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Arthritis:

Pain is a major health concern. Painful and inflamed joints become stiff affecting mobility. This condition may lead to lost work time and reduced productivity.1 Joint pain is also an overall hindrance and reduces the pleasure people get from everyday life. Inflammation of the joints is called arthritis and the incidence of arthritis increases with age.2

Arthritis may also result in structural modifications of joints. It is not a disease in itself, but an end result of a variety of conditions affecting the joints. More than a hundred conditions have been identified that cause pain and inflammation of the joints.3 The most common forms of arthritis are briefly discussed below:

Osteoarthritis (OA):

The most common form of arthritis and known as a degenerative disease of the joints, it usually affects the weight bearing joints (hips, knees and lower spine), though other joints (fingers, thumbs, shoulders) may be affected. Obese people are twice as likely as people with normal weight to suffer from OA. Seventy percent of the U.S. population older than 65 manifest radiographic evidence of the disease.2 OA involves the wear and tear of cartilage that cannot be replaced or repaired by the body. The cartilage becomes thinner and with the progression of the disease, it may ultimately disappear. The bone underneath the worn out cartilage becomes thick and hard. The synovial membrane may be inflamed and produce excessive synovial fluid that contributes to the swelling of the joints. The relationship between inflammation and pain is not clear in OA.4

Rheumatoid Arthritis (RA):

The chronic inflammatory condition of joints due mainly to the inflammation of synovial membrane. The cause of the inflammation is not known. The inflamed synovial membrane becomes thick and produces excessive fluid that contributes to swollen joints. If not checked, the inflammatory mediators produced by the cells of the synovial membrane (cytokines, prostaglandins and leukotrienes, oxygen free radicals, and degradative enzymes) can damage the structures in and around the joint (cartilage, bone, tendons and ligaments) making the joint immobile and causing erosion of the bone. RA usually affects the smaller joints symmetrically.

Psoriatic Arthritis:

Occurs in people suffering from psoriasis. It commonly affects the fingers, toes, wrists, knees and ankles though major joints, like the spine, may be affected. Psoriatic arthritis resembles rheumatoid arthritis.

Mechanisms of Arthritis:

Of the various arthritic conditions, OA and RA are the most common. Various hypotheses have been put forward to explain the etiology of arthritic conditions but finite answers are still not known.
Rheumatoid factor (IgM autoantibody) has been detected in the serum of RA patients, suggesting it is an autoimmune disease.5 The common finding in RA is the involvement of synovial fluid and membrane in pathophysiology. The cells of synovial membranes include monocytic phagocytes and fibroblasts. These cells are capable of secreting cytokines like interleukin 1 (IL-1) and tumour necrosis factor (TNF). Cellularity of synovial fluid is also increased by recruitment of polymorphonuclear leukocytes, T-cells and macrophages. These cells release inflammatory mediators including prostaglandins, leukotrienes and oxygen free radicals that damage the proteins and cellular structures, including bone and cartilage. TNF and IL-1 released by activated T-cells and phagocytic cells further amplify the inflammatory reactions by attracting and stimulating more of these cells. The expression of cyclooxygenase of series 2 (COX-2) enzyme (the enzyme responsible for production of prostaglandins) has been found to be increased in inflamed RA and OA joints.6 COX-2 expression is increased by IL-1, TNF and various growth factors. COX-2 is involved in the production of inflammatory prostaglandins (PGE2) from arachidonic acid. PGE2 is responsible for pain and inflammation.7

Conventional Treatment:

Because the cause of joint inflammation is not well understood, the treatment is far from satisfactory despite the research being done. Present treatments aim to reduce or alleviate the pain and inflammation of the affected joints and improve mobility. These treatments include analgesics, salicylates, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids and reconstructive surgery. These drugs are associated with a large number of side effects. The major side effects include gastric ulcers (salicylates, NSAIDs), renal failure (NSAIDs) and immunosuppression (corticosteroids).3,8
Nutritional Approach:

Nutritional supplements offer a safer alternative to conventional medicine. Joint Health Formula contains scientifically proven constituents that are safe, reduce inflammation and pain and promote cartilage repair.

The actions of individual ingredients are summarized in brief:

BORAGE OIL is incorporated into Joint Health Formula because it is a well-known anti-inflammatory oil. It is the richest natural source of gamma-linolenic acid (GLA), an essential fatty acid (EFA) belonging to the n-6 series. GLA is metabolised in the body to dihomo-gamma-linolenic acid (DGLA). DGLA is incorporated into membrane phospholipids and competes with arachidonic acid for cytokine synthesizing enzymes (cyclooxygenases and lipoxygenases). DGLA is metabolised to prostaglandins of series 1, including prostaglandin E1 (PGE1).9 PGE1 is a potent anti-inflammatory prostaglandin. Borage oil administration is reported to reduce the formation of inflammatory prostaglandins of series 2 (PGE2) and leukotriene B4.9 Laboratory and clinical studies have established the beneficial effects of borage oil in reducing the pain and inflammation of various arthritic conditions.9,10

FLAXSEED OIL and FISH OIL are added to Joint Health Formula as a source of n-3 essential fatty acids (EFA). Flaxseed oil is the richest vegetable source of alpha-linolenic acid (ALA). ALA is metabolised in the body to eicosapentaenoic (EPA) acid and docosahexaenoic acid (DHA). Fish oil is a direct source of EPA and DHA. These essential fatty acids are incorporated into the membrane phospholipids and compete with arachidonic acid for the enzymes responsible for the production of eicosanoids. The essential fatty acids of the n-3 series reduce the formation of pro-inflammatory prostaglandins of series 2. Laboratory and clinical studies have revealed the beneficial effects of these n-3 essential fatty acids in various forms of arthritis.11,12 The EFA rich oils improve joint mobility and reduce the severity of pain and inflammation without any short or long-term side effects.

ASHWAGANDHA EXTRACT, also known as Withania somnifera, has been used medicinally for centuries in Ayurvedic formulations as an anti-inflammatory, rejuvenating and nervine tonic.13 Laboratory and clinical studies have revealed that the constituents of this plant reduce inflammation.14 The levels of alpha-2 macroglobulin are increased in arthritic and inflammatory conditions.15 Treatment with ashwagandha reduces the alpha-2 macroglobulin levels.16 Ashwagandha has no short or long-term harmful effects. The plant also has antioxidant properties that may contribute to its usefulness in anti-arthritic therapy. Antioxidants quench free radicals that are increased in the synovial fluid of patients with arthritis and contribute to cartilage and bone damage.

BOSWELLIA SERRATA EXTRACT has a long history of use in the Ayurvedic system of medicine. It has been proven safe and effective against inflammatory conditions. Recent scientific research has revealed that boswellia is a specific inhibitor of 5-lipoxygenase enzyme,17 responsible for the production of leukotriene B4 (LTB4). LTB4 is a very potent chemotactic factor that primes the phagocytic cells to release oxygen free radicals and various degradative enzymes (elastase). These free radicals and enzymes can induce or contribute to the joint damage seen in arthritis. By reducing the production of LTB4, boswellia reduces inflammation. Boswellia also inhibits the complement system, which when activated, contributes to inflammatory response.18

GLUCOSAMINE SULFATE is an amino sugar, a component of cartilage and connective tissue. Recent research has shown that glucosamine stimulates the production of glycosaminoglycans and proteoglycans, the building blocks of cartilage. It is effective orally and possesses anti-inflammatory and chondroprotective properties. Glycosaminoglycan levels are reduced in arthritic joints. Supplementation with glucosamine sulfate stimulates the synthesis and incorporation of glucosamine into cartilage19 and reduces the pain and inflammation of arthritic joints.20

ZINC SULFATE: It has been established that arthritic patients have low plasma zinc concentrations.21 This may be due to malabsorption coupled with low dietary intake.22 Therefore, supplementation with zinc is a logical choice. Studies have shown the beneficial effects of zinc supplementation on pain and inflammation.23

Suggested Use:

Take 1 3 times a day, depending on the severity of the pain and inflammation.

Cautions:

Joint Health Formula contains proven safe constituents. No serious side effects were reported from any of the ingredients. It may cause gastrointestinal disturbances, including diarrhea. These rare side effects do not require discontinuation or dose adjustment. If a person is sensitive to any ingredient in this formulation, use of the product should be discontinued.

References:

1. Yelin EH. The economic impact of osteoarthritis. In: Baker JR, Brendt KD, editors. Reappraisal of the Management of Patients with Osteoarthritis. Springfield Mass: Scientific Therapeutic Information Inc.;1993. p. 1-92.
2. Scott JC, Hochberg MC. Arthritic and other musculoskeletal diseases. In: Brownson RC, Remington PL, Davis JL editors. Chronic Disease Epidemiology and Control. Washington DC: American Public Health Association; 1993.
3. The Merck Manual of Diagnosis and Therapy. 16th ed. Rahway, NJ: Merck & Co. Ltd.; 1992, p. 1293-1378.
4. Lane NE. Pain management in Osteoarthritis: the role of COX-2 inhibitors. J Rheumatol 1997;24 Suppl 49:20-24.
5. Maini R, Feldmann M, In: Maddison PJ, Isenberg DA, Woo P, Glass DN, editors. Oxford Textbook of Rheumatology. Vol.2. Oxford University Press; 1993. p. 621-38.
6. Sano H, Hla T, Maier JAM, Crofford LJ, Case JP, Maciag T, et al. In vivo cyclooxygenase expression in synovial tissue of patients with rheumatoid arthritis and osteoarthritis and rats with adjuvant and streptococcal cell wall arthritis. J Clin Invest 1992;89:97-108
7. Lipsky PE, Isakson PC. Outcome of specific COX-2 inhibition in rheumatoid arthritis. J Rheumatol 1997;24 Suppl 49:9-14.
8. Compendium of Pharmaceuticals and Specialities. 31st ed. Ottawa: Canadian Pharmaceutical Association; 1996. p. 123-24, 379-80, 948-49.
9. Pullman-Mooar S, Laposata-M, Lem D, Holman RT, Leventhal LJ, DeMarco D, et al. Alteration of the cellular fatty acid profile and the production of eicosanoids in human monocytes by gamma-linolenic acid. Arthritis Rheum 1990;33:1526-35
10. Zurier RB, Rosetti RG, Jacobson EW, DeMarco GM, Liu NY, Temming JE, et al. Gamma-linolenic acid treatment of rheumatoid arthritis. Arthritis Rheum 1996;39(11)1808-17.
11. Simopoulos AP. Summary of the NATO advanced research workshop on dietary ?3 and ?6 fatty acids: biological effects and nutritional essentiality. J Nutr 1989;119:521-28
12. DeLuca P, Rothman D, Zurier RB. Marine and botanical lipids as immunomodulatory and therapeutic agents in the treatment of rheumatoid arthritis. Rheum Dis Clin North Am 1995;21:759-77.
13. Dr. K.M. Nadkarni's Indian Material Medica Vol 1. Bombay: Popular Prakashan PVT Ltd.; 1976. p. 1292-4.
14. Al-Hindawi MK, al-Khafaji SH, Abdul-Nabi MH. Anti-granuloma activity of Iraqi Withania somnifera. J. Ethnopharmacol 1992;37:113-16.
15. Pejovic M, Stankovic A, Mitrovic DR. Determination of the apparent synovial permeability in the knee joint of patients suffering from osteoarthritis and rheumatoid arthritis. Br J Rheumatol 1995;34:520-24.
16. Anbalagan K and Sadique Withania somnifera (Ashwagandha), a rejuvenating herbal drug which controls alpha-2-macroglobulin synthesis during inflammation. J. Int J Crude Drug Res 1985;23:177-83.
17. Safayhi H, Mack T, Sabieraj J, Anazodo MI, Subramanian LR, Ammon HPT. Boswellic acids: novel, specific, nonredox inhibitors of 5-lipoxygenase. J Pharmacol Exp Ther 1992;261:1143-46.
18. Kapil A, Moza N. Anticomplementary activity of boswellic acids - an inhibitor of C3-convertase of the classical complement pathway. Int J Immunopharmacol. 1992;14:1139-43.
19. Axelsson S, Holmlund A, Hjerpe A. Glycosaminoglycans in normal and osteoarthrotic human temporomandibular joint disks. Acta Odontol Scand 1992;50(2):113-19.
20. Tapadinhas MJ, Rivera IC, Bignamini AA. Oral glucosamine sulphate in the management of arthrosis: report on a multi-centre open investigation in Portugal. Pharmatherapeutica 1982;3(3):157-68.
21. Naveh Y, Schapira D, Ravel Y, Geller E, Scharf Y. Zinc metabolism in rheumatoid arthritis: plasma and urinary zinc and relationship to disease activity. J Rheumatol 1997;24:643-46.
22. Krener JM, Bigaouette J. Nutrient intake of patients with rheumatoid arthritis is deficient in pyridoxine, zinc, copper, and magnesium. J Rheumatol 1996;23:990-4.
23. Simkin P. Oral zinc sulphate in rheumatoid arthritis. Lancet 1976;2:539-42.

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