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