.  The fact is, if you work out, you have tissue injury – micro trauma to the muscle tissue.  As your delayed onset muscle soreness will tell you, inflammation is involved in the healing of this micro trauma.  Furthermore, in both animal and human studies it has been shown that exercise lowers the content of arachidnoic acid in skeletal muscle tissue.  Therefore, there has been talk of arachidonic acid supplementation.  
The omega-6 and omega-3 fatty acid families form different eicosanoids with different activities.  They compete with one another for the enzyme (PLA2) that catalyzes the release of the essential fatty acids from the cell membrane.  Also, they compete for cyclooxygenase and lipoxygenase, the enzymes necessary for eicosanoid synthesis.  A proper balance of these fatty acids in the diet is therefore important for the maintenance of good health.  An increase in the consumption of one family will reduce the synthesis of eicosanoids derived from the other family, which will ultimately have an effect on overall health.  According to many sources, humans evolved on a 1:1 dietary ratio of omega-6 to omega-3.  With today’s typical “Western” dietary habits the average person consumes a dietary ratio of between 25 and 40 to 1 omega-6 to omega-3.  This highly imbalanced ratio is due to the dramatic increase in consumption of omega-6 fatty acids in vegetable oils, which contain linoleic acid, and meat and shellfish, which contain arachidonic acid.  At the same time, we are consuming less of the omega-3 fatty acids.  Since the omega-6 compete with the omega-3 fatty acids for incorporation into cell membranes and subsequent metabolism, high intake of the omega-6 fatty acids will result in an increased production of unhealthy eicosanoids derived from arachidonic acid.  Omega-3 fatty acids produce eicosanoids that are anti-inflammatory.  These eicosanoids help support normal blood pressure by relaxing the arteries and blood vessels and decreasing blood lipids.  They also decrease blood-clotting factors.  Omega-6 fatty acids can produce both anti-inflammatory and/or inflammatory and vasoconstricting eicosanoids.  Omega-6 can be good for you if you take them in the right amount with omega-3.  Omega-3 can counteract the pro-inflammatory effects of omega-6 fatty acids.  When omega-3 and omega-6 are in balance, they are both very good but when omega-6 is in excess, they become bad.  For that reason, it is essential to have a proper balance of omega-6 and omega-3 fatty acids.  A healthy ratio of omega-6 to omega-3 ranges from 1:1 to 1:3.  
Now that arachidonic acid supplements are on the market, athletes need to be aware that there needs to be a balance of omega-6 and omega-3 fatty acids in their diet.  Supplementation is acceptable only if you are consuming enough omega-3 fatty acids to balance with the added omega-6 fatty acid (arachidonic acid) from the supplement.  You have a choice to make.  If your primary concern is muscular gain supplementing arachidonic acid could help as long as you are consuming enough omega-3 to balance your diet.   However, if you suffer from one of the many inflammatory conditions that plague many people who exercise (tendonitis, bursitis, arthritis, etc.) then you should probably stay away from it since it can be pro-inflammatory.  Furthermore, if you suffer from diabetes, asthma, high blood pressure, high cholesterol, heart disease, are pregnant, or are suffering from any inflammatory disease you should not supplement arachidonic acid in your diet.  Just remember if you are going to take arachidonic acid supplements you should have a healthy ratio of omega-6 to omega 3.

-THE ACUTE INFLAMMATORY PROCESS-

The acute inflammatory process, arachidonic acid metabolism and the mode of action of anti-inflammatory drugs.- Arachidonic acid is a polyunsaturated fatty acid covalently bound in esterified form in the cell membranes of most body cells. Following irritation or injury, arachidonic acid is released and oxygenated by enzyme systems leading to the formation of an important group of inflammatory mediators, the eicosanoids. It is now recognised that eicosanoid release is fundamental to the inflammatory process. For example, the prostaglandins and other prostanoids, products of the cyclooxygenase enzyme pathway, have potent inflammatory properties and prostaglandin E2 is readily detectable in equine acute inflammatory exudates. The administration of nonsteroidal anti-inflammatory drugs results in inhibition of prostaglandin synthesis and this explains the mode of action of agents such as phenylbutazone and flunixin. Lipoxygenase enzymes metabolise arachidonic acid to a group of noncyclised eicosanoids, the leukotrienes, some of which are also important inflammatory mediators. They are probably of particular importance in leucocyte-mediated aspects of chronic inflammation. Currently available non-steroidal anti-inflammatory drugs, however, do not inhibit lipoxygenase activity. In the light of recent evidence, the inflammatory process is re-examined and the important emerging roles of both cyclo-oxygenase and lipoxygenase derived eicosanoids are explored. The mode of action of current and future anti-inflammatory drugs offered to the equine clinician can be explained by their interference with arachidonic acid metabolism. For full article : https://onlinelibrary.wiley.com/doi/abs/10.1111/j.2042-3306.1984.tb01893.x?sid=nlm%3Apubmed

References:
1.  Galli, C., Simopoulos, A.P., Tremoli.  Fatty Acids and Lipids:  Biological Aspects.  World Rev Nutr Diet 1994, 75: 1-196. 
2.  Mann and Sinclair.  Contribution of Meat Fat to Dietary Arachidonic Acid.  Lipids 1998, 33: 437-40 
3.  Phinney et al.  Reduced Arachidonate in Serum Phospholipids and Cholesterol Esters Associated with Vegetarian Diets in Humans.  Am. J. Clin. Nutr. 51: 385-92.
4.  Rodemann, Peter and Alfred Goldberg.  Arachidonic Acid, Prostaglandin E2 and F2a Influence Rates of Protein Turnover in Skeletal and Cardiac Muscle.  J Biol Chem 
1982, 257:1632-1638.  
5.  Simopoulos, A.P., Leaf, A., Salem, N. Jr.  Essentiality of and Recommended Dietary Intakes for Omega-6 and Omega-3 Fatty Acids.  Ann Nutr Metab 1999, 43: 127-130.
6.  Smith, WL.  The Eicosanoids and Their Biochemical Mechanisms of Action.  Biochem J 1989, 259:315-324.

Vegan-Stuffed Roasted Capsicum with Spinach patties

IMG_9125.JPG

So I have decided to go  plant based for a while to try and reduce the inflammation in my body and I feel that eating  meat at the moment may be impacted this considerably. This could be due to the ARACHIDONIC ACID

Arachidonic acid is an inflammatory omega-6 fatty acid. … Arachidonic acid is found in animal products, like poultry and eggs. The amount of arachidonic acid found in just one egg a day can  elevated arachidonic acid levels in the bloodstream, and increase inflammation  considerably – Japanese researchers learned. ( see next blog for more information)

RECIPE

CAPPY

  •  1 cup of cooked buckwheat
  • 1/8 bunch enoki mushrooms chopped
  • 1 Ripened Roma tomato chopped
  • Bunch Fresh Thai basil- any basil will do
  •  salt & Pepper to tast
  • 1/4 teaspoon Tumeric
  • 1 teaspoon dried vegetable stock / broth
  • MIX altogether
  • 4 red or Yellow capsicum – preferably with 4 bums ( bottom of cappy)- tops cut off and insides cleaned
  • Mix all together and stuff  the capsicum
  • Place in baking tray and bake until soft.

SPINACH PATTIES

  • one bunch of chopped and little cooked silverbeet or spinach
  • Squeeze excess water out
  • Add thyme, parsley
  • Grated vegan cheese- small handful
  • Tablespoon Chia seeds that have been soaked in 1/4 cup water 10 mins prior
  • Salt and Pepper to taste
  • 1/4 cup Tapioca or GF flour
  • Mix together – looks like a batter
  • Shallow fry until golden brown with grapeseed or Extra Virgin Olive Oil

 

Serve with Fresh Cos lettuce  with squeeze of lemon and dash of Truffle oil.

 

YUMMOOOOO  😋 😋 😋

ENJOY 😊

 

 

 

RESOLVING PAIN

 Inflammation – PAIN- Chronic Disease

Focus On: Issue 3 2016

 Did you know Chronic inflammatory diseases have reached epidemic levels in industrialised countries. According to the 2014-2015 National Health Survey, half of all Australians live with a chronic inflammatory disease such as asthma, cardiovascular disease, diabetes mellitus, obesity, arthritis, Alzheimer’s disease, autoimmune disease, and cancer.4, 5, 6

It was long assumed that an acute inflammatory process was passively self-limiting, with chemotactic factors (substances that stimulate the migration of inflammatory cytokines) simply diluting or draining away.7 However this is not the case, evidenced by the development of chronic inflammatory conditions, where inflammatory mediators persist at a site, and the resolution of the inflammatory process failing to engage.8

It is  now known that the resolution of inflammation is an active process, controlled by a family of chemicals known as specialised pro-resolving mediators (SPMs).9 SPMs promote inflammation resolution, reduce pain, encourage the clearance of pathogens and mitigate pathological inflammation, without immunosuppression. Together, these qualities make SPMs an important consideration for the treatment of chronic, unremitting inflammatory conditions.

SPMs are derivatives of omega-3 essential fatty acids (EFAs), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). They are produced during the resolution phase of an acute inflammatory response, working to switch off the inflammatory process.10, 11 Several classes of SPMs are derived from EFAs, including resolvins (e.g. RvE, RvD1), protectins (e.g. PD1), and maresins (e.g.MaR1, HDHA).12 Lipoxins, another class of SPMs, are produced from the omega-6 fatty acid, arachidonic acid.

Inflammation, initiated

At the genesis of these inflammatory states is an initial insult, such as a tissue injury, infection, or exposure to an allergen or toxin, which activates the acute inflammatory response.13, 14 Here, an influx of poly-morpho-nuclear neutrophils (PMNs) enter the affected site and produce inflammatory mediators (e.g. cytokines, chemokines and eicosanoids) needed to trigger tissue repair. PMNs also phagocytose pathogens, and finally themselves undergo apoptosis,15, 16 causing inflammation and tissue damage, which must be cleared by macrophages in a process known as efferocytosis. Clearing this cellular debris enacts the resolution of the inflammatory process,17 allowing the body to once again return to homeostasis.

SPMs: inflammation stop signs

Entering this stage of inflammatory resolution relies on the synthesis of SPMs, which reduce PMN infiltration and increase efferocytosis.18 SPMs also achieve resolution via the regulation of macrophage polarisation. Macrophages exist in two broad phenotypes; M1 macrophages, which are pro-inflammatory, and M2 macrophages, which synthesise SMPs, inhibit PMNs, and promote efferocytosis, tissue repair, and resolution. SPMs trigger the macrophage switch from the M1 to the M2 phenotype, thereby promoting resolution.19

Additionally, SPMs have specific anti-inflammatory mechanisms, decreasing pro-inflammatory and increasing anti-inflammatory mediator production.20 In animal models, resolvins demonstrate the ability to reduce the production of pro-inflammatory eicosanoids and cytokines such as prostaglandin E2 (PGE2), leukotriene B4 (LTB4), interleukin-1β (IL-1β), IL-17 and IL-6.21, 22 Resolvins have also been shown to inhibit tumour necrosis factor alpha (TNF-α) activation in vitro and in animal models.23 SPMs also counter-regulate inflammatory gene transcription, and increase the clearance of inflammatory mediators by up-regulating chemokine binding receptors on T cells and PMNs, which are then phagocytosed by macrophages.24 However, in patients experiencing chronic inflammatory conditions, SPM production can be compromised,25 preventing the resolution of their condition. Supporting their presentation with Specialised Pro-Resolving Mediators will therefore provide the body with the capacity to work toward resolution of their inflammation.

Reduce the pain too, please

Additionally, SPMs also carry standalone analgesic properties. Shown to influence signalling within the brain, the resolvin RvE1 has demonstrated capacity to inhibit glutamate release and N-methyl-D-aspartate (NMDA) receptor hyperactivity, both important targets for pain relief.26 Exhibited further in animal models of inflammatory pain, resolvins have reduced pain-associated behaviours, and produced comparable pain relieving effects to the pharmaceutical medication pregabalin.28 Whilst reducing inflammation can also provide pain relief, these additional analgesic effects of SPMs will be of particular benefit for those patients experiencing concomitant chronic pain.

The many patients of SPMs

Given their pro-resolving and anti-inflammatory actions, SPMs are indicated in any condition involving chronic, unremitting inflammation. One such example commonly presenting in clinical practice is arthritis, with the crucial role of SPMs in this condition demonstrated in several human and animal studies.29, 30, 31, 32 Beyond this, Table 1 explores further evidence-based applications of SPMs in a varying range of inflammatory conditions.

Table 1. Overview of emerging research and applications for SPMs.

Condition SPM mediator studied Research outcomes
Allergies RvD1 and 17-HDHA Inhibited immunoglobulin E (IgE) production and suppressed differentiation of naïve B cells into IgE secreting cells in vitro.33
Endometriosis RvD1 and 17(R)-RvD1 Reduced severity of vaginal hyperalgesia and reduced vascular permeability in endometrial cysts in rat model of endometriosis.34
Psoriatic dermatitis RvE1 Potently suppressed inflammatory cell infiltration and reduced expression of IL-23 in skin and dendritic cells in mouse model of psoriatic dermatitis.35
Wound healing RvD1, RvD2 and RvE1 Inhibited neutrophil migration and accelerated wound healing in mouse model; RvE1 was most effective, and caused more mature collagen organisation and reepithelialisation.36
Cancer RvD1, RvD2 and RvE1 Inhibited debris-stimulated cancer progression by enhancing macrophage phagocytosis in mouse models.37
Sjögren’s syndrome AT-RvD1 Down-regulated Sjögren’s syndrome associated inflammatory genes and reduced apoptosis in Sjögren’s syndrome mouse model.38
Periodontitis associated bone loss RvD2 Modulated gene expression, favouring bone preservation, and down-regulated interferon gamma (IFN-γ) without dampening Porphyromonas gingivalis specific immune response in mice.39
Atherosclerosis RvE1 Reduced atherosclerotic lesion size, the formation of severe lesions, and the expression of pro-atherogenic genes in mice.40
Inflammatory bowel disease RvD2, AT-RvD1, MaR1, and 17-HDHA Have been shown to help reduce intestinal tissue damage, reduce inflammation and neutrophil infiltration, maintain body weight, and increase survival in animal models of inflammatory bowel disease.41, 42, 43

SPMs and EFAs are allies

It is important to note that although EPA and DHA are precursors of SPMs, EFAs do not possess the same unique pro-resolving qualities.44 Additionally, during states of chronic inflammation,45 and with progressive ageing,46 the body’s capacity to convert EFAs into SPMs may be compromised. This is a potential explanation for why fish oil, while reducing inflammation, may not always be clinically efficacious in fully resolving established inflammatory states. Therefore, SPMs do not replace EFA therapy, and vice versa – their actions are distinct but complementary. EFA supplementation should be utilised to correct deficient dietary intake, during times of increased demand (e.g. pregnancy) and to influence the induction of the acute inflammatory cascade (preventing the development of chronic inflammation). Meanwhile, providing Specialised Pro-Resolving Mediators augments the resolution of chronic inflammatory conditions, given its targeted action in resolving chronic, unremitting inflammation. For the chronically inflamed patient, EFAs and SPMs are ideally prescribed together to resolve existing inflammation, and prevent the development of inflammation in the future.

Innovative anti-inflammatories

The reality that chronic inflammatory conditions have now reached epidemic proportions is evidenced via patients’ presentation in clinical practice. Whilst resolution of these states can often present a clinical challenge, Specialised Pro-Resolving Mediators now offer an innovative and unique solution. These lipid mediators promote the resolution of chronic, unremitting inflammation, whilst also carrying their own unique anti-inflammatory and analgesic properties. Complementing EFAs which supplement dietary intake and prevent the development of chronic inflammation, SPMs offer hope and freedom for many inflamed patients.

written by:

Metagenics

When taking any supplements you should seek professional advice and take only as prescribed 

References

  1. Prevete N, Liotti F, Amoresano A, Pucci P, de Paulis A, Melillo RM. New perspectives in cancer: Modulation of lipid metabolism and inflammation resolution. Pharmacol Res. 2018 Feb;128:80-87. doi: 10.1016/j.phrs.2017.09.024. Epub 2017 Oct 3.
  2. Wang X, Zhu M, Hjorth E, Cortés-Toro V, Eyjolfsdottir H, Graff C, et al. Resolution of inflammation is altered in Alzheimer’s disease. Alzheimer’s & Dementia. 2015 Jan; 11(1): 40-50.
  3. Fredman G, Hellmann J, Proto JD, Kuriakose G, Colas RA, Dorweiler B, et al. An imbalance between specialized pro-resolving lipid mediators and pro-inflammatory leukotrienes promotes instability of atherosclerotic plaques. Nature Communications. 2016;7:12859.
  4. Australia Institute of Health and Welfare. Australia’s Health Report 2016 [Internet]. Canberra ACT: AIHW; 2016 [updated 2016 May 16; cited 2018 Nov 14]. Available from: https://www.aihw.gov.au/reports/australias-health/australias-health-2016/contents/summary.
  5. The Walter and Eliza Hall Institute of Medical Research. Inflammation [Internet]. Parkville (VIC): The Walter and Eliza Hall Institute of Medical Research; 2018 [updated 2018 Aug 8; cited 2018 Nov 8]. Available from: https://www.wehi.edu.au/research/research-fields/inflammation.
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  7. Recchiuti A, Serhan CN. Pro-resolving lipid mediators (SPMs) and their actions in regulating miRNA in novel resolution circuits in inflammation. Front Immunol.  2012 Oct 22;3:298. doi: 10.3389/fimmu.2012.00298.
  8. Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014 Jun 5;510(7503):92-101. doi: 10.1038/nature13479.
  9. Recchiuti A, Serhan CN. Pro-resolving lipid mediators (SPMs) and their actions in regulating miRNA in novel resolution circuits in inflammation. Front Immunol.  2012 Oct 22;3:298. doi: 10.3389/fimmu.2012.00298.
  10. Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014 June 5;510(7503):92-101. doi: 10.1038/nature13479.
  11. Chiang NC, Serhan CN. Structural elucidation and physiologic functions of specialized pro-resolving mediators and their receptors. Mol Aspects Med (Internet). 2017 Dec;58:114-29. doi: 10.1016/j.mam.2017.03.005.
  12. Hirahashi J. Omega-3 polyunsaturated fatty acids for the treatment of IgA nephropathy. J Clin Med. 2017 Jul;6(7):70. doi: 10.3390/jcm6070070.
  13. Gallo J, Raska M, Kriegova E, Goodman SB. Inflammation and its resolution and  the musculoskeletal system. J Orthop Translat. 2017 Jul;10:52-67. doi: 10.1016/j.jot.2017.05.007.
  14. Souza PR, Norling LV. Implications for eicosapentaenoic acid- and docosahexaenoic acid-derived resolvins as therapeutics for arthritis. Eur J Pharmacol. 2016 Aug 15;785:165-173. doi: 10.1016/j.ejphar.2015.05.072.
  15. Souza PR, Norling LV. Implications for eicosapentaenoic acid- and docosahexaenoic acid-derived resolvins as therapeutics for arthritis. Eur J Pharmacol. 2016 Aug 15;785:165-173. doi: 10.1016/j.ejphar.2015.05.072.
  16. Spite M, Serhan CN. Novel lipid mediators promote resolution of acute inflammation: impact of aspirin and statins. Circ Res. 2010 Nov 12;107(10):1170-84. doi: 10.1161/CIRCRESAHA.110.223883.
  17. Spite M, Serhan CN. Novel lipid mediators promote resolution of acute inflammation: impact of aspirin and statins. Circ Res. 2010 Nov 12;107(10):1170-84. doi: 10.1161/CIRCRESAHA.110.223883.
  18. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014; 19: 21- 36. doi: 10.1016/j.cmet.2013.10.006.
  19. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metab. 2014 Jan 7;19(1):21-36. doi: 10.1016/j.cmet.2013.10.006.
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  24. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014; 19: 21- 36. doi: 10.1016/j.cmet.2013.10.006.
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  28. Klein CP, Sperotto ND, Maciel IS, Leite CE, Souza AH, Campos MM. Effects of D-series resolvins on behavioral and neurochemical changes in a fibromyalgia-like model in mice. Neuropharmacology. 2014 Nov;86:57-66. doi: 10.1016/j.neuropharm.2014.05.043.
  29. Arnardottir HH, Dalli J, Norling LV, Colas RA, Perretti M, Serhan CN. Resolvin D3 is dysregulated in arthritis and reduces arthritic inflammation. J Immunol. 2016 Sep 15;197(6):2362-8. doi: 10.4049/jimmunol.1502268.
  30. Perretti M, Norling LV. Actions of SPM in regulating host responses in arthritis. Mol Aspects Med. 2017 Dec;58:57-64. doi: 10.1016/j.mam.2017.04.005.
  31. Barden AE, Moghaddami M, Mas E, Phillips M, Cleland LG, Mori TA. Specialised pro-resolving mediators of inflammation in inflammatory arthritis. Prostaglandins Leukot Essent Fatty Acids. 2016 Apr;107:24-9. doi: 10.1016/j.plefa.2016.03.004.
  32. Perretti M, Norling LV. Actions of SPM in regulating host responses in arthritis. Mol Aspects Med. 2017 Dec;58:57-64. doi: 10.1016/j.mam.2017.04.005.
  33. Kim N, Ramon S, Thatcher TH, Woeller CF, Sime PJ, Phipps RP. Specialized proresolving mediators (SPMs) inhibit human B-cell IgE production. Eur J Immunol. 2016 Jan;46(1):81-91. doi: 10.1002/eji.201545673.
  34. Dmitrieva N, Suess G, Shirley R. Resolvins RvD1 and 17(R)-RvD1 alleviate signs of inflammation in a rat model of endometriosis. Fertil Steril. 2014 Oct;102(4):1191-6. doi: 10.1016/j.fertnstert.2014.06.046.
  35. Sawada Y, Honda T, Nakamizo S, Otsuka A, Ogawa N, Kobayashi Y, et al. Resolvin E1 attenuates murine psoriatic dermatitis. Sci Rep. 2018 Aug 8;8(1):11873. doi: 10.1038/s41598-018-30373-1.
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  39. Mizraji G, Heyman O, Van Dyke TE, Wilensky A. Resolvin D2 restrains Th1 immunity and prevents alveolar bone loss in murine periodontitis. Front Immunol. 2018 Apr 25;9:785. doi: 10.3389/fimmu.2018.00785.
  40. Salic K, Morrison MC, Verschuren L, Wielinga PY, Wu L, Kleemann R, et al. Resolvin E1 attenuates atherosclerosis in absence of cholesterol-lowering effects and on top of atorvastatin. Atherosclerosis. 2016 Jul;250:158-65. doi: 10.1016/j.atherosclerosis.2016.05.001.
  41. Bento AF, Claudino RF, Dutra RC, Marcon R, Calixto JB. Omega-3 fatty acid-derived mediators 17(R)-hydroxy docosahexaenoic acid, aspirin-triggered resolvin D1 and resolvin D2 prevent experimental colitis in mice. J Immunol. 2011 Aug 15;187(4):1957-69. doi: 10.4049/jimmunol.1101305.
  42. Chiu CY, Gomolka B, Dierkes C, Huang NR, Schroeder M, Purschke M, et al. Omega-6 docosapentaenoic acid-derived resolvins and 17-hydroxydocosahexaenoic acid modulate macrophage function and alleviate experimental colitis. Inflamm Res. 2012 Sep;61(9):967-76. doi: 10.1007/s00011-012-0489-8.
  43. Marcon R, Bento AF, Dutra RC, Bicca MA, Leite DF, Calixto JB. Maresin 1, a proresolving lipid mediator derived from omega-3 polyunsaturated fatty acids, exerts protective actions in murine models of colitis. J Immunol. 2013 Oct 15;191(8):4288-98. doi: 10.4049/jimmunol.1202743.
  44. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014;19:21-36. doi: 10.1016/j.cmet.2013.10.006.
  45. Spite M, Clària J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metabolism. 2014;19:21-36. doi: 10.1016/j.cmet.2013.10.006.
  46. Arnardottir HH, Dalli J, Colas RA, Shinohara M, Serhan CN. Aging delays resolution of acute inflammation in mice: reprogramming the host response with novel nano-proresolving medicines. J Immunol. 2014 Oct 15;193(8):4235-44. doi: 10.4049/jimmunol.1401313.

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Ibuprofen Vs Extra Virgin Olive Oil (EVOO) – Part One

Ibruprofen-like-activity in EVOO

 

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Have heard of many benefits of virgin and extra virgin olive oil but did you know that one of the phenolic compounds in olive oil, oleocanthal, uses the same mechanism of action as ibuprofen and has potent anti-inflammatory actions. It decreases a number of inflammatory mediators and exhibits neuroprotective properties. Researchers are looking at oleocanthal and other phenolic compounds, such as oleuropein and hydroxytyrosol, in studies investigating their impact on atherosclerosis, obesity, blood sugar control, Alzheimer’s disease and cancer among many other conditions.

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