I put this on another site for thoughts and feed back and I am in the midst of a thinking and searching process. I do believe that there is a link with viruses or bacteria, there has to be, we are probably 15-20% bacteria ourselves and the balance between good and bad bacteria and MOST importantly is the bacteria's ability to modify and adapt to the environment in a very short space of time. Bacteria can evolve their DNA in days, add DNA from their attackers eg antibiotics and immune system to avoid detection. Lots to know and the book by Stephen Buhner is amazing!!!!!! huge learning opportunity!!!!!!
I disagree with the assumptions formed in this study. There are parts that ring true with my experience on ABx in regard to the Immune System transporting CPn around the body and CNS, and also that Inflammation areas harbour the first sights for CPn to 'breed'.
The challenge is to find the 'best' method of detecting CPn infection rather than to assume that one test answers all questions about CPn involvement in MS.
Paul Thibault do you have any thoughts?https://www.facebook.com/paul.thibault.37?fref=ts
"In conclusion, our results are in line with the results reached by the meta-analysis
of other studies in this field, and may suggest that CPn probably plays a bystander role in the pathology of MS. Past exposure to CPn is nearly equal in MS and
controls, but owing to infecting immune cells, CPn is more frequently detected in
the site of inflammation (CSF) as evidenced by PCR. This view is also supported
by studies which show that use of antibiotics active against CPn is not associated
with a decreased risk of MS and that MS patients do not benefit
from antibiotic treatment against CPn. (1,24)"http://www.m-hikari.com/asb/asb2012/asb ... 8-2012.pdf
Reply from Paul;
This study supports the involvement of Cpn in MS although the authors prefer to side with the argument that it is a secondary invader. Progress in the management of MS will only occur when it is looked at in a new light. The common thread of all those that deny the new paradigm is that they avoid the reality of the involvement of the venous system in MS, and assume that the disease is pimarily one of auto-immunity against myelin - a concept that is obviously flawed when one considers all the known evidence.