When an individual gets 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. A lack 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.
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 trypsin, chymotrypsin, bromelain (also called proteolytic enzymes) can help aid to 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. 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 inhibitor. Boswelia serrata has been found to specifically inhibit the powerful pro-inflammatory enzyme, 5-lipoxygenase. 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 pre-synaptic 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.
Sub-Acute Healing: Repair and Remodeling Phase
The second phase starts at day four and includes up to approximately eight weeks, during which repair and remodeling of soft tissue takes place.
- 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 repairative nutrients that may help minimize formation of scar tissue
- Aid in connective tissue remodeling
- Reduce risk of re-injury and degeneration
- Initiate soft-tissue (extracellular matrix) support by modulating matrix metalloproteinases
- Continue controlling pain and inflammation
Nutritional Protocol for Sub-Acute Healing
An injured site never achieves the original histologic or mechanical features of a healthy, uninjured tendon with rest alone., but 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 aid in the healing process. Matrix metalloproteinase (MMP) enzymes are released at the time of injury. Unfortunately, excessive release of MMP’s can damage healthy tendon, collagen and connective tissue in the injured area. At this point, with elevated MMP’s release, 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 enzymes.
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 MMP’s. These nutrients are critical elements in a soft tissue nutritional formula. Support the growth and construction of connective tissue with the following combined nutrients:
- Glycine, proline, lysine, vitamin C, B6, B5, L-taurine, and silica
- Glucosamine/chondroitin sulfate/MSM should be consumed concurrently as well to aid in joint stability
Wellness and Prevention Phase
The goal in this final phase is to achieve optimal tissue remodeling to support wellness/prevention, and to reduce the risk of re-injury and degeneration by installing what I call my foundation nutrition:
- Phytomulti: Multivitamin/mineral complex with additional phytonutrients
- Omega-3 Fatty Acids: Aids in the reduction of inflammation (two grams of EPA/DHA)
- Vitamin D: Aids in the healing of sports injuries (2,000 IU and up)
- Probiotics (L-acidophilus and B-lactis): Helps balance immune function (approximately 15 billion live organisms)
- A Phytonutrient Green Drink: To help quench damaging free radicals and contribute to whole body alkalization.
Nutritional Protocols for Joint Health
Joint pain is the leading cause of disability among U.S. adults. 30 percent of U.S. adults report experiencing some type of joint pain in any given 30-day period. 18.1 percent of U.S. men and 23.5 percent of U.S. women less than 60 years old report some type of knee pain. As we all know, 8 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 tetrahydroiso- alpha acids (ThiAA) help revitalize joint function and performance.1-4
The impact of ADLs on joints may cause localized pain and stiffness, which are hallmark features of pathologic inflammatory disease (osteoarthritis – OA5). Studies have shown that micro trauma from everyday use of the joints can lead to significant losses in articular cartilage and glycosaminoglycans6. 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).7
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.8
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.9
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 anti-inflammatory activity. Chicken-derived type II collagen was found to regulate the immune system and prevent the attack of proteins and healthy joint cartilage.10
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. Oralinduced tolerance thus prevents an inflammatory attack, a newly recognized cause of osteoarthritis.11-12
UC-II®’s key feature 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 are 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 invader.13-15 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 food we eat. This desensitizes T-cells to new foods to avoid constant inflammatory or allergic reactions. In other words, this is the area that induces tolerance.16
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.17
The second key ingredient in revitalizing joint function is tetra-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.18
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. 19-25
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 of time before experiencing joint discomfort and to recover from joint injury faster.26-27
Recent breakthrough research at Harvard, Stanford and University of Nebraska confirms the supplemental value of the combination of UC-II® and ThiAA to maintain and revitalize joint function.28 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 are intricately related. Maintaining joint health is critical for adults through the lifespan to prevent soft tissue injury during ADL’s as well as exercise.
Proper diet, ergonomically sound body movement and nutritional supplements are keys for maintaining softtissue and joint health. Without nutritional supplements, the normal aging process of soft-tissue/joints will be exponentially increased.
1. Crowley DC, Lau FC, Sharma P, et al. Int Med Sci. 2009;6:312-321
2. Lugo JP, Saiyed ZM, Lau FC, et al. J Int Soc Sports Nutr. 2013;10(1):48
3. Marone PA, Lau FC, Gupta RC, et al. Toxicol Mech Methods. 2010;20(4):175-189
4. Barnett ML, Kremer JM, et al. Arthritis Rheum. 1998;41(2):290-297
5. Ostrowski K, Rohde T, et al. Pro- and anti-inflammatory cytokine
balance in strenuous in humans. J Physiol. 1999 Feb 15;515 (Pt1):287-91
6. 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
7. Hoff P, Buttgereit F, Burmester GR, et al. Osteoarthritis synovial fluid activates pro-inflammatory cytokines in primary human chondrocytes. Int Orthop. 2013 Jan;37(1):145-51
8. Wang Q, Rozelle AL, Lepus CM, et al. Identification of a central role for complement in osteoarthritis. Nat Med. 2011 Nov 6
9. http://med.stanford.edu/ism/2011/november/osteoarthritis.html. Accessed November 15, 2011
10. Rennard BO, Ertl RF, Gossman GL, Robbins RA, Rennard SI. Chicken soup inhibits neutrophil chemotaxis in vitro. Chest. 2000 Oct;118(4):1150-7
11. Min SY, Park KS, Cho ML, et al. Antigen-induced, tolerogenic CD11c+,CD11b+ 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.
12. Weiner HL. Oral tolerance: immune mechanisms and treatment of autoimmune diseases. Immunol Today. 1997 Jul;18(7):335-43.
13. 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
14. 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
15. 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. 1998 Aug;28(8):2580-90
16. 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
17. 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
18. Desaia A, Konda VR, et al. Inflamm Res. 2009;58(5):229-234
19. Desai A, Darland G, Bland JS, et al. Atherosclerosis. 2012;223(1):130-136
20. 20) Konda VR, Desai A, Darland G, et al. Arthritis Rheum. 2010;62(6):1683-1692
21. Tripp M, Darland G, Lerman RH et al. Presented at: Fed Am Soc Experimental Biol. 2003: April
22. Lerman RH, Liska D, et al. Proprietary Clinical Research Report. Gig Harbor, WA: Functional Medicine Research Center; 2004
23. Lerman RH, Liska D, Tripp M, et al. Proprietary Clinical Research Report. Gig Harbor, WA: Functional Medicine Research Center; 2004
24. Lukaczer D, Lerman RH, Tripp M, et al. Proprietary Clinical Research Report. Gig Harbor, WA: Functional Medicine Research Center; 2004
25. Minich DM, Bland JS, Katke J, et al. J Physiol Pharmacol. 2007;85:872-883
26. Lerman RH. Proprietary Clinical Research Report. Gig Harbor, WA: Functional Medicine Research Center; 2013
27. 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
28. 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