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The road toward further proliferation of drugs for treatment has no logical ending... we may castigate the notion of this sort of treatment with a variety of pointed adjectives, among them "dangerous", "expensive", "prone to obsolescence," and "lacking credibility."

This new path (open up the veins, get the blood sugar and insulin resistance under control) however will have a logical ending and I sincerely hope that the medical community will take all necessary steps to move ahead in this direction expeditiously: http://www.thisisms.com/ftopict-15188.html

It is hypothesised that multiple sclerosis (MS) is caused by an insufficient glucose level in the brain or parts of the brain.

Patients with MS are consuming more sugar than the average person, to get it elevated in our blood streams, to try and meet the unmet needs of the brain. And the result of greater sugar consumption is a greater prevalence of chronic yeast infections and symptoms as candida . Also the faster recovery of motor functions of MS patients on the intake of sugar/glucose, in particular in the beginning, would seem to suggest a glucose link. Furthermore, it is an explanation for the fast recovery of some patients post- ccsvi liberation and a post-liberation increase in dreams and REM sleep, since REM has high glucose demands.

The blood flow delivers oxygen and glucose to the very hungry brain as well as other nutrients, and takes away waste products. A lack of glucose puts the neurons in a dormant state; they become under-nourished. The consequence is demyelination and, if seriously under-nourished for a longer period of time, myelin and neuronal death. When this happens, the microglia jump on this and clean up the mess. Once they get out of the BBB, the T-cells jump on them and we start see the scars and the inflammation. That is when MS shows up.

Why are the cells under-nourished? There are at least two reasons: iron deposits on the vessel walls that inhibit the transport of glucose across the BBB and; insulin resistance that inhibits this same transport of glucose. The iron deposition may develop at a young age as a result of problems with the drainage, its origin is probably pre-congenital. The insulin resistance may develop at a later age. MS is probably a consequence of both, in a wide variety of cases among the population. One effect may be a more important for an early age onset and the other for a later age onset. The double peak in the age of onset of MS would indeed suggest the possibility of such underlying mechanism [there are two peaks on the age of onset graph at 25-30 and 40-45 http://newsgroups.derkeiler.com/Archive ... 01256.html ].

Stenoses in the veins draining the brain and spinal column (ccsvi, Zamboni) cause refluxes in the deep cerebral veins and will lead to iron deposition on the vessel walls (you can see this on 7T MRI) and this inhibits glucose transport through the affected parts of the BBB. Iron deposition is a normal phenomenon in organs and limbs in case of problems with the drainage that has been known for a long time. By opening up the blockages in the veins by angioplasty, the blood flow can restore to normal, and eventually as the iron is taken away the BBB function may restore to normal. The increased blood flow during pregnancy and stop of MS progression adds to the plausibility of the concept. The low fat/Swank diet and the use of blood thinners/anti-clotting (effect Copaxone?) may also help improve the blood flow with the same positive effects.

Some persons may already have a fairly weak glucose condition in their brain due to the low blood flow through the head and the iron depositions. At mid age then, the insulin resistance starts to develop and the glucose transport will be further weakened. The Vitamine D relationship, well known in MS, plays its role here.

As studies found, higher levels of Vitamine D (childhood and/or during pre-congenital phase) may delay the onset of MS a bit because of lower intra-cellular calcium levels where insulin resistance and problems with glucose transport will develop a bit later on. Conversely, lower levels of Vitamine D will elevate intra-cellular calcium levels where insulin resistance develops earlier on and thus impaired glucose transport across the BBB will develop earlier.

This may explain the differences found among MS patients and a control group that were screened for ccsvi: people who have stenoses and therefore a low blood flow but high Vitamine D will still provide enough glucose to their neurons and myeline, and therefore will not experience the MS symptoms, or at the very least not as quick as those with low Vitamine D. The prevalence of diabetes type 2 in MS patients would further suggest a link with the insulin resistance. It is also known that this insulin resistance develops long before the signs of diabetes become apparent and the diabetes type 2 is diagnosed, further adding to this part of the hypothesis.

Studies have also found that a low-glucose condition causes or at the very least it is likely to cause demyelination. The process of demyelination is already well underway before diabetes type 2 shows up.

Also it ties in with the effect of heat on glucose in the bloodstream (it fluctuates more wildly; diabetics have to account for this in the summer) and, if overheated, the brain will endure worse damage from this lack of glucose.


What lessons may we draw:

1. get the veins opened and restore the normal blood flow. This will increase the volume of blood, and improve the cerebral hypoxia side of the equation, and the cerebral hypoglycemia side. The iron deposits may be taken away (?)

2. if appropriate and confirmed, start taking (diabetes type 2?) medication early on to overcome insulin resistance and improve the glucose transport across the BBB. And also, get the blood sugar level back to normal.

Leonard wrote:The road toward further proliferation of drugs for treatment has no logical ending... we may castigate the notion of this sort of treatment with a variety of pointed adjectives, among them "dangerous", "expensive", "prone to obsolescence," and "lacking credibility."

This new path (open up the veins, get the blood sugar and insulin resistance under control) however will have a logical ending and I sincerely hope that the medical community will take all necessary steps to move ahead in this direction expeditiously: http://www.thisisms.com/ftopict-15188.html

I would add that it is not "the new path". It is the ONLY path. The theory behind the drugs was "I don't know why this works, but we have make a trial and by our statistics it works"

This could be statistics but no science. Science needs to have first a model and later, use statistics to validate. By now the only model we have is the CCSVI theory.

And in science a model is valid until a new model appears. Newton gravity was considered valid until general relativity appeared. It was wrong, but it would have been absurd not to consider it valid in absence of something better.

Until something better appears, CCSVI should be considered the ONLY valid theory for MS.

frodo wrote: ...Until something better appears, CCSVI should be considered the ONLY valid theory for MS.

may be this is enough further evidence to consider a broader low-glucose based theorie: http://www.ncbi.nlm.nih.gov/pubmed/12938635

of course ccsvi is part, in fact it causes the low glucose condition that sets off the whole process.

Here's another one, although they're drawing a different conclusion (assuming that the lowered glucose use in the brain is a result of "a deterioration of cortical activity" as the disease progresses, meaning we use less glucose because our brains are not doing as much. Seems like that is one possibility and the glucose-ccsvi-theory is another):
http://www.ncbi.nlm.nih.gov/pubmed/10408551

Cece wrote: Seems like that is one possibility and the glucose-ccsvi-theory is another

Cece, you are right, this is the question.

The discussion should concentrate neither on the neurological nor on the vascular dimension. The reason why we have taken this discussion so far is that we have been able and willing to look outside the box, that is the box of the neurologists. Now we should not make the same systemic failure of locking ourselves into the vascular box. Our primary goal must be to solve the mystery of MS, to find what causes MS and how to best treat it. In my view that should be done somewhere in the triangle between the three disciplines involved.

So then, how do we get vascular specialists/interventional radiologists, endrocrinologists/diabetologists and neurologists in one room to discuss the question?

Insulin-resistant states might be associated with dysfunction of the vascular endothelium.

http://www.ncbi.nlm.nih.gov/pubmed/21122687

J Clin Lipidol. 2010 Sep-Oct;4(5):427-34. Epub 2010 Aug 8.
Diet-supported aerobic exercise reduces blood endothelin-1 and nitric oxide levels in individuals with impaired glucose tolerance.
Kasımay O, Ergen N, Bilsel S, Kaçar O, Deyneli O, Gogas D, Akalın S, Yeğen BÇ, Kurtel H.

Department of Physiology, Sports Physiology, Marmara University School of Medicine, Tıbbiye Street, Haydarpaşa, Istanbul 34668, Turkey. ozgurkasimay@hotmail.com

BACKGROUND: Impaired glucose tolerance (IGT) forms an intermediate stage in the natural history of diabetes mellitus. Insulin-resistant states might be associated with dysfunction of the vascular endothelium.

CONCLUSION: Our results demonstrate that exercise, along with low-calorie diet, induced reductions in the plasma of both ET-1 and NO. Beneficial effects were observed on anthropometric measurements and plasma oxidant stress markers, indicating weight loss associated with exercise training and calorie restriction may effectively improve endothelial dysfunction in patients with IGT.

Copyright © 2010 National Lipid Association. Published by Elsevier Inc. All rights reserved.

Makes instinctive sense to me. For ten years I was thought to be hypoglycemic. Turns out I just had CCSVI.

Interesting about the cortisol...some of the issues I've had have recently landed me in an endocrin. chair but none of my tests are out of range. However my a.m. cortisol is right at the low end cut-off. And I've always had trouble if I go too long without eating somthing but my blood glucose levels and A1C are always within the norm on blood tests too. Trying to pinpoint a true cause for my problems has been like trying to nail jello to a wall. Interesting.

Completing the picture with the last piece of the puzzle: the effect of immuno-suppressive drugs

It seems that we are faced now with a chicken and egg problem: which is there first, the MS or the ccsvi-insulin low glucose condition?

Let's recollect the facts:

1. Zamboni worked as a junior doctor on the island of Sardinia. He diagnosed many young people with vascular problems in the neck. 20 years later - he was already back for some time on the Italian mainland - he found that >90% of these young people had developed MS when adults.

2. In December 2009, a consensus position was agreed (in fact by unanimity) by the vascular experts of 47 countries that ccsvi is there first and causes MS later on. Also it was agreed that the venous strictures are pre-congenital in origin. http://www.ncbi.nlm.nih.gov/pubmed/20087280

3. The autoimmune concept for MS is a hypothesis that even today - after 60 years - is still a hypothesis. However, with the low glucose condition, all pieces of the puzzle fit together neatly (double peak in the age of onset, vitamine D relation, MS and diabetes relation ..)

With these facts, let's assume that the ccsvi-insulin low glucose condition is there first.

What happens when there is a sustained shortage of nutrition of the brain cells for many years? We will start to see an inflammation of the vessels /BBB as the immune system is starting to clean up the mess caused by the death of myeline cells and neurons. This inflammation then will further deteriorate the transport of glucose /nutritution along the BBB. That is where the vascular dimension and the neurological dimension start to interact.

The effect of immuno-suppressive drugs will dampen the inflammation and may slightly improve the functioning of the BBB, I guess in particular for RR. However, the situation of malnutrition caused by the poor blood flow, the iron depositions and the insulin resistance, will sustain; and the underlying process of demyelination and axonal death will continue; and as a result the progression of the disease with a further debilitation will carry on. I think the papers on the glucose transport and the BBB (see above postings) may perfectly fit within such concept of the issue.

All the major pieces of the puzzle are now known, and the full picture can be put together. The solution lies somewhere around the intersection of 3 disciplines: vascular specialists/interventional radiologists, endrocrinologists/diabetologists and neurologists. I hope they pick up this message and solve the problem expeditiously and with force.

frodo wrote:

Leonard wrote:The road toward further proliferation of drugs for treatment has no logical ending... we may castigate the notion of this sort of treatment with a variety of pointed adjectives, among them "dangerous", "expensive", "prone to obsolescence," and "lacking credibility."

This new path (open up the veins, get the blood sugar and insulin resistance under control) however will have a logical ending and I sincerely hope that the medical community will take all necessary steps to move ahead in this direction expeditiously: http://www.thisisms.com/ftopict-15188.html

I would add that it is not "the new path". It is the ONLY path. The theory behind the drugs was "I don't know why this works, but we have make a trial and by our statistics it works"

This could be statistics but no science. Science needs to have first a model and later, use statistics to validate. By now the only model we have is the CCSVI theory.

And in science a model is valid until a new model appears. Newton gravity was considered valid until general relativity appeared. It was wrong, but it would have been absurd not to consider it valid in absence of something better.

Until something better appears, CCSVI should be considered the ONLY valid theory for MS.

exhuberant, aren't we. Perhaps we should hold back just a tad until there is some evidence beyond anecdote. One theory's inferiority should not elevate another.

let hope you are correct that a mechanical treatment is the fix, but i doubt it will be that simple

drsclafani wrote:
let hope you are correct that a mechanical treatment is the fix, but i doubt it will be that simple

that is not what I claim: see http://www.thisisms.com/ftopic-15188-da ... asc-0.html
and please read/analyse the thread from beginning to end. thanks

This morning I got a mail from Lyndacarol. As it is the crown on the ccsvi-low glucose hypothesis, I take liberty to post an extract here.

quote: … I have believed for a long time that MS is NOT autoimmune and that insulin plays a STRONG role in my disease. The posting of your ideas causes me to extend my insulin hypothesis. Along with your mention of "malnutrition" in the cells and the understanding that insulin is the "key" that unlocks the cell door and allows the fuel source (glucose) to enter,

http://www.sharecare.com/question/what- ... rtner=droz

I now consider my insulin problem is part of a larger Metabolic Hypothesis. It seems quite logical that cells which are crying out for an energy source, but which are resistant to letting insulin unlock the door, would continue to call for the necessary nutrition (fuel). In response, the pancreas secretes more insulin. It is the insulin that damages the inside of the blood vessels, resulting in stiffening and thickening of the walls (a known fact) and probably narrowing and stenosis of veins (implicated in CCSVI). As I consider the symptoms of MS, it seems to me that all can be traced to one of the steps along the way – "starving" cells, excess insulin, insulin resistance.

uquote

Sorry Lynda, I could not resist.
Please add as you wish.

Thank you, we should be grateful to you forever!!

Leonard wrote:

drsclafani wrote:
let hope you are correct that a mechanical treatment is the fix, but i doubt it will be that simple

that is not what I claim: see http://www.thisisms.com/ftopic-15188-da ... asc-0.html
and please read/analyse the thread from beginning to end. thanks

His response came after frodo's, who I believe was talking about just CCSVI.

I am exuberant too.

CCSVI theory dovetails well with the original autoimmune theory. There never was an answer for why everything was getting past the blood-brain barrier in the first place.

As Leonard and lynda-carol have been doing, looking into insulin resistance and the role of glucose fits well with CCSVI too if it's true that the refluxing blood has not just less oxygen but also less glucose to meet the needs of the very hungry brain.

I do not exclude the possibility that some MS patients who have been liberated are experiencing further degradation of their condition because of increased insulin secretion and resistance. Restoring the normal blood flow may increase the insulin secretion by the pancreas that washes blood sugar away and also the increased blood flow may increase the insulin resistance of the cerebro-spinal. This is sufficient reason to investigate further the link of ccsvi and insulin.

This does not change the principle goal of liberation but may add an important and necessary second step to bring the sugar level and insulin resistance under control.

Cece wrote:As Leonard and lynda-carol have been doing, looking into insulin resistance and the role of glucose fits well with CCSVI too if it's true that the refluxing blood has not just less oxygen but also less glucose to meet the needs of the very hungry brain.

Cece, it is not only less glucose, it is also that this smaller amount/flow of glucose will pass (the affected parts of) the BBB more difficult due to iron depositions, insulin resistance, thickened vessel walls, and last the inflammation related to the MS.