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Hi Lib,

Uric acid is low in MS patients and even lower during relapse. They attribute the low levels to peroxynitrite scavenging. I'm not sure if the levels are even lower in SPMS or PPMS. Here are a few studies I've dug up about it (copied from aldosterone and MS thread). I'm leaving the aldo connection in there because pwms release errant aldosterone constantly. By controlling this release, you might be able to improve uric acid levels. I'm currently inhibiting aldosterone with clonidine and hibiscus tea with very good results. I should have had my uric acid tested before I started but I didn't think of it!

Uric Acid and Aldosterone
Serum uric acid levels in multiple sclerosis patients correlate with activity of disease and blood-brain barrier dysfunction.
http://www.ncbi.nlm.nih.gov/pubmed/11985629

Uric acid in multiple sclerosis
http://www.ingentaconnect.com/content/m ... 3/art00015

“In animal models, aldosterone infusion causes endothelial dysfunction via the generation of ROS (reactive oxygen species) [22–24]. Aldosterone increases expression of NADPH oxidase subunits p22pbox and gp91phox through an MR-dependent mechanism, whereas aldosterone stimulates expression of p47phox mRNA through both AT1 receptor and MR-dependent mechanisms (Figure 2) [25,26]. The resultant generation of ROS leads to the formation of peroxynitrite”
http://submit.clinsci.org/cs/113/0267/cs1130267.htm

Uric Acid: Eplerenone (aldosterone blocker) produced increases in uric
acid to greater than 9 mg/dL in approximately 0.3%
http://www.hsc.wvu.edu/Charleston/sop/C ... /jun04.pdf

edited to fix links

Hi Liberation,

I haven't thought of Inosine, or anything I'm trying against MS, as more than a rear guard defensive action. If we gain an extra year or three or five of better health than we would without it, that helps.

I'm putting together as many of these 'little steps' as I can, hoping to combine them into a delaying action against the disease.

Regarding whether it helps with secondary progression, I wish I knew. I don't see harm. More ATP is good. More uric acid cleaning up free radicals (ROS) that would otherwise cause damage is good. New axons, if that promise plays out from rats to humans, would be very good helping the brain cope with and compensate for damaged nerves.

CaliReader wrote:Hi Liberation,

I haven't thought of Inosine, or anything I'm trying against MS, as more than a rear guard defensive action. If we gain an extra year or three or five of better health than we would without it, that helps.

I'm putting together as many of these 'little steps' as I can, hoping to combine them into a delaying action against the disease.

Regarding whether it helps with secondary progression, I wish I knew. I don't see harm. More ATP is good. More uric acid cleaning up free radicals (ROS) that would otherwise cause damage is good. New axons, if that promise plays out from rats to humans, would be very good helping the brain cope with and compensate for damaged nerves.

In addition it is very cheap. 500mg a day will cost around $50 a year.

I use 500mg about 5x per week but am prepared to go up to 4000mg for a limited period in the event I feel an attack coming on.

I am taking 1 gram twice a day with 8 glasses of water per day. I had serum UA and Zinc measured before starting, will have serum UA measured again in a month. Phase II trial suggested 2-3 grams per day were typical to get and keep UA in the study's target range (7 - 9 I think).

As this thread points out, inosine has promise beyond just raising UA levels. UA levels are pretty important though. Another inosine thread noted that MS and gout were nearly mutually exclusive. Since high UA can cause gout, it would seem that high UA may protect against MS.

hey jp do you have those zinc and ua results?

I will get them Friday. I know they didn't concern my doctor (she wants to see me about very low cholesterol) but that doesn't mean they may not be low-normal. I will likely continue the inosine regardless.