Joint Health

By Dr. Greg Fors, DC, DIBCN
Board Certified Neurologist

According to the World Health Organization, DJD or degenerative joint disease is one of the top 10 global disease burdens in the world today. Approximately 1 in 3 adults between 25 to 74 years old in the US have radiological evidence of Osteoarthritis (OA) in at least one joint. In the US, 25% of all visits to primary care physicians and half of all NSAIDs prescriptions are for OA. However, degenerative joint disease is not an inevitable consequence of growing older. It develops when trauma, and/or biochemical changes trigger a shift between joint cartilage synthesis and degradation.(1) Primarily, when the cartilage synthesis of any joint cannot keep pace with the background degradation of the cartilage, the joint will degenerate. Two very important factors in the joint play a primary role in joint deterioration. The first factor is the reduction in proteoglycan production in the joint cartilage. The second factor is the rate of production of inflammatory catabolic cytokines in the chondrocytes and synovial cells.(2) The driving force behind these two factors is of course multifactorial, but genetics play a primary role, which is influenced by the quality of the macro and micro nutrient intake of the individual.

Low vitamin D levels are now linked to multiple health problems, including degenerative disc disease of the spine.(3) A 2006 study showed that an inherited polymorphism of a vitamin D receptor in the spinal disc was associated with a high risk of degenerative disc disease and disc bulge developing, especially in individuals younger than 40 years.(4) In a future Clinical Update, I will dedicate an entire issue to the importance of and clinical use of vitamin D3.

Early Assessment of Optimal Joint Health
Even in today's "modern medicine", early diagnosis of degenerative joint disease is still based on keen clinical observation and radiographic changes. However, when you make the diagnosis at this point, your patient has already fully developed the disease. There has always been the hope of finding inexpensive clinical lab tests that would help indicate when a patient is heading for degenerative joint disease. From the previously cited studies, low Vitamin D3 levels may be indicative of spinal degeneration problems in the future. It may be prudent to keep your patients' serum levels of Vitamin D, 25-hydroxycalciferol above the 40 ng per milliliter.

However, exciting work is now being done on the diagnostic relevance of high sensitivity C reactive protein to osteoarthritis. New ultrasensitive methods for C-reactive protein (hsCRP) have improved the usefulness of this marker, especially in the assessment of systemic inflammation. One study found that patients with erosive OA averaged hsCRP levels of 4.7mg/L, and individuals with non-erosive OA averaged 2.2 mg/L.(5) What is important to realize here is that both patient groups were above the threshold for increased risk for systemic inflammation, and the erosive OA group was well above the significant risk profile. What is indicated here is that patients well above ideal levels of hsCRP of 0.5 mg/L may be on the road to the development of osteoarthritis. Fibrinogen is also an inexpensive clinical marker of low-grade systemic inflammation in the tissues and may be helpful in assessing the risk for the development of degenerative joint disease.

Nutritional Support for Healthy Joints
To properly treat the underlying metabolic causes of degenerative joint disease, it is vital to treat the underlying chronic catabolic inflammation, oxidative stress, and poor cartilage repair. For the management of the inflammatory catabolic cytokines of degenerative joint disease, concentrated standardized herbal extracts of Ginger, Curcumin, Nettle leaf, and Boswellia have been shown to help manage this inflammatory cascade. Specifically, standardized extracts of these herbs have been shown to manage the pro-inflammatory cytokines and prostaglandins involved in the pain, swelling, and cartilage destruction of OA. These herbs also reduce oxidative stress and support healthy and muscle joint tissue function. To help improve your management of inflammatory catabolic cytokines it is beneficial to combine these standardized herbal extracts with high levels of EPA/DHA fatty acids.

To help improve proteoglycan production and cartilage synthesis in the joints, supplement 1.5 to 2 g of glucosamine sulfate. Glucosamine sulfate has been found to stimulate the synthesis of GAGs, proteoglycans, and collagen within the joint complex. It has also been shown to support healthy synovial fluid through synthesis of hyaluronic acid, which may increase the mobility of joints and enhance their lubrication. It may also assist in the inhibition of many enzymes that break down the cartilage matrix.

For best results always combine nutraceuticals that manage inflammatory catabolic cytokines and those that promote proteoglycan production and cartilage synthesis. To be successful, make sure these nutraceuticals contain sufficient quantities of quality ingredients. Standardized extracts of ginger should reach 2 g per day and Curcumin a minimum of 1 g per day to reach clinical results. Research studies also show that glucosamine should reach levels of 1 to 2 g daily to be effective and chondroitin should reach approximately 1000 mg. As you can see from these studies, it is vital to get formulations that are highly concentrated. Both products should be supplemented for a minimum of 12 weeks before therapeutic effects can be evaluated.

Copyrighted 2007 by Dr. Greg Fors-Article or portions of this article cannot be used without the authors permission click here to obtain permission
1. Silver FH, Bradica G, Tria A. Relationship among biomechanical, biochemical, and cellular changes associated with osteoarthritis. Crit Rev Biomed
2. Notoya K, Jovanovic DV, Reboul P, Martel-Pelletier J, Mineau F, Pelletier JP. The induction of cell death in human osteoarthritis chondrocytes by nitric oxide is related to the production of prostaglandin E2 via the induction of cyclooxygenase-2. J Immunol. 2000 Sep 15; 165(6):3402-10
3. Videman T, Gibbons LE, Battie MC, et al. The relative roles of intragenic polymorphisms of the vitamin d receptor gene in lumbar spine degeneration and bone density. Spine. 2001 Feb 1;
4. Cheung KM, Chan D, Karppinen J, ET. Al. Association of the Taq I allele in vitamin D receptor with degenerative disc disease and disc bulge in a Chinese population. Spine. 2006 May 1; 31(10):1143-8.
5. Punzi L, Ramonda R, Oliviero F et al. Value of C reactive protein in the assessment of erosive osteoarthritis of the hand Ann Rheum Dis. 2005 Jun; 64(6):955-7

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