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There would be another way: Living donor liver transplantation An example: MS father with a MS child. Then in many cases one could use part of the liver of the mother to treat /cure? the MS child. This would be a feasible way for a study and possible treatment. But it's clearly a high risk surgery -...

Maybe this is part of the puzzle:

http://www.msrc.co.uk/index.cfm/fuseact ... ageid/1775

R.

That's interisting. I am not an expert, but is seems that from time to time there are no recipients found for donor organs. In a study with an appropriate database one could try to match such a liver to someone with MS. I think there would be enough MS volunteers (EDSS>5) for a liver transplant stud...

Infection ALONE must be wrong.

Because the probability that MS parents transfer the disease to their children is close to 10%.

http://www.neurology.org/content/69/12/1208.abstract

So there must be a congenital part (a metabolism dysfunction?).

But may be it's an/the important trigger.

R.

You are right, there are many problems and open questions for such a study.

But if such a study would show that some pwMS are cured, that would be one of the hugest steps in MS research ever.

R.

Thanks for this link. "CONCLUSIONS: Combination immunosuppression with tacrolimus may have a beneficial effect on MS.” reflects the mainstream thinking. The phrase ….beneficial effect on MS … is misleading, because the result was extremely positive. So, immunosuppression with tacrolimus should ...

Because this one case is so outstanding, a small study should be done - let's say with 10 pwMS (EDSS>5).

It will be hard to find many other cases with EDSS 5 to symptom free after 3 years.

R.

If one looks into the linked paper from cheerleader http://endo.endojournals.org/content/144/6/2201.full.pdf one can see in the images that the liver plays an important role in the metabolism chain. So again: After a liver transplant the EDSS of a woman decreased from 5 to less than 2. After 3 years...

Venous leg diseases are often congenital. First symptoms / problems start in many cases in the age of 20-30. MS has the same “timing”. This is a strong argument pro CCSVI as a major risk factor for triggering MS but clearly no proof. Perhaps CCSVI may be caused by MS and the treatment only optimizes...

I think different risk factors may trigger different forms of MS:

gene
and/or
CCSVI
and/or
Virus
and/or
….
and/or
liver metabolism defect (my guess)

Because a woman went from EDSS 5 to zero in 3 years after a liver transplant.

R.

Very interesting.

Before talking about CCSVI one should give this to a "sceptical" neuro.

R.

If MS is triggered by some type of drainage disorder, a trauma may be an additional risk factor nothing more. When one identical twin has MS the other will get it with a chance of 30%. There is a STRONG genetic correlation. The important point in this study is that it points to a drainage / pressure...

This is very interisting.

So the autoimmune response could be the inheritable co-morbidity (typically in RRMS), that is trigged by some biomechanical disorder from CSF flow and/or CCSVI.

Trauma alone can not explain the inheritable part.

R.

@ badcopy: Give him this link :
http://www.ccsvi-tracking.com/index.php

Here are graphs for balance, mobility, edss.... from over 800 treatments.

I think it is a better idea to concentrate all data at one place (ccsvi-tracking.com)
because the largest database is the most reliable.

R.

There is an interesting point in his story: His blood test showed that he has a deficit of Glutathione. Look here for more information: http://en.wikipedia.org/wiki/Glutathione http://en.wikipedia.org/wiki/Glutathione_synthetase_deficiency http://www.ei-resource.org/treatment-options/treatment-infor...