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One Theory To Explain Them All? The Vagus Nerve Infection Hypothesis for Chronic Fatigue Syndrome -

Gijs

Senior Member
Messages
690
Yes - infections and other 'stressors' can prime and/or activate microglia which can be measured using a PET scan.

This poster presentation claims to have confirmed microglial activation in ME/CFS which would be A BIG THING :

http://ras.ni.brain.riken.jp/neuros...keyword=&key_start_disp_num=0&key_disp_num=10

Unfortunately I've not come across a full published paper.

Hi Marco, i don't see any 'confirmation' i only see an old study from 2011, is this correct or do you mention another upcumming new study?
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
Hi Marco, i don't see any 'confirmation' i only see an old study from 2011, is this correct or do you mention another upcumming new study?

Sorry Gijs - bad choice of words. I meant microglial activation has been a suspicion of mine and others and this appeared to have 'confirmed' that suspicion (subject to replication of course).
 

ramakentesh

Senior Member
Messages
534
Viral infection of the nerves is also a leading hypothesis for a common complication in fibro and ME, small fiber polyneuropathy. It would also explain why antivirals work, but its harder to explain why Rituximab works using this model.

Actually no, nearly all etiological theories in relation to pathological small fiber neuropathies are based on genetic abnormalities and an autoimmune etiology in many (b cell mediated inflammatory response via cytokines).
 

ramakentesh

Senior Member
Messages
534
If it quacks like a duck, it probably is a duck. CFS acts like an autoimmune disease - triggering stressor, fluctuating relapsing remitting course, preliminary response to b cell depletion, increased female to male ratio.
 

ramakentesh

Senior Member
Messages
534
there is some evidence that the vagus nerve can mediate central parasympathetic withdrawal, cns vasoconstriction and reduced brain blood flow. But its very preliminary
 

lansbergen

Senior Member
Messages
2,512
If it quacks like a duck, it probably is a duck. CFS acts like an autoimmune disease - triggering stressor, fluctuating relapsing remitting course, preliminary response to b cell depletion, increased female to male ratio.

Would you call a reaction to a misfolded form of a cellulair protein, an autoimmune disease?
 

Legendrew

Senior Member
Messages
541
Location
UK
When I first read this hypothesis I found it intriguing however I think it too novel an idea to prove true in the majority of patients. As Ramakentesh stated above, ME just seems too much like an autoimmune condition for something like this to be a leading hypothesis. However I do still feel the vagus nerve is adversely effected hence resulting in symptoms such as ibs type problems due to the link with the enteric nervous systems. The more I read the more I feel the autoimmune response is targeted towards the functioning of the HPA axis, specifically small peptides that activate the hypothalamus; this as a result could cause a vast array of autonomic dysfunction, a dysfunctional stress response and vascular issues - all without an inflammatory problem and without any major organic damage.
 

Wally

Senior Member
Messages
1,167
It will be interesting to see when the Montoya/Lipkin cytokine findings are released if any of the theories that have been floating around become clearer or seem less likely. I have no opinion either way, since my science brain was left back in my college biology class about 40 years ago. :nerd: However, I am hopeful that some of the new findings coming down the pike will open up new and/or old avenues to explore. :balanced:
 

rosie26

Senior Member
Messages
2,446
Location
NZ
@Wally did Montoya/Lipkin say when they were going to publish.? I don't know how these things work. Would it be less than 2 months away.
 

Wally

Senior Member
Messages
1,167
They are hoping to be published before the symposium/conference they have planned at Stanford on March 19th. Here is the thread about this event. http://forums.phoenixrising.me/inde...and-translational-research.27055/#post-418719

You will be able to see from the agenda that Ian Lipkin is slated to talk, as well as a few other notable people (i.e. 1) Phil Bronstein - former editor of the S.F. Chronicle, former husband of Sharon Stone, and an unfortunate victim of a painful bite by a Komoda dragon (see, http://www.sfgate.com/news/article/Chronicle-editor-bitten-at-L-A-zoo-Komodo-2910148.php), 2) Dave Tuller - former staff writer for the S.F. Chronicle and the N.Y. Times, I believe Dave is currently a freelance writer who is also a visiting or associate professor at U.C. Berkeley's School of Journalism and Public Health (see, http://www.theopennotebook.com/2012/01/18/david-tuller-cfs/) and, 3) Erin Allday (medical/health writer for the S.F. Chronicle (http://www.sfchronicle.com/author/erin-allday/) and the reporter who wrote a story for the Chronicle back in May 2011 about the ME/CFS Patient Demonstration held in front of the HHS Offices in S.F (see, the blog "Thoughts About Me" at http://thoughtsaboutme.com/2011/06/...stration-at-hhs-san-francisco-on-may-25-2011/), where this article is discussed) - unfortunately I have been told that this article (and the multitude of comments received in response to the article) is no longer available from Chronicle's online newspaper site (SFGate.com). Some day, I will see if I can dig out my hardcopy of the article and post it online unless someone else can find a copy already floating out in cyberspace that can be copied and filed away in the Forums "wiki" stash :nerd:).

Wally

P.S. Seems to me that you would not bring this group of people together for such a symposium unless you thought you could release some important information to the news media, the medical community and the public. Just my guess - but in the past I have had some fairly good guesses about what may be simmering on the stove. ;)
 

Wally

Senior Member
Messages
1,167
Yes. I will also be attending the 4 day ICFSME Conference in S.F. on the 4 days that follow the event at Stanford. :hug:
 
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MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
When I first read this hypothesis I found it intriguing however I think it too novel an idea to prove true in the majority of patients. As Ramakentesh stated above, ME just seems too much like an autoimmune condition for something like this to be a leading hypothesis. However I do still feel the vagus nerve is adversely effected hence resulting in symptoms such as ibs type problems due to the link with the enteric nervous systems. The more I read the more I feel the autoimmune response is targeted towards the functioning of the HPA axis, specifically small peptides that activate the hypothalamus; this as a result could cause a vast array of autonomic dysfunction, a dysfunctional stress response and vascular issues - all without an inflammatory problem and without any major organic damage.

There is a theory that autoantibodies to ACTH, which is required to produce cortisol, are a factor in ME. We know that there is a mechanism whereby leaky gut can lead to autoimmunity, so it could be: leaky gut leads to autoimmunity which leads to autonomic dysfunction (and other dysfunctions such as mitochondrial dysfunction, perhaps due to autoantibodies against HSP60).

There's a thread about the ACTH issue here.