Terry wrote:Hey Bob,
This seems a good time to ask. Where do I find info on Faroe Island/MS that includes timeframes? I always just find an overview, but I'd like to see more detail.
finn wrote:Lyon wrote:...and Finn from the grave!
"The rumors of my death have been greatly exaggerated".
It's great that dignan's posts have kept this thread alive. Now at least it's clear that Prineas et al are questioning both autoimmunity and Lucchinetti's theory. Interesting.
dignan wrote:It's not "MS 101"
I dropped the Zamboni paper published in Dec 08, on Prof Pollards Desk, so we know he has at least seen this one.dignan wrote:... or it could be that they wrote this paper before some of the more recent Zamboni and Simka papers were published.
as some of you might remember, after a serious disagreement on this board eighteen months ago, I got angry and removed all my messages. After reposting one of them few days ago, I checked them all to see if there was something else worth reposting. IMO, there was. As a member of "MS is not an autoimmune disease -camp" I'd like to share following two posts with you again.
The first post underlines the issues and questions related to MS research that I still find important. The second post contains selected quotes of a hypothesis published two and a half years ago. In it Maggs and Palace challenge the theory of inflammation as a cause of demyelination and axonal injury. They state that "suppressing inflammation does not appear to significantly slow disability – inflammation may even be protective for nerves."
This is how I summarized my own opinion then, and I still think the same way:
"What if axonal damage causes demyelination and inflammation, not vice versa, and inflammation occurs only when the system is still able to protect itself? In the light of my current knowledge it seems to me that the less inflammation in lesions, the more progression of disability. So the amount of possible protective elements such as hormones, endorphin, unsaturated fatty acids, and vitamin D in the system at the disease onset - and maybe sometimes also during the disease course - together with the level of genetic susceptibility to MS might have a crucial effect on disease severity.
I tend to believe in the Occam's razor, and think that usually "one should not make more assumptions than the minimum needed". So my guess about the pathology of MS is this: One cause, one trigger, but multiple factors that have an effect on disease progression and severity. I am just glad I don't have to try to prove it "
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