This Is MS Multiple Sclerosis Knowledge & Support Community

I think that MS may have several underlying causes; and that there is not one solution for MS.

One of the causes of MS is definitely a mitochondrial energy failure as I have described on this thread - the whole picture just fits together too good; but another cause could well be an aggressive immune system. The latter could be treated by bone marrow transplantation (as in the Toronto experiment – another thread on TIMS refers) or by the manipulation of white blood cells (see the link below); the former by FMT or diet (FMT stands for Feacal Microbiota Transplantation of feces transplantation).

As the article under the link below says, it is likely that it is not only MS but also a host of other autoimmune and allergic diseases that could be treated in a similar way. The matrix then turns from diseases described by their symptom syndromes (MS, rheuma arthritis, diabetes, perhaps ALS…) to disease groups that are cause orientated (mitochondrial energy failure, aggressive immune cells, …).

This re-classification of diseases will be a big step forward and at the same time imply a huge change for the medical world. The latter may give resistance, and that would be unfortunate because the patient is to benefit...

http://www.northwestern.edu/newscenter/ ... m_campaign

I think with Lyndacarol and Vesta that gluten is an issue; I know several people who do better after they started a gluten-free diet, who are even on a recovery path...

I think that complex long-chain carbohydrates are the problem. Just like (very) long chain fatty acids can be a problem. The gut microbiota does not break down these molecules sufficiently and -just like with (very) long chain fatty acids - immune complexes then leak into the blood stream leading to low grade inflammation. All the rest follows...

I think that the Carnitine production by the liver (or the depletion thereof) and other regulatory functions come into the picture here as well. It may explain why the new liver of the Caucasian women helped her overcome MS...

I had myself tested on gluten intolerance/coeliac disease. The blood test did not show a gluten intolerance though. Notwithstanding, in the meanwhile I understand that the blood test is far from reliable and that up to 80% of the population may have some form of intolerance...

The finding of this study is earthshaking; it is basically what I have argued since January 2011 and what underlies the thinking on this whole thread.

http://www.ncbi.nlm.nih.gov/pubmed/23595117

quote TRAF2 elevation in RRMS reinforces the concept that different pathophysiological and immunological processes sustain RRMS and SPMS or PPMS.

As far as I'm concerned, you may find how the story ends on page 1, 1st posting....

The new concept for MS already mentions the Boston study in relation to environmental factors such as exposure to heavy metals (even of previous generations) and related genetic factors of veins.

This link gives an another study on the same subject and concludes "The number of people with MS among former Mesita students is twice as high as expected, based on national estimates."

http://www.dshs.state.tx.us/epitox/elpasostudy.shtm

the story of my family's exposure to heavy metals on
http://www.thisisms.com/forum/general-d ... 22492.html

The new concept for MS claims that "Many years of venous obstruction in the drainage of the cerebro-spinal (CCSVI) will weaken the important tissue (endothelium) in the finest capillaries and the lymphatic system of the most affected areas in brain and spinal column".

This statement by Paolo Zamboni goes into that same direction:
... the venous system is closely related to cerebrospinal fluid dynamics, as well as to the arterial and lymphatic system of the head.

http://www.pagepressjournals.org/index. ... 013.1/1255

The CCSVI concept has raised a great deal of controversy and debate in the medical community, see e.g. http://msj.sagepub.com/content/19/7/855.full versus http://msj.sagepub.com/content/19/7/858.full

MS should be looked at as a bigger concept, in a holistic manner. It does not make any sense to look at individual conditions such as CCSVI in isolation. As the conclusion under the second link says: The introduction of quantitative criteria that can define the degree of extra-cranial venous structural and hemodynamic impairment in future multimodal approach studies should be preferred to the use of a binary CCSVI diagnosis.

I think the first posting of this thread gives a holistic picture of what is MS which is plausible, highly consistent. I feel sad to see a medical community struggling and only grudgingly coming along with such view, thereby loosing so much valuable time and energy.

Leonard wrote:This article postulates that bacteria in the sinus flora may be a factor in MS. In particular staphylococcal immune complexes are suspect.
http://www.sciencedirect.com/science/ar ... 4813000059

....

I do believe that the sinus infection is a factor in MS although it is not clear to me whether the sinus infection is causal or whether the infection is part of a bigger syndrome caused by weakened endothelial conditions in a bigger part of the head...

Whow, this is a beautiful article! It gives an answer to the above question and a whole lot more. In fact, the many years of ccsvi causes distortion of the venous hemodynamics in the head, preparing the condition for neurological disorders including MS...
The dural sinuses empty into the internal jugular vein. Needless the say what happens if they are blocked...

http://www.biomedcentral.com/1741-7015/11/142

quote:

The cerebral venous system is often viewed simply as a series of collecting vessels channeling blood back to the heart, yet it also plays an important role in the intracranial hemodynamic/cerebrospinal fluid (CSF) regulatory system (hereafter simply referred to as the hydrodynamic regulatory system), a role that is often overlooked and that appears to influence both perfusion of the brain parenchyma [1,2] and the dynamics of the CSF system [3-5]. Although the physiological mechanisms associated with cerebral-venous outflow are poorly understood, abnormalities of the venous system have been implicated in a variety of neurological disorders, including multiple sclerosis (MS) [4,6-11], leukoaraiosis [3,12-16], vascular dementia [5,17], and normal-pressure hydrocephalus (NPH) [2,3]. This raises intriguing questions about the involvement of the venous system in these pathophysiologies.
...

From the data it can be seen that in patients with MS, there is a general reduction in the volume of the vascular bed, which, if approximated to a series of parallel round tubes, equates to a mean reduction in cross-sectional area of the vessels of about 8.4% in patients with MS. According to Poiseuille’s Law, it can be calculated that the 8.4% reduction in average cross-sectional area equates to an approximately 19.3% increase in hydraulic resistance. Given that the blood-flow rate is directly proportional to the hydraulic resistance, this means that the reduction in CBV seen in patients with MS, is more than enough to account for the 15.6% reduction in CBF reported by Varga et al.. According to equation 1, hypertension in the dural sinuses would tend to reduce the pressure gradient pushing the blood through the cerebral veins, which in turn would tend to inhibit blood flow. However, when we consider that the CPP is normally in the region of 70 to 90 mmHg, it is unlikely that venous hypertension of less than 5 mmHg, such as that associated with CCSVI, could account for the large reduction in WM CBF reported in patients with MS [18-21]. Hence, this suggests that the reduction in CBF in patients with MS is probably due to morphological changes in the cerebral vascular bed, rather than a straightforward reduction in perfusion pressure arising from raised pressure in the venous sinuses. However, this does not preclude the possibility that the reduction in CBF may also be due to changes in behavior of the Starling resistor associated with the cortical bridging veins.

unquote.

well, in my own case the reduction in cross-sectional area was over 90% relative to normal where I think a much higher degree of obstruction than 8.4% is typically true for many MS patients.

MS then is caused by a combination of ccsvi and - after mid age - a bad gut as explained in the first posting of page 1 of this thread.

The informative postings of Caveman on the last several pages of this thread still resonate through my head. It is useful to read the postings a few times to fully appreciate the flavour of the comments and the thinking behind. I am sure we have only just begun to understand the influence of our diet on the health of our gut micro biota and how this may affect human health, even across the boundaries of generations.

In this same context, the influence of (highly-dense) a-cellular carbohydrates in particular gluten on the gut working is intriguing. I searched a bit more on this and found that "no real epidemiological studies support the theory that for populations who eat whole grains the incidence of MS is higher than in populations who don’t; indeed the reverse seems to be true" (see page 2 of http://www.overcomingmultiplesclerosis. ... Code=11098 , with all respect for George Jelinek, I love his work and much appreciate what he has done for us and is still doing for us)

But I believe this analysis is fun-da-men-tal-ly flawed. Patients with MS have a fundamentally different condition than the average citizen, in the sense that their BBB is compromised. Large epidemiological studies on big populations, although they can be very powerful in themselves, will never reveal that effect as it is not statistically significant and side conditions are extremely difficult to manage and thus these studies may easily lead to erroneous or misleading conclusions.

The theory on the gluten intolerance is very interesting. If particles are not sufficiently broken down by enzymes in the small intestine (the body food supply) T-cells will be produced and these T-cells continue to multiply. The epithelial layer of the small intestine is damaged and becomes permeable. T-cells proliferate and cause endothelial cells to release cytokines. The bad working of the small intestine probably also influences the micro biota in the next part of the intestine (which is for vitamin production and absorption, minerals etc).

The theory on coeliac disease seems very interesting and appropriate here. Actually, it is surprising that people have not made a much stronger connection between MS and coeliac disease.

some strong zinc connections there - structural integrity of the gut, required to digest gluten, diversity/composotion of gut biota, building block of enzymes, etc etc etc

I picked up this article from one of Caveman's last postings above http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402009/

The article explains why either the Swank diet (low fat) or the coeliac diet (avoid dense acellular carbohydrates) or a combination of both work for people with MS, and it explains a whole lot more.

I think you can also turn things around and argue that the fact that the Swank diet and the coeliac diet work for people with MS reinforces the theory under the article.

The article leaves me speechless...
In combination with the broken BBB which results from ccsvi, I think we have come here to the root cause of MS in its progressive form...

here is one more of the same category
http://www.wheatbellyblog.com/about-the-author/
http://www.amazon.com/Wheat-Belly-Lose- ... 1609611543

you might ask: what has this got to do with MS?
to which I would say: E-VE-RY-THING! for the second progressive phase.

if you open the book on Amazon, you can see from the table of contents the diseases mentioned: diabetes, asthma, arthritis..
well, progressive MS falls into that same category.

Toward a unified theory of receptor blockage?

The theory so far has been that a weakened endothelium is vulnerable to further (insulin and leptin) receptor blockage, causing problems to cellular nutrition (see 1 st posting on 1 st page). This happens in the RR phase by infectious agents (Cpn, EBV, sinus induced staphylococcal infection). The theory also holds that inflammation then is a re-action to poor cellular nutritional conditions, and designed to remove the infectious agent.

Extending this line of thought, in the progressive phase lectin activity from (highly dense) cereal grains may also impair insulin receptor and leptin receptor activity http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1326203/ , cause poor cellular nutrition and – as a re-action – raise inflammation.

Again, inflammation is not seen as a direct causal factor but a re-active phenomenon to poor nutritional conditions, fully commensurate with earlier thinking on this thread. Furthermore, while insulin has been the primary focus for study, leptin regulation (the "fat thermostat") may be as important and wiped out before the insulin regulation degrades.

The effect of blocking receptors may be aggravated by Lipopolysaccharide (LPS) and non-LPS making receptor blockage more "sticky" and persistent (re: the double hit of highly dense a-cellular carbohydrates and fat). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402009/ A strong immune reaction to LPS would seem to hint into that direction. Also, the lectin binding properties apparently involve saccharide on cell membranes suggesting it is the complex of things (above paper contains very interesting thoughts on the role of lectin in evolution and why it binds as it does).

The immune system reacts with endothelial cells being bombarded by "auto" reactive T-cells produced and multiplied in the gut and trained to fight wheat/gluten/lectin particles which break through the gut lining as of mid age. This might explain the T-cell "recognition" of the lectin agents on the cell membranes / receptors, in fact crack the "auto-immunity" nut. The fact that many immune diseases start as of mid-age when the gut lining breaks and the fact that different pathophysiological conditions underly the RR and progressive phase of MS are a powerful confirmation of this line of thinking...

The process of cleaning up damages the receptors/cell membranes and hence impairs mitochondrial working. More and more mitochondria will fail, maintaining the charging of the ion pump becomes increasingly more difficult, eventually if enough mitochondria fail the cell will die and if enough cells die the nerve will disintegrate.

Of course, the compromised BBB caused by ccsvi and an overstreched windkessel mechanism is a pre-requisite for the processes to take place as they do.

Leonard wrote:Terry Wahls writes in her book Minding My Mitochondria that "The health of our mitochondria affects the health of nearly every cell in the body. … Mitochondrial failure drives the development of diabetes, heart disease, lung disease, heartburn from stomach acidity, Alzheimer's, Parkinson's, many psychiatric disorders, and Multiple Sclerosis." …

I think this is true, very true. I think that mitochondrial stress and eventually failure underlies the progression for a majority of MS cases. Where an over-active immune system as is now being addressed by bone marrow transplantation (e.g. in Toronto, see another thread on this forum) is responsible only for a minority of MS cases. In addition, there are obviously the infectious agents, mainly responsible during the RR phase (see e.g. 1st posting page 1 on New Concept for MS).

The mitochondrial energy failure can be addressed by feces transplantation. In fact, and that point is also mentioned in the above article from the NYT but it is not further developed, the insulin sensitivity and the leptin sensitivity of all cells in the body can be greatly increased by feces transplantation. As the Amsterdam experiment shows ( http://www.cvgk.nl/legacy/bestanden/cvc ... rp-def.pdf ), even doubled in 6 weeks time. At the same time the permeability of the gut barrier will be reduced. As the NYT article elaborates and as can be found in the links below, the fat metabolism in the gut holds the key. (I guess Swank's low fat diet comes into the picture here as well).

If you do a Google search on mitochondrial energy failure insulin sensitivity leptin sensitivity you find many articles on how the gut microbiota influences the sensitivity of the cells.

http://www.plosbiology.org/article/info ... io.1001212
Our results emphasize the role of microbiota in the complex network of molecular and cellular interactions that link genotype to phenotype and have potential implications for common human disorders involving obesity, diabetes, and even other immunological disorders.

http://care.diabetesjournals.org/conten ... /2277.long
connect an altered microbiota composition to the development of obesity, insulin resistance, and diabetes in the host through several mechanisms: increased energy harvest from the diet, altered fatty acid metabolism and composition in adipose tissue and liver,..

http://bfg.oxfordjournals.org/content/e ... 4.abstract
The contribution of the gut microbiota to the development of several diseases (e.g. obesity, type 2 diabetes, steatosis, cardiovascular diseases and inflammatory bowel diseases)..

http://www.ncbi.nlm.nih.gov/pubmed/21933985
We conclude that specific gut microbiota modulation improves glucose homeostasis, leptin sensitivity, and target enteroendocrine cell activity in obese and diabetic mice. By profiling the gut microbiota, we identified a catalog of putative bacterial targets that may affect host metabolism in obesity and diabetes.

I haven't been following this thread but i found this article as it relates to gut microbiota....

14. Conclusion
This paper presents an exhaustive review of the toxic effects of the herbicide, glyphosate, the active ingredient in Roundup®, in humans, and demonstrates how glyphosate's adverse effects on the gut microbiota, in conjunction with its established ability to inhibit the activity of cytochrome P450 enzymes, and its likely impairment of sulfate transport, can remarkably explain a great number of the diseases and conditions that are prevalent in the modern industrialized world. Its effects are insidious, because the long-term effects are often not immediately apparent. The pathologies to which glyphosate could plausibly contribute, through its known biosemiotic effects, include inflammatory bowel disease, obesity, depression, ADHD, autism, Alzheimer's disease, Parkinson's disease, ALS, multiple sclerosis, cancer, cachexia, infertility, and developmental malformations. Glyphosate works synergistically with other factors, such as insufficient sun exposure, dietary deficiencies in critical nutrients such as sulfur and zinc, and synergistic exposure to other xenobiotics whose detoxification is impaired by glyphosate. Given the known toxic effects of glyphosate reviewed here and the plausibility that they are negatively impacting health worldwide, it is imperative for more independent research to take place to validate the ideas presented here, and to take immediate action, if they are verified, to drastically curtail the use of glyphosate in agriculture. Glyphosate is likely to be pervasive in our food supply, and, contrary to being essentially nontoxic, it may in fact be the most biologically disruptive chemical in our environment.

http://www.gmfreecymru.org/pivotal_pape ... ial37.html

Any thoughts..???

Sorry my quotes are not coming out right

Bob

I am not sure about the toxic effect of herbicides.
I think the problem lies deeper, in what mother nature has designed as protective mechanisms as this video tells:


gluten, grain, lectins, it is all in the same basket:
http://trulyglutenfree.co.uk/2013/01/15 ... all-three/
http://www.greenmedinfo.com/blog/gluten ... ult-health

if you search a bit on lectin gluten the response is just amazing.

as the last link tells, it would not surprise me if lectin would in some way lie at the basis of what is called "auto-immunity" and indeed MS.
see also my previous posting above that explains how properly trained T-cells in the gut cause havoc in the brain.

whow, please have a look at this book! this book puts a wider and good historic perspective on our carb society. I read it during my holidays.

http://www.amazon.com/Good-Calories-Bad ... d+calories

In the book, which was on the NYT best seller list, Gary Taubes argues that the problem lies in refined carbohydrates, like white flour, easily digested starches, and sugars, and that the key to good health is the kind of calories we take in, not the number.

we should amalgamate this account with the recent knowledge and perspective on lectins, pick up the pieces and rebuild the Lego house.

I don't know whether any of this matters but I feel a bit like these wonderful people must have felt when they had recorded this beautiful song.