Nevertheless, there is NO PROOF of an autoimmune connection to MS. So as soon as a doctor shows me that, I will shut up.
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fact there is no proof that MS is autoimmune.
There are myelin active T cells................ but there are myelin active T cells in any kind of trauma to the brain, spinal cord injury and stroke both have large increases in myelin active T cells.
Ongoing trauma would result in ongoing myelin active T cells.
Oligoclonal bands are also not specific to MS.
The most recent research on the cutting edge in multiple sclerosis is done Barnett et al in 2009 and they confirm yet again that the oligodendrocytes died when there are no immune cells at all in the area.(their first paper was in 04)
It appears that the macrophage that goes into the lesion area -- so frequently offered as "proof" that MS is autoimmune-- is actually there to clean up the oligodendrocyte that died first.
Such activity by the immune system is a normal reaction to damage.
When I say "it appears" that's a fact. No one has disputed the Barnett et al research however and there is no counter research, but theoretically you can apparently still find a way for autoimmunity to be part of this process that appears to be normal immune reactivity.
Dr. prineas himself in an interview with the Australian multiple sclerosis society after he received the Charcot award mentioned that he thought perhaps the oligodendrocytes could have died as a result of "standby damage" such as what is seen in Devic disease.
In Devic disease, the astrocytes is attacked by a very specific cell but the oligodendrocyte ends up dying as a side effect of that.
Dr. Prineas was wondering if there is some factor in the serum that causes the oligodendrocyte to die, then the immune system goes in to clean up starting the whole process that we have always been told is MS but with this other as yet undescribed and theoretical factor in the serum as the real culprit in MS.
in this case it is an elaborate Rube Goldberg type of deal that they have no idea what the first event was.
Is it possible it is hypoxic damage caused by venous insufficiency that is the first event?
I have been waiting for Prineas to say what he thinks. I wrote to Barnett at his public email about 12 months ago and got a one sentence response of no he didn't see how veins could have anything to do with MS....
it is a lot to get your head around when you never ever read any research in the field of venous insufficiency. If not, you cannot know how it triggers immune system activity that damages the tissue and is very VERY similar to MS immune system activity, and instead you just think of venous insufficiency as vericose veins that make ankles puff up.
Of course puffy ankles seem ridiculously unrelated to anything like MS which is viewed as orders of magnitude more complex.
The problem is specialization and clique-ish medical specialties.
I am writing a book it is under contract already.
It is about 300 pages and is about all this stuff and nearly done.
I am never here any more because I am darned busy........
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