Is there a connnection between gcMAF and the Marshall protocol?

[richvank]

Hi, all.

Here's something to ponder:

It occurs to me that both gcMAF and the Marshall protocol involve the vitamin D receptor and the macrophages.

In Dr. Trevor Marshall's concept, there is too much conversion of 25 OH vitamin D into the hormone form 1,25 OH2 vitamin D, and this overloads the vitamin D receptors and prevents the macrophages from activating. The result is that intracellular bacteria are able to live inside the macrophages, where they produce granulomas and the disease that results.

With gcMAF, the gc protein is the vitamin D receptor. In the case of tumors and some pathogens, the enzyme nagalase is produced, and it chops a piece off of the gc protein, so that it is not able to activate the macrophages. In Dr. Yamamoto's technique, the gc protein is extracted, purified, and treated ex vivo, and then put back into the body, where it activates the macrophages to go after the tumor cells or pathogens.

What if these two disease mechanisms are two different ways of inactivating the gc protein? If this is true, perhaps the gcMAF treatment of Yamamoto would also work on sarcoidosis and the other diseases Marshall has been treating by lowering vitamin D and giving antibiotics.

Best regards,

Rich

 

[RivkaRivka]

interesting, rich.

thinking like a puzzlemaster, as always!

 

[alex3619]

Hi Rich, all very good points. The vit D connection I have also thought about then completely forgotten about it, doh! The implication of the full range of illness treatment is also interesting, and one I have not thought about.

A further implication is that the Marshall protocol, in combination with GcMAF, might have synergistic effects, as might other protocols that assist macrophages through cytokine shifts, nutrition or antioxidant status. I hope we are heading into a time when combinations of protocols can be tested on patients, and we don't base treatment on one single simplified hypothesis. I have long thought that attacking a multisystem disease with multiple targets at many places at the same time is a good alternative to picking just one subsystem and hoping it will be enough.

Bye
Alex

 

[FunkOdyssey]

Rich please be careful here, it sounds like you may be on the verge of believing the Marshall Protocol to be efficacious, backed by evidence, or in some way legitimate or proven. None of these things are true. I invite you to review the following site for a comprehensive deconstruction of the protocol and it's claims: http://stuff.mit.edu/people/london/universe.htm

Your own simplified methylation protocol, preliminary as it is, has made infinitely more public data available demonstrating its efficacy: Treatment Study of Methylation Cycle Support in Patients with Chronic Fatigue Syndrome and Fibromyalgia. And it is supported rather than contradicted by available science. Not remotely in the same league as Marshall.

 

[richvank]

Hi, Rivka, Alex and Funk.

Thanks for the responses.

Rivka--Yes, this is a fascinating puzzle!

Alex--Yes, I agree that a multipronged attack is a promising concept, so long as we can understand the mechanisms well enough that we can be sure that the modalities used will support and not counteract each other.

Funk--Please be assured that I am aware of the history and issues involved with the Marshall protocol, and Mark London's critique of it. I have interacted in person and by email with Trevor Marshall over the past few years, and at one time was active on his website, until my views were soundly rejected there! I am not advocating this protocol, and particularly not for the treatment of ME/CFS.

Having said this, I think there is an element of truth in Trevor's concept, particularly as it relates to sarcoidosis, which he suffered from himself, and into which he put a lot of study. I'm keeping an open mind about this. There has been a lot of research activity on vitamin D and its role in immunity in recent years. All I'm saying is that vitamin D and its receptor have popped up both in Trevor's concept and in the newer Yamamoto gcMAF work, and in both cases the blocked activation of macrophages seems to be involved. I expect that we will be hearing more about this.

I'm glad that you think the methylation protocol is well-supported. I like to think it is, too, but I can tell you that that view is not shared by orthodox researchers and clinicians, who insist on double-blind, placebo-controlled, randomized clinical trials of high statistical significance, approved by institutional review groups, and published in highly respected peer-reviewed journals. These are high hurdles to be surmounted.

Thanks again.

Rich

 

[Hip]

I found Trevor Marshall's ideas very fascinating, and I think it may well turn out that, in a large percentage of chronic diseases like CFS, autism, Lyme, lupus, etc, that have been associated with chronic infections, it is the immune-evasion tactics employed by microbes (like VDR blocking) that are responsible for not only allowing these microbes to survive long-term, but also, as a side effect, these immune-evasion tactics are likely responsible throwing out major metabolic systems in our bodies (like all the major metabolic systems thrown out of kilter in CFS). There are many, many other different types of immune-evasion tactics employed by microbes, in addition to VDR-blocking.

But Trevor Marshall thinks that VDR-blocking is central in sarcoidosis, the disease that the Marshall Protocol was originally designed to treat.

The VDR is the switch that releases the anti-microbial peptides cathelicidin and beta-defensins inside humans cells. These anti-microbial peptides form part of the cell's internal immune system. Trevor Marshall theorizes that in sarcoidosis, L-form intracellular bacteria live inside human cells, and secrete chemicals to block the VDR switch, as their main immune-evasion tactic.

(Other well-known immune-evasion tactics employed by microbes are: making "fake" cytokines, in order to divert, or switch off, the immune response, so that the microbes are not destroyed by the adaptive immune system.)

The role of the main drug used in the Marshall Protocol, Benicar (olmesartan), is to push the blocking chemical off the VDR receptor, and bind to this receptor itself, thereby activating the VDR. Benicar's activation of the VDR then causes the release of the anti-microbial peptides cathelicidin and beta-defensins, which then act to kill off the L-form bacteria inside the human cell.

Only later did Trevor Marshall start to consider and begin to test whether the Marshall Protocol might work for other conditions such as chronic fatigue syndrome.

Trevor Marshall himself thinks that CFS is uniquely caused by these same intracellular L-form bacteria, not viruses. Of course, most people would disagree with this, myself included. It is true that Chlamydia pneumoniae is an example of an intracellular bacterium that can cause CFS, but this is only one of many pathogens that are suspected of being able to cause CFS.

The interesting thing is that these anti-microbial peptides, cathelicidin and beta-defensins, although their main target is intracellular bacteria, they do have some antiviral efficacy; so it is conceivable that ramping up cathelicidin and beta-defensins production will help eliminate viruses inside cells: viruses like Chia's/Chapman's noncytolytic enteroviruses, which remain mainly intracellular; or viruses like EBV in its latent state inside a cell.

I have found that Trevor Marshall is not interested in entertaining the possibility of these viral etiologies of CFS; nevertheless, it would be good if someone else started to research the effects of using the Marshall Protocol as an antiviral protocol in CFS, for each of the major viruses implicated in CFS (enteroviruses, HHV-6, EBV, cytomegalovirus, etc).

One other thing I find lacking in the Marshall Protocol world: the so-called "immunopathology" side-effects that occur while taking Benicar on the MP (such as the great sensitivity to light, requiring that you wear special sunglasses while on the MP); well, blithely labeling this as immunopathology is not a good thing, when in fact nobody really has any idea of why these side-effects arise.

Perhaps these so-called "immunopathology" side-effects are in fact caused by something quite simple, that could be easily fixed via a bit of biochemical investigation, and fixing these sides-effects may not only make the MP much easier to do, but may possibly make it more effective too.

(In fact, Mark London notes that the MP side-effects may conceivably result from temporary acidosis, arising from type 4 renal tubular acidosis, which can be caused by taking Angiotensin II receptor blocker drugs such as Benicar.)

 

[ukxmrv]

Hip,

Marshall and associates started posting to one of the CFS groups quite early on (10 years?) but then left. At that stage the posts were concerned with Vit D avoidance. Over time the MP grew and grew. It added parts that came from other CFS protocols and treatments as they learned from them. The MP that was being described to CFS patients way back then is different to the MP that exists today and I think that this is because different CFS treatments have been incorporated.