I Bloss, Thanks for checking in
I am making my way through the treatment slowly. There probably won't be any positives as such for a while yet. The bacterial or infection load takes time to gradually be removed. If it is done too fast the endo-toxin load can kill. So the Protocol is designed to be gradual and safe.
There are side effects from both the ABx and the secondary effect on body systems.
The Abx is quite minor things like very acute sun sensitivity and some rashes.
The secondary stuff is from the endo-toxins produced by the bacteria when they die. It's quite an interesting science lesson to understand and it is this that causes the more severe symptoms.
Sadly there is no magic pills and you have to go with flow.
We have 6 NZers on the Protocol now and we have our own online private support group and direct link to Paul Thibault as well. So there is a warm feeling amongst the group.
I am very positive that something good will come of all this there are many research papers to explain the process which is a relief to know that the method is working, who I will be in a year or two is an unknown of course, the Goal for me is to stop the progression.
Hope you are doing ok too Blossom, I often think about the Family here when I hear of News around the World
Not sure if I put this link on this thread, and it helps to connect the article about ALs, MS etc and CPn. Keeping in mind that Medical Science understands the processes of 0.04% of Bacteria and we have well over many Trillion that make up our 'body'.
When you think about it there are more bacteria than our 'own' cells, if they all talked we would be in the shit!
"Endothelial cells in CCSVI are stressed by the Vascular dysfunctions in MS and other de-generative diseases, when you add an infective bacteria there will be complications and symptoms.
Monocyte Stickiness and heart disease
Monocytes are large immune cells that eventually turn into
macrophages, the garbage collectors of the immune system. Before
they turn into macrophages, monocytes drift along in the
bloodstream, eating a germ here, a dead cell there, and generally
behaving themselves. In the course of their travels they brush
against the endothelial cells in our arteries, bounce off, and continue
to drift. Occasionally, however, a monocyte will stick to an
endothelial cell, then creep into the wall of the artery where it turns
into a macrophage and where, sometimes, it becomes a foam cell.
When millions of macrophages have become foam cells in one area,
we have an atherosclerotic plaque.
Researchers from the University of Wisconsin designed a study
to find out why some monocytes, but not others, stick to endothelial
cells. They found that monocytes infected with CPN were stickier
than uninfected monocytes.
Furthermore, the more heavily infected
the monocytes were, and the longer they had been infected, the
stickier they became. The CPN didn't have to be alive--monocytes
that ate dead CPN organisms also became sticky.http://www.potbellysyndrome.com/attach/CPN.pdf