This Is MS Multiple Sclerosis Knowledge & Support Community

Cece wrote:Sorry, 1eye, you are right. The others seemed to have steered the conversation back on track; I was hoping for scatological humor next....

I know a music-therapist who used to work in a rock and roll band played by all doctors. They were called the Star-tools. For some reason or other.

1eye wrote:I know a music-therapist who used to work in a rock and roll band played by all doctors. They were called the Star-tools. For some reason or other.

Dr. House in that band?

1eye wrote:Here's a study: Have 1000 MS patients pee in a bottle.

Have 1000 normals pee in a bottle.

Measure for MS prevalence by taking a reading of the hemosiderin levels.

Blind the test so that nobody knows who is who.

If anyone has abnormally high hemosiderin and 'MS" offer them the Liberation treatment. Do this blinded. See who says yes.

I wonder why that hasn't been done already? Sounds like a quick, relatively inexpensive procedure.

It would also be interesting to measure the hemosiderin levels of healthy people who also have CCSVI. Sorry to go on about this other group (indications are that between 10% and 22.4% of all healthy people have CCSVI) but they interest me so much. If Zamboni's claim is true, that CCSVI raises hemosiderin levels in urine, then surely they must have the same hemosiderin levels as MSrs (assuming the severity of the CCSVI is the same). If they do, it would be interesting to know if they also have the same kind of free iron deposits close to the vascular system that have been found in all MS patients, and if not, why not?

There's no doubt whatsoever that free iron deposits are present in the brains of everyone with MS - but are they there because of CCSVI? If non MSrs with CCSVI were found to have the same kind of iron deposits it would suggest that the iron deposits are there as a result of CCSVI, not MS.

If, on the other hand, non MSrs with CCSVI were found not to have the same kind of iron deposits seen in those with MS, it would suggest that CCSVI doesn't give you the iron deposits - MS does.

Unless...just thinking aloud here...there is a "special type" of CCSVI that causes MS, perhaps the most severe cases of CCSVI, or CCSVI that occurs in certain veins? That seems pushing it a bit, but there's still the possibility that there's some other factor, or unknown catalyst, that crucially occurs in a minority of CCSVI cases which then results in the free iron deposits and MS. That crucial other factor could be something like a gene or virus.
But on the otjher hand, why would this gene or virus need a weakened venous system to work its way into the equation? If it were a virus, or faulty metabolic process in the mitochondria of nerve cells, would it not be just as likely to pick on a healthy vascular system?

If you switch all this round and imagine that the gene, virus, or faulty metabolic process comes first in the genesis of MS, then for me in all gets just that little bit more plausible, e.g. the presence of a virus like EBV somehow activates the immune system > this causes inflammation and disrupts nerve metabolism > this results in poor iron metabolism > free iron deposits > diseased nerves > altered blood flow

It's still the chicken and egg thing. I'm not completely dismissing the theory that CCSVI is a factor in the cause of MS, but the only way it could possibly make sense would be if there is another, as yet unknown, factor to make it all happen in the first place. What worries me about that - is that even if the veins are fixed, that same factor could make the disease come back again.


gainsbourg

so is hemosirin hard to test for? Could I say run down to my gp's today and get it looked at?

concerned wrote: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?

First they'd need to establish that hemosiderin is indicative of CCSVI. That would be an easy enough study as well. Am I right in understanding that it's been proven to an indicator of CVI? Are levels markedly raised in CVI, all the time or only some of the time?

Cece wrote:First they'd need to establish that hemosiderin is indicative of CCSVI. That would be an easy enough study as well. Am I right in understanding that it's been proven to an indicator of CVI? Are levels markedly raised in CVI, all the time or only some of the time?

Yep. A little wee wee in a cup and walla.... results! At least I think

http://www.jvascsurg.org/article/S0741- ... 1/abstract

Edit: Oh! Take a look at the authors!

Edit2: Wow, this is interesting:

A score of 0 or 1 was associated with successful surgery, whereas a score of 2 or 3 reflected persistence of reflux.

So hemosiderin test could not only be a simple test for CCSVI, but also for a successful treatment!

lol and wow, cah! So Zamboni at least is aware of this as a test!

But would hemosiderin be present in CCSVI for the same reasons as it is in CVI?

BRILLIANT with it being used as a test for whether the venoplasty was successful or not.

If I've got this right, hemosiderin is a form of iron that builds up when blood hangs around where it's not supposed be. It happens in Chronic Venous Insufficiency (CVI) and is now thought to also happen in CCSVI.

You'd expect that the longer venous reflux goes on the more iron would build up. What puzzles me about all this is that if MS is caused by venous weakness, why does MS not get more common as people age? After all, incidence of CVI, which is also thought to be congenital, gradually increases with age.

The older people get, the weaker the vascular system becomes, and the more common venous problems like CVI get - therefore you'd expect MS to become much more common as people go into middle and old age as the venous system stops performing so well. Incidence of CVI gradually increases and peaks at around 50, whereas the average age of MS onset is much younger, between 20-40, peaking around age 34.

On the other hand you could say it accounts for why MS often worsens with age.

gainsbourg

gainsbourg wrote:If I've got this right, hemosiderin is a form of iron that builds up when blood hangs around where it's not supposed be. It happens in Chronic Venous Insufficiency (CVI) and is now thought to also happen in CCSVI.

Thought by us here on the forum or by the actual docs?

Sometimes we are ahead of them....

People with chronic venous insufficiency have:

* Redness of the legs and ankles
* Skin color changes around the ankles
* Varicose veins on the surface (superficial)
* Thickening and hardening of the skin on the legs and ankles (lipodermatosclerosis)
* Ulcers on the legs and ankles

Anyone have redness or color changes on their neck? Also the use of doppler is very effective at diagnosing chronic venous insufficiency. I looked and found nothing online stating that people with chronic venous insufficiency have an excess of iron in their body. Maybe I am comparing apple to oranges but it does seem that this thread is comparing CVI to CCCSVI.

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

Do you have a search filter that excludes all results containing Zamboni?

http://www.ncbi.nlm.nih.gov/pubmed/12514590

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? Based on his previous research, wouldn't a simple urine test have confirmed his reflux hypothesis? Unless I missing something.