The Marshall Protocol: Part II

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The Marshall Protocol: Part II

Sunday, September 5th, 2010 | health blog

In part one, we discussed how Dr. Marshall has developed a protocol, which has been implemented by a few physicians, to treat autoimmune diseases.  Further we discussed his interesting and not implausible idea, for which there is currently very little evidence, that auto-immune diseases are the result of chronic intracellular infection with wall less bacteria.  From here we have to look at Dr. Marshall’s interpretation of microbiology to see how he comes up with the Marshall Protocol treatment.  Dr. Marshall hypothesizes that chronic intracellular infection leads to “dysregulation” of the Vitamin D Receptor (VDR) protein.  Okay, that’s another neat idea but we need to be careful with the definition of dysregulation.  We do know that some pathogens are able to modify both the degree of expression and the distribution of the VDR protein.

Let’s jump ahead now directly to the Marshall Protocol as defined on the Marshall Protocol Knowledge Database.

At its essence, the MP involves four key elements, each of which is supported by the latest insights in molecular science:

take 4 doses of olmesartan (Benicar) per day

take varying combinations of pulsed, low doses of specific bacteriostatic antibiotics

wean off any immunosuppressive or potentially immunosuppressive therapies

avoid the consumption of vitamin D, as well as certain other immunosuppressive foods; note that photosensitive patients must also restrict exposure to light

As regards point four Dr. Marshall states “A 25-D level of 12 ng/ml or less indicates successful avoidance of ingested vitamin D.” Such a blood level of vitamin D indicates a deficiency state with all its attendant health consequences. It is also noted the treatment often lasts, “multiple years.”

As is further emphasized at the same site, “The most important medication Marshall Protocol patients take is not the low doses of antibiotics, but the Benicar. MP patients take 40mg of Benicar – also known by its substance name, olmesartan – every six hours.”  Okay so olmesartan is central to the Marshall Protocol (MP).  Here is where things begin to unwind in such confusing irrationality that one might wish to pull one′s hair out.

Dr. Marshall states that olmesartan is a partial agonist (activator) of the VDR receptor.  Unfortunately however there is no published experimental evidence for this, there is only speculation based off of computer modeling simulations. That is why olmesartan is spoken of and marketed as an “angiontensin II inhibitor”, a blood pressure medication.  Still what another “science fictiony cool” sort of unlikely idea, which to have any clinical usefulness needs to be part now of a string of possibly true ideas.  There is no direct evidence that olmesartan interacts with the VDR receptor.

However, if one took the position that olmesartan is a clinically usefull agonist to VDR why is one giving it and restricting the more powerful agonist vitamin D itself at the same time? As we mentioned earlier, if the dysregulation of the VDR is downregulation caused by infection then vitamin D would work better at improving the situation than the partial agonist olmesartan.

I see two possible ways around this problem of the anti-hypertensive/partial VDR agonist not being less effective than vitamin D itself.  One, is that the bacterium actually changes the configuration (say through methylation) of the VDR such that vitamin D is no longer effective.  That isn’t Trevor’s neat idea, it’s mine, maybe he should update his site.  The other is the one he pulled out of a hat.  “Like 1,25-D, Benicar turns on the VDR, but unlike 1,25-D, it does not interfere with the activity of the body′s other nuclear receptors.”  Quite a molecule that Benicar.  And really the pathology now is not so much related to the VDR (i.e what happened to VDR dysregulation) as to the undefined other nuclear receptors which vitamin D is now supposed to be errantly activating.  But I thought the issue (per Marshall) was that vitamin D is lowered in autoimmune diseases as a compensatory protective mechanism (and needs to be lowered further by treatment).  So how were lowered vitamin D levels causing such a problem in various undefined nuclear receptors.  Is the pathology in the “dysregulated″ VDR or in the undefined other receptors?

Sounds like a fun guy to have a beer with.  Things could go on like this in perpetuity.  At some point though the rubber has to hit the road.  You give a treatment, people get better or not.  Despite having been promoting this treatment since at least 2002 there is not a single published study showing it does any good.  I mentioned in the last post my understanding of the evaluation of any unpublished data by an FDA reviewer.  I do enjoy this other quote from his Marshall Protocol Knowledge Base, “According to one rough estimate, 25% of patients who begin the MP experience immediate symptomatic relief when they begin the olmesartan blockade, about 25% feel no different, and the other 50% will experience some adjustment symptoms.“  hmmm, say that again.

But wait, you see when patient’s get worse, they aren′t actually getting worse they are experiencing the rare and obscure, “Herxheimer reaction″ a flooding of endotoxins when a large bacterial infection is rapidly killed off.&nbsp Ah, thanks for explaining that Dr. Marshall.&nbsp And as this is a chronic infection, this “Herxheimer reaction″ may go on for quite a long time.&nbsp But really it means your getting better.

To summarize: we have an unidentified pathogen or pathogens responsible for multiple disease states, diabetes, sarcodosis, Lupus, Crohns disease, Sjogrens disease, rheumatoid arthritis, etc, etc.  These unidentified pathogens work through a hypothesized dysregulation of the vitamin D receptor.  A vitamin D analogue, which no one considers to actually be a vitamin D analogue, is used, in place of vitamin D to “partially activate” the vitamin D receptor.  Exogenous vitamin D is to the extent possible eliminated.  Vitamin D itself wouldn’t work because of an unexplained pathology involving other nuclear receptors.  The largest percentage of patients starting the therapy apparently feel worse.  After a number of years, and government Orphan incentives, there is no published evidence of any clinical benefit in any auto-immune disease. The “therapy” involves a massive dose of a presription blood pressure reducing medication, long term use of multiple presription antibiotics and inducing a state of chronic, long term, severe vitamin D deficiency.

At what point does a Herxheimer reaction actually become, “someone is getting worse?”&nbsp I mention this last question because it may explain much of the thrust of the article we looked at a few days ago.&nbsp You see a few years back before more of the evidence for the likely usefulness of vitamin D supplementation in autoimmune diseases, there was no premise of, “well vitamin D makes things better now but you’ll get worse latter, just look at the unlabeled figure in our paper.”&nbsp So now in the converse of the “you’re getting worse now with vitamin D restriction but it is a Herxheimer reaction, that paper took the position of, “yes patients are getting better with vitamin D normalization but they’ll get worse later”

Trevor Marshall has a brief curriculum vitae online at his site http://www.trevormarshall.com/ Oddly he has attached a disclaimer to his CV. As someone who, while not directly prescribing, has directly affected the health of 100s if not thousands of people with serious chronic diseases a disclaimer of some sort seems in order, though I′ve never seen one attached to a CV before. I thought I might reproduce this disclaimer here. If you care to try and read between the lines you might get a very good idea of my opinion of Dr. Marshall.

DISCLAIMER: Any resemblance between the above views and those of my employer(s) are purely coincidental. Any resemblance between the above and my own views is non-deterministic. My existence can be challenged. The question of the existence of views in the absence of anyone to hold them is left as an exercise for the reader. The question of the existence of the reader is left as an exercise in the second order coefficient.