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Once in a while, a breakthrough occurs in the natural medicine world and Metagenics OmegaGenics SPM Active is showing initial evidence that it may be a very powerful supplement for those suffering from inflammatory conditions. At this time, the process of inflammation and its consequences is one of the most widely studied areas of research in both traditional and alternative medicine. Its resolution may be the most important concept in improving outcomes for our patients with any inflammatory condition.

So, let’s discuss this the easy way and also the detailed way.

The Easy Explanation

Briefly, the concept addressed with Metagenics OmegaGenics SPM Active is that it promotes the resolution phase of inflammatory conditions after a number of other steps are taken to address the initiation phase (acute phase) of inflammation…and this occurs in any inflammatory condition.

If I asked you if you knew that fish oil is anti-inflammatory, most people would say yes. If I asked you what it is about fish oil or is in fish oil that makes it anti-inflammatory, most people would not have any idea. That included me till a few months ago. Then someone very smart decided to research that concept.

The research showed that there are compounds in fish oil that are taken by the body’s chemistry and converted into other substances that promote the resolution phase of inflammation. But, there is very little in a piece of fish or in fish oil capsules. The compounds were identified and then concentrated from fish oil to a level 100’s of times more than in fish oil capsules. Maybe 1000 time more concentrated.

Testing reveals that inflammatory conditions responded positively to the taking of this new product. In fact…though there are no studies that confirm this, it’s all anecdotal evidence…that higher doses are a potent pain reliever, and in very short time frame.

These findings have led holistic doctors to begin applying the use of Metagenics OmegaGenics SPM Active to their patients with any number of inflammatory conditions. And with great success.

The Detailed Explanation

Acute inflammation is a localized, protective immune response that occurs in an attempt to eliminate invading pathogens and/or repair injured tissue as in a sprained ankle.1 Poor foods choices have also been linked to inflammation.2 Hopefully, the initiation phase or acute inflammatory response is self-limited and leads to a resolution that allows tissue to heal and return to normal.3

If left unresolved a prolonged state of chronic inflammation that causes damage to the patient can occur and result in pain and/or a chronic disease. Many chronic diseases such as cardiovascular disease, arthritis, osteoporosis, diabetes, metabolic syndrome, inflammatory bowel disease, periodontal disease, asthma, and age-related macular degeneration, as well as some neurological disorders such as dementia and Alzheimers, have been linked to chronic inflammation.14-9 Aging may also be associated with a chronic pro-inflammatory state and has been termed “inflammaging.”10

The acute inflammatory response (initiation phase) begins within seconds to minutes following the presence of harmful stimuli such as pathogens, injuries, or irritants. It is controlled by pro-inflammatory eicosanoids, cytokines, chemokines, and other chemical messengers.11,12 The most well known responders are white blood cells that travel from the blood stream into the inflamed site and forms exudates like whitish creamy pus) to surround the area.3,13 This is called phagocytosis.

Then comes the resolution phase.14 Always thought to be a passive process, the new research shows resolution is an active process controlled by specialized pro-resolving mediators (SPMs) that are produced in tissue exudates during the resolution phase and function as “resolution agonists” to accelerate the return to normal.13,14

To return to normal, the white blood cells present in the area of damage need to be removed from the inflamed site and white blood cells on their way to the site need to be stopped. If they are allowed to continue to the site, they would cause additional tissue damage and continued inflammation.15 Extensive experimental research has shown that SPMs block excessive infiltration of white blood cells and control a timely cell death of existing white blood cells, and stimulate macrophages to remove dead white blood cells, debris, and microbes.16,17

In the resolution phase of acute inflammation, long-chain polyunsaturated fatty acids (PUFAs) in tissue are converted into SPMs.22,24 The majority of SPMs are biosynthesized from omega-3 fatty acids such as EPA and DHA. 25

SPMs have shown to be pro-resolving when administered to animal models with human disease. 25,27

Although EPA and DHA (ingredients of typical fish oil capsules) can be converted to SPMs, they do not have the properties of SPMs. For decades, blocking initiation-phase pro-inflammatory mediators or enzymes such as COX-2 enzyme by drugs like non-steroidal anti-inflammatory drugs (NSAIDs) has been the therapy of choice for many acute and chronic inflammatory conditions. Keep in mind that anti-inflammation is not the same as pro-resolution.

Because initiation phase activities are required to ever get to the resolution phase, traditional COX-2 and lipoxygenase inhibitors may delay resolution activities and prevent the bodyʼs attempt to return to normal and allow tissue healing.19,29,30 Unresolved inflammation and unhealed tissue can lead to fibrosis that can impair organ function.1

Thus, an important key to controlling/resolving inflammation and subsequently preventing chronic inflammatory conditions lies in SPMs and their pro-resolving properties that switch an inflammatory response toward resolution and balance. The fact that SPMs are enzymatically produced from long-chain PUFA (especially EPA and DHA) in tissue exudates indicates the indispensable role of nutrition in regulating inflammation and promoting resolution.

Don’t suffer. All inflammatory conditions can be addressed naturally using dietary changes and all natural supplementation. Please download Dr. Dahlman’s Autoimmune Inflammatory free report and learn more about his treatment plan to address your health concerns.

 

References

1. Majno G, Joris I. Cells, Tissues, and Disease: Principles of General Pathology: Oxford University Press, USA; 2004.

2. Giugliano D, Ceriello A, Esposito K. The effects of diet on inflammation: emphasis on the metabolic syndrome. J Am Coll Cardiol. 2006;48:677-685.

3. Recchiuti A. Immunoresolving Lipid Mediators and Resolution of Inflammation in Aging. J Gerontol Geriat Res. 2014;3:151.

4. Nathan C, Ding A. Nonresolving inflammation. Cell. 2010;140:871-882.

5. Tabas I, Glass CK. Anti-inflammatory therapy in chronic disease: challenges and opportunities. Science. 2013;339:166-172.

6. Libby P. Atherosclerosis: the new view. Sci Am. 2002;286:46-55.

7. Mushtaq G, Khan JA, Kumosani TA, Kamal MA. Alzheimer’s disease and type 2 diabetes via chronic inflammatory mechanisms. Saudi J Biol Sci. 2015;22:4-13.

8. Fuentes E, Fuentes F, Vilahur G, Badimon L, Palomo I. Mechanisms of chronic state of inflammation as mediators that link obese adipose tissue and metabolic syndrome. Mediators Inflamm. 2013;2013:136584.

9. Parmeggiani F, Romano MR, Costagliola C, et al. Mechanism of inflammation in age-related macular degeneration. Mediators Inflamm. 2012;2012:546786.

10. Franceschi C. Inflammaging as a major characteristic of old people: can it be prevented or cured? Nutr Rev. 2007;65:S173-176.

11. Lawrence T, Willoughby DA, Gilroy DW. Anti-inflammatory lipid mediators and insights into the resolution of inflammation. Nat Rev Immunol. 2002;2:787-795.

12. Samuelsson B, Dahlen SE, Lindgren JA, Rouzer CA, Serhan CN. Leukotrienes and lipoxins: structures, biosynthesis, and biological effects. Science. 1987;237:1171-1176.

13. Spite M, Claria J, Serhan CN. Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metab. 2014;19:21-36.

14. Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014;510:92-101.

15. Serhan CN, Brain SD, Buckley CD, et al. Resolution of inflammation: state of the art, definitions and terms. Faseb J. 2007;21:325-332.

16. Serhan CN. A search for endogenous mechanisms of anti-inflammation uncovers novel chemical mediators: missing links to resolution. Histochem Cell Biol. 2004;122:305-321.

17. Maddox JF, Hachicha M, Takano T, et al. Lipoxin A4 stable analogs are potent mimetics that stimulate human monocytes and THP-1 cells via a Gprotein- linked lipoxin A4 receptor. J Biol Chem. 1997;272:6972-6978.

18. Ariel A, Fredman G, Sun YP, et al. Apoptotic neutrophils and T cells sequester chemokines during immune response resolution through modulation of CCR5 expression. Nat Immunol. 2006;7:1209-1216.

19. Schwab JM, Chiang N, Arita M, Serhan CN. Resolvin E1 and protectin D1 activate inflammation-resolution programmes. Nature. 2007;447:869-874.

20. Chiang N, Fredman G, Backhed F, et al. Infection regulates pro-resolving mediators that lower antibiotic requirements. Nature. 2012;484:524-528.

21. Serhan CN, Savill J. Resolution of inflammation: the beginning programs the end. Nat Immunol. 2005;6:1191-1197.

22. Levy BD, Clish CB, Schmidt B, Gronert K, Serhan CN. Lipid mediator class switching during acute inflammation: signals in resolution. Nat Immunol. 2001;2:612-619.

23. Hong S, Gronert K, Devchand PR, Moussignac RL, Serhan CN. Novel docosatrienes and 17S-resolvins generated from docosahexaenoic acid in murine brain, human blood, and glial cells. Autacoids in anti-inflammation. J Biol Chem. 2003;278:14677-14687.

24. Serhan CN, Clish CB, Brannon J, et al. Novel functional sets of lipid-derived mediators with antiinflammatory actions generated from omega-3 fatty acids via cyclooxygenase 2-nonsteroidal antiinflammatory drugs and transcellular processing. J Exp Med. 2000;192:1197-1204.

25. Serhan CN, Petasis NA. Resolvins and protectins in inflammation resolution. Chem Rev. 2011;111:5922-5943.

26. Serhan CN. Lipoxins and aspirin-triggered 15-epi-lipoxins are the first lipid mediators of endogenous anti-inflammation and resolution. Prostaglandins Leukot Essent Fatty Acids. 2005;73:141-612.

27. Serhan CN. Novel lipid mediators and resolution mechanisms in acute inflammation: to resolve or not? Am J Pathol. 2010;177:1576-1591.

28. Serhan CN, Chiang N. Resolution phase lipid mediators of inflammation: agonists of resolution. Curr Opin Pharmacol. 2013;13:632-640.

29. Navarro-Xavier RA, Newson J, Silveira VL, et al. A new strategy for the identification of novel molecules with targeted proresolution of inflammation properties. J Immunol. 2010;184:1516-1525.

30. Chan MM, Moore AR. Resolution of inflammation in murine autoimmune arthritis is disrupted by cyclooxygenase-2 inhibition and restored by prostaglandin E2-mediated lipoxin A4 production. J Immunol. 2010;184:6418-6426.

 

 

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