This Is MS Multiple Sclerosis Knowledge & Support Community

jerrygallow wrote:All those people who think they have gout and ms need to take a serious look at Lyme disease. Many docs don't understand Lyme and they stigmatize each other for diagnosing it because quacks say everything is Lyme. Plus there are no good tests for it. After a while the blood work looks normal. One study sent known samples to the labs and half the time the labs reported negative results though all samples were positive. Gout and ms almost never occur together while joint pain is a classic Lyme symptom

Multiple sclerosis and Uric acid levels

Lower serum values of uric acid have been associated with multiple sclerosis (MS). MS patients have been found to have serum levels ~194 µmol/L, with patients in relapse averaging ~160 µmol/L and patients in remission averaging ~230 µmol/L. Serum uric acid in healthy controls was ~290 µmol/L. Conversion factor: 1 mg/dL=59.48 µmol/L

A 1998 study completed a statistical analysis of 20 million patient records, comparing serum uric acid values in patients with gout and patients with multiple sclerosis. Almost no overlap between the groups was found.
Uric acid has been successfully used in the treatment and prevention of the animal (murine) model of MS.

A 2006 study found elevation of serum uric acid values in multiple sclerosis patients, by oral supplementation with Inosine, resulted in lower relapse rates, and no adverse effects.

Normalising low uric acid

Correcting low or deficient zinc levels can help elevate serum uric acid. Inosine can be used to elevate uric acid levels. Zn inhibits Cu absorption, helping to reduce the high Cu/Fe in some people with hypouricemia. Fe supplements can ensure adequate Fe reserves (ferritin above 25 ng/dl), also correcting the high Cu/Fe.

Hi,

The other point to remember is Uric acid is a potent scavenger of Peroxynitrite which can cause serious problems with cell respiration. Peroxynitrite can be elevated by an infectious agent such as EBV or expand when an abundance of iNOS exists in the endothelial layer.
JL is right that elevating Purine levels will raise the Uric acid levels but it is hard to do. I took a gram a day of Valtrex (a purine nucleotide analogue) for 10 years before I got gout. That is a very large amount!
Do look to lift your uric acid level but try to work on lowering the Peroxynitrite as well a that is a major issue.

Regards

@jack - you don't boost the uric acid levels to gout levels! just to healthy control levels.

@scott - I spent a couple years trying to use dietary purines to boost my uric acid levels. I got absolutely nowhere. when your urea cycle is broken, it's broken. I probably just sent my ammonia levels through the roof. it took the identification and correction of zinc deficiency to sort out the uric acid scenario in my case.

@amir - LOL I recognize your Wikipedia content .. I wrote most of that a few yrs ago

@amir - LOL I recognize your Wikipedia content .. I wrote most of that a few yrs ago

Apologies!

nonsense - none required!

Hi JL,

I agree. Diet isn't enough. Happy with the zinc but I would be cranking up the Q10 as well in my case and definitely intervening with an anti viral to attack the peroxynitrite. Particularly, in light of the research published this week on EBV.

Regards

I wonder if I could have fixed the zinc situation successfully with diet. to me it seems like the purine foods I ate to try to drive up uric acid should have had decent zinc content. but, in the end for whatever reason it had to be supplements.

I personally favour nutritional support for synthesis of things like coq10, glutathione peroxidase, and so on. zinc is antiviral itself, as is selenium.

neat stuff on some familiar nutrients involved in CoQ10 synthesis (all of the nutrients listed below are included in the good old klenner protocol for ms):

http://medicinemosul.uomosul.edu.iq/fil ... 485647.pdf
The quinone portion of CoQ10 is synthesized from tyrosine and indispensably requires vitamins B2, B3, B5, B6, B12, folic acid, tetrahydrobiopterin and vitamin C.
The isoprenyl side chain is synthesized from acetyl-CoA through the mevalonate pathway, which also requires zinc.

low coq10 occurs with impaired nutrient status:

Lower plasma Coenzyme Q 10 in depression: a marker for treatment resistance and chronic fatigue in depression and a risk factor to cardiovascular disorder in that illness
http://www.researchgate.net/publication ... be5a42.pdf
We found that plasma CoQ10 was significantly (p=0.0002) lower in depressed patients than in normal controls... The findings of this study reinforce the existent literature which shows that depression is accompanied by a significantly decreased antioxidant status, as evidenced by lower serum zinc, vitamin E and C, glutathione peroxidase, tryptophan and tyrosine and albumin (see Introduction). It is safe to posit that the “low CoQ10 syndrome” in depression and the more general reduced antioxidative capacity in those patients may have impaired the anti-oxidative protection against the damaging effects IO&NS and, consequently, may be involved in the neurotoxic damage which occurs in depression (Maes et al. 2009b).

The pathways are all so interconnected.

"The quinone portion of CoQ10 is synthesized from tyrosine and indispensably requires vitamins B2, B3, B5, B6, B12, folic acid, tetrahydrobiopterin and vitamin C."

Tetrahydrobiopterin is easily oxidized by Peroxynitrite but it can be boosted by folic acid and vitamin C infusions in animal models. It can correct eNOS dysfunction but if it's depleted you get iNOS which can promoted peroxynitrite. To get round that you need arginine.

To quote- Endothelial Nitric Oxide Synthase in Vascular Disease : From Marvel to Menace Ulrich Förstermann and Thomas Münzel Circulation. 2006;113:1708-1714 doi: 10.1161/CIRCULATIONAHA.105.602532

"All NOS isozymes catalyze flavin-mediated electron transfer from the C-terminally bound NADPH to the heme on the N terminus. Calmodulin (on calcium-induced binding) increases the rate of electron transfer from NADPH via the reductase domain flavins to the heme center . At the heme, the electrons are used to reduce and activate O2. To synthesize NO•, the enzyme needs to cycle twice. In a first step, NOS hydroxylates L-arginine to N- hydroxy-L-arginine (which remains largely bound to the enzyme). In a second step, NOS oxidizes N-hydroxy-Larginine to L-citrulline and NO• .3 In human eNOS, Cys99, which is part of the zinc-thiolate cluster, is thought to represent (or largely contribute to) the binding site for BH4; zinc itself does not contribute to BH4 binding. "

and on it goes.................