I am opening this thread to discuss possible connections between the material on the CCVI thread in the general discussion forum and CPn.
Rather than quote all the material for that 16 page forum thread, I'll assume readers have read the discussion over there, found here
1. Zamboni did blinded research on large numbers of patients in three studies that shows venous abnormalities in 100% of MS patients. There appear to be strictures in the azygous or jugular vein that "back up" blood flow in the same way a stricture in the femoral vein "backs up" blood flow in the leg and causes venous ulcers.
2. Zamboni and Schelling do not say where the strictures that cause the venous back up come from.
3. Several researchers have proposed that MS lesions and venous ulcers are the same kind of injury, supporting the idea venous backups play a role
4. venous ulcers, while they are known to be related to a stricture in the femoral vein, are not well understood. Exactly what causes the minute changes that eventually mean an ulcer is not known, but relieving the femoral stricture helps a lot.
While my personal belief is that MS is a CPn connected problem and that the intriguing results of Zamboni's work shows that MSers have venous problems in the brain, I see these problems as not at all mutually exclusive. Here I paste something I posted on the other thread that shows Dr Stratton's work on venous ulcers in a published paper:
The stratton work on venous ulcers is here http://www.nature.com/jidsp/journal/v6/ ... 0063a.html
the genus, Chlamydophilia, as obligate intracellular pathogens, induce chronic scarring in humans. Chlamydia pneumoniae, a common cause of pneumonia, infects endothelial cells and circulating macrophages. Evidence that C. pneumoniae is an opportunistic pathogen in chronic skin ulcers and other inflammatory skin conditions analogous to its role in atherosclerosis is reviewed.
That was added to the thread because NAPAY asked for the research Stratton did on venous ulcers and CPn. This shows that Stratton at least has proposed a connection between these venous ulcers and CPn. If venous ulcers are like MS lesions as Zamboni proposes, this is expected isn't it?
There is absolutely every reason to imagine CPn COULD be involved in this pathology (the strictures and the proposed "venous ulcer-like" idea of MS lesions)
CPn is present in arterial plaques always and for years has been considered an emerging pathogen in cardiac disease by the CDC.
So CPn is a good candidate for being involved with several known issues in this pathology we are talking about on this thread: endothelium is directly impacted by CPn, CPn is known to be involved with vascular plaques, etc etc. I hope they look for it if they send any removed tissue from the stricture area to pathology if such is needed in an individual case.
NO signaling and CPn and atherosclerotic plaques
from here http://circ.ahajournals.org/cgi/content ... 102/9/1039
Conclusions—C pneumoniae impairs arterial endothelial function, and the NO pathway is principally involved. Cyclooxygenase-dependent vasoconstricting products may also account for the infection-induced impaired relaxation. These findings further support the role of C pneumoniae infection in atherosclerosis development.
S with regards to CPn/MS/venous strictures I am thinking that;
1. the strictures might be caused by CPn--atherosclerotic plaques are caused by CPn, why not venous ones?
2. if venous ulcers can be caused by CPn in some research like Stratton and Mitchell's, and we already know MS lesions are caused by CPn in those same minds, there is no reason at all to assume the overall BIG PICTURE pathology is not similar....both a stricture AND a CPn induced lesion at the area of the backup.
It is obvious that some people can, and do, get better with just abx. There is no reason to assume this somehow negates the idea of MS being treatable with abx, obviously Sarah, Katman, Mack and others have had great results. Perhaps they can dissolve the plaque that causes the stricture as well as stopping that "something unknown"
that causes the MS lesion.
But as Stratton mentions above "scarring" is caused by CPn, it is entirely possible that some people have too much scarring so the venous issue remains stubbornly in place in spite of CPn treatment. THUS, BY THIS PROPOSED TOTALLY UNPROVEN MECHANISM BY TOTALL Y SPECULATIVE ME, IT IS POSSIBLE THIS IS THE REASON SOME PEOPLE HAVE TREATMENT FAILURE ON CAP. I am one of those people.
I see the way forward as this:
1 get the venous issue assessed and see if I have a blockage as Zamboni proposed.
2 Get treatment if possible to restore blood flow
3 continue abx and expect a much better outcome with blood flow normal
There is absolutely no way success in my case can prove anything at all: the Zamboni people will see it as success of the venous issue, and any abx I use will be seen as of uncertain value. And I am certain some people will get right in there to remind me that abx are antiinflammatory.....
Empirical treatment is fraught with problems because you can't prove cause by effect: just cause I get better does not mean the reason I am better is what I suppose it is.
But in the end, if I'm better, who cares?!
I'm following my own lights for MS treatment and my main criteria for doing something is that it is safe, has a resonable and supported hypothesis and its side effects are in line with its PROVEN effectivenss.....That's where the "standard" therapies beyond the first tier CRABS fail. the side effect profile is way to terrible for the minimal results they offer.
While CAP is light on the clinical study side of things because no one has put 100 MSers on either abx or placebo for 4 years to see what happens, it is way high on the safety side.
Plus abx have shown effectiveness in terms of them to ther therapies like Mino to copaxone or doxy to interferon, so there is additional reason to look at it in a positive light.
I hope others will add to the ideas I have offered here.