Osteoarthritis is the most common cause of musculo-skeletal disability in the elderly and, within the secondary care system, its management is primarily focused on palliative relief using pharmaceutical drugs such as non-steroidal anti-inflammatory drugs (NSAIDs) and analgesics. As with many pharmaceutical drugs, there are potential side effects, with treatment regimens also failing to address the progressive and complex nature of the condition.
The potential role of pharmaconutrients
Not surprisingly, given the safety profile of the majority of nutritional interventions, practitioners are continually striving to identify disease-modifying pharmaconutrients that are capable of both improving symptoms and preventing, slowing, or even reversing the degenerative process. Clinically, osteoarthritis is characterised by joint pain, crepitus (grating or cracking sounds on movement), stiffness after immobility and general limited movement. Identifying nutrients that can aid and support these symptoms are crucial to providing both relief from pain and treating the condition itself [1, 2].
Fatty acids as immunomodulators
Marine omega-3 fatty acids such as eicosapentaenoic acid (EPA) and the omega-6 fatty acid gamma-linolenic acid (GLA) exhibit anti-inflammatory effects through the production of eicosanoids – substances with both anti-inflammatory and immunoregulatory properties. As such, both are well documented as useful natural agents to help treat inflammatory diseases, alone and in combination.
GLA is found in certain plant-seed oils, including evening primrose seed oil, and is metabolised to dihomo-gamma-linolenic acid (DGLA) the direct precursor to anti-inflammatory and immunoregulatory products. Supplemental GLA has been shown to suppress acute and chronic inflammation in several conditions, including arthritis .
The specific ratio of the principal omega-3 and omega-6 fatty acids AA (arachidonic acid) and EPA provides valuable information on the measure of the body’s eicosanoid balance and the AA:EPA ratio provides a direct indication of the inflammatory state of the body. Developing an anti-inflammatory treatment regime means preventing or reducing the accumulation of AA from the diet. By reducing AA through EPA supplementation, we reduce the substrate for the formation of inflammatory eicosanoids and increase the production of anti-inflammatory eicosanoids directly from EPA. Interestingly, whilst the benefits of EPA as a potent anti-inflammatory and immune-regulating fatty acid are well established,  these benefits are significantly superior for osteoarthritis sufferers when combined with glucosamine .
As well as pain and joint degeneration, osteoarthritis also involves progressive loss of cartilage. Glucosamine is an amino monosaccharide believed to stimulate production of compounds called glycosaminoglycans and proteoglycans, the ‘building blocks’ of cartilage. Whilst glucosamine is important as a structural component, it is also known to exert specific pharmacologic effects by decreasing the production of inflammatory products. Glucosamine does this by regulating their production at the genetic level, by switching off genes that are directly involved in their production, thereby interfering with the inflammatory signalling cascade. When administered exogenously, it is used for the treatment of osteoarthritis as a prescription drug or a dietary supplement .
The synovial fluid within joints contains calcium, as does the cartilage lining the joints. When that calcium crystallises, the resulting tiny shards wear away the joint surface and spur the release of enzymes that further break down cartilage. Not surprisingly, it is sometimes thought that because osteoarthritis is aggravated by calcium deposition in joints, osteoarthritis patients should avoid taking calcium. Formation of calcium crystals can, however, result in calcium deficiency and, whilst calcium serves to maintain healthy bones and teeth, it is also essential for the normal functioning of muscles, blood vessels and nerves. If proper management of calcium is not carried out, this could be harmful for osteoarthritis patients, who may be at a higher risk of also developing osteoporosis, especially if they are long-term users of NSAIDs .
Written by Dr Nina Bailey
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