What is Broccoli good for ???

Grown all over the world and enjoyed as a versatile ingredient for various dishes, broccoli is a member of the cruciferous family, along with cauliflower, kale and cabbage. It has a light green stalk topped with dark green florets tightly clustered together, giving it the appearance of a tree.”1,2

Broccoli means “little arms” or “little shoots” in Italy, where it’s believed to originate from. Every part of this vegetable is edible — from its stem to the gray-green leaves that surround its head, which are usually removed before the broccoli is sold. You can eat it raw in a salad or in a crudités platter, puree it to make soup or serve it sautéed, grilled, steamed, roasted or stir-fried.3  

The flavor of broccoli depends on which part you’re using and how you prepare it. The florets tend to have a stronger taste than the stem, but they’re milder compared to the leaves. Cooked broccoli is also sweeter than raw.4 Additionally, the method of cooking affects the compounds found in this vegetable; One study showed that steaming is the best way to preserve broccoli’s nutrients.5

To determine if a broccoli is fresh, look for tightly closed and springy florets as well as thin stalks. Avoid those with flowering heads, yellowing florets or thick stems, as they indicate maturity. Fresh broccoli can be kept for up to five days when wrapped in a reusable or perforated bag and stored in the crisper of your fridge. Meanwhile, cooked broccoli can last for up to three days in the refrigerator.6,7

Health Benefits of Broccoli 

Broccoli is a nutritional powerhouse of vitamins, minerals and bioactive phytochemicals. One of its major chemical constituents is sulforaphane, which is found to have antioxidant, anti-inflammatory, anticancer, antimicrobial, antiaging, antidiabetic and neuroprotective properties.8

An article published in the Experimental and Clinical Sciences Journal highlights the chemoprotective property of sulforaphane against various cancers, including breast, colon, stomach and lung cancer. It may also help lower the risk for diabetes, cardiovascular disease9 and osteoporosis.10

The flavonoids kaempfrol and quercetin contribute to the anti-inflammatory, cardioprotective and anticancer actions of broccoli.11,12,13 In terms of vitamins and minerals, broccoli is an excellent source of vitamin A,14 a necessary nutrient for eye health,15and vitamin C,16 which plays a role in various biological functions in the human body, including the biosynthesis of collagen and neurotransmitters.17

Other high-amount, health-boosting nutrients present in broccoli include vitamins K and B6, folate, potassium and manganese. For more information about the nutritional value of this cruciferous vegetable, check out the nutrition facts table below:18

 Amt. Per 
Serving
% Daily 
Value*
Calories34 
Total Fat0.37 g 
Saturated Fat0.114 g 
Trans Fat
Cholesterol0 mg 
Sodium33 mg 
Total Carbohydrates6.64 g 
Dietary Fiber2.6 g 
Sugar1.7 g 
Protein2.82 g 
Vitamin A31 mcgVitamin C89.2 mg
Calcium47 mgIron0.73 mg

Studies Done on Broccoli

Broccoli has been widely studied for its cancer-fighting potential over the years. One 2013 study, published in the Topics in Current Chemistry, found that the sulforaphane in broccoli may help stimulate the detoxification of airborne toxins and aflatoxins, a type of poisonous toxin produced by certain kinds of mold, thereby protecting exposed individuals from associated health risks like cancer.19,20

Another study published in the Nutrition and Cancer evaluated the anticancer property of broccoli on smokers and nonsmokers. The study involved a group of 10 smokers and 10 nonsmokers, both of which were given 200 grams of broccoli or put under a controlled diet within 10 days. Results showed that DNA strand breaks “decreased significantly after the broccoli diet in smokers as well as in nonsmokers,” highlighting the importance of eating broccoli for protecting cells against DNA damage.21

Broccoli Fun Facts

The use of broccoli as a nutritional food source dates back to the Roman Empire, where it was considered very valuable. Thomas Jefferson, an American Founding Father who was also an avid gardener, began experimenting with broccoli seeds he brought home from in Italy as early as the late 1700s. However, it wasn’t until the 1920s that this vegetable became popular in the United States.23

Summary

Broccoli is not just a versatile ingredient. It’s proven to be beneficial for your health too, as it contains a wide range of bioactive compounds, vitamin and minerals, including sulforaphane, kaempfrol, quercetin, vitamin C, vitamin K and potassium, to name a few. These powerful compounds work together to help reduce your risk of health disorders, such as cancer and cardiovascular disease.24

Every part of broccoli can be eaten, from the florets to the stalk. There are many ways to enjoy this vegetable: Toss it into salads, steam and serve it with dip, puree it into soup or serve it as a side dish to complement recipes with strong flavors.25

reference: https://foodfacts.mercola.com/broccoli.html

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BENEFITS OF OLIVES

Delicious olives offer an amazing array of health benefits that humans have likely been enjoying for thousands of years. Historians note that olives were part of the diet for people as far back as 6,000 years ago in the early Bronze Age. Although the Mediterranean region is particularly note for their delectable olives and high-quality olive oil, olives also grow in regions of Portugal and the Middle East. There are many different varieties of olives, but the research is suggests that each variety offers spectacular health benefits. Whether you’re a fan of green olives or black olives or all the wonderful olive varieties that exist, you should add them to your weekly diet to obtain their many health benefits.

Good for Your Brain

With their brain-supportive antioxidants, olives provide support for strong cognitive function. Because your brain requires so much oxygen, it’s more prone to the development of free radicals than other parts of your body. Antioxidants neutralize these disease-causing free radicals to protect brain health. Additionally, olives contain vitamin K; a lack of vitamin K has been linked to diseases like Alzheimer’s. As if those benefits weren’t enough, there is research that suggests that olives can reduce the risk for depression. So, simply be eating olives, you could elevate your mood and protect your brain health at the same time.

Antioxidants

Olives, whether they be black, green, or stuffed with blue cheese, are loaded with Vitamin E and polyphenols, both of which are powerful antioxidants. To break that down a little, antioxidants are potent compounds that fight free radicals in the body, which can help protect cells and prevent cardiovascular diseases and cancer. Antioxidants also help protect your immune system, helping you avoid getting sick and keep you healthy as you age. Vitamin E is fat soluble, meaning that .Olives are a great source of vitamin E, which has the ability to neutralize free radicals in body fat. Especially when working with the stable monounsaturated fats found in olives, vitamin E can make cellular processes safer. If the DNA of a cell is damaged, it can mutate and become cancerous. Studies have shown that a diet supplemented with olives and olive oil leads to a lower risk of colon cancer, almost as low a risk as a diet rich in fish oil.it’s better absorbed into your bloodstream when combined with fat—just like in that perfect little olive package that nature cleverly designed.

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

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  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.
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  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.
  20. 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.
  21. Serhan CN, Petasis NA. Resolvins and protectins in inflammation resolution. Chem Rev. 2011 Oct 12;111(10):5922-43. doi: 10.1021/cr100396c.
  22. 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.
  23. 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.
  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.
  25. 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.
  26. Sommer C, Birklein F. Resolvins and inflammatory pain. F1000 Med Rep. 2011 Oct;3:19. doi: 10.3410/M3-19.
  27. Xu ZZ, Zhang L, Liu T, Park JY, Berta T, Yang R, et al. Resolvins RvE1 and RvD1 attenuate inflammatory pain via central and peripheral actions. Nat Med. 2010 May;16(5):592-7. doi: 10.1038/nm.2123
  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.
  36. Menon R, Krzyszczyk P, Berthiaume F. Pro-resolution potency of resolvins D1, D2 and E1 on neutrophil migration and in dermal wound healing. Nano Life. 2017 Mar;7(1). pii: 1750002. doi: 10.1142/S1793984417500027.
  37. Sulciner ML, Serhan CN, Gilligan MM, Mudge DK, Chang J, Gartung A, et al. Resolvins suppress tumor growth and enhance cancer therapy. J Exp Med. 2018 Jan 2;215(1):115-140. doi: 10.1084/jem.20170681.
  38. Easley JT, Nelson JW, Mellas RE, Sommakia S, Wu C, Trump B, et al. Aspirin-Triggered Resolvin D1 Versus Dexamethasone in the Treatment of Sjögren’s Syndrome-Like NOD/ShiLtJ Mice – A Pilot Study. J Rheum Dis Treat. 2015;1(4). pii: 027.
  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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