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it will be interesting to see whether my zinc supplementation can help boost the uric acid level when i next get some bloodwork done. i wonder if anyone has ever looked at dietary or supplementary zinc absorption and levels, in patients supplementing with inosine?

My wife takes the last 5 months 50mg zinc daily and this hasn't increase her uric acid levels!
On the other hand inosine isn't a medicine so why you expect from it to completely stop your relapses, it helps with one or other way but seems very optimistic if it could stop relapses!

interesting, has she been supplementing inosine too? if so, in what amounts and for how long? what was her UA level before, and what is it now?

i'm also curious as to your wife's zinc level prior to supplementing 50mg per day for 5 months? was she actually deficient? what is her zinc level now?

i'm asking in order to assess starting and ending levels of zinc and UA in your wife's case, for comparison to my case once i have some current post-zinc-treatment bloodwork.

cheers

had another peek into it to see if there is any more backup to the zinc-UA notion...

http://www.diagnose-me.com/glossary/G563.html

it looks like a complicated bit of reading to back up these statements succinctly with easy abstracts, but in the meantime:

Multiple Sclerosis
Recommendation Test Serum Uric Acid Levels
"...Uric acid levels should be monitored and, if low, raised by supplemental molybdenum and reducing any copper toxicity..."

Copper Toxicity
"Since high levels of copper in the body or diet may result in molybdenum insufficiency and cause low uric acid levels, reducing copper toxicity can result in normalizing uric acid and molybdenum levels..."
"Zinc and manganese with vitamin C remove copper from the tissues..."

http://linkinghub.elsevier.com/retrieve ... 6306002269

Approximately 12% of Americans do not consume the estimated average requirement for zinc and could be at risk for zinc deficiency. Since zinc has proposed antioxidant function, inadequate zinc consumption may lead to an enhanced susceptibility to oxidative stress through several mechanisms, including altered antioxidant defenses. In this study, we hypothesized that dietary zinc restriction would result in lower antioxidant status and increased oxidative damage.

Collectively, zinc deficiency increased oxidative stress, which may be partially explained by increased CYP activity and reductions in hepatic alpha-tocopherol and gamma-tocopherol and in plasma uric acid.

jimmylegs wrote:interesting, has she been supplementing inosine too? if so, in what amounts and for how long? what was her UA level before, and what is it now?

i'm also curious as to your wife's zinc level prior to supplementing 50mg per day for 5 months? was she actually deficient? what is her zinc level now?

i'm asking in order to assess starting and ending levels of zinc and UA in your wife's case, for comparison to my case once i have some current post-zinc-treatment bloodwork.

cheers

Her UA levels were quite low 2.9 (1.9-7) but probably in the "normal" MS range.
She hasn't had ever a zinc test but I guess it is at least normal if not above.
There is a zinc taste test that every one can do by himself but haven't tried it yet.
This Saturday she has her blood tests for UA, B, D, hormones, hepatic enzymes etc so I'll tell you.
I expect her UA to be @ 4.5-5 range.

Purinergic modulation of microglial cell activation :

Abstract Microglial cells are resident macrophages in the brain and their activation is an important part of the brain immune response and the pathology of the major CNS diseases. Microglial activation is triggered by pathological signals and is characterized by morphological changes, proliferation, phagocytosis and the secretion of various cytokines and inflammatory mediators, which could be both destructive and protective for the nervous tissue. Purines are one of the most important mediators which regulate different aspects of microglial function. They could be released to the extracellular space from neurons, astrocytes and from the microglia itself, upon physiological neuronal activity and in response to pathological stimuli and cellular damage. Microglial activation is regulated by various subtypes of nucleotide (P2X, P2Y) and adenosine (A1, A2A and A3) receptors, which control ionic conductances, membrane potential, gene transcription, the production of inflammatory mediators and cell survival. Among them, the role of P2X7 receptors is especially well delineated, but P2X4, various P2Y, A1, A2A and A3 receptors also powerfully participate in the microglial response. The pathological role of microglial purine receptors has also been demonstrated in disease models; e.g., in ischemia, sclerosis multiplex and neuropathic pain. Due to their upregulation and selective activation under pathological conditions, they provide new avenues in the treatment of neurodegenerative and neuroinflammatory illnesses.

Receptor-Mediated Interaction Between the Sympathetic Nervous System and Immune System in Inflammation

(1) Department of Surgery, UMD-New Jersey Medical School, Newark, NJ, 07103


Abstract The sympathetic nervous system plays a central role in establishing communication between the central nervous system and the immune system during inflammation. Inflammation activates the sympathetic nervous system, which causes release of the transmitters of the sympathetic nerv-ous system in the periphery. The transmitters of the sympathetic nervous system are the cate-cholamines noradrenaline and adrenaline and the purines ATP, adenosine, and inosine. Once these transmitters are released, they stimulate both presynaptic receptors on nerve terminals and post-synaptic receptors on immune cells. The receptors that are sensitive to catecholamines are termed adrenoceptors, whereas the receptors that bind purines are called purinoceptors. Stimulation of the presynaptic receptors exerts an autoregulatory effect on the release of transmitters. Ligation of the postsynaptic receptors on inflammatory cells modulates the inflammatory ac-tivities of these cells. The present review summarizes some of the most important aspects of the current state of knowledge about the interactions between the sympathetic nervous system and the immune system during inflammation with a special emphasis on the role of adreno and purinoceptors.

jimmylegs wrote:so sounds like cure is right on track at 1mg 2x per day in the normal routine. i will keep this in mind for if i ever get around to taking inosine myself :S
maybe one more crappy result will tip me over the edge?

Just for your info Jimmy wife's uric acid levels are now at 344 µmol/L (5.8 mg/dL) exactly double than before a month with 2X1gr/day inosine supplementation, which means her levels are in the "optimal for MS without inducing gout" zone - PERFECT!
I start give her 1gr/day every other day in case her levels go sky high.
My problem now is that I can't lower her hepatic enzymes although she takes all the antioxidants, choline, sylibum, dandelion etc next week (hope) I'll receive the N-acetyl cysteine that helps liver function!
But she had blood tests 6 days after a bacterial (or virus) infection, could this be the reason for the levated enzymes?
Where are you Cheerleader when I need you, what did you do with your husband to lower his liver enzymes?

good info DIM thx i know i'll only be going for about 290 µmol/L myself but 344 definitely sounds safe too. cheers!

In the exchanges for inosine I see 1 to 2 mg/day and 1 to 2 g/day. Which one is the correct dose?

K

i just read it wrong k it's grams by the looks of it

I'm here, DIM... I'm Here!

High liver enzymes could be related to infection, toxins, and her liver's inability to cleanse itself. Most MSers have high liver enzymes, and don't even know it.

Milk thistle was the way I healed Jeff's high liver enzymes. 500 mg. supplement every day for one month with plenty of fresh water. His enzymes came down in a month's time. I still give him milk thistle one week out of every month, to continue to cleanse. Milk thistle has anti-inflammatory affects, as well. It really works!


http://www.newhope.com/nutritionscience ... _herbs.cfm

best to you and your wife,
AC

i don't have any supporting numbers but i still think milk thistle is a good idea
i was taking milk thistle blend for liver protection when i was just dxd in '06 and worried about the imminent effects of rebif...
but my baseline enzyme tests were okay and i've never had them re-tested coz i never ended up taking any rebif anyway.
i am finishing up this other non liver-related herbal blend right now (i have this rule not to mix herbal blends with each other because i know it's hard enough balancing the vitamins!) but certainly plan another round of milk thistle blend soon, i reckon it's time - missed 2007 altogether!

Go for it Jimmylegs! As I keep saying...what in the hell do you have to lose??? And gee, it just might help (as it has for my daughter and you!) Someone just might find that proverbial needle in the haystack. Why not you?

bromley wrote:ABX has worked for Sarah and some others

..... and who has had a long-term sustained reversal of disability on Avonex, Betaseron, Copaxone or Rebif?

Has anyone done better than Sarah on one of those.

I honestly don't understand what seems to me to be a double standard. I'm not looking for an argument and my typing can't express my quizical feeling. I just want to be clear that I'm not trying to be a smart ***.

As I see it the score is at least:


CRABs - 0 ABX - 1


Ken