In researching alternatives to mainstream-medicine’s approach to treating MS, I’ve come across many articles and scholarly papers denoting the relationship between serum (blood) uric acid levels and the incidence and severity of MS. The most telling anecdotal evidence suggesting a relationship is that in a review of 20,000,000 medical records, the diseases of gout and MS are virtually mutually exclusive: that is, if you have gout, you do not have MS; and if you have MS, you do not have gout. For those unaware, gout sufferers have very high uric acid levels while those with MS have quite low levels of uric acid.
Acting on this information, researchers have studied the effects of raising serum uric acids levels both in mice induced with EAE and in people with MS. From what I can glean from the articles and papers, they’ve had what I would consider nearly miraculous results, from prevention of the disease in mice to reducing gadolinium-enhanced brain lesions in human patients to the point of being no longer detectable.
Without getting into too much detail, oral administration of inosine (a precursor of uric acid) raised serum levels safely and effectively, and regularly produced the results mentioned previously. In studying inosine’s mechanism of action, it appears inosine, by raising uric acid levels, inhibits the damaging effects of peroxynitrite, a powerful oxidant. Interestingly, uric acid levels are also significantly increased individually by methylpredisolone and copaxone. (Note of interest: inosine is incredibly cheap, predisolone and copaxone are not.)
I have just started taking inosine (also used by athletes to improve performance) and am tempted to say I have noticed improvement in sensations in the tips of my fingers and less fatigue. I would like to know, has anybody else either researched inosine or incorporated it into their treatment protocol.
Let's not turn this thread into a debate like my last thread about Inosine. http://www.direct-ms.org/pdf/UricAcidMS ... AcidMS.pdf