A lot of people recovered during the timeframe, the recovery time is typically 4..6 years for light or normal case.
Is there any summary of the success rate?
For example, when Dr Chia uses tenofovir to treat ME/CFS, he notes that less than 1 out of 3 patients respond (but when they do respond, the results are significant. See these posts:
1 2 Then if you take something like low-dose naltrexone, maybe only 10% or 20% of patients benefit from that, but when they do benefit, again the results are significant. Ref:
1.
It's always useful to have some details of the success rate like these.
Have more severe ME/CFS patients tried the Marshall Protocol to your knowledge? Since the MP can worsen symptoms, it may unbearable for severe patients (by severe, I mean severe on the ME/CFS scale of:
mild, moderate and severe).
Its a herx .. basically same herx people experience on antibiotics when treating their Lyme(treating Lyme with abx can bring ton of herx, especially if level of D25 is low), just more powerful and I hope, more productive...
The so-called immunopathology of the Marshall Protocol might be similar to Herxheimer reaction, but by definition Herx is caused by the release of bacterial endotoxins like LPS when bacteria are killed by antibiotics, etc. Endotoxins come from the cell wall of bacteria, but
L-form bacteria which live inside cells do not have a cell wall when inside the cell (L-forms discard their cell walls in order to live inside cells).
Alternatively the immunopathology might be similar to the
immune reconstitution inflammatory syndrome.
Marshall Protocol would weaken bones...
I would not have thought that would be the case. Benicar (olmesartan), the drug used in the MP, is a potent activator of the vitamin D receptor (VDR). The reason that vitamin D is avoided in the MP is paradoxically to allow for
more VDR activation, via the effects of Benicar on the VDR (though I don't understand the precise mechanics).
In Prof Marhsall's original theory, intracellular L-form bacteria are blocking the VDR as an immune evasion strategy; they do this because the VDR is the ON switch for a part of the intracellular immune system. So this is how these bacteria are thought to survive inside the cell, by blocking the VDR, and thus turning of some of the intracellular immune response. The idea of the MP is to switch on this de-activated VDR (by means of Benicar) so that this part of intracellular immune system is once again activated, and can then kill the intracellular bacteria.
However, the intracellular immune system activated by the VDR involves the release of antimicrobial peptides cathelicidin (LL-37) and beta-defensin, and I believe these peptides are better at fighting intracellular L-form bacteria than they are intracellular viruses. Thus the Marshall Protocol may work better for diseases like sarcoidosis which are linked to L-form bacteria, than for virus-associated ME/CFS.
Though some cases of ME/CFS are linked to or involve Chlamydia pneumoniae, which is an intracellular bacterium (an obligate intracellular pathogen rather than an L-form). So it may be that the MP works better for those cases where Chlamydia pneumoniae is involved.
