Inflammation is the body’s immune response to injury or infection which is an important part of innate immunity. When damage occurs in the body, an acute inflammatory response helps to respond quickly to the damage to limit the spread of damage while also initiating repair. The inflammatory process is a complex cascade of molecular and cellular signals that result in familiar symptoms of pain, swelling, redness, and heat (Libby P., 2007). This acute inflammation is a normal process that protects the body and helps to heal the body. The site of damage is invaded by several different immune cells and several changes also occur including increased blood flow, and increased vascular permeability; however, if this inflammatory response lingers to long or does not turn off or the system misfires it can lead to low grade chronic inflammation. Many studies suggest low grade chronic inflammation could have a serious role in a wide variety of medical conditions (Khansari et al., 2009). Beyond such conditions some of the major risk factors for chronic inflammation include age, obesity, smoking, and diet. One’s diet can affect the inflammatory response on the body so nutrition can play an important role. Dietary strategies to manage inflammation include eating oily fish, reduction trans and saturated fats, consuming fruits and vegetables, nuts, and whole grains (Giugliano et al., 2006). Importantly, there are some nutritional compounds that provide benefits which are attributed to improving inflammatory balance as well. C-reactive protein (CRP) is a common clinical and general biomarker of inflammation studied in clinical literature and in used in clinical practice, although there are other markers of inflammation such as various cytokines, white blood cells, and so forth. Because there is significant evidence that certain inflammatory markers are involved in the initiation but also the persistence of chronic pain (Watkins et al., 2003) strategies to support a healthy inflammatory response may also help to support pain management. Pain is a common reason for seeking medical and alternative care. About 100 million adults in the United States are affected by chronic pain which costs over $500 billion a year in health care costs and productivity costs (Gaskin et al., 2011). The types of pain can be divided into categories including neuropathic pain or nerve pain, nociceptive pain or damage to body tissue, or psychogenic pain or physical pain caused or prolonged by emotional or behavioral factors.
Libby P: Inflammatory mechanisms: the molecular basis of inflammation and disease. Nutr Rev 2007; 65(12 Pt 2): S140-6
Khansari N, Shakiba Y, Mahmoudi M. Chronic inflammation and oxidative stress as a major cause of age-related diseases and cancer. Recent Pat Inflamm Allergy Drug Discov. 2009 Jan;3(1):73-80. Review.
Giugliano D, Ceriello A, Esposito K. The effects of diet on inflammation: emphasis on the metabolic syndrome. J Am Coll Cardiol. 2006 Aug 15;48(4):677-85. Review.
Watkins LR, Milligan ED, Maier SF. Glial proinflammatory cytokines mediate exaggerated pain states: implications for clinical pain. Adv Exp Med Biol. 2003;521:1-21. Review.
Gaskin DJ, Richard P. The Economic Costs of Pain in the United States. In: Institute of Medicine (US) Committee on Advancing Pain Research, Care, and Education. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. Washington (DC): National Academies Press (US); 2011. Appendix C. Available from: https://www.ncbi.nlm.nih.gov/books/NBK92521/
Calder PC (2010) Omega-3 fatty acids and inflammatory processes. Nutrients 2, 355-374.
Cawood AL, Ding R, Napper FL et al. (2010) Eicosapentaenoic acid (EPA) from highly concentrated n-3 fatty acid ethyl esters is incorporated into advanced atherosclerotic plaques and higher plaque EPA is associated with decreased plaque inflammation and increased stability. Atherosclerosis 212, 252-259.
Malekshahi Moghadam A, Saedisomeolia A, Djalali M et al. (2012) Efficacy of omega-3 fatty acid supplementation on serum levels of tumour necrosis factor-alpha, C-reactive protein and interleukin-2 in type 2 diabetes mellitus patients. Singapore medical journal 53, 615-619.
Wood AD, Strachan AA, Thies F, Aucott LS, Reid DM, Hardcastle AC, Mavroeidi A, Simpson WG, Duthie GG, Macdonald HM. Patterns of dietary intake and serum carotenoid and tocopherol status are associated with biomarkers of chronic low-grade systemic inflammation and cardiovascular risk. Br J Nutr. 2014 Oct 28;112(8):1341-52.
Kaulmann A, Bohn T. Carotenoids, inflammation, and oxidative stress–implications of cellular signaling pathways and relation to chronic disease prevention. Nutr Res. 2014 Nov;34(11):907-29. doi: 10.1016/j.nutres.2014.07.010. Review.
Guest J, Grant R, Garg M, Mori TA, Croft KD, Bilgin A. Cerebrospinal fluid levels of inflammation, oxidative stress and NAD+ are linked to differences in plasma carotenoid concentrations. J Neuroinflammation. 2014 Jul 1;11:117.
D’Adamo CR, Miller RR, Shardell MD, Orwig DL, Hochberg MC, Ferrucci L, Semba RD, Yu-Yahiro JA, Magaziner J, Hicks GE. Higher serum concentrations of dietary antioxidants are associated with lower levels of inflammatory biomarkers during the year after hip fracture. Clin Nutr. 2012 Oct;31(5):659-65.
van Herpen-Broekmans WM, Klopping-Ketelaars IA, Bots ML, et al.: Serum carotenoids and vitamins in relation to markers of endothelial function and inflammation. Eur J Epidemiol 2004; 19(10): 915-21
Kritchevsky SB, Bush AJ, Pahor M, Gross MD: Serum carotenoids and markers of inflammation in nonsmokers. Am J Epidemiol 2000; 152(11): 1065-71
King DE, Mainous AG, 3rd, Geesey ME, Woolson RF: Dietary magnesium and C-reactive protein levels. J Am Coll Nutr 2005; 24(3): 166-71.
Wannamethee SG, Lowe GD, Rumley A, Bruckdorfer KR, Whincup PH: Associations of vitamin C status, fruit and vegetable intakes, and markers of inflammation and hemostasis. Am J Clin Nutr 2006; 83(3): 567-74; quiz 726-7. Abstract at: http://www.ncbi.nlm.nih.gov/pubmed/16522902
Singh U, Devaraj S, Jialal I: Vitamin E, oxidative stress, and inflammation. Annu Rev Nutr 2005; 25: 151-74. Abstract at: http://www.ncbi.nlm.nih.gov/pubmed/16011463
Church TS, Earnest CP, Wood KA, Kampert JB: Reduction of C-reactive protein levels through use of a multivitamin. Am J Med 2003; 115(9): 702-7.
Tipoe GL, Leung TM, Hung MW, Fung ML. Green tea polyphenols as an anti-oxidant and anti-inflammatory agent for cardiovascular protection. Cardiovasc Hematol Disord Drug Targets. 2007 Jun;7(2):135-44. Review.
Ohishi T, Goto S, Monira P, Isemura M, Nakamura Y. Anti-inflammatory Action of Green Tea. Antiinflamm Antiallergy Agents Med Chem. 2016 Sep 15.
Mota MA, Landim JS, Targino TS, Silva SF, Silva SL, Pereira MR. Evaluation of the anti-inflammatory and analgesic effects of green tea (Camellia sinensis) in mice. Acta Cir Bras. 2015 Apr;30(4):242-6.
Tome-Carneiro J, Gonzalvez M, Larrosa M et al. (2012) One-year consumption of a grape nutraceutical containing resveratrol improves the inflammatory and fibrinolytic status of patients in primary prevention of cardiovascular disease. The American journal of cardiology 110, 356-363.
Ghanim H, Sia CL, Abuaysheh S et al. (2010) An antiinflammatory and reactive oxygen species suppressive effects of an extract of Polygonum cuspidatum containing resveratrol. The Journal of clinical endocrinology and metabolism 95, E1-8.
Zahedi HS, Jazayeri S, Ghiasvand R et al. (2013) Effects of polygonum cuspidatum containing resveratrol on inflammation in male professional basketball players. International journal of preventive medicine 4, S1-4.
Gonzales AM, Orlando RA (2008) Curcumin and resveratrol inhibit nuclear factor-kappaB-mediated cytokine expression in adipocytes. Nutrition & metabolism 5, 17
Maroon JC, Bost JW, Maroon A. Natural anti-inflammatory agents for pain relief. Surg Neurol Int. 2010 Dec 13;1:80. doi: 10.4103/2152-7806.73804. PubMed PMID: 21206541; PubMed Central PMCID: PMC3011108
Healing is a complex series of interactions that includes coagulation, inflammation, proliferation, and remodeling (Velnar et al., 2009). The wound healing process begins with vascular constriction and clot formation, followed by the release of pro-inflammatory cytokines and the migration of inflammatory cells including neutrophils and macrophages to the site of damage. Following a robust proliferation process in which the wound begins to be rebuilt with new tissue, the remodeling phase begins which can last for years making healing a process more than an event (Guo, S., et al., 2010). Healing wounds is necessary for any damage to the normal anatomical structure and function of the body. Many people might associate wounds with cuts or bruises on the skin, but wounds can occur throughout the entire body. Much effort has focused on understanding the process of healing and developing approaches and strategies wound management. Many factors are involved in our ability to heal including but not limited to age, stress, obesity, alcohol, smoking and nutrition (Guo, S., et al., 2010). Thus, strategies to reduce stress, manage weight, limit alcohol and smoking, and improved nutrition (among other therapeutic strategies including physical therapy to strengthen the damaged area and restoring range of motion and flexibility) can all be beneficial to effective healing. Also, strategies to manage inflammation can provide a benefit to healing because inflammation is part of the healing. Acute wounds are more easily managed, but if the healing does not progress it can convert into more of a chronic wound which is more difficult to manage so taking steps to heal properly are important (Natarajan S et al., 2000). Of interest is the full-length journal review article by MacKay and Miller available at the following link, entitled “Nutritional Support for Wound Healing” for more information specific to nutrition and wound healing: http://www.altmedrev.com/publications/8/4/359.pdf which lists nutrients such as protein intake, vitamins and minerals and others as being supportive of the different phases of the healing process. Other researchers have published findings on nutrition and select nutrients to support the healing process as well (Kavalukas et al., 2011; Wild et al., 2010; Stechmiller et al., 2010; Molnar et al., 2014). Additional references below are in support of complementary strategies to healing associated primarily with issues related to stress and weight management.
Velnar T, Bailey T, Smrkolj V. The wound healing process: an overview of the cellular and molecular mechanisms. J Int Med Res. 2009 Sep-Oct;37(5):1528-42. Review.
Guo, S., and L.A. DiPietro. “Factors Affecting Wound Healing.” Journal of Dental Research 89.3 (2010): 219–229. PMC. Web. 8 Nov. 2016.
Natarajan S, Williamson D, Stiltz AJ, Harding K. Advances in wound care and healing technology. Am J Clin Dermatol. 2000 Sep-Oct;1(5):269-75. Review.
Kavalukas SL, Barbul A. Nutrition and wound healing: an update. Plast Reconstr Surg. 2011 Jan;127 Suppl 1:38S-43S.
Wild T, Rahbarnia A, Kellner M, Sobotka L, Eberlein T. Basics in nutrition and wound healing. Nutrition. 2010 Sep;26(9):862-6.
Stechmiller JK. Understanding the role of nutrition and wound healing. Nutr Clin Pract. 2010 Feb;25(1):61-8.
Molnar, Joseph Andrew, Mary Jane Underdown, and William Andrew Clark. “Nutrition and Chronic Wounds.” Advances in Wound Care 3.11 (2014): 663–681. PMC.
Devkota S, Layman DK. Increased ratio of dietary carbohydrate to protein shifts the focus of metabolic signaling from skeletal muscle to adipose. Nutr Metab (Lond). 2011 Mar 4;8(1):13.
Devkota S, Layman DK. Protein metabolic roles in treatment of obesity. Curr Opin Clin Nutr Metab Care. 2010 Jul;13(4):403-7.
Westerterp-Plantenga MS, Nieuwenhuizen A, Tomé D, Soenen S, Westerterp KR. Dietary protein, weight loss, and weight maintenance. Annu Rev Nutr. 2009;29:21-41.
Paddon-Jones D, Rasmussen BB. Dietary protein recommendations and the prevention of sarcopenia. Curr Opin Clin Nutr Metab Care. 2009 Jan;12(1):86-90.
Layman DK. Dietary Guidelines should reflect new understandings about adult protein needs. Nutr Metab (Lond). 2009 Mar 13;6:12.
Gannon MC, Nuttall FQ, Saeed A, Jordan K, Hoover H. An increase in dietary protein improves the blood glucose response in persons with type 2 diabetes. Am J Clin Nutr. 2003 Oct;78(4):734-41. Abstract available at: http://www.ncbi.nlm.nih.gov/pubmed/12566475
Kobayashi K, Nagato Y, Aoi N, et al. Effects of l-theanine on the release of alpha-brain waves in human volunteers. Nippon Nogeikagaku Kaishi 1998;72:153-7.
Yoto A, Motoki M, Murao S, Yokogoshi H. Effects of L-theanine or caffeine intake on changes in blood pressure under physical and psychological stresses. J Physiol Anthropol. 2012 Oct 29;31(1):28. doi: 10.1186/1880-6805-31-28. PubMed PMID: 23107346; PubMed Central PMCID: PMC3518171.
Zheng G, Sayama K, Okubo T, Juneja LR, Oguni I. Anti-obesity effects of three major components of green tea, catechins, caffeine and theanine, in mice. In Vivo. 2004 Jan-Feb;18(1):55-62. PubMed PMID: 15011752.
Tart Cherry fruit powder
Seymour EM, LEWIS SK, Urcuyo-Llanes DE et al. Regular tart cherry intake alters abdominal adiposity, adipose gene transcription, and inflammation in obesity-prone rats fed a high fat diet. J Med Food 2009;12:935-42.
Kuehl KS, Perrier ET, Elliot DL, Chesnutt JC. Efficacy of tart cherry juice in reducing muscle pain during running: a randomized controlled trial. J Int Soc Sports Nutr 2010;7:17.
Cayenne fruit powder
Leung FW. Capsaicin-sensitive intestinal mucosal afferent mechanism and body fat distribution. Life Sci 2008;83:1-5.
Ludy MJ, Moore GE, Mattes RD. The effects of capsaicin and capsiate on energy balance: critical review and meta-analyses of studies in humans. Chem Senses 2012;37:103-21.
Joo JI, Kim DH, Choi JW, Yun JW. Proteomic analysis for antiobesity potential of capsaicin on white adipose tissue in rats fed with a high fat diet. J Proteome Res 2010;9:2977-87
Ludy MJ, Moore GE, Mattes RD. The effects of capsaicin and capsiate on energy balance: critical review and meta-analyses of studies in humans. Chem Senses 2012;37:103-21.
Shin KO, Moritani T. Alterations of autonomic nervous activity and energy metabolism by capsaicin ingestion during aerobic exercise in healthy men. J Nutr Sci Vitaminol (Tokyo) 2007;53:124-32.
Westerterp-Plantenga MS, Smeets A, Lejeune MP. Sensory and gastrointestinal satiety effects of capsaicin on food intake. Int J Obes Relat Metab Disord 2004;29:682-6.
Joints are where two or more bones that are connected like the shoulder and the knee. Bones are kept from grinding together by cartilage which acts as a cushion. Muscles connect to bones through tendons and are important to keep strong because they can help to protect joints which is one of the many reasons why exercise to strengthen muscles is important for joint support. Because individuals with poor joint mobility often have increased levels of free radicals, antioxidants may provide a benefit to combat these free radicals to help fight against oxidative stress (Wang et al., 2007). In trials involving patients with joint issues it was shown that glucosamine can reduce pain and provide functional improvement (Black et al. 2009; Richy et al., 2003) so dietary ingredients have been shown to provide some relief and functional benefits for those suffering from joint issues.
Wang Y, Hodge AM, Wluka AE, English DR, Giles GG, O’Sullivan R, Forbes A, Cicuttini FM. Effect of antioxidants on knee cartilage and bone in healthy, middle-aged subjects: a cross-sectional study. Arthritis Res Ther. 2007;9(4):R66.
Black C, Clar C, Henderson R, MacEachern C, McNamee P, Quayyum Z, Royle P, Thomas S. The clinical effectiveness of glucosamine and chondroitin supplements in slowing or arresting progression of osteoarthritis of the knee: a systematic review and economic evaluation. Health Technol Assess. 2009 Nov;13(52):1-148. doi: 10.3310/hta13520. Review.
Richy F, Bruyere O, Ethgen O, Cucherat M, Henrotin Y, Reginster JY. Structural and symptomatic efficacy of glucosamine and chondroitin in knee osteoarthritis: a comprehensive meta-analysis. Arch Intern Med. 2003;163:1514–1522.
Müller-Fassbender H, Bach GL, Haase W, Rovati LC, Setnikar I. Glucosamine sulfate compared to ibuprofen in osteoarthritis of the knee. Osteoarthritis Cartilage. 1994 Mar;2(1):61-9.
Reginster JY, Deroisy R, Rovati LC, Lee RL, Lejeune E, Bruyere O, Giacovelli G, Henrotin Y, Dacre JE, Gossett C. Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, placebo-controlled clinical trial. Lancet. 2001 Jan 27;357(9252):251-6.
McAlindon TE, LaValley MP, Gulin JP, Felson DT. Glucosamine and chondroitin for treatment of osteoarthritis: a systematic quality assessment and meta-analysis. JAMA. 2000 Mar 15;283(11):1469-75. Review.
Towheed TE, Maxwell L, Anastassiades TP, Shea B, Houpt J, Robinson V, Hochberg MC, Wells G. Glucosamine therapy for treating osteoarthritis. Cochrane Database Syst Rev. 2005. p. CD002946
Qiu, G. X., X. S. Weng, K. Zhang, Y. X. Zhou, S. Q. Lou, Y. P. Wang, W. Li, H. Zhang and Y. Liu (2005). “[A multi-central, randomized, controlled clinical trial of glucosamine hydrochloride/sulfate in the treatment of knee osteoarthritis].” Zhonghua Yi Xue Za Zhi 85(43): 3067-3070
Siddiqui MZ. Boswellia serrata, a potential antiinflammatory agent: an overview. Indian J Pharm Sci. 2011 May;73(3):255-61. doi: 10.4103/0250-474X.93507.
Abdel-Tawab, M., O. Werz and M. Schubert-Zsilavecz (2011). “Boswellia serrata: an overall assessment of in vitro, preclinical, pharmacokinetic and clinical data.” Clin Pharmacokinet 50(6): 349-369.
Jurenka JS. Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review of preclinical and clinical research. Altern Med Rev. 2009 Jun;14(2):141-53. Review.
McAlindon, T. E., P. Jacques, Y. Zhang, M. T. Hannan, P. Aliabadi, B. Weissman, D. Rush, D. Levy and D. T. Felson (1996). “Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis?” Arthritis Rheum 39(4): 648-656.
Pattison, D. J., A. J. Silman, N. J. Goodson, M. Lunt, D. Bunn, R. Luben, A. Welch, S. Bingham, K. T. Khaw, N. Day and D. P. Symmons (2004). “Vitamin C and the risk of developing inflammatory polyarthritis: prospective nested case-control study.” Ann Rheum Dis 63(7): 843-847.
Canter, P. H., B. Wider and E. Ernst (2007). “The antioxidant vitamins A, C, E and selenium in the treatment of arthritis: a systematic review of randomized clinical trials.” Rheumatology (Oxford) 46(8): 1223-1233.
Nerves carry signals to and from different areas of the nervous system and between the nervous system and other tissues and organs. The nervous system includes cranial nerves from the brain to parts of the head, central nerves that are in the brain and spinal cord, peripheral nerves that go from the spinal cord to extremities, and autonomic nerves that go from the spinal cord to internal organs. This entire system helps to sense our surroundings and communicate information between our brain and spinal cord and other tissues along with coordinating voluntary movements and involuntary functions like blood pressure and heart rate. Neuropathy is a nerve problem that can cause pain, tingling, swelling, or even muscle weakness. Such nerve problems can be caused by physical injury, infection, metabolic problems, certain medical conditions and treatments, vitamin deficiencies, and more although sometimes the cause of nerve issues including nerve pain are not fully understood (Head, 2006). Because the pain is difficult to treat and standard analgesics are usually not effective enough (Bansal et al., 2006) many people look for alternative treatments. Some alternative strategies depend on the underlying problem but include controlling blood sugar levels, correcting vitamin deficiencies, treating infections, exercise to improve muscle strength and more.
Head KA. Peripheral neuropathy: pathogenic mechanisms and alternative therapies. Altern Med Rev. 2006 Dec;11(4):294-329. Review.
Bansal V, Kalita J, Misra UK. Diabetic neuropathy. Postgrad Med J. 2006 Feb;82(964):95-100. Review.
Ko GD, Nowacki NB, Arseneau L, Eitel M, Hum A. Omega-3 fatty acids for neuropathic pain: case series. Clin J Pain. 2010 Feb;26(2):168-72.
Alpha Lipoic Acid
Ziegler D, Nowak H, Kempler P, Vargha P, Low PA. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: a meta-analysis. Diabet Med. 2004 Feb;21(2):114-21.
Shay, Kate Petersen et al. “Alpha-Lipoic Acid as a Dietary Supplement: Molecular Mechanisms and Therapeutic Potential.” Biochimica et biophysica acta 1790.10 (2009): 1149–1160. PMC. Web. 11 Nov. 2016.
Hammond, Nancy et al. “Nutritional Neuropathies.” Neurologic clinics 31.2 (2013): 477–489. PMC. Web. 11 Nov. 2016.