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I have spoke to Dr. Danna Spence at Michigan State University-
Dr.Spence's group was first to report that the RBCs obtained from people with type 2 (or adult-onset) diabetes released less ATP(50%) upon stimulation in comparison to RBCs obtained from non-diabetic subjects. The importance of this finding is due to the role of ATP in controlling blood flow, endothelial cell function, and platelet function.
When doing research on Red Blood Cells in subjects with MS it and found that blood samples from subjects with MS - have much higher levels of ATP (300% More) in their blood .

His research has shown when RBC's flow thru restrictive passages (as with CCSVI) they produce ATP- signaling for increasing NO2 ( Nitric Oxide ) in the blood.
This NO2 causes veins to dilate promoting easier passage for RBC's.

Unfortunately the NO2 leaks thru vein walls and damages (Inflammation) the Myelin on nerves (they run alongside the veins)promoting the Immune Cells to remove "defective" Myelin, leaving nerves even more exposed !

Normal NO2 levels,and in in less dilated veins' would prevent /reduce leakage and so Myelin inflammation.
Removing defective cells is normal for the immune system in MS , not a directed attack on myelin as in "EAE " where immune cells are produced that target even normal Myelin.

EAE - is a "Autoimmune Disease"that has been created injecting various myelin components into animal brains to provide differing myelin seeking immune cells for EAE and has misdirected research toward only different competing Immune Suppressing med's.

MS - is better labeled as a "Vascular Restriction Disease"

- that reduces blood draining from the CNS and causes Ruflux back to the brain - leaving inflammation producing Iron deposits.

The restricted RBC's produce - Very high levels of ATP causing - Very high amounts of NO2 leaking thru dilated vein walls to "Inflame" Myelin throughout the body, causing the Immune system to target the damaged cells.

This is just a normal function of the Imm.Sys. and depressing it - only Slows - it's Progress in MS.

Multiple amounts of restriction in different locations would produce toxic Iron deposits from Reflux with a variety of patterns of Plaques in the Brain.
And so the different types of MS and progression patterns as veins become restricted, intermittently reopened,or totally blocked throughout the CNS.

The greater the levels of Venous restriction - the higher the amounts of NO2 is produced because of higher levels of ATP with increased Myelin inflammation and targeting for it's removal.

This explains also,why all the Immune Suppressant MS med.'s help reduce ( the frequency ) of immune -"attack"- and only slowing the progress (for some) of MS.

The Neuro damage would then be "side effect" of 3-times the normal levels of NO2 stimulating ATP for years attempting to relieve restricted RBC's

All the-$-is in various competing drug research to suppress the Imm.Sys. while they only slow it's progress enough to help some.

If CCSVI Angioplasty treatment - reduces restrictions it would seem this would reduce ATP and so lower NO2 levels .

I should be standard to test ATP levels of all MS patients .
With ATP levels tested before and after CCSVI Angioplasty,with frequent monitoring to warn of returning blockage.

Patients suspected to have MS should have ATP levels tested before more $ expensive MRI tests are requested.
-doctors more willing to prescribe lower costing blood test-to screen for MRI & MRV (save $)
-everyone could be routinely have a blood test of ATP levels at a physical
-early CCSVI detection (or any venus restrictive problems)=less permanent damage

This is a very interesting writeup. This theory nicely explains how NO2 is a double edged sword - both good and bad for ms.

I wonder what the ATP levels would be for diabetic MSer's if ATP is low in diabetics but high in MSer's?

How would this theory account for the secondary progressive phase of MS where there is no longer an inflammatory component? Why and how does that happen then?

Do you have research links for the ATP info?

Thanks, this is very interesting ..

I am also convinced that MS and diabetes type 2 (adult onset) are not very far apart (see also http://www.thisisms.com/ftopic-15188-da ... asc-0.html ). Apparently, so I was told by doctors, in the early 1980's there has been a intense discussion in the medical world on this topic. Eventually, for reasons unclear to me, the topic disappeared in the background.

Perhaps now, due to these new insights, both as reagrds the venous strictures in the neck and reduced blood flow in teh cerebro-spinal, as well new insights in endocrinology and cellular processes and feeding mechanisms, this discussion should be re-opened.

I searched a bit on the terms like ATP endothelin1 glucose Ca2+ nitric oxide generation STIM1 and find many hits, also with the terms in combination. And there are clear links to cellular feeding e.g. with glucose and the "mobilisation" of the Calcium channel. But then I hit a barrier there because the complexity of the matter is such that it is beyond my grasp as a semi-literate MS patient.

Perhaps we should launch a new thread on this forum to give our global college a chance to emerge in this field as well. Apart from that, I have indications that professionals in the medical world are looking into these things now as well.

Very very interesting, thank you for the info.

Does Dr. Spence know about CCSVI?

Sounds like Dr. Spence needs to hop on a plane to Italy next month.

EAE in mice is not the same disease as MS in humans. Search for work by Behan if you are a info techie.
EAE has probably caused more wasted hours of research on MS than any other mouse model.

MarkW

this is excelllent ! Food for thought in order to answer a very important question to continue to unveil claimed mistery of MS. This would be the second act being CCSVI the first. The question is: what are the damaging biological processes ocurring in the brain in presence of a chronic blood reflux that humankind hs grouped under the name of MS on planet earth fo the last 150 years!
i think some of these issues will be approched in ISNVD this march.
I hope so.

Another question is, if we produce so much ATP (which is the "energy currency" in the body), where is all that energy?

I am as fatigued as any MSer and having hard time figuring out how can that be with extra production of ATP.

NotFound wrote:Another question is, if we produce so much ATP (which is the "energy currency" in the body), where is all that energy?

I am as fatigued as any MSer and having hard time figuring out how can that be with extra production of ATP.

Yes, I would have thought excess ATP would be a good thing, helpful to those who have trouble with muscle strength. Something seems to be missing in the actuation.

With the talk here recently of ATP, I took particular notice when reading an e-mail newsletter from Dr. Joseph Mercola today. I was especially intrigued with the connection between fibromyalgia and hypothyroidism, and the comment that "Low thyroid hormone reduces ATP" – I encourage you to read

http://articles.mercola.com/sites/artic ... art-1.aspx

The last sentence, "A one-line summary of Dr. Lowe’s research would be that thyroid hormone is the missing ingredient in the treatment of fibromyalgia that is nearly universally overlooked," was particularly important to me since I believe there is a connection between fibromyalgia and MS – the author Kathryn R. Simpson, in her book The MS Solution, feels the answer for her MS is in endocrine malfunctions.

As Leonard has stated in his postings, I too wish we could get the endocrinologists investigating our problem of MS. I think we have had the wrong medical specialist in charge all these many decades!