This Is MS Multiple Sclerosis Knowledge & Support Community

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In the other direction, I'd be interested to hear some ideas about how MS might lead to occluded jugular veins ... the other direction makes more sense to me but I am open to ideas.

I can't find much about how the veins might close up, but perhaps somehow the veins are damaged, made stiff or brittle and prone to collapse and stenosis?

Bob-
The following is the story of how my vascular studies affected my view of MS. It is a work in progress. You are giving me an opportunity to share it again. Thank you for that!

Have you ever read the paper I put together on my research of the endothelial layer of blood vessels, and how our modern society has radically changed nitric oxide levels in just the last 100 years? Almost 500 people have downloaded it- I'll post it again-
link to Endothelial Health Paper

I wrote it well before the Zamboni was published, and I stand by it. This paper is how I met Dr. John C. Cooke at Stanford University, I sent it to him for his feedback. Dr. Cooke, an endothelial researcher, addresses these issues about modern man and our hampered vascular systems in his book, The Cardiovascular Cure. At the time he read my paper, he wasn't sure there was a connection to MS, but he thought it looked like a good program. Months later, I sent him the Zamboni research, and he immediatly connected me to Dr. Dake.

I spent several months on that research, and what I learned was that many of the nitric oxide disrupters that change the endothelial layer and affect vasodilation and coagulation are things such as:
depressed vitamin D levels, saturated and man made fats, viruses, bacterial infections, plastics and PCBs, diesel fuel, heavy metals used in oil refining and mining, mercury in amalgam fillings, cortisol created by stress, high glucose levels, pesticides. The list of nitric oxide disrupters is a veritable list of modern life.

I believe that there is a genetic defect- as Marie says, like crooked teeth in a tight jaw - there is a tight space for the jugular and azygos veins in a very small percentage of the population. It takes a long time for these congenital venous anomalies to result in reflux and damage to the brain and spine. Modern life adds a new level of strain, as the endothelium is damaged, blood is hypercoagulated and the lining of the veins is repeatedly injured.

This is a scientific theorum....although the research regarding the endothelium is proven fact in reference to the cardiovascular system- the connection to MS is still being made. If you or anyone else have any questions after reading my paper, I'll be pleased to answer them.

cheer

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Lyon wrote:So that there isn't a long, pregnant pause here, I'm responding that I'll read your paper and afterwards will edit this post with the response.
Bob

Terrific! And the response was to the line-
"not that there is any possible way that CCSVI can be the cause of MS..."
just so we're clear. I have spent over a year of my life on the vascular connection, my husband is healing and doing well after his stent procedure, and I continue to work for the healing of MS patients. I found that offensive.
cheer

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Lyon wrote:
Interesting paper. I like and respect, but disagree, with the line of reasoning. Not to seem dense or persistent for the sake of being annoying, but how does any of that prove "cause" even if CCSVI is found in 100% of people with MS?

Bob

Thanks, Bob. Now that you've read the paper, I can address your questions from the vascular viewpoint. Remember, I understand venous occlusions/stenosis to be congenital, and the endothelial disrupters to be the variable in the equation. This is only a theorum....
Also, I should preface this all with the comment that I think it is funny to try and take the new peg of CCSVI and make it fit into the hole of MS studies. Nothing has been shown to be 100% in all of MS studies...except CCSVI. And I've often said, my California husband, with lots of sun, just shouldn't have MS according to the "studies". But he does. He also had closed jugular veins.

Considering that MS was so rare as to be almost unheard of before the 20th century what led to the drastically increased incidence of CCSVI/MS rate in the "developed" populations, yet left the MS incidence to remain almost unheard of in the undeveloped populations?

Aside from genetic propensity in northern European populations to venous insufficiency (chronic venous insufficiency is more common in this population) endothelial disrupters of modern living as noted in paper.

What factors of the British occupation led to the CCSVI/MS outbreaks among the previously unaffected Faroese natives?

Again, genetic predisposition (the Faroese are northern European) to venous stenosis with added endothelial dysfunction created by industrialization, mining, higher viral rates due to intercourse with British -STDs- see paper

How is CCSVI responsible for the fact that someone migrating from a low MS incidence area to a high MS incidence area before the age of 14 will share the lifetime incidence rate of the area they migrated to and how is CCSVI responsible for the fact that someone migrating from a low MS incidence area to a high incidence area after the age of 14 will enjoy the low MS incidence rate of the area they migrated from?

Genetic predisposition + higher incidence areas tend to be at higher elevations, ie: Colorado (affecting nitric oxide/oxygen balance) with less sunshine (affecting vitamin D) both create endothelial disruption

How is CCSVI responsible for low MS incidence among indigent populations who live in close proximity to genetically similar populations living in "developed" conditions with much higher MS rates?

Less opportunity for MS diagnosis in impoverished communities, more exposure to endothelial disrupters in developed communities...wealthier people have access to alcohol, cigarettes, processed food, chemicals- all change nitric oxide balance.

How is CCSVI responsible for the increasing MS incidence among groups which, not too long ago, were considered not to have the genetic predisposition? (worldwide aboriginals, minorities in the developed populations, increasing oriental and populations on the African continent)

again- see paper re: industrialization and increasing endothelial dysfunction

And that is why I believe CCSVI is the cause of MS, and that better tools for diagnosis of MS (ie: more readliy available MRI technology) and the endothelial dysfunction of modern society leads to more cases diagnosed, and more people affected in the 21st century.

This is a new path, and there are many more connections to be made. Thanks again for the opportunity to reiterate these points, Bob-
cheer

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Please let me clarify what I was trying to say early and I will zip it. I just feel that we have so many newcomers to this forum looking for answers that we need to be careful how we represent our own personal beliefs. To share info on new studies, clinical trials, updates on how each of us are responding to different treatments,etc. is valuable to this site and everyone who reads our posts. I hope that Thisisms remains a place that we can challenge each other beliefs and theories in a way that is respectful. We also need to be careful that we do not start stating our beliefs as though they are facts unless there is scientific support to back it up that has been EMPIRICALLY proven. Please keep the discussion going Bob and Cheer because you guys bring out the best in each other (haha)! I read and reread your arguments and must say it took me awhile to process all the info but I think I got it! That Jesus analogy however.......

Lyon wrote: Proving that something is the cause of MS requires ALL of the pieces of the to fit, not just some, but I honor your efforts and I agree that it's still early and research in that regards continues.

No it doesn't. While I've been viewing the CCSVI theory with some healthy skepticism, if it proves out by showing refuced relapse rates and improved MRIs, I really don't care what happened on the Faroe Islands 60 years ago, or what happens in the southern hemisphere.

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Gollllleeeee. A peson can't go spend the day at the country getting a permit for a deck without everyone doing everything while you're gone.

it took me ages to finish this please excuse that it is about 10 posts late...

OK I am a big part of this because I have spent hundreds of hours on TIMS posting research and abstracts related to medical science for years. Years.

First and importantly.

Epidemiological evidence is the WEAKEST form of science. Epidemiology is the starting point for something to give you and idea where to look for your problem, not the ending point. So, when you talk about migration or increasing incidences of MS, you do not know why those things are happening only that they do happen.

For example: the increase in incidence in MS might be hygiene. Or pesticides. Or hydrogenated oils. Or antibiotics in our food supply. Or......

We do not know which of these play a role. And since you don't know which of these play a role, you also don't know how they impact the disease. It is just as likely that hydrogenated oils cause stenosis as is that it causes autoimmunity. The epidemiological evidence is not selective about which theory it endorses, it is up to further research to answer those questions. It is not scientific to say one theory about why that seems to be happening is smart and another one is a pipe dream without further research to further elucidate what is important about that.

Second, I have posted easily 50 references on this CCSVI forum related to how stasis ulcers develop and relating this speculatively potentially/theoretically to the MS lesion. People obviously have not read these and have not understood that this is what directs my interest in this. Somehow people seem to think it is merely that fact that stenoses occur that makes me think that MS lesions could possibly be caused by CCSVI, which is ridiculous and absurd in the extreme. that is not how I operate at all. The thread is full of scientific information and thought not mindless chat.

The literature such as what was posted in volume by me and Cheer here is the basis for all the research and theory to date. Don't kid yourselves, this is the model; CCSVI causing MS lesions and there are reams of reasons to think it is working that way not just the fact that lesions are present. These people are world class researchers, not janitors. They are looking at it from a very complex perspective. Dr Dake had a pile of papers on his floor that he had read that was at least 4 feet across and 10 inches deep when I was there. Hundreds and hundreds of papers. My gift to him was, believe it or not, three of my favorite papers.

For Bob who now all of a sudden wants to know something rather than to just throw "you are being dumb" rocks, (yes they hurt and that tone came from "ouch" sorry ) I say read the threads herein because it is clear you have not done so becasue you do not seem to understand this. 54 pages on the big thread it is not that much and a lot of research is in there. Both Cheer and I have posted a lot of material supporting this.

But you remind me of the person who comes on here and says 'bottom line this for me in one paragraph how does this cause MS?' You can't do that, it is unproven material as I have said time and time again (to the point of people telling me to quit saying that; we get it). You HAVE TO READ THE PAPERS, not just the Zamboni papers but the ones in the threads that discuss how the lesion MAY....MAY.....be the same as a stasis ulcer.

NHE I respect you very much and never have felt you to be unkind or provoking for no good reason but the bulk of MS knowledge to date is based on hypothesis and supporting scientific facts that seem to endorse the hypothesis...NOT on direct MS patient experiments.

For example, why do we think MS lesions are autoimmune? Is it because we gave people myelin and they developed MS? No; it is because the postulated theory is that MS is autoimmune, this deduced based on inflammation and the fact that in animals we can induce EAE and it is sort of similar. We also see that there is MMP9 and t cells and b cells in both so we assume that this too supports immunity being at fault. We also look at MS lesions and see macrophages full of myelin at the sites and this too we assume is the fault of immune activation. We also give people immune suppressives and some of them seem to do better at least a little better than placebo treated patients. All of this "circumstantial" evidence supports the idea that MS is autoimmune...and the bulk of it is inference.

BUT we have never, ever found the direct evidence of autoimmunity....the antigenic target and antibody that is primed to go into the brain and attack perfectly healthy tissue and destroy it. We have been perfectly capable of finding this in other AI diseases, so why not MS?

People are being treated based on a theory that is supported in general but not directly

SO let's apply the same standard to CCSVI.

First it appears all people have stenoses. And since this is new MS has not been evaluated from this perspective meaning that researchers need to take that into account FIRST and see what it has to do with other facts we know about MS like vitamin D and other epidemiological material.

Second, these stenoses are exactly like stenoses in other parts of the body. They act the same in that the body creates collateral circulation to try to get around them. They have pressure differentials across them so that the pressure on the back side of the stenosis is much greater than it should be.

Thirdly, stenoses with collateral circulation and pressure differentials CAUSE venous ulcers in the lower leg. There is absolutely NO dispute to that. You can't argue it. IT is fact and insurance companies pay to have such stenoses repaired. it does not matter that TIMS members or neuros never heard of it. It is fact. Hard and fast.

What happens IN LEGS is this:
The pressure differential because of the stenosis allows changes in the endothelium, this allows microcirculatory changes and tiny channels through the endothelium, which essentially makes it leaky. Endothelium is the blood vessel "skin" to make it easy to understand. Now the blood vessel leaks iron and other plasma and fluid into the tissue. These things DO NOT BELONG in the tissue so they are aggressively attacked by the immune system as foreign; all of a sudden t cells, b cells macrophages, MMP9 is upregualted, TIMP1 is downregulated ICAM1 is activated etc are invited to the area to clean it up. The result is a stasis ulcer that eventually scars into a hard tissue. Many of the abstracts I posted were related to these facts in leg ulcers.

We do not know what causes MS lesions but the extensive research into MS lesions shows exactly the same profile MMP9 up regulations, iron leaking into the tissue, TIMP down regulation, t cell b cells etc etc all in the MS lesion. In light of the research showing that CCSVI is present in all MS patients and knowing that such a stenosis CAUSES similar lesions in the legs is it not naive to say that this CAN'T be the cause of MS lesions?

The Big Idea by Zamboni on table one shows the lesion similarities. They are astonishing.

It does not prove that MS lesions are caused by CCSVI and we have never said it did, in fact I have said repeatedly it does not prove this. but

How can someone say that CCSVI CAN'T cause MS lesions when leg stenosis causes lesions that look the same from a pathology perspective..... you just do not have enough information to make that determination and it is premature and naive to say that.

Why is MMP9 upregulation in a stasis ulcer understood to be a normal reaction to the venous pressure to experts in the field when in an MS lesion it is considered evidence of autoimmunity------AND once you know ccsvi is present, doesn't this change everything? Doesn't it demand that everything we thought we knew about MS lesions be reevaluated in light of this new material?

Is it foolish for a person who is aware of the fact that there is stenosis and a lesion in head and who also knows the stenosis in legs causes a lesion that is pathologically similar to the head lesion to think they are the same pathology possibly? Isn't it likely that they ARE the same pathology? At some point isn't it incumbent on the person saying they are not the same to prove that--?

The fact is that I have understood from about the first week how these were probably related and saw the possibility therein and have posted and posted reams of material on this to either explain or debunk it.

I find it ironic that people seem to say that we are only NOW having a real debate about this when I was dying for people to read those papers and comment on it...........

I did so because I don't have any options left and I wanted to know for myself if this was at all possible. It appears that it is absolutely possible, thank God. I am not saying this is the cause of MS, I am saying it MAY BE and scientists will need to do more on this.

People who have volunteered to be seen and treated have put themselves out there the same way that anyone in any trial has done. Did you know the people who signed up for the early Campath trial with SPMS got worse? you have to be brave to get out in front like that.

New ideas are new. Not proven but some of us with little to hope for but a bed need new ideas.

I am not trying to be unkind just to clarify. Please forgive anything that seems to have tone to it, I don't mean it to be that way.

Stasis ulcers have been increasing in incidence by the way.
Stasis ulcers also have increased prevalence in spring and fall. MS does that too.
Just food for thought.

Lyon wrote: What I've done my best to point out and what keeps getting overlooked is that I'm NOT saying that CCSVI isn't something to hold high hopes for or that treating CCSVI can't offer improvement in MS, but that CCSVI is far from being proven the "cause" of MS and even if it's shown to have 100% association with MS and even if treating it does offer symptom relief doesn't prove or even strongly hint causation.

Again....Proving that something is the cause of MS requires ALL of the pieces of the puzzle to fit, not just some

Actually you've gone further than this:

but that there is no reason to consider CCSVI the "cause" of MS.

Although they are theories, there have been reasons put forth to consider how CCSVI might cause MS. Although the CCSVI theory has been pushed pretty hard in this forum, from what I have seen, no one is saying this is definitely the cause of MS. But I don't see how it can be dismissed either. True, it doesn't fit with all the pieces of the puzzle. But science rarely does. Maybe some day it will. But, if you're waiting for some grand unified theory of MS, which answers all the questions, I'm afraid you'll be waiting for a very long time.

Marie said:

Epidemiological evidence is the WEAKEST form of science. Epidemiology is the starting point for something to give you and idea where to look for your problem, not the ending point. So, when you talk about migration or increasing incidences of MS, you do not know why those things are happening only that they do happen.

Thanks for that point, Marie. Epidemiology- the study of "what is upon the people"- is meant to help us understand where to look for causation. It is not meant to be construed as puzzle pieces that must fit for an answer as to cause. These environmental studies were merely made to illumine the path, but they are not the path itself.

And you are correct to remind us that we have disease models for lesions in CCSVI already documented: stasis venous ulcers and congestive venous myelopathy. They are a scientific fact, not theory.

Here are the papers and research Marie has compiled for us. Before picking up the next stone, please read them.
http://www.thisisms.com/ftopict-7098.html


cheer