A more physiologically relevant observation was discussed by Peacock (see above link, NY annals paper), where their controlled trial found that the beneficial effect of calcium supplementation was blunted in those with higher 25-D.

The second, 1976 reference you mention is quite old –more current researchers state that 1,25-D is the only active metabolite. Overall, I think the modelling and our clinical data is a viable alternative to what others propose.

You are right that we don’t yet have enough corraborative data of the sort that you require, but hopefully we will in future.

If you read the article at this link: http://synergyhn.com/lesions you will see that the PTH issue isn’t nearly as simple or clear as many portray it. Look at the paper by Aloia that is discussed there. Many people have extremely low 25-D and do not have elevated PTH. If you look at his graph, they are by far the majority (probably 85%). I give an alternative explanation for the PTH — 25-D relationship that is often discussed.

If you observe the types of responses people have to Benicar, you will see that they really are not particularly similar to low aldosterone symptoms in most cases. In fact, the majority of patients feel no worse or feel considerably better on Benicar and raising the dosage of Benicar can reduce symptoms more in some patients due to its effects on receptors other than the VDR.

In those who do experience symptoms similar to hypoaldosteronism, the symptoms usually closely parallel antibiotic dosage increases rather than Benicar dosage and resolve as the treatment progresses, thus they appear to be primarily due to bacterial die-off.

Also, healthy people, typically feel no negative effect from very high dosages of Benicar and other ARBs.

As to the 32 ng/ml vs. 20 or less, I believe the 32 ng/ml was the level Dr. Marshall found that the modelling indicated the VDR blockage was more or less complete. The lower levels unblock it more and are preferred, leading to statements that you mention. You also have to consider that the VDR is also blocked by bacterial ligands, which would probably mean that an even lower 25-D level would be desirable in infected patients. In addition, Dr. Marshall has identified other means by which there is a blockage of the immune system when 25-D is high, via the very high 1,25-D levels that often occur.

Our work is so new that one isn’t likely to find adequate support in other’s work yet. For more support, I can only refer you to our data (Tom Perez’ presentation, the interviews on this site, the alumni forum on the MP site, also the case histories in part two of this article: http://winmlm.neostrada.pl/mp/townsend/Townsend_Apr07.PartOne.pdf
http://winmlm.neostrada.pl/mp/townsend/Townsend_Letter_May2007.Part2.pdf and our future work).

If you really spend time reading on the site and the above links, then you can judge whether your hypotheses that IP reactions are hypoaldosteronism and that lowering 25-D is crippling immune function are really the better explanation for patient’s responses. I don’t see how it could be consistent with the data.

Best wishes to you in your research and to your sister,

Joyce Waterhouse, PhD

I was a bit harsh. Sorry for that. You really care about this, and you’re looking for answers. That’s admirable.

Best,
Paul

This paper looks vaguely familiar.

Thanks for your interest.

Amy

The researchers specifically performed an entire study before this one to rule out the possibility that fat could have played a role in lesions. While it’s possible that another component of milk could be contributing to the lesions, many variables were analyzed and vitamin D was the only one that was statistically associated with the lesions. Because it was significant, unless the research was flawed, it has a relationship to the development of lesions.

I have no idea if they used D2 and D3. You may want to email the researchers.

From where we stand vitamin D2 and D3 are the same in terms of their ability to suppress the immune response. In the future, please don’t post your comment twice. There is a message right above the comment box that says it may take a while to get back to you, because I am school right now.

Thanks for your patience.

Amy

http://www.ncbi.nlm.nih.gov/pubmed/19758226?itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum&ordinalpos=50

Ann N Y Acad Sci. 2009 Sep;1173:757-65.

Reversing bacteria-induced vitamin D receptor dysfunction is key to autoimmune disease.
Waterhouse JC, Perez TH, Albert PJ.

Autoimmunity Research Foundation, Thousand Oaks, California 91360, USA. jcw@autoimmunityresearch.org

Vitamin D research is discussed in light of the hypothesis that the lower average levels of vitamin D frequently observed in autoimmune disease are not a sign of deficiency. Instead, it is proposed that the lower levels result from chronic infection with intracellular bacteria that dysregulate vitamin D metabolism by causing vitamin D receptor (VDR) dysfunction within phagocytes. The VDR dysfunction causes a decline in innate immune function that causes susceptibility to additional infections that contribute to disease progression. Evidence has been accumulating that indicates that a number of autoimmune diseases can be reversed by gradually restoring VDR function with the VDR agonist olmesartan and subinhibitory dosages of certain bacteriostatic antibiotics. Diseases showing favorable responses to treatment so far include systemic lupus erythematosis, rheumatoid arthritis, scleroderma, sarcoidosis, Sjogren’s syndrome, autoimmune thyroid disease, psoriasis, ankylosing spondylitis, Reiter’s syndrome, type I and II diabetes mellitus, and uveitis. Disease reversal using this approach requires limitation of vitamin D in order to avoid contributing to dysfunction of nuclear receptors and subsequent negative consequences for immune and endocrine function. Immunopathological reactions accompanying bacterial cell death require a gradual elimination of pathogens over several years. Practical and theoretical implications are discussed, along with the compatibility of this model with current research.

PMID: 19758226 [PubMed - indexed for MEDLINE]

Thank you for this

I’d like to know what kind of Vit D they used. Fortified Vit D in milk is Synthetic Vit D – D2. The information being out on the benefits of Vit D is D3.

Second, was it synthetic D2 that was supplemented or natural Vit D3?

Third, drinking pasteurized milk from sick cows on factory farms that are fed GMO corn and soy, ground up roadkill, rBGH, antibiotics and steroids is poison IMO.

So this in my opinion, although interesting, doesn’t hold a lot of weight….Payne and team had found that individuals who consumed more high-fat dairy products had more brain lesions than those who did not follow such a diet but determined that fat intake in general was not a significant factor. However vitamin D is found in high fat dairy products, and a large number of dairy products are fortified with extra vitamin D. Hence the team’s idea to investigate the effect of vitamin D on brain lesions.

How do the researchers know it wasn’t something else in the cow’s milk like bovine spongiform that is causing these lesions?

I haven’t had pasteurized milk in almost 2 decades an dont recommend it for my clients.

Would you please comment— thank you Amy!!

Dan

Joyce – I’d be careful with using data based on lifeguards, since exposure to chlorine compounds is a complicating factor. http://en.wikipedia.org/wiki/Pool_chlorine_hypothesis

(Yes, I know wikipedia isn’t authoritative. But it’s a good starting point for those who need more info.)

Bill – Be aware that the ‘in silico’ computer modeling data often referred to by supporters of the Marshall Protocol in support of the immunosuppressive properties of 25D above a certain threshold is, to the best of my knowledge, not peer reviewed.

As a side note; Production of cholecalciferol is not the only biological result of exposure to light. Sunlight can kill microbes, break down bilirubin, increase serotonin levels, and so forth.

that there may be something to higher vitamin D supplementation and immunity to flu.

I agree. For what it’s worth, I’ve known a few people who take oral cholecalciferol (D3) in response to specific temporary sicknesses like the flu and seem to have good results. I think you hit the nail on the head in that AMP levels need to be studied in various people with different 25D3 levels to see what’s actually going on. As of about a year ago, I couldn’t find any studies which really spoke to that point.

It seems to me like several different groups; those who cannot produce enough cholecalciferol, those who use up cholecalciferol too rapidly and those with a dysregulated VDR are being lumped into a single group when 25D3 is measured.

The weakest point of the dominant paradigm and the easiest to support with in vivo and in vitro studies seems to be 25D3 and its relation to heart disease. Many studies assert that high 25D3 is associated with lower cardiac risk. But D3 supplementation (particularly when K1 is suppressed and in the absence of K2 or menaquinone) can lead to arterial calcification (which would require activation of the VDR.) That does support the notion that low 25D3 in some cases is the result of an infection rather than a ‘deficiency.’ But I’m not sure whether those studies concerned levels of 25D3 high enough to test the assertion that high levels of 25D3 blocks the VDR.

In a healthy person without this autoimmune disease causing VDR dysfunction, could a person tank up on enough steroid D3 to cause an autoimmune disease as I suspect? Is all of it stored in the fat cells and the liver or does some of it proliferate out and effect the rest of the immune system?

Nick D.