A new concept and treatment options for MS

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Postby Leonard » Fri Jan 21, 2011 8:51 am

copy form the thread on ccsvi:

Cece wrote: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, 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?
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Postby Leonard » Sat Jan 22, 2011 12:07 am

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 the 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.
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Postby jgkarob » Sun Jan 23, 2011 3:41 am

There is a piece missing from this hypothesis puzzle.
What is your opinion on the different types of MS?

Your theory doesn't once mention relapses.

I'm a low-carb diet MSer. I've been low carbing for many years after several blood tests revealed that my very low fat diet wasn't working.

Since eating a gluten-free low carb diet, my health has been good. However, my relapses are sudden and debilitating.
In the year following my conversion to low-carbing, I had two knee operations and a massive reaction to a drug (Hyaluronic acid for meniscal supplementation) and my MS was diagnosed the next year.

Since diagnosis, I have had some on-off periods with the diet, until 2006, when I became very strict.
I have had only one relapse since then, in 2009 after some months without beta-interferon.
I've been on Rebif for 10 years now and that relapse in 09 was bad enough to put me in hospital for 2 weeks. After which, I went back to my regime of Rebif/LDN/gluten-free/low-carb/vitamin D3 supplementation.

My particular flavour of MS is non-progressive but marked by many relapses. Beta-interferon has worked very well. Diet has worked well and moving to a country with more sunlight has had an effect.
I don't have the money to be tested for CCSVI. I'm fairly sure I have it, but it's just supposition right now.

So, as there are several types of MS, PRRMS, RRMS, Benign RRMS, SPMS, PPMS. There are quite big differences in presentation.
What's your theory on this?
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Postby Leonard » Sun Jan 23, 2011 5:51 am

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!!
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Postby Leonard » Mon Jan 24, 2011 7:27 am

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.
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Postby Leonard » Tue Jan 25, 2011 2:54 am

from the thread on ccsvi/a logical ending?

1eye 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.


If the blood is slow getting through the brain it stands to reason that it not only gets very very low on oxygen but glucose as well by the time it gets back into the heart.

Might go towards explaining why exercise makes such a difference. The faster pumping heart will at least mix the overused venous blood faster with blood that isn't so exhausted, and maybe increase arterial pressure towards the brain.

The cognitive problems and fatigue might have something to do with bad brain nutrition. Not to mention atrophy and cell death (brain starvation?).


@1eye: thank you, this is yet another piece of the puzzle! It may help explain why the drainage side of the brain is more affected. Clearly the iron depositions on the drainage side is one thing, it will be a fact that the oxygen/glucose level in the blood will be poorest on the drainage side as well further weakening the already low glucose condition of that part of the brain.

And exercise may help, for the reasons you mention. I think many MS patients may confirm this including myself, but at the same time it should not be too much exercise either because then the glucose build-up in the cells (or in any case what is left of that) will be used up...

the low-glucose hypothesis goes beyond plausibility!
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Postby Leonard » Wed Jan 26, 2011 1:13 am

The article from the Medical Director of the National Multiple Sclerosis Society of Australia from 2006 states:
.... there are two peaks on the age of onset graph at 25-30 and 40-45. This is presumably due to a small number in the intermediate age group 35-40. Since this statistic has not previously been reported, it may simply reflect some non-random feature in the case selection process.

http://newsgroups.derkeiler.com/Archive ... 01256.html

I have seen the observation that there are two peaks in the age of onset graph before; there must be more evidence because I have seen it! The explanation given however "This is presumably due to a ... etc " is not correct. There actually is a double peak.

Why? How is this double peak explained? Young people who get MS have serious stenoses and get MS onset already by 25-30 years of age. Others who have stenoses but less severe do have a low glucose condition of their brain but not enough to suffer from MS yet. At mid age (around 40) when the insulin resistance start to develop in about 8% of the general population, this will affect these "stenosed patients". Because these people already have a fairly weak glucose condition, they will detoriate further quickly and MS will show up.

The explanation is as simple as it is beautiful and it confirms the picture that MS is the result of a low-glucose condition of the brain. It also confirms the picture found by Zivadinov and others that stenoses are not confined to MS patients only but that they occur more frequently in the general population.

If you have these stenoses, and you are among the 8% of the population which develops insulin resistance (where there may clearly be a genetic predisposition), you may get MS, just like me. I had the stenoses in the left and right IJV and in the Azygos, and I had onset at 47 years of age, and my farther has diabetes 2 just like his mother..

I believe there is no way around this concept. The double peak is not fake, it is not invented, it is real and explained by the ccsvi - low glucose/insulin concept.
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Postby Leonard » Fri Jan 28, 2011 3:54 am

I start to believe that the detoriation of the glucose transport at mid age is caused by a calcification of the veins and not primarily due to increased insulin resistance.

I am convinced that the double peak in the graph of MS onset is explained by:
1. at young age (first peak in graph of age of onset 25-30): by iron deposits on the vessel wall and an insufficient blood flow for a good supply of glucose.
2. at middle age (second peak in graph of age of onset 40-45), patients who already have a low glucose condition in their brains will now be affected by the normal process of atherosclerosis (of the veins). Years later they may develop diabetes, possibly due to increased insulin resistance also caused by the same atherosclerosis. This also explains the prevalence of diabetes in MS.

In summary, it is the developing atherosclerosis that constitutes the primary process for the detoriation of the glucose supply, not an increased insulin resistance as such.

Whether an early start with the anti-diabetes drug metformin ( http://www.metformine.com/ ) would help is a very interesting question. In any case, my triglyceride levels, and prior to my low fat diet, also my cholesterol were too high. And the risks/side effedts of this drug seem to be very low.

I think the answer to the question about the early start with metformin is very important! But I also sense a reluctance/resistance from medical practitioners that we (as patients) bring new concepts and insights that do not fall within the existing protocols. Like with CCSVI where we saw a huge resistance from the established order (from neurologists), it is not impossible that we will see again a resistance to this new insight from the established order (from endocrinologists/diabetologist).

Last night, I saw an interesting program on the Belgian TV on reserach into Alzheimer that talked about the competition between research teams worldwide over the last 20 years. In our case, we also see a lot of envy and competition. On top of that, we see the traditional vertical silo's of neurologists, vascular experts and endocrinologists, different micro-cosmos's as we saw, each with their own interests, motivations etc.

These vertical silo's have now been replaced by a bigger cloud or clouds of knowledge and ideas that fork into thousands of thin lines and pockets of information that proliferate as far as every remote corner of the world. With a very hungry and motivated public at the other end, that is us, and we are learning fast.

Just like with ccsvi, with the help the Internet and these social fora, this global circulation of ideas and brains will prove to be unstoppable.
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MCT for brain

Postby aDifferentDrS » Sat Jan 29, 2011 3:49 pm

Hi, all, I came to this forum to look for a speaker for a conference who could talk about the treatment for CCSVI, but was drawn in by this thread on glucose metabolism with MS.
There's been some discussion on alzheimer's disease being an issue with glucose metabolism by the brain, and some have proposed using medium chain triglycerides (MCT) for this and have had good results. There is even a "medical food" called Axona ($86 for 30 packets) that is basically just MCT. It turns out, however, that coconut oil is a rich source of MCT and also lasts longer than Axona (8 hours vs 6 hours).
However, the Swank diet for MS is very specific about what fats are better for MS and that people who followed the Swank diet survived longer than those who didn't, and that diet lowers fat overall and specifically recommends against saturated fats, so would tend to argue that MCT might not be the best idea.
There has been another theory floated recently that biofilms accumulating in the bloodstream may play a role in the development of CCSVI. Apparently, the inhabitants of the biofilm may use fats for their nutrition, so a low-fat diet may help to limit growth. I have heard that one piece of evidence of the biofilm hypothesis is an ultrasound of a constriction on a vein that had little trails coming off it like algae in a stream.
So, I don't know if this adds anything to the discussion, but thought it might add some additional pieces to the puzzle.
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Postby Leonard » Sun Jan 30, 2011 12:11 am

Let's recap the facts and see whether we can find some conclusions:

- there are two peaks in the graph of the age of onset: at 25-30 and at 40-45. Young people who get MS have serious narrowings in the neck veins. The supply of nutrition/glucose will be insufficient because of slow blood flow and iron depositions (mainly on the draining side). At mid age when hardening of arteries and veins occurs (a normal process for every one), those people who have narrowings in the neck veins and already a weak glucose condition of their brain but not yet MS will suffer because the supply of nutrition/glucose will now become insufficient. This explains the double peak in the graph of age of onset. The double peak is mentioned for instance in: http://newsgroups.derkeiler.com/Archive ... 01256.html

- when the supply of glucose gets insufficient, cells will die (including myeline and neurons) and the immune system cleans up the mess. That is when MS shows up. The correlation between MS and a (low) supply of glucose is reported in this originally Russian paper of 2003: http://www.ncbi.nlm.nih.gov/pubmed/12938635

- the relation of MS and Vitamin D is well known. High Vitamin D during the time your mother was pregnant from you and your youth (in the period your cells were growing) reduces the risk for MS. The intra-cellular calcium will be lower if there was a high Vitamin D level; conversely, the intra-cellular calcium will be elevated if there was a lack of Vitamin D. Sustained elevations of intracellular calcium may inhibit insulin-target cells from sensing the brisk intracellular calcium fluxes necessary for insulin action, such as in particular glucose transport. See this recent article in the International Journal of Endocrinology:
http://www.hindawi.com/journals/ije/2010/351385.html


- Diabetes 2 (old age diabetes) and MS have very similar symptoms. It is known that in case of diabetes 2, the process of demyelination is already well underway for many years (I found a recent article in a journal with good reputation on the net but I can not find it back now but it is there). The same is true for MS, the process of demyelination started much earlier. Although they are not the same disease, they may well have a common cause i.e. a common underlying metabolic mechanism namely a lack of glucose supply due to the hardening of the arteries and veins, and in fact they may be two sides of the same coin. Diabetes may affect the whole body, in our case the disease is concentrated around the cerebro-spinal. See this link for the remarkable resemblance of effects: http://diabetes.niddk.nih.gov/dm/pubs/neuropathies/ It may also help to explain the prevalence of diabetes in MS. This report states: Several investigators have found some metabolic disorders linking both diseases, such as abnormalities in fat, calcium, and vitamin D metabolism. Also, there is evidence of disruption of myelin due to changes in glucose levels. http://care.diabetesjournals.org/conten ... 984.1.full

If we take all these facts together, and also consider how people who have been liberated from ccsvi recover, the link of MS with the glucose condition of the cerebro-spinal goes beyond doubt.

There is an effective medication for diabetes 2 that is called metformin. It is made from the French lilac, a plant used in folk medicine for several centuries, and it is safe and widely prescribed for diabetes. http://en.wikipedia.org/wiki/Metformin

What is more interesting for us is that the medication has been investigated for other diseases where insulin resistance may be an important factor. Or may be I should write here where glucose transport is an issue. I do therefore not exclude the possibility that metformin will not only help diabetes 2 patients to overcome their insulin resistance, but also that metformin will help improve glucose transport to hungry cells in MS patients in particular at mid age and later when hardening of the veins/calcification becomes a factor. Therefore, besides the opening of narrowed veins by balloon agioplasty, metformin could be a useful medication for us to improve the glucose transport and help overcome MS.

I would be very interested in your views and/or reactions.
Last edited by Leonard on Mon Jan 31, 2011 2:53 am, edited 3 times in total.
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Postby Daisy3 » Sun Jan 30, 2011 8:03 am

Are you taking Metformin? If so, how are you finding it?
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Postby Yodi » Sun Jan 30, 2011 11:41 am

Hello everyone, I never posted on here before but I do follow this forum for quite a while.

I wanted to add an amazing discovery that was made in Berlin. Metformin can help against Alzheimer's disease (AD). As a diabetes drug metformin stimulates insulin production. Now scientists have found out that the drug also activates an enzyme in the brain, which could prevent the death of certain brain cells. Metformin would become a cost-effective tool in the fight against AD
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Postby lyndacarol » Sun Jan 30, 2011 12:16 pm

Yodi – It has been my understanding that all the diabetes drugs (rosiglitazone, etc.), EXCEPT metformin, operate by stimulating insulin production. As the "insulin girl," I think stimulating insulin production is exactly the wrong thing to do.

Metformin may be helpful because it does NOT stimulate insulin production, but works by another mechanism which actually reduces the insulin level in the bloodstream by making the cells receive it (and the glucose) more effectively.
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Postby Leonard » Mon Jan 31, 2011 3:45 am

from the thread on ccsvi:

Cece wrote:Leonard, wouldn't people in the first peak (age 25-30) then get hit harder when their arteries or veins age and interfere even further with the glucose issues?


YES, I think this is known by neurologists. Of course it depends on the degree of hardening. If you have diabetes 2 in the family, clearly there is a genetic predisposition and you should be alerted.

Cece wrote: I think the vitamin D link with intra-cellular calcium and glucose transfer is fascinating, I still need to read up on that.


YES, it is fascinating isn't it and -besides the double peak in the graph of age of onset- a centre piece in the thesis. No one will be able to get around it

Cece wrote: Are you or any other MSer thinking of trying Metformin? I am curious if it will work.


YES, and I am sure that it will work. My father had weakening of his legs when he was around 58 years old. He never had MS though, but may have some venous problems. He was diagnosed with diabetes 2 at more or less the same time. We are now 25 years later, he is 83 years old and in good health. The weakening seems to have evaporated... But he takes Metformin... already for 25 years...

My blood sugar and my fast serum insulin response under stress were tested last week. Things were normal or a sort of normal. So from the diabetics side, I am OK, at least up till now. But I have another problem (=MS) and the medical protocols of endocrinologists do not say anything about that... So the doctor can not prescribe...

What is happening here has never been seen before. We go at the speed of light, the medical system goes at glacial speed, or at best the speed of a plane. We have a global college and brains circulating, they have at best pockets of information that they may share at conferences, meetings, .. When we share information, it is "us for us", in their world there is a lot of envy and competition (not in the least for the intellectual property). We are motivated by our own health situation (which is even more powerful than the $) and we are experienced (we know what it is and what the symptoms are from the inside), they may have different motivations, experiences and expectations. And -in all fairness-, we have the freedom to think and express ourselves (which we do), for them that may be different ("primum non nocere").

We are witnessing an intellectual transformation here that is more sweeping than anything we have seen in the past. The technological revolution of the Internet and these social fora provide extraordinary tools for searching, ordering and processing information. The monopoly of information enjoyed by the medical sector or its various disciplines disintegrates. This makes that we are light-years ahead (and some doctors have literally told me precisely this).

The systemic problem is one of cultural preparation, the challenge is to graduate the computer age. That may be an issue that transcends the medical sector. And perhaps here lies a role for governments.
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Postby Algis » Mon Jan 31, 2011 4:59 am

Did you (or do you know anyone who) tried metformin in any form or dosage and did you (or do you know anyone who) see any "changes" (not even improvements or worse) in their disease/symptoms?

If yes: what dosage and what symptoms.

If not: I can start metformin in a 500mg a day as a test - After consult with relevant physicians - If it seems to be a road to exploit.
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