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.

group of experts

Postby Leonard » Tue Feb 14, 2012 3:40 am

I want to try something new. There is no future in being cynical, voicing complaints and resigning ourselves to pessimism. Looking forward, what we must do instead is to improve upon what we know and further the new insights.

I am an engineer by training, graduated from university 30 years ago, and since then worked in a wide variety of jobs. That background has certainly helped me to move this matter forward, to take a fresh look at things or with a totally different slant if needed, to connect things together in an unorthodox manner sometimes perhaps even with a bit of reverse engineering. Now don't say it is all wrong because it is not..

But I have come to a point where I have reached my limits; I do not have the deep understanding or expertise necessary to progress the matter further. Therefore, I wonder whether there are medical people, physicians, doctors, researchers reading here that would like to positively and constructively help me to produce a joint paper. I think there is enough material in this thread and if necessary on the Internet. My idea would be to produce a paper for public consumption i.e. that is sound, understandable, easy digestable and that makes appeal to a wider public. Time horizon: a few months. As far as I am concerned, your participation and contributions could be anonymous.

If you are interested, please send me a PM with just a few lines (max 5!) of your expertise and an email contact point where I can reach you (which as I said could be anonymous for instance using a gmail or hotmail address). I would suggest that common sense and consensus prevails when preparing such joint paper. And if you are happy with the final result, those of you who contributed in an anonymous fashion could add their full names to the paper as well if they wish to do so.
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Postby Leonard » Mon Feb 20, 2012 7:24 am

This study is interesting because it suggests innate immune activation by "latent" EBV infection. It strengthens the sketch for the new concept explained on top of page 1 of this thread.
http://www.ncbi.nlm.nih.gov/pubmed/22156987

The article mentions yet another receptor, the Toll-like receptor-3. When I searched wikipedia, I learned that there is a whole family of Toll-like receptors of which TLR3 is a member. And that these receptors play a fundamental role in pathogen recognition and activation of innate immunity.
http://en.wikipedia.org/wiki/Toll_like_receptor-3

In an earlier posting, there was a link between EBV and vitamin D receptor dysfunction. And also, we saw a link between the vitamin D metabolism and the innate immune system.
http://www.ncbi.nlm.nih.gov/pubmed/20593215

So now we are faced with a multitude of receptors, some of which with a direct link to innate immunity. Where I start to think that there may be much more to it that we have not seen so far, let alone understood how it all works together... And perhaps that -at the end of the day- it is not the one molecule that will do the trick (there simply isn't such a solution) but that it is a complex of issues, fats, vitamines, minerals etc as well as clean receptors that is needed for our recovery.

The very interesting video under the first link would indeed suggest such path: to note the chart with the daily intakes of our predecessors. And the path is advocated by many others.
http://www.wimp.com/mindingmitochondria/ and http://www.terrywahls.com/ForumRetrieve ... rumID=3749
http://www.swankmsdiet.org/ a plan for the treatment of multiple sclerosis that absolutely anyone can do
http://www.overcomingmultiplesclerosis. ... ntId=20084 Swank in the Lancet
http://www.overcomingmultiplesclerosis.org/ with recommendations aiming at overcoming multiple sclerosis and recovering
http://www.overcomingmultiplesclerosis. ... trumpets!/
http://www.ncbi.nlm.nih.gov/pubmed/19209185 Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet

I believe that future MS research should focus primarily on this path. However, the pharma industry will lack the commercial incentives and the clinical sector may become luke warm at best as this risks to be so disruptive to their world. But for public health it is a very promising path: it gives a healthier society and will dramatically lower costs. Therefore, a substantial share of public money should be allocated to exploring this path further rather than the search for one or the other molecule or genetic defect... If we take all the information on this thread together, such path would seem to have much better chances for success than the traditional search for new medication and offers the prospect of bringing real benefits to the individual patients and society in the short to medium term.
Last edited by Leonard on Mon Feb 27, 2012 4:14 am, edited 1 time in total.
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Vitamin D and the intestine

Postby Leonard » Wed Feb 22, 2012 4:55 am

In the sketch of the new concept for MS in the first posting of this thread, a link was established between the vitamin D metabolism and commensal intestinal bacteria. Ligands of these bacteria may block vitamin D receptors and other receptors which would lead to a cascade of events causing poor cellular nutrition and a disintegration of myelin. Vitamin D 25OH supplementation could cause adverse effects as it would raise 1,25D levels in the blood that bind to vitamin D receptors and displace other receptors that are supposed to activate from them.

However, there is another vitamin D relationship to MS. And that is to do with the role of vitamin D in the intestine. To this end, this poster is really very interesting: http://www.vitamindandms.org/resources/ ... -in-MS.pdf

As this clearly points to a positive effect of vitamin D supplementation, the question whether or not to supplement vitamin D then becomes an issue. In fact, some patients report significant improved health with vitamin D supplementation. Others see things turning worse after some initial improvements. Perhaps, but this is still a big perhaps, a genetic predisposition for diabetes could be a possible indicator for T/B cell problems originating from the gut, and for this category of MS patients, vitamin D supplementation could be beneficial...

The following publications are also interesting in this regard:

Intestine is Crucial to the Function of Immune Cells, Research Shows

The researchers found that some B cells—a type of white blood cell that produces antibodies—acquire functions that allow them to neutralize pathogens only while spending time in the gut. Moreover, this subset of B cells is critical to health.

..found that as B cells differentiate into plasma cells in the gut, they adopt characteristics of innate immune cells—despite their traditional association with the adaptive immune system. Specifically, they begin to look and act like inflammatory cells called monocytes, while maintaining their ability to produce a key antibody called Immunoglobulin A.
"What intrigued us was that this theme—B cells behaving like monocytes—had been seen before in fish and in vitro. But now we have a living example in a mammalian system, where this kind of bipotentiality is realized," says Gommerman.

This B-cell plasticity provides a potential explanation how cells dedicated to controlling pathogens can respond to a large burden of harmful bacteria without damaging beneficial bacteria and other cells essential for proper function of the intestine.

It also may explain how scientists had failed to appreciate the multi-functionality of some B cells. "There are classical markers immunologists use to identify B cells—receptors that are displayed on their surface—and most of them are absent from plasma cells," says Gommerman. "So in some cases, what people thought was a monocyte could have been a plasma cell because it had changed its surface identity, although monocytes play an important role in innate immunity as well."

This transformational ability [of T-B cells], the researchers also found, is dependent on bacteria called commensal microflora that digests food and provides nutrients. etc

http://www.infectioncontroltoday.com/ne ... shows.aspx

Scientists Find Vitamin D Crucial in Human Immune Response to TB

…researchers found that although both the innate and acquired immune systems start out by using different receptors to trigger a complex chain reaction in infected cells to kill the tuberculosis bacteria, both converge early on to follow the same pathway that utilizes vitamin D.

Previous research by the team found that vitamin D played a key role in the production of a molecule called cathelicidin, which helps the innate immune system kill the tuberculosis bacteria. Humans are born with innate immunity, which is the pre-programmed part of the immune system. The team notes that vitamin D may help both innate and adaptive immunity, two systems that work synergistically together to fight infections.

http://www.infectioncontroltoday.com/ne ... to-tb.aspx


A final intriguing question: Could one or all of these - Vitamin D, diet or a transplant with gut bacteria from a ‘healthy’ human - cure MS? Again, I believe this is where the future MS research should focus.
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Vitamin D for MS is becoming mainstream

Postby Leonard » Sun Feb 26, 2012 1:40 am

and the vitamin D story continues
http://www.vitamindwiki.com/tiki-view_b ... ?postId=62

I quote
MS is in a vicious cycle with vitamin D:
Low vitamin D ==>MS ==> lower vitamin D ==> many more vitamin D deficiency diseases

This certainly matches my own experience..
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Re: I think I found it: This Is MS

Postby Leonard » Mon Feb 27, 2012 3:45 am

nice video: MS-Wars: Hope, Science and the Internet

http://vimeo.com/37484943

The fact that progressive patients have less benefit from the liberation procedure, as mentioned in the video, is of course because the attacks from the manipulated gut T/B cells will continue after liberation.

So one needs to do both: to unblock the veins and to get the gut flora back in balance.

The risk is that if both dimensions are not picked up and addressed simultaneously, ccsvi alone will fail to break through or at least that a treatment scheme will be significantly delayed ... I think that is precisely what is currently happening, in Canada and elsewhere.


Politicians and doctors may ask: there will be many people in our society with an unhealthy gut flora, so why is this so bad for MS patients? The answer to that question is simple: because in MS patients, the BBB will be (at least partly) compromised due to many years of ccsvi. And hence, in our case these bad T/B cells from the gut can enter our brain and continue to do their destructive work. Liberation from ccsvi will reduce the pressure on the brain, on the cell walls of the veins and improve the blood flow and conditions, but the BBB function will not be [immediately] restored. Therefore these bad T/B cells (which incidently may cause many other chronic "immune" diseases such as diabetes) can continue to enter the brain and do their destructive work.. So you need to do both.

I think this is where the difficulty comes is: MS is a complex multi-facetted disease that needs to be tackled by a complex of treatment options..
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insulin

Postby Leonard » Mon Mar 05, 2012 3:42 am

MS is a multi-facetted disease.
One factor is the glucose metabolism.

The link refers to Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet
http://www.ncbi.nlm.nih.gov/pubmed/19209185
From the conclusion: Even short-term consumption of a paleolithic type diet improves BP and glucose tolerance, decreases insulin secretion, increases insulin sensitivity and improves lipid profiles ..

Many years of ccsvi will have significantly weakened the glucose transport across the BBB. Under these conditions, optimizing insulin sensitivity of cells you have left over would seem an absolute necessity. High peaks of insulin are devastating while low levels will increase insulin sensitivity and hence improve micro-cellular feeding. The same can be said about the need to optimise lipid profiles across the barrier.

The working mechanism of Metformin is not well understood, many effects have been suggested. But most important in this particular context seems to be the fact that Metformin keeps the blood sugar level down and -I guess- insulin levels as well. And precisely this will improve the sensitivity of your cells to insulin and maintain good cellular health (Terry Walsh would say Minding your mitochondria..).
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transplant gut flora

Postby Leonard » Mon Mar 05, 2012 3:43 am

http://www.vitamindandms.org/resources/ ... -in-MS.pdf

From the above link: Could one or all of these - Vitamin D, diet (e.g. to keep insulin peaks down :-D ) or a transplant with gut bacteria from a ‘healthy’ human - cure MS?

I understand that the transplantion of gut flora is now being practiced in California but other countries such as for instance the Netherlands. Some links to gut flora inbalances and transplantation may be found on this thread, it was around Summer time.

It is clear that the debate is shifting from unravelling / understanding MS towards finding a cure or the best possible conditions for managing MS...
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sun exposure

Postby Leonard » Mon Mar 05, 2012 3:56 am

The skin produces vitamin D from cholesterol when exposed to sunlight.
The process works until about 50 years of age.
But what other pathways are there besides the vitamin D pathway that we have not yet seen or understood?

As the link below suggests, there are other pathways that are activated by sun exposure than just the vitamin D pathway.
And in fact these other pathways may be as important..
And thus a daily dose of sunshine seems important and is not directly substitutable by vitamin D supplements..

http://www.overcomingmultiplesclerosis. ... vitamin+D/
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more on the gut

Postby Leonard » Tue Mar 06, 2012 6:57 am

MS is a complex two-stage disease.
The first RR stage is caused by ccsvi that breaks the BBB and weakens many metabolic processes...
An infection and contamination of receptors then is enough to slow these processes further...

The second progressive stage is caused by the gut that manipulates T/B cells.
As the BBB is broken, these cells get free access to the intercellular space..
Here is more recent links on this gut induced stage:

http://www.sciencedaily.com/releases/20 ... 112520.htm
https://www.facebook.com/notes/ncs-the- ... 5274823676
http://natmednews.posterous.com/faecal- ... -parkinson
http://www.medicaldiscoverynews.com/sho ... types.html
http://www.ncbi.nlm.nih.gov/pubmed/21508958
http://www.secondgenome.com/2011/05/gut ... lammation/
http://www.medicalnewstoday.com/releases/239176.php
http://www.ncbi.nlm.nih.gov/pubmed/10377132
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the gut microbiome and MS

Postby Leonard » Mon Mar 12, 2012 1:56 am

Further to the last posting on the two-stage disease concept and the role of the gut:

http://www.lecomprime.com/wp-content/up ... -20111.pdf
Immune-cell-associated sensors use information about the local nutrient or metabolite milieu to organize local immune responses
The microbiome component could also help to define a previously uncharacterized axis of human genetic evolution (our microbiome evolution), reflecting in part our changing dietary habits. It could also produce testable hypotheses about unappreciated aspects of the pathophysiology of Western diseases, and yield new microbiome-based strategies for disease prevention or treatment.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158464/
The Lifestyle of the Segmented Filamentous Bacterium: A Non-Culturable Gut-Associated Immunostimulating Microbe Inferred by Whole-Genome Sequencing

http://www.nature.com/nature/journal/v4 ... 10213.html
Marked changes in socio-economic status, cultural traditions, population growth and agriculture are affecting diets worldwide. Understanding how our diet and nutritional status influence the composition and dynamic operations of our gut microbial communities, and the innate and adaptive arms of our immune system, represents an area of scientific need, opportunity and challenge. The insights gleaned should help to address several pressing global health problems.

This article is really very interesting and I urge you all to read it carefully:
http://www.secondgenome.com/2011/05/gut ... lammation/
I quote: The presence of this single type of bacteria (Segmented Filamentous Bacteria) induced a Th17 cell response with an associated rise in systemic IL-17 levels and ..
Prof. Mazmanian’s research suggests that targeting the source of the auto-immune response (gut microbes) rather than the end result (elevated levels of IL-17) may be a valid approach to treating MS.
But, as he says, “this research opens the door for examining these concepts in patients, but potential therapies for MS stemming from this research would require many additional studies…"
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there is risk of paralysis by analysis

Postby Leonard » Mon Mar 12, 2012 2:29 am

Further to the last posting, I would agree with Prof. Mazmanian that targeting the source of the auto-immune response (gut microbes) rather than the end result (elevated levels of IL-17) is probably the valid approach to treating MS.

Where I would disagree with him is when he says, “this research opens the door for examining these concepts in patients, but potential therapies for MS stemming from this research would require many additional studies ..."

If you take the information collected and analysed on this thread, there is no denying that MS is a two-stage disease with an important role for CCSVI and a significant influence of the intestinal bacteria... And there is no denying that certain diets can change the course of MS... Therefore, it would be a shame for all if this matter would need many years of further study. In fact, things to improve the gut microbiota could be implemented tomorrow: a good diet could be the start of a recovery programme. And perhaps -and this may indeed need a bit of experimentation - a gut flora transplant ..

I can see two possible scenarios from here. That is 1. either the neurology embraces the new insights and pro-actively helps to move things forward; or 2. the neurology remains at its base, deserters are earmarked as 'also ran' and meanwhile the world moves on in parallel tracks exploring the new insights...

The Internet causes revolutions all around us (re: the book of Brafman and Beckstrom titled the Starfish and the Spider). I've seen it happen in several sectors and it is currently happening in others. And unfortunately, in most cases, the latter scenario is followed. Ultimately, the own world just dries up, the pedestal on which they had placed themselves falls apart, tenured lecture spots shift elsewhere etc. At that point, the old constituancy discovers that the dynamics has gone elsewhere and they retire...

But in the other disciplines that I have seen, it was all about business. Here is about people. Therefore, I would hope that this time it will be different ... But the weight of the status quo is enormous, and change will be very difficult because they all have to climb down the ladder and that hurts. Therefore I am afraid that the second scenario is likely to happen here too.. Where there is risk of paralysis by analysis, leading to a new situation of indecision.. And that things get deferred, deterred, delayed, and possibly destroyed (don't worry, that is not possible anymore...)

We have seen in an earlier posting that the arguments for further study so often used by the medical sector are way oversold. It is symptomatic; they will use that again.

This article under the link below would seem appropriate as well: http://www.forbes.com/sites/stevenbergl ... ecision/2/
One particular lesson I would like to stress from here: Accept The Limits Of Analysis
The road to hell, we’re told, is paved with good intentions, judicious decisions and exhaustively analyzed strategies. Wars have been lost owing to unexpected weather conditions; data-wielding sports scouts draft college players who fail in the pros.
Bottom line: Avoid paralysis by analysis. Act, examine your results, make adjustments, and move on.

To which I would add: Don't analyse this thing to hell, there are millions of people waiting for you every day..
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recap

Postby Leonard » Wed Mar 14, 2012 2:26 am

I think it works like this:

The condition to develop MS is prepared by venous insufficiency of the neck veins draining the brains.
This breaks the BBB (in certain areas) and slows all sort of processes important in the vessel walls: feeding, transcription.

If you then get a bacteria outbreak like the Cpn (of which it is known that it may be sleeping in your body for years) or a virus (like EBV also latent), even a vaccination for Hepatitis is suspect, these [or their ligands] will attach to cellular receptors. As these dysfunction, their important role for feeding (cells, ion pump) or transcription (oligodendrocytes that then should compete to maintain the myeline and axons) gets impaired. And if severe enough, you get MS (RR).

But some may 'survive' this first stage of attack, stay reasonably ok and not get MS. But you are not there yet. Because at mid age, the gut comes up. Bacteria in the gut (you have more bacteria in your gut than cells in your body) manipulate T/B cells (the immune system). Some people get diabetes or a rheumatic disorder from this. But our problem is a compromised BBB. And these bad T/B cells are misguided and can get on the myeline. This is the second progressive phase.



In this second phase things like insulin, insulin sensitivity, cytokines, insulin resistance, etc become important.
See for example: http://www.stemcelltherapies.org/multip ... osis_3.htm the paragraph on the leaky gut syndrome
or http://www.kennislink.nl/publicaties/af ... -donorpoep the paragraph on LPS-productie (In Dutch but Google Translate version below)
LPS-producing
Besides the effect on weight Vrieze also examines the influence of intestinal flora on insulin sensitivity. They, inter alia, investigates whether the composition of the intestinal flora influence on the production of lipopolysaccharide (LPS) in the intestine. This substance is released during the fermentation process. LPS, which stimulates inflammatory responses via cytokines, contributes to insulin resistance. Thus the body responds less well to insulin, leading to type 2 diabetes.

Vrieze: "I ​​wonder if the new intestinal flora after the transplantation of poop in lean men also affects the LPS-production and thus on the sugar. If so, then we may have a new target to inhibit the production and type 2 diabetes to address. "
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take things out of their narrow neurological context!!

Postby Leonard » Fri Mar 16, 2012 2:21 am

Biogen Idec takes option to MAKScientific MS program

general-discussion-f1/topic19495.html

interesting, they are going down the path of receptor health/functioning.
and interesting to see that lipids play their role here too..

http://en.wikipedia.org/wiki/Cannabinoid_receptor

still, I remain convinced that a narrow neurological approach is not the right way.
where the problem really originates in the gut and that it is precisely there where 'they' should start..

in my view, 'they' should take things out of their narrow neurological context!
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the pedagogic form determines the image

Postby Leonard » Mon Mar 19, 2012 3:44 am

.. Science does not deal in all possible laboratory manipulations. Instead, it selects those relevant to the juxtaposition of a paradigm with the immediate experience that that paradigm has partially determined. As a result, scientists with different paradigms engage in different laboratory manipulations. The measurements to be performed on a pendulum are not the ones relevant to a case of constrained fall..

... This is not to suggest that pendulums, for example, are the only things a scientist could possibly see when looking at a swinging stone. We have already noted that members of another scientific community could see constrained fall. But it is to suggest that the scientist who looks at a swinging stone can have no experience that is in principle more elementary than seeing a pendulum. The alternative is not some hypothetical "fixed" vision, but vision through another paradigm, one which makes the swinging stone something else...

... it is hard to make nature fit a paradigm. That is why the puzzles of normal science are so challenging and also why measurements undertaken without a paradigm so seldom lead to any conclusions are all. Chemists could not, therefore, simply accept Dalton's theory [of chemical reactions between atoms] on the evidence, for much of that was still negative. Instead, even after accepting the theory, they had still to beat nature into line, a process which, in the event, took almost another generation. When it was done, even the percentage composition of well-known compounds was different. The data themselves had changed. That is the last of the senses in which we may want to say that after revolutions scientists work in a different world.

quoted from the intellectually highly stimulating book The Structure of Scientific Revolutions, Revolutions as Changes of World View, Thomas S. Kuhn

The book then carries on with The invisibility of Revolutions, "We must still ask how scientific revolutions close. .."

Drawing a parallel with our little world, my own "opinion" (as described in the first posting) is probably as good as the "opinion" of neurologists who have built a huge model around 'auto-immunity' that has never been proven however. My own opinion certainly matches my own experiences during my MS "career", it fits within the factual observations and a vast amount of literature, it fits with the diabetic predisposition seen in my family etc etc etc. 'Auto-immunity' does not.

Let's just hope that it will not take another generation "to beat nature into line" this time.
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different mechanisms underlie

Postby Leonard » Mon Mar 19, 2012 6:57 am

From: http://onlinelibrary.wiley.com/doi/10.1 ... 3596.x/pdf

Conclusion: .... These findings allow to support the hypothesis that different mechanisms
might underlie progression of disability in relapsing and progressive onset MS.


Well, to hear this conclusion from the horse's mouth is earthshaking ...
They are (re)inventing the wheel here.
For further background: see this entire thread....


Incidently, it strikes me that the article is a bit peculiar in several ways. Firstly, I find that the contents of the article is somewhat disconnected from the Conclusion. Almost as if this part of the Conclusion was introduced at a later stage...

Also the use of the word "allow" is strange because the conclusion could have been written perfectly well without.
Then, why would you write it like that? I think you do that if someone has raised the specific question (possibly from a negative attitude) about whether different mechanisms might underlie MS where the authors felt they needed to respond to that question, be it very cautiously (allow to support ... the hypothesis ... might ...) ...

So great, the good thing is they are thinking! :smile:
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