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#21 |
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Professional
Join Date: Jun 2010
Location: NorCal
Posts: 1,029
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I tried some of these supplements a few years ago,,after taking just a few of them I felt lubricated all over-all joints were feeling really good,,I dont want to bore you all with the brand. it worked for me, however, from the time I was 16 to 18 y.o I ran 10 miles a day every day rain or shine and never missed one day, if that has a bearing on it.
Last edited by 3fees : 11-13-2012 at 07:26 PM. |
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#22 |
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Legend
Join Date: Feb 2009
Posts: 5,504
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There are no "magical" medications that "turn on" cartilage repair, though the quest continues.
"The need for novel pharmacological agents which provide effective long-term pain relief and have disease modifying properties for OA treatments is, as yet, unmet. Direct delivery of drugs such as glucocorticoid and hyaluronic acid formulations into the affected joint, do not retard the disease process and may provide only short-term pain relief [155]. The development of novel drugs such as lipid-based formulations and nanoparticles in combination with controlled exercise therapy may provide an alternative strategy in this challenging area of research. Such therapies may be aimed at blocking the pro-inflammatory and proteolytic pathways, thereby allowing the beneficial effects of targeted anabolic exercise regimens. Experimental studies suggest that such options may be of value." - http://www.hindawi.com/journals/arth/2011/979032/ Never underestimate the power of exercise! Interestingly, low load or even moderate stress loads done slowly (such as weight lifting) which induce mechanical stress on cartilage initiates a biochemical series of events that results in decreasing inflammation at joints, and even stimulates the synthesis of extracellular matrix which composes 99% of cartilage!!! "Evidence from in vitro studies demonstrate that mechanical signals within a physiological range of intensity, duration and frequency have potent anti-inflammatory effects which counteract the catabolic signals induced by IL-1β or TNFα (Figure 2)... The critical mechanosensitive components include the integrins and cytoskeletal proteins (Figure 2). Previous in vitro studies have shown a role for the integrins in mediating the compression-induced synthesis of matrix components [136–140]... These studies clearly identify a number of routes involved in chondroprotection and are illustrated in Figure 2." - http://www.hindawi.com/journals/arth/2011/979032/ "7. Conclusions The importance of mechanical loading in maintaining healthy joints and normal tissue remodelling has long been recognised. Previous in vitro studies continue to support the hypothesis that moderate mechanical loading is necessary to maintain healthy cartilage. If joints are insufficiently loaded, chondrocyte metabolism shifts in favour of catabolism. Similarly, traumatic or excessive joint loading leads to cartilage degeneration and OA. Emerging evidence suggests that physiological joint loading could be used to counteract the inflammatory pathways and restore anabolic activities. - http://www.hindawi.com/journals/arth/2011/979032/ Hence the answer in the future may be to incorporate exercise to "turn on" cartilage synthesis and "turn off" excess inflammation. Then to dose in some yet to be determined medication(s) to augment this process to return chondrocytes [the living cells in cartilage] to return to a state of making more extracellular matrix, and therefore increasing the amount of cartilage present. "A further option is to develop agents which synergise with physiological mechanical loading or which block the signal transduction pathways activated by abnormal mechanical stimuli. Stimulation of mechanoreceptors releases several soluble mediators in chondrocytes including ROS, prostaglandins, cytokines, growth factors, and neuropeptides... Normal and OA chondrocytes from diseased joints transmit mechanical signals via the α5β1 integrin, resulting in markedly different downstream signalling events. For example, mechanical stimulation of normal chondrocytes release the chondroprotective IL-4 in contrast to OA cells which produce IL-1β [169]. It is possible that chondrocytes from OA cartilage have been reprogrammed to respond differently to their altered mechanical environment, and it may be necessary to target structural components of the cell such as the actin cytoskeleton [170] This may allow reversal of biomechanical changes developed during OA disease progression allowing the beneficial effects of moderate exercise to be gained at the tissue level." - http://www.hindawi.com/journals/arth/2011/979032/ |
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