Nutritional Protocols for Soft-Tissue Injuries and Joint Health
INTEGRATIVE CARE
Robert G. Silverman
When an individual is injured, the typical treatment response does not include proper supplementation necessary to help the body heal itself. In the times of physiological stress or injury, diet alone may not meet the body’s nutritional needs. The use of nutritional supplements in addition to a proper diet creates a physiological environment for healing. Therefore, understanding the role and use of micronutrients can improve the quality of your practice. The following article will talk about micronutrients and how they can promote injury healing.
A continually contracting muscle requires specific nutrients and oxygen. Alack of nutrient supply to a muscle/tendon region will lead to overuse, soft tissue injuries. Therefore, let’s ensure
that patients get a healthy nutrient supply to the body through proper diet and supplementation that will assist the body with its natural function and repair processes.
The initial injury stage is called the acute phase, characterized by visual swelling, inflammation, and spasm in the surrounding tissues. Typically, there is limited range of motion and potential loss of function. The objective of nutritional supplements in this phase should be to aid in managing pain, reducing swelling, and relaxing tight muscles.
Tissue trauma causes an inflammatory process, which releases certain inflammatory response mediators called cytokines and chemokines. These chemicals release PLA2 and arachidonic acid, which then stimulate prostaglandins and thromboxanes. These hormones signal pain and induce rapid inflammation.1
Management of the Acute Phase: Reducing Pain, Swelling, and Inflammation
The typical acute phase lasts for three days. Effective treatment begins immediately with nutritional supplementation. Nutrients to address swelling, such as tiypsin, chymotrypsin, and bromelain (also called proteolytic enzymes), can help reduce pain and inflammation. In fact, it is evidenced that patients experience faster recovery rates with proteolytic enzymes. These enzymes must be consumed on an empty stomach for full effectiveness.2"4 Numerous studies conclude that both ginger and turmeric (curcumin) inhibit inflammation by moderating excessive cyclooxygenase and lipoxygenase response. Turmeric stimulates muscle tissue repair and is an NF-KB inhibitor5-7. Boswellia serrata has been found to specifically inhibit the powerful proinflammatory enzyme, 5-lipoxygenase8. The objective of taking these nutrients is to reduce pain and modulate inflammation.
Muscle Tissue Repair
Calcium and magnesium are excellent additions to assist muscle tissue relaxation; calcium acts via presynaptic inhibition at neuromuscular junctions to reduce spasm, while magnesium promotes muscle relaxation. In a typical multivitamin/ mineral, calcium to magnesium is taken in a 2:1 ratio. However, for muscle injury, they should be consumed at a 1:2 ratio for purposes of muscle relaxation.910
Subacute Healing: Repair and Remodeling Phase
The second phase starts at day four and includes up to approximately eight weeks, during which repair and remodeling and soft tissue takes place.
Patient Symptoms
• Continued joint or muscle pain
• Palpable inflammation surrounding injury may still be present
• Range of motion possibly compromised
• Tissue repair and remodeling have begun
Therapeutic Objectives for the Repair/Remodeling Phase
• Provide reparative nutrients that may help minimize formation
of scar tissue
• Aid in connective tissue remodeling
• Reduce risk of reinjury and degeneration
• Initiate soft-tissue (extracellular matrix) support by modulating matrix metalloproteinases
• Continue controlling pain and inflammation
Nutritional Protocol for Subacute Healing
An injured site never achieves the original histologic or mechanical features of a healthy, uninjured tendon with rest alone. However, chiropractors can make a real difference in the healing of a tendon. Chiropractic treatment, including low-level laser therapy, exercise, manipulation, and crucial nutritional supplements, aids in the healing process. Matrix metalloproteinase (MMP) enzymes are released at the time of injury. Unfortunately, excessive release of MMPs can damage healthy tendon, collagen, and connective tissue in the injured area. At this point, with the release of elevated MMPs, the body goes from an inflammatory process into a degenerative state, accelerating from “itis” to “osis.” The goal at this point is to modulate the explosion of these enzymes11'13. Certain compounds (iso-alpha acids such as ThiAA) signal inhibition and stimulate positive messages into the cell. Berberine, selenium, and folic acid are nutrients that also positively impact MMPs. These nutrients are critical elements in a soft-tissue nutritional formula14'15.
Support the growth and construction of connective tissue with the following combined nutrients:
• Glycine, proline, lysine, vitamin C, B6, B5, L-taurine, and silica.1617
• Glucosamine/chondroitin sulfate/MSM should be consumed concurrently as well to aid in joint stability.18
Wellness and Prevention Phase
The goal in this final phase is to achieve optimal tissue remodeling to support wellness and prevention, and to reduce the risk of reinjury and degeneration by installing what I call my foundation nutrition:
•Phytomulti: Multivitamin/mineral complex with additional phytonutrients.19
• Omega-3 F atty Acids : Aid in the reduction of inflammation (two grams of EPA/DHA).20'23
•Vitamin D: Aids in the healing of sports injuries (2,000 IU and up)24'25.
•Probiotics (L-acidophilus and B-lactis): Help balance immune function (approximately 15 billion live organisms).26"27
•A phytonutrient green drink: Helps quench damaging free radicals and contributes to whole body alkalization.
Nutritional Protocols for Joint Health
Joint pain is the leading cause of disability among US adults. Thirty percent of US adults report experiencing some type of joint pain in any given 30-day period28. In addition, 18.1 % of US men and 23.5 % of US women younger than 60 report some type of knee pain.29 As we all know, eight out of 10 adults at some point in their lives complain of lower back pain. A recent
innovation in nutrition supplemental medicine has proven to be a breakthrough in maintaining joint health. Research has shown that a combination of undenatured type II collagen (UC-II®) and tetrahydro-iso-alpha acids (ThiAA) help revitalize joint function and performance.30"33
The impact of ADLs on joints may cause localized pain and stiffness, which are hallmark features of pathologic inflammatory disease (osteoarthritis, or OA34). Studies have shown that microtrauma from everyday use of the joints can lead to significant losses in articular cartilage and glycosaminoglycans35. In fact, some studies have shown that many of the cytokines implicated in the onset and progression of OA also appear to regulate the remodeling of normal extracellular matrix (ECM).36 Conventional medical wisdom has long held that osteoarthritis results from age-related “wear and tear.” For the first time, a team of researchers at Stanford University has demonstrated that this is not true. Their research has shown that a nutritional intervention has been identified to safely regulate the immune system to protect aging/stressed joint tissue from autoimmune attacks.37 A team of 25 scientists at Stanford University concluded that the development of osteoarthritis is in great part driven by low-grade inflammatory processes. Specifically, the researchers discovered low-grade inflammation launches an orchestrated, powerful attack on the synovial joints via signaling proteins normally used to fight infections. This autoimmune response, they reported, plays a key role in osteoarthritis onset. Fortunately, scientists have discovered a substance called undenatured type II collagen, or UC-II®, that retrains killer T cells (which destroy target cells) so that they recognize collagen as a harmless substance, preventing the joint damage seen in osteoarthritis.38
UC-II® was discovered when a team of scientists at the University of Nebraska found that chicken soup prevented the mobilization of immune system cells to sites of inflammation. Upon further analysis, they found it was not vegetables, but a component of the chicken broth itself that exerted this antiinflammatory activity. Chicken-derived type II collagen was found to regulate the immune system and prevent the attack of proteins and healthy joint cartilage.39 UC-II® has been proven to activate a pathway known as “induced oral tolerance,” which teaches the immune system to correctly recognize cartilage proteins as the body’s own tissues instead of foreign microbes. Oral-induced tolerance thus prevents an inflammatory attack, a newly recognized cause of osteoarthritis.40'41
The key feature UC-II® is that it results in “induced-specific oral tolerance.” T cells are, in part, immune system watchdogs, constantly assessing the three-dimensional structure of proteins they encounter in order to distinguish between harmless “self’ proteins and potentially deadly “foreign” proteins. If T cells ai e exposed in the blood to a new protein structure—such as an unrecognized protein on separated collagen fiber—they react violently and trigger an inflammatory response to destroy what is presumed to be a disease-causing invader42-44. However, scientists have learned that it is possible to teach T cells that the collagen molecule is a friend rather than a foe. Induced
specific oral tolerance retrains T cells to ignore collagen fibers when they are encountered in joints. Rich collections of immune tissue located in the lower end of the small intestine (called Peyer’s patches) act as “training centers” for the immune system. Peyer’s patches expose T cells to a vast variety of molecular shapes among the natural components in the foods we eat. This desensitizes T cells to new foods to avoid constant inflammatory or allergic reactions. In other words, this area induces tolerance.45
Native collagen introduced into the digestive tract—rather than directly into the bloodstream—can “educate” T cells to ignore collagen fibers when they are encountered in the joints. In scientific terms, the result is “induced specific oral tolerance.” This oral tolerance to collagen powerfully suppresses joint inflammation, as has been shown in numerous studies. In order to induce tolerance to exposed joint collagen, the orally introduced product must be type II collagen—the same form of collagen found in the cartilage matrix—and must have the exact same three-dimensional structure. Undenatured type II collagen retains its molecular structure, allowing it to induce oral tolerance.46
The second key ingredient in revitalizing joint function is tetrahydro-iso-alpha acids (ThiAA). Research has shown that ThiAA modulates kinases to prevent the expression of the NF-KB pathway. This pathway is the signal transducer of
inflammation in a cell. In other words, it reduces the level of inflammation.47
ThiAA contributes to maintaining joint health by decreasing inducible inflammation (cell production of inflammation at the time of injury). In addition, studies have shown it to reduce swelling of acute inflammation and inhibit bone/cartilage degeneration with chronic inflammation.48'54
In a landmark study, the combination of UC-II® and ThiAA was shown to promote joint health, specifically by positively influencing knee extension (knee extension is necessary for daily function and sports activities). Additional findings reveal the combination allowed individuals to exercise for longer periods before experiencing joint discomfort and to recover from joint injury faster.55'56
Recent breakthrough research at Harvard University, Stanford University, and the University of Nebraska confirms the supplemental value of the combination of UC-II® and ThiAA to maintain and revitalize joint function57. These results can make a profound impact on joint health.
Based on the numerous research studies conducted, there is a definitive need to augment soft-tissue healing by adding proper supplementation because soft tissues do not heal properly by themselves. The three phases of care outlined in this
article have been formulated for doctors of chiropractic to follow as a template for soft-tissue injuries to ensure proper healing. In my opinion, soft-tissue and joint injury are not two separate units but aie intricately related. Maintaining joint health is critical for adults through the lifespan to prevent soft-tissue injury during ADLs as well as exercise.
Proper diet, ergonomically sound body movement, and nutritional supplements aie keys for maintaining soft-tissue and joint health. Without nutritional supplements, the normal aging process of soft ti s su e/j oints will be exponentially increased.
Reference
1. Bucci LR. (1995). Nutrition applied to injury rehabilitation and sports medicine. CRC Press: Boca Raton.
2. Rathgeber WR The use of proteolytic enzymes in sporting injuries. SAfrMed J. 1971;45(7): 181-3.
3. Masson M. Bromelain in blunt injuries of the locomotor system. A study of observed applications in general practice. Fortschr Med. 1995;113(19):303-306.
4. Tricket P. Proteolytic enzymes in treatment of athletic injury. Appl Uier. 1964;30:647-652. '
5. Flynn, etal. Inhibition of human neutrophil 5lipoxygenase activity by gingerdione, shogaol, capsaicin and related pungent compounds. Prostaglandins LeukotMed. 1986;24(2-3): 195-8.
6. Satoskar, et al. Evaluation of anti-inflammatory property of curcumin (diferuloyl methane) in patients with postoperative inflammation. Int J Clin Pharmacol Ther Toxicol. 1986;24(12):651-4.
7. Buhrmann C, Mobasheri A, Busch F, et al. Curcumin modulates nuclear factor kappaB (NF-kappaB)-mediated inflammation in human tenocytes in vitro. J Biol Chem. 2011;286(32): 28556-66.
8. Etzel, et al. Special extract of Boswellia serrata (H 15 ) in the treatment of rheumatoid arthritis. Phytomed. 1996;3:91-94.
9. Weeks BS. Formulations of dietary supplements and herbal extracts for relaxation and anxiolytic action. Med Sci Monit. 2009;15(ll):RA256-62.
10. 0 Iseri LT, French JH. Magnesium: nature’s physiologic calcium blocker. Am Heart J. 1984;108(1): 188-194.
11. Amoczky, et al. Matrix Metalloproteinase inhibitors prevent a decrease in the mechanical properties of stress-deprived tendons: an in vitro experimental study. Am J Sports Med. 2007;35(5):763-9.
12. Litherland GJ, Dixon C, Lakey RL, et al. Synergistic Collagenase Expression and Cartilage Collagenolysis Are Phosphatidylinositol 3-Kinase/Akt Signaling-dependent. J Biol Chem. 2008;283:1422114229.
13. McCarthy MM, Hannafin JA. The Mature Athlete: Aging Tendon and Ligament. Sports Health. 2014;6(l):41-48.
14. Desai A et al. META060 inhibits multiple kinases in the NF-kB pathway and suppressed LPS-mediated inflammation in vitro and ex vivo. Inflammation Research. 2009;58(5):229-34.
15. Konda VR, et al. META060 inhibits osteoclastogenesis and matrix metalloproteinases in vitro and reduces bone and cartilage degradation in a mouse model rheumatoid arthritis. Arthritis & Rheumatism. 2010;62(6):1683-92.
16. Tinker D, Recker RB. Role of selected nutrients in synthesis, accumulation, and chemical modification of connective tissue proteins. Physio Rev. 1965,65(3):607-657.
17. RingsdorfWM, Cheraskin E. Vitamin C and human wound healing. Oral Surg. 1982;53(3):231-236.
18. Arsenault J. Kennedy J. Dietary supplement use in U.S. Army Special Operations candidates. Military Medicine. Í999;164(7):495-501.
19. 9 Global Advances in Health and Medicine. 2014;3(2):34-39.
20. Terano T, Salmon JA, Higgs GA, Moneada S. Eicosapentaenoic acid as a modulator of inflammation: Effect on prostaglandin and leukotriene synthesis. Biochem Pharmacol. 1986;35(5):779-85.
21. Marwick C. Learning How Phytochemicals Help Fight Disease. JAMA. 1995;274( 17) : 13281330
22. Noreen EE, Sass MJ, Crowe ML, et al. Effects of supplemental fish oil on resting metabolic rate, body composition, and salivary cortisol in healthy adults. JISSN. 2010;7:31.
23. Yates Anthony, Norwig J, Maroon JC, et al. Evaluation of Lipid Profiles and the Use of Omega-3 Essential Fatty Acid in Professional Football Players. Sports Health. 2009;l(l):21-30.
24. American Ortho Soc for Sports Medicine. Annual meeting, July
10, 2011.
25. Angeline ME, Ma R, Pascual-Garrido C, et al. Effect of dietinduced vitamin D deficiency on rotator cuff healing in a rat model. Am J Sports Med. 2014 Jan;42(l):27-34.
26. Collier, SR, Casey DP, Kanaley JA. Growth hormone responses to varving doses of oral arginine. Growth Horm IGF Res. 2005;15(2): 136-9.
27. Cox AJ, Pyne DB, Saunders PU, Fricker PA. Oral administration of file probiotic Lactobacillus fennentum VRI-003 and mucosal immunity in endurance athletes. Br J Sports Med. 2010;44(4):222-
6. Epub 2008 Feb 13.
28. NationalHealthInterviewSurvey2006.MMWR.2008;57(17):467. www.cdc.gov/nchs/nhis.htm
29. Andersen RE et al. Prevalence of significant knee pain among older Americans; results from NHANES III. J Am Geriatr Soc. 1999;47( 12): 1435-8.
30. Crowley DC, Lau FC, Sharma P, et al. Int Med Sci. 2009;6:312321.
31. Lugo JP, Saiyed ZM, Lau FC, et al. J Int Soc Sports Nutr. 2013 ; 10( 1 ) : 48.
32. Marone PA, Lau FC, Gupta RC, et al. Toxicol Mech Methods. 2010;20(4): 175-189.
33. Barnett ML, Kremer JM, et al. Arthritis Rheum. 1998;41(2):290297.
34. Ostrowski K, Rohde T, et al. Proand anti-inflammatory cytokine balance in strenuous in humans. J Physiol. 1999 Feb 15;515(Pt 1):287-91.
35. Kiviranta I, Tammi M, Jurvelin J, et al. Articular cartilage thickness and glycosaminoglycan distribution in the canine knee joint after strenuous running exercise. Clin Orthop Relat Res. 1992 Oct;(283):302-8.
36. Hoff P, Buttgereit F, Burmester GR, et al. Osteoarthritis synovial fluid activates pro-inflammatory cytokines in primary human chondrocytes. Int Orthop. 2013 Jan;37(l):145-51.
37. Wang Q, Rozelle AL, Lepus CM, et al. Identification of a central role for complement in osteoarthritis. Nat Med. 2011 Nov 6.
38. http://med.stanford.edu/ism/2011/november/osteoarthritis.html. Accessed November 15, 2011.
39. Rennard BO, Ertl RF, Gossman GL, Robbins RA, Rennard SI. Chicken soup inhibits neutrophil chemotaxis in vitro. Chest. 2000 Oct;118(4):1150-7.
40. Min SY, Park KS. Cho ML, et al. Antigen-induced, tolerogenic CDllc+,CDllb+ dendritic cells are abundant in Peyer’s patches during the induction of oral tolerance to type II collagen and suppress experimental collagen-induced arthritis. Arthritis Rheum. 2006 Mar;54(3):887-98.
4L Weiner HL. Oral tolerance: immune mechanisms and treatment of autoimmune diseases. Immunol Today. 1997 Jul;18(7):335-43.
42. Bagchi D, Misner B, Bagchi M, et al. Effects of orally administered undenatured type II collagen against arthritic inflammatory diseases: a mechanistic exploration. Int J Clin Pharmacol Res. 2002;22(3-4): 101-10.
43. Cremer MA, Rosloniec EF, Kang AH. The cartilage collagens: a review of their structure, organization, and role in the pathogenesis of experimental arthritis in animals and in human rheumatic disease. J Mol Med (Berl). 1998 Mar;76(3-4):275-88.
44. Corthay A, Backlund J, Broddefalk J, et al. Epitope glycosylation plays a critical role for T cell recognition of type II collagen in collagen-induced arthritis. Eur J Immunol. 1998Aug;28(8):2580-90.
45. Recommendations for the medical management of osteoarthritis of the hip and knee: 2000 update. American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. Arthritis Rheum. 2000 Sep;43(9):1905-15.
46. Park KS, Park MJ, Cho ML, et al. Type II collagen oral tolerance; mechanism and role in collagen-induced arthritis and rheumatoid arthritis. Mod Rheumatol. 2009;19(6):581-9.
47. Desaia A, Konda VR, et al. Inflamm Res. 2009;58(5):229-234.
48. Desai A, Darland G, Bland JS, et al. Atherosclerosis. 2012;223(1): 130-136.
49. Konda VR, Desai A, Darland G, et al. Arthritis Rheum. 2010;62(6): 1683-1692.
50. Tripp M, Darland G, Lerman RH et al. Presented at: Fed Am Soc Experimental Biol. 2003: April.
51. Lerman RH, Liska D, et al. Proprietary Clinical Research Report. Gig Harbor, WA: Functional Medicine Research Center; 2004.
52. Lerman RH, Liska D, Tripp M, et al. Proprietary Clinical Research Report. Gig Harbor, WA: Functional Medicine Research Center; 2004.
53. Lukaczer D, Lerman RH, Tripp M, et al. Proprietary Clinical Research Report. Gig Harbor, WA: Functional Medicine Research Center; 2004.
54. Minich DM, Bland JS, Katke J, et al. J Physiol Pharmacol. 2007;85:872-883.
55. Lerman RH. Proprietary Clinical Research Report. Gig Harbor, WA: Functional Medicine Research Center; 2013.
56. JP Lugo, ZM Saiyed, FC Lau, et al. Undenatured type II collagen (UC-II®) for joint support: a randomized, double-blind, placebocontrolled study in healthy volunteers. Journal of the International Society of Sports Nutrition. 2013;10:48.
57. Trentham DE, Dynesius-Trentham RA, Orav EJ, et al. Effects of oral administration of type II collagen on rheumatoid arthritis. Science. 1993 Sep 24;261(5129): 1727-30.
Dr. Robert G. Silverman. DC, DACBN, DCBCN, MS, CCN, CNS, CSCS, CIISN, CKTP, CES, HKC, SASTM graduated Magna cum Laude from the University of Bridgeport, College of Chiropractic. He holds a Masters of Science in Human Nutrition and is a Diplomate with the American Clinical Board of Nutrition and the Chiropractic Board of Clinical Nutrition. He is certified as a sports nutritionist, Certified Nutrition Specialist, and Certified Clinical Nutritionist. Dr. Robert G. Silverman (914) 287-6464 e-mail: [email protected] website: www.DrRobertSilverman.com * You can see Dr. Silverman at the 2015 Metagenic's Lifestyle Medicine Summit on Sept. 25th held in Phoenix, Arizona!