This Is MS Multiple Sclerosis Community: Knowledge & Support

Vitamin K-2, also known as menaquinone, helps to remove calcium from the blood vessels by activating Gla protein.


NHE

I seem to remember having seen in the past the proposition that the myeline in the brain is different from the myeline in the rest of the body. The myeline in the brain should behave differently or has a different composition. Certainly it was argued that it is more sensitive to demyelination. I am very positive that I have seen that.

But is this true? I invite you to have a look at http://www.phschool.com/science/science ... escue.html

This article is absolutely great and suggests that the mechanism for feeding the cells of the brain is different from that of the other parts of the body. Unlike the other parts, the brain can only be fed by glucose. The barrier or filter must be the BBB. And therefore I conclude that if the glucose transport mechanism across the BBB is impaired (for whatever reason – many reasons have been suggested on this thread) the cells deeper in the brain will suffer. In other words, the composition of the myeline itself is no different at all, it is the feeding of the cells that is different.

I believe this is yet another very important piece of the puzzle that would fully confirm the ccsvi / low-glucose hypothesis.

To what extent the back-up mechanism of ketones would be useful for us is probably an interesting research question.

This PhD study from 2009 seems to support the ccsvi / low-glucose hypothesis of this thread:

This PhD project explores the hypothesis that the deficits arise because the nerve fibres passing through inflammatory lesions are relatively starved of oxygen and glucose. The hypothesis is strongly supported by historical evidence, currently largely forgotten, that drugs that open blood vessels (e.g. amyl nitrite) can restore function in MS within an hour.

http://www.mssociety.org.uk/research/re ... t_824.html

Hello Leonard and other interested parties,

I have read this thread with interest. I am an RN x almost 40 years (OMG does that say 40?)
I have a few comments to add and some more data to add.
1. Glucose is the only fuel of brain cells. It cannot be stored so it is at the mercy of the circulatory system.
2. 70% ( on average) of the bodies glucose is used as fuel by the brain cells.
During complex thinking we use more.
3. 70% of the brains blood is in the veins (venules and veins)
4. The brain (3 lbs) holds about 1.5 pints of blood at any given time.
5. 25% of our oxygen is used by the brain to burn the fuel
6. There is a polypeptide (protein) called Endothelin1. It's made by endothelium as a signaler to maintain the vessel integrity.
7. Sheer stress is the force on the endothelium when the flow is going the wrong way.
8. Hypoxia is a level of oxygen lower than what is considered normal for metabolic (cell) activity to occur at the normal rate
9. Hypoglycemia is a lower than normal glucose level . This being lower means the cell can not perform at the normal level.
10. If you block the venous outflow the glucose and the oxygen get used up by the brain cells , the blood cannot exit the desired way and the mixed blood levels of oxygen and glucose and other nutrients dip.
11. Endothelin1 rises when sheer stress goes up and hypoxia occurs.
12. Endothelin1 in high levels causes fibrosis and hypertrophy of the vessels....including vessel walls and valves.
13. PwMS have levels of Endothelin1 that are hundreds of times the normal.
14. Chronic blood turbulence will fracture red blood cells and cause deposits of iron. This can cause iron to be imbeded in the porous stressed BBB vessel walls.
15. Maybe pwCCSVI vein anomalies from birth would see the anomalies get progressively worse as the ENDOTHELIN1 levels rise in response to the chronic hypoglycemia and hypoxia and sheer stress.
16. At a tipping point the CCSVI gets to the point where the brain environment (cerebral hypoxia, hypoglycemia, oxidation of iron, etc) causes myelin and Axonai damage and death. During this phase the immune system attempts to correct the damage.
17. Eventually the immune system calls out the big guns ( B and T cells).
18. Some MS symptoms are CCSVI symptoms.

_________________
Cat (Catherine Somerville on FB)
MegansMom
My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-

Thanks for that Megans Mom

I am in a very similar position as your Daughter. I was dianosed with CIS in November 2010. I am 38 years old.

Can you tell me more about her CCSVI?

I am going to have a scan when I am back in the Uk in May but still undecided. If my Neuro wasn't a Muslim he would hold a cross up everytime I mention CCSVI!

MegansMom, thank you VERY much for all that very helpful, concise info, for us medical semi-literates trying to comprehend all this. And thank you, Leonard, for sharing your very interesting lines of thinking. Wouldn't it be nice if "someone" out there would pick up on your ideas and do some research on them?

I am concerned less with myself (dxed SPMS in 2000) than with my teen daughter, with Raynaud's and other symptoms suggestive of CCSVI. My hope: successful, early-stage CCSVI treatments will be shown to prevent MS from ever developing. Not unrealistic, in my view. Waiting with bated breath on CCSVI and MS research developments, while approaching my health holistically, and encouraging daughter to do the same.

Meanwhile, also waiting for CCSVI treatment for myself. Getting close!

Liz

_________________
CCSVI:  Making Sense of MS

Thank you for these insights! This global college is really unbeatable. This adds yet another very important piece of the puzzle, perhaps even the final crowning piece!




be patient.. (I know, that is not easy, I have MS myself..)
but I think things are going faster now than ever before...

This thread argues that an impaired glucose transport is the cause of MS. There are a number of remarkable features of MS that would seem to suggest such relation: the double peak in the graph of the age of onset of MS and the hardening/calcification of veins at mid age; the vitamin D relationship and intracellular calcium levels; the feeding of cells through the BBB only by glucose and the relation with the quality of the myelin in teh cerebro-spinal as opposed to other parts of the body; the prevalence of diabetes in MS.

The high consumption of sugar among MS patients is known. Also, the short term improvement of motor functions on the intake of sugar is known. But on the long term, this sugar intake may be devastating for the functioning of the endothelium (the inside of the vessel walls) and indeed the functioning of the BBB; and cause a further calcification of endothelial cells. This article from 2009 would seem to suggest such course:

http://ajpheart.physiology.org/content/298/1/H171.full

I quote from the article: Collectively, these results suggest that endothelial cells may react in a biphasic way to HG conditions with a short-term exposure resulting in an enhanced Cai2+ response to Ca2+ mobilizing agents and an increase in NO generation while chronic exposure to HG impairs function. Reports that NO generation and blood flow increased and peripheral resistance decreased in the early stages of diabetes (32, 51) whereas long-term diabetes leads to macro- and microangiopathy with reduced vascular reactivity (3, 52) lend support to the concept of HG-induced time-dependent changes in endothelial function.

The devastating effects of sugar can be found on many websites, and include suggestions for the onset of neuro-inflammatory diseases as MS: http://answers.yahoo.com/question/index ... 105AAjkonM
http://www.mvholisticretreat.com/articl ... eet-poison

On the Dutch webforum, a reaction to my suggestion on the glucose link said: When I was diagnosed in 1995, my neurologist at the time (a man who was already in his 60's) told me to stop immediately with the consumption of sugar … according to him, this was very bad … Perhaps, there is some wisdom in his advice. And indeed, as has been suggested above in this thread, the high consumption of sugar, although giving some immediate alleviation, could well cause a vicious circle with a further calcification of the endothelial cells that would further impair glucose transport etc.

Many of these processes can go on long before any signs of diabetes type 2 show up in the form of high blood sugar and increased insulin resistance.

I have seen on www.ccsvi-tracking.com that some patients get worse after liberation. My theory goes as follows: when liberated, the blood flow is much stronger, also the supply of glucose. Things like REM sleep and dreaming (high glucose demand) and some motor functions improve. But the same time, particularly for mid-age and older patients, the calcification of the endothelium may increase as a result of the improved blood flow and glucose content. With detrimental consequences on the longer term.

It would be very interesting so see the age of those people that report worsening of functions.

The advice to stop sugar intake should therefore be taken very serious. And perhaps things like Metformin that help glucose transport (and help stop further calcification?) should be studied as a matter of urgency.

I've had similar thoughts on glucose but not centered on the transport but the actual use in "aerobic glycolysis". That is glycolysis that takes place even in the presence of oxygen.

thanks. can you explain?

From Wikipedia: Cellular respiration (redirected from Aerobic glycolysis) is the set of the metabolic reactions and processes that take place in the cells of organisms to convert biochemical energy from nutrients into adenosine triphosphate (ATP), and then release waste products.
Aerobic respiration requires oxygen in order to generate energy (ATP). Glycolysis is a metabolic pathway that is found in the cytosol of cells in all living organisms. The process converts one molecule of glucose into two molecules of pyruvate(pyruvic acid), it makes energy in the form of two net molecules of ATP.
The energy released in respiration is used to synthesize ATP to store this energy. The energy stored in ATP can then be used to drive processes requiring energy, including biosynthesis, locomotion or transportation of molecules across cell membranes.

ATP rings a bell. See this very recent thread on MS not "auto-immune"--it is "normal-immune&qu http://www.thisisms.com/ftopict-15694.html

Here significantly elevated ATP levels in the Red Blood Cells of MS patients are signalled; while for diabetes type 2 it should be lower than normal. Also there is the ATP signalling role causing increased NO2 in the blood, which leaks through vein walls and causes inflammation of the myelin and the immune system to target the inflammated myeline. Liberation from ccsvi should reduce ATP level, reduce NO2 level and thus stop the inflammation.

Apparently there is a role of ATP in controlling blood flow and the endothelial cell function. But for what? For glucose transport? Or is it for ATP transport?
I would much welcome any expert advice.

MS patients seem to have high level ATP (up to 300%).
high levels of ATP may add to further hardening of the veins

http://www.vitamins-supplements.org/die ... phorus.php

PwMS also have high levels of Endothelin1 that are hundreds of times the normal.
ET – 1 inhibits the release of ATP.

http://cat.inist.fr/?aModele=afficheN&cpsidt=16798385

Is here a mechanism at work that is trying to control the metabolism?
If the ATP level drops (as in diabetes type 2 patients), is this control mechanism also quietening down?

On the medication side:
http://www.rsc.org/Publishing/Journals/ ... active.asp

They found that, when they administered zinc-activated C-peptide with metformin, the type 2 diabetic red blood cells released ATP at levels comparable to healthy ones. Diabetic red blood cells are more rigid and so normally release less ATP than normal cells. As metformin is positively charged at physiological pH, Spence suggests the metformin neutralises the phosphatidyl serine groups on the outer cell membrane, making it less negative and more able to interact with the C-peptide.


I think it is about time for a true multi-disciplinary cooperation involving neurologists, vascular specialists and endocrinologists. In our own interest, it must be avoided that energies in the medical world are spent on abstruse debates of identity and status.

MS Made Simple

All in all, including information that was posted recently here on TIMS, I come to the following explanation for MS:

1. There is a high correlation of MS and narrowing of veins in the neck that drain blood from the brains.

2. This causes a slow blood flow in the brains and excess iron deposits on the walls of the vessels near the outlet (a normal phenomenon which occurs also in other "organs").

3. The transport of food for the brain becomes progressively inadequate.

4. The endotholium (inside of the wall of the veins) reacts and increases the secretion of Endotholin-1 (ET-1); in MS patients, the concentration of ET-1 is many times higher than in normal people.

5. In response the ATP level increases in the red blood cells; the ATP is the basic carrier of energy and the product of glucose and oxygen molecules. The ATP level in MS patients is much higher (300%) than normal.

6. The nitrogen oxide level rises (NO2) as a result too. This has a relaxing effect on the vascular wall and is a natural reaction against the strictures.

7. By a persistently high NO2 level (which can and does not resolve the strictures), especially around these strictures NO2 will leak slowly through the vessel wall. This NO2 causes an inflammation of the myelin.

8. Our immune system sees the inflammation and cleans the infected cells of the myelin, which is what we have always seen as MS.

9. By opening up the narrowed veins, the process will stop and reverse. In young patients with RR-MS with very good results.

10. At mid age yet another phenomenon strikes and that is the hardening of the veins / diabetes 2 (This also explains the double peak in the graph that we see when if we plot the age when patients got diagnosed with MS. In young patients, the inflammation is caused solely by serious strictures, in patients at mid age who already have a weak nutritional condition due to (less severe) strictures, the nutritional condition becomes now even weaker by the vein hardening / diabetes 2 and thsi causes the late onset MS).

11. The vein hardening / diabetes 2 hinders the transport of nutrition because the red blood cells do not release ATP as easy anymore. Also, it is more difficult for the insulin to get to grips with the cells and do its job due to the calcification of the veins (this is also the explanation of the known vitamin D relationship with MS, i.e. that people who move south at young age are less likely to develop MS; also here lies the explanation of the higher prevalence of diabetes in MS).

12. By opening the veins, the process of vein hardening does not stop. In some cases it may even be that the hardening of the endotholium goes even faster due to a higher supply of calcium and forsfor (in the much higher concentration of ATP). This hardening might also be related to high sugar consumption.

13. The process that now arises is not much different from diabetes2 (in the early 1980's there was already a discussion in the medical field whether or not MS and diabetes2 are two sides of the same coin).

14. In diabetic 2 patients, the ATP is lower than in normal people, and they use drugs that help the red blood cells to release the ATP, and the insulin to do its work (such as Metformin). Perhaps this is also indicated for MS patients who are freed from the vein narrowing, particularly middle-aged and older patients that have a predisposition for diabetes 2.

15. On a parallel thread, it is suggested that all patients with MS should be tested on ATP.


Maybe it is an idea to submit this line of thinking to associations in various medical disciplines (e.g. neurology, vascular specialists, endocrinology) to ask for their opinion.

Leonard,

Can you answer the following questions with regards to points 7 and 8 of your hypothesis.

1. Why is it only that the myelin (white matter) is inflamed and not other tissue such as the grey matter?

2. I could see that if the inflamed meylin tissue eventually dies, it would be removed by the inate immune system.

However, if this tissue is just inflamed it would require a cell mediated response to attack it in a normally functioning immune system. This means the myelin would need to be infected with a virus such that its antigen would be presented on the cell surface to notify the adaptive immune system to attack it.

I am sorry, CVfactor. You are overasking me.

You may well be right that there needs to be some sort of virus around there as well. In fact, I believe that studies have indeed revealed the presence of a virus infection in MS.

Notwithstanding, I am convinced of the diabetes 2 link for late onset MS (which was the case for me). My farther who is genetically not very far from me had problems walking the stairs when he was about 58. He was diagnosed with diabetes around the same time, got his medication (Metformin and Glimperide) and his diabetes under control, and the symptoms diappeared. He 83 years old now and in good health.

Of course I had the stenoses in my neck that were opened. With that, I believe the "real MS" was overcome. But the diabetes predisposition remains and needs to be addressed.

I know that I have to become very humble. Matters are probably a bit more complex as they may seem at first hand. I am fascinated by this thread on the ccsvi chapter of this forum:
http://www.thisisms.com/ftopict-15731.html