JAD Journal Paper:

Bill,
Your "food for thought" is a "red herring."

I have laid out the detailed reasons that Borrelia has to be a co-infection.
I have laid out the reasons that what you find in autopsy tissue may have no relevance to the clinical disease that caused the patient's death. And most of all, I have explained that Alzheimers and Dementia occur in regions of the world where there are no ticks carrying Borrelia spirochetes.

Chronic disease is caused by Th1 bacteria, but not by the obvious species (eg, Borrelia, Treponema). Focus on the spirochetes is counter-productive, as it paints the Lyme community into a remote corner of the medical landscape.

Yes, the Th1 pathogens induce production of amyloids, and yes, they also stop the body from dealing effectively with co-infections like Borrelia, Bartonella and Rickettsia. But chronic disease (including Alzheimers) will persist after the spirochete has been eliminated. This is the same problem that folks with AIDS find when they get rid of HIV. When the DVDs of my recent conference presentation are available please review very carefully how I explain the problems devising an effective cure for that disease. Modern medicine has not been very good dealing with multifactorial disease.

..Trevor..
ps: I have been working with a clinic in Germany treating selected Alzheimer patients with a version of the MP. I am told this group of patients generally exhibit Rickettsia infection (a coccoid, not a spirochete) (as tested by Jardin Labs) and very few have a positive Borrelia titre (as tested by Bowen Labs). And, most important, they herx, their disease relapses after a day soaking in the sun, and some show (very) tentative signs of recovery. ....

Just search this MP database for what I have written about "plasmids" and "polymicrobial" and you should find more detail.

Borrelia most certainly do harm. They are just not causal. If you could get rid of the Borrelia then you would still have the underlying Th1 disease, the disease which weakens the immune system so that it can easily become parasitized by Borrelia and the other identifiable viruses and bacteria. You find Epstein-Barr Virus (EBV), for example, in all the Th1 diseases - search PubMed you will find folks saying it causes just about all of them. But it is most likely a bystander, throwing its plasmids into 'the infectious soup'. The real answer lies in the genomics, in the DNA (and RNA) and the intermixing thereof, and it is possible we may never know the totality of species involved.

Oh - if you want some names - Strep appears frequently in Dr Andy Wright's microscopy, Staph (because Mino works and Doxy doesn't), E-coli, Propionibacteria, Bacillus, M.leprae, all the other common species nobody uses PCR to look for. They accumulate and share plasmids and chromosomal DNA and viral/bacteriophage RNA as the chronic infection progresses from stage to stage. The chronic Th1 syndromes are the result of a lifetime of sequential infections.

.. Cathelidicin, which is produced when the Vitamin D receptor is activated, is certainly capable of killing pathogens. Trevor Marshall has developed a good model for sarcoidosis. It remains to be seen how well that model can be generalized to other chronic diseases where the vitamin D receptor is not dysregulated. I think Marshall's criticism of the 'vitamin D' are crucial. Excessive activation of the vitamin D receptor by 1,25D (calcitrionol) can lead to calcification of soft tissue and heart disease. But I think Marshall's devotees overstate their claims in terms of how widely people's vitamin D receptors are dysregulated.

In violation of conventional wisdom, Vitamin D supplementation does increase arterial calcification in those susceptible to it (those with insufficient vitamin K in their diet.)
http://cat.inist.fr/?aModele=afficheN&cpsidt=1262915

1,25D puts calcium into the bloodstream, not the bones.
The relationship of d3 and calcium metabolism is horribly misunderstood.

see my comment on this post.
nutrition.about.com/.../vitamin-d-for-pain-relief.htm

Low 25D is sometimes associated with increased risk of heart disease because high production of 1,25D depletes 25D, not because of actual deficiency.

So raising 25D won't always help.

People need to differentiate between low 25D cause by kidney or liver problems or lack of sunlight, and low 25D caused by chronic infection.

...Because so many people being tested have chronic inflammatory conditions, the typical lab ranges are skewed upward (Merck’s upper value is 45 pg/mL). However, the medical literature clearly states that a 1,25(OH)D level above 42 pg/mL is so far beyond “normal” that it will induce osteoporosis over time. I’m living proof of that, with a -2.9% DEXA T-score for my spine and a 1,25(OH)D value of 63 pg/mL this past May.

So it appears that Vitamin D dysregulation is quite widespread in the populace, with, for many people like myself, most of this chronic, underlying Th1 inflammation being “hidden” for many decades of life until the “diseases of aging” set in.

See this video of Dr. Marshall’s presentation on this subject just 3 months ago, which has applicability to just about every one of us:

Defeating the Diseases of Aging: http://vimeo.com/1268542

... detail for you to understand the whole picture regarding the ARB modeling, in particular Olmesartan’s (trade name Benicar) action on the VDR (Vitamin D Nuclear Receptor). Here’s some further clarification by Marshall:

“The agonist effect of Olmesartan occurs at higher doses, and the degree of effect can be adjusted by adjusting the dose. Whereas with a drug which is too high an affinity, like Telmisartan as an antagonist, you cannot adjust the dose to modulate the degree of the effect. So Olmesartan is able to displace 1,25-D, or capnine, from the VDR LBP in a controlled manner, dependent on Olmesartan dose (and the concentration of capnine or 1,25-D). This is called "homologous displacement" in most pharmacology texts. It follows a characteristic S-shaped curve.”

Also see these articles:
Simple explanation of the action of Benicar:
http://www.marshallprotocol.com/forum2/364.html

Cell Wall Deficient Bacteria and the MP:
http://www.marshallprotocol.com/forum2/2810.html

Re cancer, you may be interested to know that of the hundreds of people past and present who are following the Marshall Protocol, many of whom are at middle-age or older with multiple health problems, there have been no reports of someone developing a metastasis that was not previously present when they began the protocol. See this interesting interview with Gene Johnson and his defeat of bladder cancer:
http://bacteriality.com/2008/07/18/interview24/

Finally, here is a more complete exposition of Marshall’s genomic and molecular modeling research which you may find more comprehensive:
autoimmunityresearch.org/.../marshall_bio21_2006.pdf

Dr. Trevor Marshall's work has clearly demonstrated the fallacy of this reasoning--it is the inflammatory disease process which CAUSES the low D, not the other way around. Dr. Marshall cured himself of (often-fatal) cardiac sarcoidosis after he discovered that his disease, as well as ALL the chronic inflammatory diseases, are caused by intra-phagocytic, meta-genomic cell-wall deficient bacterial forms:
http://www.trevormarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf ..