remodeling to support wellness/prevention, and to reduce the risk of re-inury 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 inammation (two grams of EPA/DHA)


 itamin D Aids in the healing of sports inuries (,000 I and up) Probiotics


 (L-acidophilus and -lactis) Helps


balance immune function (approximately 1 billion live organisms)


 A Phytonutrient reen Drink To help uench damaging free radicals and contribute to whole body alkaliation.


Nutritional Protocols for Joint Health Joint pain is the leading cause of disability among .S. adults. 30 percent of .S. adults report experiencing some type of oint pain in any given 30-day period. 18.1 percent of .S. men and 3. percent of .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 oint health. Research has shown that a combination of undenatured type-II collagen (C-II) and tetrahydro- iso-alpha acids (ThiAA) help revitalie oint function and performance.1-


The impact of ADLs on oints may cause localied pain and stiffness, which are hallmark features of pathologic inammatory disease (osteoarthritis  OA


that many of the cytokines implicated in the onset and progression of OA also appear to regulate the remodeling of normal extracellular matrix (ECM).


Conventional medical wisdom has long held that osteo- arthritis results from age-related “wear and tear.” For the rst time a team of researchers at Stanford niversity has demonstrated that this is not true. Their research has shown that a nutritional intervention has been identied to safely regulate the immune system to protect aging/ stressed oint tissue from autoimmune attacks.8


A team of  scientists at Stanford niversity concluded that the development of osteoarthritis is in great part driven by low-grade inammatory processes. Specically, the researchers discovered low grade inammation launches an orchestrated, powerful attack on the synovial oints via signaling proteins normally used to ght 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 C-II, that retrains killer T-cells (which destroy target cells) so that they recognie collagen as a harmless substancepreventing the oint damage seen in osteoarthritis.9


THE ORIGINAL INTERNIST MARCH 01


shown that micro trauma from everyday use of the oints can lead to signicant losses in articular cartilage and glycosaminoglycans6


. In fact, some studies have shown ). Studies have


C-II was discovered when a team of scientists at the niversity of ebraska found that chicken soup prevented the mobiliation of immune system cells to sites of inammation. pon further analysis, they found it was not vegetables, but a component of the chicken broth itself that exerted this anti-inammatory activity. Chicken-derived type II collagen was found to regulate the immune system and prevent the attack of proteins and healthy oint cartilage.10


C-II has been proven to activate a pathway known as “induced oral tolerance” which teaches the immune system to correctly recognie cartilage proteins as the body’s own tissues instead of foreign microbes. Oral- induced tolerance thus prevents an inammatory attack, a newly recognied cause of osteoarthritis.11-1


C-II’s key feature is that it results in “induced-specic oral tolerance.”


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 unrecognied protein on separated collagen berthey react violently and trigger an inammatory response to destroy what is presumed to be a disease-causing invader.13-1


scientists have learned that it is possible to teach T-cells that the collagen molecule is a friend rather than a foe.


Induced-specic oral tolerance retrains T-cells to ignore collagen bers when they are encountered in oints. 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 desensities T-cells to new foods to avoid constant inammatory or allergic reactions. In other words, this is the area that induces tolerance.16


ative collagen introduced into the digestive tractrather than directly into the bloodstreamcan “educate” T-cells to ignore collagen bers when they are encountered in the oints. In scientic terms, the result is “induced specic oral tolerance.” This oral tolerance to collagen powerfully suppresses oint inammation, as has been shown in numerous studies. In order to induce tolerance to exposed oint 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. ndenatured type II collagen retains its molecular structure, allowing it to induce oral tolerance.1


The second key ingredient in revitaliing oint function is tetra-iso-alpha acids (ThiAA). Research has shown that ThiAA modulates kinases to prevent the expression of the F-k pathway. This pathway is the signal transducer of inammation in a cell. In other words, it reduces the level of inammation.18


ThiAA contributes to maintaining oint health by decreasing inducible inammation (cell production of (Continued on next page)


11 However, T-cells are in part, immune system


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