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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.
Terry

Just a note, this is also considered in the ABX discussion, regarding the introduction of new bacteria.

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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.

-finn

Thanks for stopping back in, Finn. You left TIMS around the time I started learning, reading, researching...and your posts always confounded me and subsequently inspired me to learn more. Hope this means you'll rejoin the discussion!
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Bob, I'd like to read that. I would very much appreciate your sleuthing through this issue. I think David mentions it here.

Finn! It's good to see you post again. As you may have noticed, I'm a fan of this thread you started. It's not "MS 101", but once you get through learning some of the basics about MS, I think this thread provides so many good links and posts for anyone wanting to get a rundown on a lot of significant MS research.

dignan wrote:It's not "MS 101"

Hey! That was my thread, soooooo long ago. Still linked below. Ken

dignan wrote:... or it could be that they wrote this paper before some of the more recent Zamboni and Simka papers were published.

I dropped the Zamboni paper published in Dec 08, on Prof Pollards Desk, so we know he has at least seen this one.

Thank you Cure, that could turn out to be the pivotal moment in the history of MS...or at least a pretty good one...

Well, just got back from my consult with Prof. Pollard. He remembered the original paper I dropped, but does not see how it could cause MS, and hence is not a convert. I quickly tried to described Dr Simka's original response to Zamboni's article explaining how (non laminar flow ect ect). I dropped & left the preliminary results paper on his desk this time.

Prof Pollard's basic response was that he is going to ECTRIMS in 4 weeks in Düsseldorf, and if its new and exciting in MS, it will be presented there. I had no idea of ECTRIMS, so when I got home I checked, and found CCSVI is only presented as part of the "Poster Viewing" section. ie no specific session is allocated. DOH!

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Lyon wrote:Bump, because I'm trying to re-read it and I can't find it otherwise.

Why not just bookmark it in your browser?

NHE

These 4 functional medicine practitioners all mention inflammation as fundamental to diabetes, obesity, fatigue (thyroid hormone problems), Alzheimer's, menopause problems due to hormone imbalance.

Dr. Susan Blum suggests most important minerals for thyroid function: zinc, selenium, iodine

http://www.doctoroz.com/videos/fatigue- ... age=2#copy


Because of the common tie of inflammation with MS this information may fit with this thread, "Inflammation vs. neurodegeneration."

The mention of insulin comes up often, as in "estrogen causes insulin production" (per Dr. Wendy Werner).

finn wrote:Hi,

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 "

be well.

-finn

Just wanted to bump Finn's wonderful thread from many moons ago. As more researchers looks at gray matter loss and neurodegeneration (which precede demyelination and inflammation, and continue after they are long gone in progressive MS) it appears Finn's thesis is being confirmed.

I've compiled research showing how hypoperfusion can lead to ischemic injury, mitochondrial dysfunction and neurodegeneration. And how reperfusion injury, the body's attempt to return blood, glucose and O2 to tissue, mirrors what happens in RRMS. It's on Facebook, for those who are over there. If anyone isn't, and would like a copy, let me know. Won't take up space on Finn's thread.


it's one explanation (certainly not the only one) of how neurodegeneration precedes the immune activation, and why inflammation is a temporary process. Thanks again to Finn for coming back and returning his thread...it's a good one.
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