Does MS cause CCSVI?

[cah]

I looked and found nothing online stating that people with chronic venous insufficiency have an excess of iron in their body.

That's exactly what the study I mentioned above says.

To Redness and Thickening and things like that: I think the main difference simply is gravity. If you have a slight blockage in the veins in your neck, then gravity still does a part of the job. But if you have a blockage in the veins of your legs, the "pumping" might be insufficient and so the problems are more "physical".

But maybe that's just an oversimplified view from a layperson.

[gainsbourg]

Since Zamboni presumably would be aware of his own research, isn't the lack of hemosiderin testing in his CCSVI study conspicuous by its absence?

The same things bugs me about Zamboni's initial finding that all 177 healthy people in his first study did not have CCSVI - why hasn't he attempted to replicate this finding and silence the critics? Especially when so much of his argument depends on it.

We know that there are iron clusters around the vasculature in MS - these clusters may or may not be there because of poor venous drainage. Some believe that this iron is causing MS (CCSVI > IRON > MS) but there is also the possibilty that the MS disease process is causing the iron clusters in some other way. Zamboni's argument is that CVI is associated with similar iron clusters, so why not CCSVI? However, there is also the possibility that the clusters are there for a completely different reason, or that even if they were found to be there because of CCSVI, they are not involved in actually causing MS.

What other reason could there be for the iron clusters? Perhaps because of iron overload as a result of faulty iron metabolism. It was discovered a couple of years ago, that there is metabolic disregulation causing iron overload in MS (Abo-Kryshna 2008). It's a hugely complicated area to understand unless you are an expert in iron. Every nerve cell needs oxygen to work properly - so hemoglobin (oxygen bound to iron) is used to transport oxygen to wherever it is needed. Once the hemoglobin gets to the neurons things seem to go wrong in the metabolic process in those with MS. There is a protein called transferrin receptor (TfR) that is found in the endothelium wall of capillaries. It is a kind of docking mechanism for iron within each cell - the means by which iron is allowed in, for example to facilitate energy release. TfR decides the amount of iron taken up by nerve cells. Abo-Kryshna and his team discovered that iron overload was occuring in the brains of those with MS, and that this was due to very much higher levels of TfR.

http://www.ncbi.nlm.nih.gov/pubmed/18408021

Does this metabolic difference occur as a result of the MS disease process? Could it be part of MS pathology? Does it result in an overspill of iron in surrounding tissues? Could it be intended as a benign balancing act, e.g. to provide extra iron for myelin repair? Who knows, but I can't make this discovery fit in with the venous reflux theory of MS - maybe someone else can .

Faulty iron metabolism causes a demyelinating disease very similar to MS. Friedreich's Ataxia is a rare, hereditary disease that has syptoms very similar to MS. The faulty iron metabolism is caused by a defective gene.

Restless Leg Syndrome (common in those with MS) is also now known to be caused by faulty iron metabolism.

Similar free iron deposits to those in MS are found in Parkinson's Disease, Alzheimer's and other neurological diseases.



gainsbourg

[Billmeik]

lots of talk along these lines in sweden today

cheers take:

http://www.facebook.com/note.php?note_id=447000732210

[Bethr]

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

"Hemosiderin may deposit in diseases associated with iron overload. These diseases are typically diseases in which chronic blood loss requires frequent blood transfusions, such as sickle cell anemia and thalassemia."

Hmmm not sure where the chronic blood loss fits into the MS equation. Would anyone like to clarify?

The whole piece from wiki:

Hemosiderin deposition in the lungs is often seen after diffuse alveolar hemorrhage, which occurs in diseases such as Goodpasture's syndrome, Wegener's granulomatosis, and idiopathic pulmonary haemosiderosis. Mitral stenosis can also lead to pulmonary hemosiderosis. Hemosiderin collects throughout the body in hemochromatosis. Hemosiderin deposition in the liver is a common feature of hemochromatosis and is the cause of liver failure in the disease. Deposition in the pancreas leads to diabetes and in the skin leads to hyperpigmentation. Hemosiderin deposition in the brain is seen after bleeds from any source, including chronic subdural hemorrhage, Cerebral arteriovenous malformations, cavernous hemangiomata. Hemosiderin collects in the skin and is slowly removed after bruising; hemosiderin may remain in some conditions such as stasis dermatitis. Hemosiderin in the kidneys have been associated with marked hemolysis and a rare blood disorder called paroxysmal nocturnal hemoglobinuria.

Hemosiderin may deposit in diseases associated with iron overload. These diseases are typically diseases in which chronic blood loss requires frequent blood transfusions, such as sickle cell anemia and thalassemia.

[Billmeik]

Problem is...CCSVI exists. And it exists early in the MS disease process. Other doctors are finding it in early MS and clinically isolated syndrome. I've told the story of Dr. Dake testing the daughter of one of his first patients, and finding she had occluded veins, even though she did not have an MS diagnosis. She later had an MRI, and there were the white matter lesions. Dr. Dake treated her with angioplasty, even before she ever had an official MS diagnosis. The other daughter had great veins, no CCSVI and no MS. And Dr. Zivadinov told a similar story in Bologna, about the daughter of an MS patient in his study who was part of the healthy control group. Sure enough, she had CCSVI and it was a few months later she showed white matter lesions on MRI and received an MS diagnosis. And this is happening world wide.

another tale that comes to mind is from georgetown where a kid presented with mild ms and bad ccsvi. These anecdotes need to be collected in a paper that counters the one presented the other day in sweden . Along with the bone stuff, and the fact that the study on cis patients was done by someone who coesnt have a lot of experience finding ccsvi in general...it's close.

[Billmeik]

ok lets say ms does cause ccsvi. The question beomes why does the blood stop in the jugulars? why wouldn't the stenosis occur in the heart and cause ms patients to have bad hearts.

I mean if there are no congenital blockages, but just scarr cells washed down from the brain that have a 'clenching' effect they use to close wounds but also cuse stenosis..

So this theory of ms->ccsvi needs a reason for why the blood would stop and cause stenosis where it is. My idea is that blood becomes stopped in some people while asleep. Mini apnea. The stopped blood has time to play havoc on the veins.

hmm. is there literature on blood flow while sleeping?Proving blood doesnt stop proves ms->ccsvi is a long shot.