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Pure Wellness Medical Supplements

PURE Wellness Inflamm Support

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$53.50 USD
Regular price
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$53.50 USD
  • Description
  • Serving Size: 3 capsules - 240 capsules per bottle   80-day supply

    Directions: As a dietary supplement, take three (3) capsules with 8-12 fl oz of water daily.

    BENEFITS: Ingredients have been shown to reduce inflammatory markers, possess antioxidant properties, and help to decrease cellular damage. This special combination is formulated to reduce inflammation locally and throughout the entire body.

    IMPORTANT FACTS:

    QUERCETIN: Plant pigment and long-lasting anti-inflammatory that contains strong anti-inflammatory capacities across multiple kinds of cells.

    BOSWELLIA SERRATA: Strong anti-inflammatory agent used to treat various chronic inflammatory diseases.

    TURMERIC(CURCUMIN): Powerful anti-inflammatories and antioxidants that aid in reducing and preventing systemic and localized inflammation.

    ALPHA-LIPOIC ACID: Antioxidant nutrient that assists in nutrient breakdown and has been found to contain strong anti-inflammatory properties.

    RESVERATROL: Found to increase metabolic rate and inhibit triggers of inflammation throughout the body.

    GREEN TEA: Contains antioxidants and EFCF,which have been found to naturally reduce inflammation.

    BROMELAIN: Encourages the body to produce vital substances to support a healthy immune system.

    ZINC: Crucial for normal development and function of cells. 

  • Clinical evidence
  • Two specific studies showed Quercetin was reported as a long-lasting anti-inflammatory substance that possesses strong anti-inflammatory capacities (1,2). Several studies shoe quercetin to possess anti-inflammatory potential that can be expressed on different cell types, both in animal and human models (3,4,5,6,7,8,9,10,11). Quercetin possess both mast cell stabilizing and gastrointestinal cytoprotective activity (12). It can also play a modulating, biphasic and regulatory action on inflammation and immunity (11). Additionally, quercetin has an immunosuppressive effect on dendritic cells function (13). Boswellia serrata has been traditionally used in folk medicine for centuries to treat various chronic inflammatory diseases. The resinous part of Boswellia serrata possesses monoterpenes, diterpenes, triterpenes, tetracyclic triterpenic acids and four major pentacyclic triterpenic acids (14). In Several in-vitro studies and animal models show that boswellic acids were found to inhibit the synthesis of pro-inflammatory enzyme, 5-lipoxygenase [5-LO] including 5-hydroxyeicosatetraenoic acid [5-HETE] and leukotriene B4 [LTB-4], which cause bronchoconstriction, chemotaxis, and increased vascular permeability (15-20). Boswellic acids seem to be specific inhibitor of 5-LO (21). 5-LO generates inflammatory leukotrienes, which cause inflammation by promoting free radical damage, calcium dislocation, cell-adhesion and migration of inflammation-producing cells to the inflamed body area. Boswellic acids have been shown to significantly reduce glycosaminoglycan degradation (22–25). Clinical trials of gum-resin of Boswellia alone have shown to improve symptoms in patients with osteoarthritis, and rheumatoid arthritis (26,27). A clinical trial conducted by Raychaudhuri and co-workers in India has shown that the extract of the plant, Boswellia serrata, can reduce pain and improve knee-joint functions, in some cases providing relief even within seven days. Raychaudhuri and her colleagues described their study as the first to evaluate the efficacy of the extract enriched with a form of boswellic acid on osteoarthritis (28). Very recently, Pawar et al. in 2011 have reported a simple, rapid, accurate, reproducible, selective and economic HPTLC method for routine quality control analysis as also quantitative determination of β-boswellic acid from Boswellia serrata Roxb. (exudate) and its formulations (29). Turmeric is the spice that gives curry its yellow color. It has been used in India for thousands of years as both a spice and medicinal herb. These compounds are called curcuminoids. Curcumin is the main active ingredient in turmeric. It has powerful anti-inflammatory effects and is an extraordinarily strong antioxidant (30,31). Extensive research has demonstrated the mechanism by which persistent oxidative stress can lead to chronic inflammation, which in turn could cause many chronic diseases including cardiovascular diseases, neurological diseases, pulmonary diseases, diabetes, and cancers (32). Alpha-lipoic acid or ALA is a naturally occurring compound that is made in the body. Increased pro-inflammatory markers and oxidative stress occurs in adipose tissues are the two factors that may play a key role in the incidence of metabolic-related comorbidities among patients with metabolic disorders (33). Increased chronic inflammation is associated with increased risk of metabolic disorders, including type 2 diabetes mellitus (T2DM) (34) and arteriosclerosis, endothelial dysfunction, vascular calcification, increased activity of metalloproteinases, oxidative damage, and degradation of collagen (35-37). Increased levels of CRP are associated with increased risk of CVD and diabetes (38,39). In addition to CRP, other inflammatory biomarkers such as IL-6 and TNF-α may be correlated with the development of CVD in diabetic patients (40). The results of current meta-analysis showed that ALA supplementation significantly decreased CRP, IL-6, and TNF-α levels in patients with MetS and related disorders. In a large meta-analysis of eighteen different studies showed that ALA supplementation significantly decreased CRP, IL-6, and TNF-α levels in patients with MetS and related disorders (41). Resveratrol is produced by plants as a phytoalexin in response to a stressful stimulus, or to a microbial or fungal infection, providing the plant resistance (42). Chronic, low-grade inflammation can underlie the development of several non-communicable diseases, including cancer, and neurodegenerative, respiratory, metabolic, and cardiovascular diseases. Accumulating data strongly suggest that phytochemicals can interact with multiple targets, and alter the dysregulated inflammatory pathways and mediators, indicating treatment of the inflammatory processes underlying chronic diseases (43). RSV treatment also leads to increases in the metabolic rate and mitochondrial number, which might be correlated with increases in peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) activity and expression, which control mitochondrial biogenesis in the liver and muscle (44-47). Green tea has been shown to have beneficial effects against a variety of diseases such as cancer, obesity, diabetes, cardiovascular disease, and neurodegenerative diseases. Green tea and its major component, epigallocatechin-3-gallate (EGCG) have been demonstrated to have anti-inflammatory effects (48). Green tea and EGCG have multiple targets and act in a pleiotropic manner, it is essential to consider their usage to improve the quality of life in patients with inflammatory disease. Green tea and EGCG have beneficial health effects and no severe adverse effects (48). Bromelain is a mixture of different thiol endopeptidases and other, and several protease inhibitors (49). In vitro and in vivo studies demonstrate that bromelain exhibits various fibrinolytic, antiedematous, antithrombotic, and anti-inflammatory activities (49). Bromelain accounts for many therapeutic benefits like the treatment of angina pectoris, bronchitis, sinusitis, surgical trauma, and thrombophlebitis, debridement of wounds, and enhanced absorption of drugs, particularly antibiotics (49). It also relieves osteoarthritis, diarrhea, and various cardiovascular disorders. Bromelain also possesses some anti-cancerous activities and promotes apoptotic cell death (49). Shankar et al. in one study showed Zinc to be crucial for normal development and function of cells mediating nonspecific immunity such as neutrophils and natural killer cells (50). They also found Zinc deficiency to affect development of acquired immunity by preventing both the outgrowth and certain functions of T lymphocytes such as activation, Th1 cytokine production, and B lymphocyte help. The study also showed B lymphocyte development and antibody production, particularly immunoglobulin G, to be compromised with Zinc deficiency (50). They showed how the macrophage, a pivotal cell in many immunologic functions, is adversely affected by zinc deficiency, which can dysregulate intracellular killing, cytokine production, and phagocytosis (50). Shankar et al. explained zinc to be a key immunologic mediator that is rooted in the myriad roles for zinc in basic cellular functions such as DNA replication, RNA transcription, cell division, and cell activation (50). Zinc also functions as an antioxidant and can stabilize membranes (50).

  • Reference
  • 1. Read M.A. Flavonoids: Naturally occurring anti-inflammatory agents. Am. J. Pathol. 1995;147:235–237. [PMC free article] [PubMed] [Google Scholar]
    2. Orsolic N., Knezevic A.H., Sver L., Terzic S., Basic I. Immunomodulatory and antimetastatic action of propolis and related polyphenolic compounds. J. Ethnopharmacol. 2004;94:307–315. doi: 10.1016/j.jep.2004.06.006. [PubMed] [CrossRef] [Google Scholar]
    3. Manjeet K.R., Ghosh B. Quercetin inhibits LPS-induced nitric oxide and tumor necrosis factor-alpha production in murine macrophages. Int. J. Immunopharmocol. 1999;21:435–443. [PubMed] [Google Scholar]
    4. Gerates L., Moonen H.J.J., Brauers K., Wouters E.F.M., Bast A., Hageman G.J. Dietary flavones and flavonols are inhibitor of poly (ADP-ribose) polymerase-1 in pulmonary epithelial cells. J. Nutr. 2007;137:2190–2195. [PubMed] [Google Scholar]
    5. Bureau G., Longpre F., Martinoli M.G. Resveratrol and quercetin, two natural polyphenols, reduce apoptotic neuronal cell death induced by neuroinflammation. J. Neurosci. Res. 2008;86:403–410. doi: 10.1002/jnr.21503. [PubMed] [CrossRef] [Google Scholar]
    6. Kim H.P., Mani I., Iversen L., Ziboh V.A. Effects of naturally-occurring flavonoids and bioflavonoids on epidermal cyclooxygenase and lipoxygenase from guinea-pigs. Prostaglandins Leukot. Essent. Fat. Acids. 1998;58:17–24. doi: 10.1016/S0952-3278(98)90125-9. [PubMed] [CrossRef] [Google Scholar]
    7. Lee K.M., Hwang M.K., Lee D.E., Lee K.W., Lee H.J. Protective effect of quercetin against arsenite-induced COX-2 expression by targeting PI3K in rat liver epithelial cells. J. Agric. Food Chem. 2010;58:5815–5820. doi: 10.1021/jf903698s. [PubMed] [CrossRef] [Google Scholar]
    8. Endale M., Park S.C., Kim S., Kim S.H., Yang Y., Cho J.Y., Rhee M.H. Quercetin disrupts tyrosine-phosphorylated phosphatidylinositol 3-kinase and myeloid differentiation factor-88 association, and inhibits MAPK/AP-1 and IKK/NF-κB-induced inflammatory mediators production in RAW 264.7 cells. Immunobiology. 2013;218:1452–1467. doi: 10.1016/j.imbio.2013.04.019. [PubMed] [CrossRef] [Google Scholar]
    9. Kempuraj D., Madhappan B., Christodoulou S., Boucher W., Cao J., Papadopoulou N., Cetrulo C.L., Theoharides T.C. Flavonols inhibit proinflammatory mediator release, intracellular calcium ion levels and protein kinase C theta phosphorylation in human mast cells. Br. J. Pharmacol. 2005;145:934–944. doi: 10.1038/sj.bjp.0706246. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
    10. Yang D., Liu X., Liu M., Chi H., Liu J., Han H. Protective effects of quercetin and taraxasterol against H2O2-induced human umbilical vein endothelial cell injury in vitro. Exp. Ther. Med. 2015;10:1253–1260. doi: 10.3892/etm.2015.2713. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
    11. Chirumbolo S. The role of quercetin, flavonols and flavones in modulating inflammatory cell function. Inflamm. Allergy Drug Targets. 2010;9:263–285. [PubMed] [Google Scholar]
    12. Penissi A.B., Rudolph M.I., Piezzi R.S. Role of mast cells in gastrointestinal mucosal defense. Biocell. 2003;27:163–172. [PubMed] [Google Scholar]
    13. Huang R.Y., Yu Y.L., Cheng W.C., OuYang C.N., Fu E., Chu C.L. Immunosuppressive effect of quercetin on dendritic cell activiation and function. J. Immunol. 2010;184:6815–6821. doi: 10.4049/jimmunol.0903991. [PubMed] [CrossRef] [Google Scholar]
    14. M. Z. Siddiqui. Boswellia Serrata, A Potential Antiinflammatory Agent: An Overview Indian J Pharm Sci. 2011 May-Jun; 73(3): 255–261.doi: 10.4103/0250-474X.93507
    15. Ammon HP, Mack T, Singh GB, Safayhi H. Inhibition of leukotriene B4 formation in rat peritoneal neutrophils by an ethanolic extract of gum-resin exudates of Boswellia serrata. Planta Med. 1991;57:203–7. [PubMed] [Google Scholar]
    16. Wildfeuer A, Neu IS, Safayhi H, Metzger G, Wehrmann M, Vogel U, et al. Effects of boswellic acids extracted from a herbal medicine on the biosynthesis of leukotrienes and the course of experimental autoimmune encephalomyelitis. Arzneim Forsch. 1998;48:668–74. [PubMed] [Google Scholar]
    17. Ammon HP. Boswellic acids (components of frankincense) as the active principle in treatment of chronic inflammatory diseases. Wien Med Wochenschr. 2002;152:337–78. [PubMed] [Google Scholar]
    18. Ammon HP. Boswellic acids in chronic inflammatory diseases. Planta Med. 2006;72:1100–16. [PubMed] [Google Scholar]
    19. Schweizer S, von Brocke AF, Boden SE, Bayer E, Ammon HP, Safayhi H. Workup-dependent formation of 5-lipoxygenase inhibitory boswellic acids analogues. J Nat Prod. 2000;63:1058–61. [PubMed] [Google Scholar]
    20. Etzel R. Special extract of boswellia serrata (H15) in the treatment of rheumatoid arthritis. Phytomedicine. 1996;3:91–4. [PubMed] [Google Scholar]
    21. Ammon HP. Salai guggul-Boswellia serrata from a herbal medicine to a specific inhibitor of leukotriene biosynthesis. Phytomedicine. 1996;3:67–70. [PubMed] [Google Scholar]
    22. Lee KH, Spencer MR. Studies on mechanism of action of salicylates V: Effect of salicylic acid on enzymes involved in mucopolysaccharide synthesis. J Pharmacol Sci. 1969;58:464–8. [PubMed] [Google Scholar]
    23. Palmowski MJ, Brandt KD. Effect of salicylate on proteoglycan metabolism in normal canine articular cartilage in vitro. Arthritis Rheum. 1979;22:746–54. [PubMed] [Google Scholar]
    24. Dekel S, Falconer J, Francis MJ. The effect of anti-inflammatory drugs on glycosaminoglycan sulphation in pig cartilage. Prostaglandins Med. 1980;4:133–40. [PubMed] [Google Scholar]
    25. Brandt KD, Palmowski MJ. Effect of salicylates and other non-steroidal anti-inflammatory drugs on articular cartilage. Am J Med. 1984;77:65–9. [PubMed] [Google Scholar]
    26. Murray MT. Rocklin, CA: Prima Publishing; 1995. The Healing Power of Herbs; pp. 327–35. [Google Scholar]
    27. Arora RB, Kapoor V, Basu N, Jain AP. Anti-inflammatory studies on Curcuma longa (turmeric) Indian J Med Res. 1971;50:1289–95. [PubMed] [Google Scholar]
    28. Anonymous. Indian herb hope for arthritis relief. The Telegraph Calcutta. 2008. Aug 4, [Last accessed on 2011 May 18]. p. 7. Available from: http://www.telegraphindia.com/1080804/jsp/nation/story_9643877.jsp#top,
    29. Pawar RK, Sharma S, Singh KC, Sharma RK. Physico-chemical standardization and development of HPTLC method for the determination of β-boswellic acid from Boswellia serrata Roxb.(exudate) Int J App Pharm. 2011;3:8–13. [Google Scholar]
    30. Yan He, Yuan Yue, Xi Zheng, Kun Zhang, Shaohua Chen, Zhiyun Du. Curcumin, inflammation, and chronic diseases: how are they linked? Molecules. 2015 May 20;20(5):9183-213.  doi: 10.3390/molecules20059183. 
    31. Rebecca L Edwards, Paula B Luis, Paolo V Varuzza, Akil I Joseph, Sai Han Presley, Rupesh Chaturvedi, Claus Schneider. The anti-inflammatory activity of curcumin is mediated by its oxidative metabolites J Biol Chem. 2017 Dec 29;292(52):21243-21252. doi: 10.1074/jbc.RA117.000123. Epub 2017 Nov 2.
    32. Reuter S., Gupta S.C., Chaturvedi M.M., Aggarwal B.B. Oxidative stress, inflammation, and cancer, How are they linked? Free Radic. Biol. Med. 2010;49:1603–1616. doi: 10.1016/j.freeradbiomed.2010.09.006. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
    33. Furukawa S, Fujita T, Shimabukuro M, Iwaki M, Yamada Y, Nakajima Y, et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest. 2004;114:1752–1761. doi: 10.1172/JCI21625. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
    34. Liu C, Feng X, Li Q, Wang Y, Hua M. Adiponectin, TNF-alpha and inflammatory cytokines and risk of type 2 diabetes: a systematic review and meta-analysis. Cytokine. 2016;86:100–109. doi: 10.1016/j.cyto.2016.06.028. [PubMed] [CrossRef] [Google Scholar]
    35. Mozos I, Malainer C, Horbanczuk J, Gug C, Stoian D, Luca CT, et al. Inflammatory markers for arterial stiffness in cardiovascular diseases. Front Immunol. 2017;8:1058. doi: 10.3389/fimmu.2017.01058. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
    36. Dinh QN, Chrissobolis S, Diep H, Chan CT, Ferens D, Drummond GR, et al. Advanced atherosclerosis is associated with inflammation, vascular dysfunction and oxidative stress, but not hypertension. Pharmacol Res. 2017;116:70–76. doi: 10.1016/j.phrs.2016.12.032. [PubMed] [CrossRef] [Google Scholar]
    37. Elcioglu OC, Afsar B, Bakan A, Takir M, Ozkok A, Oral A, et al. Chronic rhinosinusitis, endothelial dysfunction, and atherosclerosis. Am J Rhinol Allergy. 2016;30:58–61. doi: 10.2500/ajra.2016.30.4325. [PubMed] [CrossRef] [Google Scholar]
    38. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA. 2001;286:327–334. doi: 10.1001/jama.286.3.327. [PubMed] [CrossRef] [Google Scholar]
    39. Danesh J, Wheeler JG, Hirschfield GM, Eda S, Eiriksdottir G, Rumley A, et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med. 2004;350:1387–1397. doi: 10.1056/NEJMoa032804. [PubMed] [CrossRef] [Google Scholar]
    40. Haffner SM. The metabolic syndrome: inflammation, diabetes mellitus, and cardiovascular disease. Am J Cardiol. 2006;97:3a–11a. doi: 10.1016/j.amjcard.2005.11.010. [PubMed] [CrossRef] [Google Scholar]
    41. Maryam Akbari, Vahidreza Ostadmohammadi, Reza Tabrizi, Moein Mobini, Kamran B. Lankarani, Mahmood Moosazadeh, Seyed Taghi Heydari, Maryam Chamani, Fariba Kolahdooz, Zatollah AsemiThe effects of alpha-lipoic acid supplementation on inflammatory markers among patients with metabolic syndrome and related disorders: a systematic review and meta-analysis of randomized controlled trials. Nutr Metab (Lond). 2018; 15: 39. Published online 2018 Jun 5. doi: 10.1186/s12986-018-0274-y, PMCID: PMC5989440
    42. Chedea V.S., Vicas S.I., Sticozzi C., Pessina F., Frosini M., Maioli E., Valacchi G. Resveratrol: From diet to topical usage. Food Funct. 2017;8:3879–3892. doi: 10.1039/C7FO01086A. [PubMed] [CrossRef] [Google Scholar]
    43. Diego de Sá Coutinho, Maria Talita Pacheco, Rudimar Luiz Frozza, Andressa Bernardi1. Anti-Inflammatory Effects of Resveratrol: Mechanistic Insights Int J Mol Sci. 2018 Jun; 19(6): 1812.Published online 2018 Jun 20. doi: 10.3390/ijms19061812
    44. Baur J.A., Pearson K.J., Price N.L., Jamieson H.A., Lerin C., Kalra A., Prabhu V.V., Allard J.S., Lopez-Lluch G., Lewis K., et al. Resveratrol improves health and survival of mice on a high-calorie diet. Nature. 2006;444:337–342. doi: 10.1038/nature05354. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
    45. Pirola L., Frojdo S. Resveratrol: One molecule, many targets. IUBMB Life. 2008;60:323–332. doi: 10.1002/iub.47. [PubMed] [CrossRef] [Google Scholar]
    46. Rauf A., Imran M., Suleria H.A.R., Ahmad B., Peters D.G., Mubarak M.S. A comprehensive review of the health perspectives of resveratrol. Food Funct. 2017;8:4284–4305. doi: 10.1039/C7FO01300K. [PubMed] [CrossRef] [Google Scholar]
    47. Um J.H., Park S.J., Kang H., Yang S., Foretz M., McBurney M.W., Kim M.K., Viollet B., Chung J.H. AMP-activated protein kinase-deficient mice are resistant to the metabolic effects of resveratrol. Diabetes. 2010;59:554–563. doi: 10.2337/db09-0482. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
    48. Tomokazu Ohishi, Shingo Goto, Pervin Monira, Mamoru Isemura, Yoriyuki Nakamura. Anti-inflammatory Action of Green Tea Anti-inflamm Antiallergy Agents Med. Chem  2016;15(2):7490.  doi:0.2174/1871523015666160915154443.  
    49. Rajendra Pavan, Sapna Jain, Shraddha, and Ajay Kumar. Properties and Therapeutic Application of Bromelain: A Review Biotechnol Res Int. 2012; 2012: 976203.Published online 2012 Dec 10. doi: 10.1155/2012/976203  
    50. A H Shankar, A S Prasad. Zinc and immune function: the biological basis of altered resistance to infection. Am J Clin Nutr 1998 Aug;68(2 Suppl):447S-463S. doi: 10.1093/ajcn/68.2.447S.