This Is MS Multiple Sclerosis Knowledge & Support Community

cheerleader wrote: Therefore, it may well be that CVI is a potential trigger factor for localized scleroderma. In addition, localized scleroderma may only develop if a certain amount of trigger factors are present – and resolves if one or more of the contributing factors (i.e. CVI) can be treated.

Replace "localized scleroderma" with "multiple sclerosis" and that's how we should think about MS, imho.

Anyway, here's more on CVI and collagen.

Varicose vein disease is a common condition. Its pathology is not well characterized. A disor ganization of smooth muscle cells and extracellular matrix components in the venous wall have been described. The objective of this paper is to offer an explanation for the abnormal distensibility of varicose veins. The content of hydroxyproline was quantified in control and varicose human saphenous veins. The synthesis of collagen types I, III, and V was quantified in cultured venous smooth muscle cells and dermal fibroblasts of control subjects and patients with varicose veins. The proportion of collagen type III in the heterofibrils composed by collagen types I, III, and V was calculated. The level of hydroxyproline was increased in varicose veins, suggesting an increased content of collagen. This augmentation of collagen in diseased tissues appears to be correlated with an increase of collagen type I since the collagen I mRNA was overexpressed in varicose veins, whereas collagen type III mRNA was not altered. The quan tification of collagen synthesis in cultured cells shows that proportion of collagen type III was significantly decreased in cultured smooth muscle cells and dermal fibroblasts derived from patients with varicose veins. The results indicate a deficiency in collagen type III in patients with varicose veins. Since collagen type III is involved in tissue elasticity, these results offer an explanation for the abnormal distensibility of varicose veins. Moreover, this defect seems to be generalized in different tissues and argues in favor of a genetic alteration of remodeling in these patients.

Perhaps the lower collagen III in the vein explains why sometimes the vein won't expand with angioplasty. (I'm sure it's more complicated than that, just trying to sound smart )

Last night PBS ran a show called "A sense of Wonder" about Rachel Carson, she wrote Silent Spring - a warning about the dangers associated with the indiscriminate use of chemical pesticides and their potentially adverse effect on the environment and human health. A couple of memorable quotes were,

"I was assembling wildly scattered facts never before looked at together in relationship to one another."

"Work was fun, like putting together an enormous jigsaw puzzle!"

I know I’ve read Dr. Zamboni saying the same two sentiments above in his own personal way.

And I’ll leave you with this last, exact quote of hers.

“If facts are the seeds that later produce knowledge and wisdom, then the emotions and the impressions of the senses are the fertile soil in which the seeds must grow.”

Loved the quiet confidence, wonder, grace and undettered determination of that women. Kind of reminded me of a few of the traits I admire in one of our own members here at TIMS.

Lora

cheerleader wrote:And Dr. Dake's comment to Jeff sticks with me, "Your veins are sticky, the lining is like glue. Never seen anything like this."

This sounds worrying.

"This collagen switch between type 1 and type 3 occurs in some genetic connective tissue disorders, and is present at birth."

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If for some of us the vascular problems are due to pathological reasons (i mean other than bones pinching veins,malformed veins from birth and such) as these findings suggest, wouldnt the problem exist in all our veins? By Dr Dake's comment i do not understand if the same situation could be present anywhere in the vein system. Did he say anything about that?

"Connective tissue in MS switches from collagen I to collagen III and this takes place in the IJVs"
Why only the IJVs?
What about the Azy?

For some reason it looks like a long shot to me. I cant imagine for only 2 veins to get affected by "something" genetic or not. Such kind of disease would manifest elsewhere too leading to another diag on top of ms. Except if i cant read so good in this case.
On the other hand, Sclafani says that he has encountered problems in smaller CNS veins also...right on!!!


Thoughts by someone who apparently does not know better.

Thanks Cheer,
I always found this information very interesting. Thanks for bringing it back in front of us

costumenastional wrote:wouldnt the problem exist in all our veins?

For all we know it does. MSers could just as well have a systemic venous issue that leads to a host of other problems (hemorrhoids, CVI in the legs...?), but the jugular veins and azygos vein just cause the most immediate and disabling symptoms.

Costume....
this switch in collagen could be congenital, or it could be secondary, due to inflammation or venous hypertension. I think it will be important going forward to understand why some veins are different. Not all will be affected by the congenital nature of a connective tissue disorder. I don't think anyone should freak out about Jeff's "sticky veins" and the possibility of this affecting everyone in the same way. Dr. Dake said it to Jeff...not everyone he saw. As the study Ikulo posted states...varicose vein disorder is still not completely understood. Why the collagen switch? Is it genetic or situational? More research needs to be done.

In CCSVI, we've seen cysts, bone impingement, veins damaged by accident or injury, malformed valves, fibrous blockage, missing veins, and transient stenosis--I really believe every situation will be unique, and every solution for treatment will be unique, as well. THis is why it is so important to have a relationship with a local vascular doctor. CCSVI treatment is turning out to be far from one size fits all. And this is why it is important to have doctors like Dr. Gabbiani looking at jugular veins in MS patients. And more research.
cheer

Thank you both!!!
Check this out if not already:


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Hi Dr Sclafani

Thanks for all the time you give us!

My question is and you may have covered this before - but it is a real anxiety I have about the treatment - Is it possible for the valves to be damaged during the procedure thus making the situation worse as one poster on this site reports. I think his vein was found on initial examination to be wider than normal.

My brother when treated for blood cloths was found to have an abnormal venous system in his abdominal cavity and sticky blood syndrome so Im hopeful that Dr Simka will find something to explain my ms.

Thanks and regards

Maureen
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not to mention my hemorhoids...
sweet!

Me too! I'm shouting out in my corner, thank you cheer and everyone adding to the research. I'm trying my best to make sense of it all, (cheer you mentioned you talked your way though high school science lab..I cheated my way through senior chemistry...a lot of good that does me now), but I'm following as best I can.
I am astonished at how the relationships are starting to be seen, and by people, laymen and women on this site. And like Barbara I too feel stimulated by being so involved in my own disease!

Peace,
Z

This is so interesting. I remember seeing more than a few folks who had really large jugulars in their MRVs, and then there are those with none, those with really tiny jugulars like my wife's.

I wonder, is it possible that that over time, as a vein tries to compensate for the venous hypertension due to stenosis, that the body initiates this change in collagen to make the veins more rigid and resilient. A person with CCSVI could start out with fairly normal size veins, then over time they could get larger due to the venous hypertension, then perhaps the collagen alteration occurs to compensate for the extra pressure on the vein, and again over time this change could in-turn compound the effect of CCSVI making the veins less pliable, more prone to re-stenosis after ballooning, and less responsive to angioplasty in general.

Very interesting to see where this thread of research goes.

That is an interesting abstraction, Johnnymac. I never cease to be amazed at the incredible intelligence, and adaptability of our bodies.

I have MS and Ehlers-Danlos Syndrome (Type III - hypermobility) and find this collagen connection fascinating! I've met several people online who have both MS and EDS and it seems that incidents of MS are higher in those with EDS (EDS tends to get diagnosed sooner than MS, which I suppose is why they say it in that order.) I know my jugulars are constricted and am trying to find someone to open them. If I can ever find a doctor willing to talk with me, I cannot wait to hear what they think of this!

bluesky63 wrote:Cheerleader, I really appreciate your efforts -- everyone's efforts! -- in bringing out this research. I have a son diagnosed with Ehlers-Danlos, as well as many, many family members with varying issues that all make sense when viewed through this lens.

It is so exciting to think that we are getting closer and closer to understanding how everything fits together -- and most important -- how to get healthy and keep the kids healthy.

I would do anything to keep my children from going through what I have experienced.

Hi Mseds--
thanks for posting...I'm sure you know much more about EDS, having lived with it. There's a vascular form of EDS, and I know the cardiovascular side of it has been studied, but not the potential affects on the venous system. Might be something to talk about with your doc who diagnosed you with EDS?
take care,
cheer

Though I am not a reasearcher, to me the answer seems very obvious: MS starts with a substantial decrease in Type I collagen production, the one that is mainly found in the 3 enveloppes of the brain, the blood-brain barrier, and the blood vessels... Following this decrease, the body tries to compensate and uses the main type of collagen present in the body which is type III. So basically, there is NO conversion but rather a COMPENSATION... The other possible way of compensating is that the body uses type II collagen, thus creating a shortage in that one too and resulting in bones and articulation problems. That is the reason why many MS sufferers develop rhumatoid arthritis also, which a lack of type II collagen...
So instead of asking wrong anjd endless questions, we have to get the doctors work on the right ones:
-what goes wrong with the production of type I collagen that results in MS?
-Is it an autoimmune process where the body destroys it or is it a decrease of its production like diabetes can be a decrease of insulin.... by the way, isn t it interesting that diabetes can result in nerve pain, blindness, loss of sensation and paralysis... doesn t that sound familiar?....But although there are at least two types of diabetis, they can be well managed if not cured...
- How does the compensation process impact the brain and venous tissues? in the whole body and not just in the jugular veins of course...
- finally wouldn t this be the best track to follow? I am absoulutely certain that the solution to MS is as "simple" as insulin to diabetis... with carefull monitoring....
Najat