This discussion is going nowhere. It’s clear you still have not read much of the vital information discussed on this site and in Dr. Marshall’s papers- information that is necessary if you and I are going to have a reasonable discussion.

For one thing, BioEssays is a peer-reviewed journal, and a very prestigious one at that. So clearly you haven’t even looked at Marshall’s model of vitamin D metabolism. If you haven’t taken the time to understand his model, then how can you criticize it?

What about the fact that Marshall just gave a presentation on vitamin D at Karolinska or the fact that he will be chairing an entire session about vitamin D, the VDR, and the MP pathogenesis at the upcoming 6th International Conference on Autoimmunity. Apparently enough of his peers are interested in his work to offer him such opportunities.

And you seem unable to grasp the fact that the Marshall Protocol phase II study trial is putting Marshall’s molecular model to the test, and in thousands of human patients no less. Patients on the MP don’t experience immunopathology unless they remove vitamin D from their diets, allowing the VDR to be activated once again. Every aspect of Marshall’s model is backed up daily by living, breathing, patient data.

The rest of what you are putting forth is simply speculative dogma, the same stuff pushed forth by vitamin D proponents that I’ve heard a million times over. Believe me, I’ve heard your arguments before such as the notion that our ancestors scorched themselves in the sun. Personally, I think they had the wits to find a cave or at least a tree.

You say molecular data can’t be trusted and yet your strongest argument for why humans should be consuming vitamin D is based on a hypothetical ancestor from millions of years ago that nobody really knows even existed.

This site looks at vitamin D through a new lens, and if you are unwilling to try to adjust your viewpoint then you’d be better off posting comments on the Vitamin D Council website or somewhere else where you and everyone can all agree that vitamin D is a wonder drug, while ignoring the fact that while we increase supplementation of the secosteroid, the rate of chronic disease is escalating.

Sorry to come off as harsh, it’s just that when all your concerns are essentially addressed in articles on this site, arguing with you takes away time that I need to answer the questions of people who are open-minded towards this new research.

Best,

Amy

Blacks and South Asians among others do not tan. They do however require a little longer than whites to meet their maximum day’s intake of vitamin D via UVB, but even then whites create all the vitamin D they need before turning darker.

I understand that there are people who have symptom flares related to vitamin D, linked to macrophages releasing very excessive amounts of 1,25D.

I’m not aware of any studies that suggest UVA facilitates vitamin D production, please show me these.
A perfectly logical reason as to why sunscreens fail to completely inhibit vitamin D production is that no one applies sunscreen that liberally all over their skin. You will always miss spots no matter how hard you try.

NICE (or the National Institute for Health and Clinical Excellence) in England and Wales classifies rickets as caused by a deficiency of calcium *and* vitamin D. This is logical due to the fact that 25D increases intestinal absorption, a small amount of calcium with a certain dosage of vitamin D is as or more effective than a large amount of calcium on it’s own. I do not believe he is immunosuppressed as immunosuppression clearly is complete inability to fight or arrest illness - yet the reverse happened in him. All blood test markers indicate so.

Since a lot of Black and Asian children in Europe have rickets - trends show it’s more common than in white counterparts - and there is no dietary sourcing problems here, it suggests that D is the missing link. Calcium in Africa where UVB is abundant, vitamin D in Europe where UVB isn’t; but both are needed together.

Molecular technology can be flawed. One wrong variable and it’s all insignificant. I also want to point out again that I said public, peer-reviewed studies - not opinions as per that BioEssays link. I could setup a website saying chewing pen caps is beneficial but who’d believe me unless my *data* was verified by peers? I’m not trying to mock, but you follow what I’m saying.

It’s clear why many people with abundant sunlight can have low levels of D, simply because very little of us live as nature intended - hunter/gathering in birthday suits - whether in low or high UVB conditions. You’ll find concrete data where lifeguards in abundant UVB areas have high vitamin D, more than the 24/7 clothed, indoor working population.

Since it’s becoming clear that most if not all people are insufficient in D, this would mean that everyone is potentially ill. I was D deficient - and wasn’t ill - and what separates me from a person who’s currently ill is my potential in future to be more likely to become a patient if I didn’t address my D status.

Even if the disease process down-regulates 25-D, why do our bodies push cholesterol into the skin for conversion? It would be prudent if our bodies shut off pushing cholesterol to the skin - yet they don’t. Same in other animals.
Another explanation of the disease process down regulating D is the fact an ill person will stay indoors more so.
Furthermore Professor Joanne Lappe proved in a PCRT that low levels of vitamin *influence* cancer risk and not the other way around.

I intend to follow Marshall’s developments from time to time but will end my participation here. What I really want to say is that despite your enthusiasm for Marshall’s work it would be unscientific to not entertain that mainstream findings on this issue have merit.

One last thing, since other animals synthesize D; one example being cats who create D3 when UVB hits the oils in their fur which they then ingest on cleaning (or by livers of prey), would they be immunosuppressing themselves? I mean does the MP have designs to offer this protocol to veterinarians say for diabetic, house bound, cats?

Best wishes,

HC.

You say you have no problems grasping Marshall’s hypothesis, but your comments suggest otherwise. If you were truly familiar with the Marshall Protocol you would know that a tan absolutely promotes the production of vitamin D. None of our study subjects can get any form of sunlight without creating the vitamin D that causes symptom flares. Why else would our patients have to make such concerted efforts to protect themselves from the sun? Not to mention the fact that there are many studies showing that both UVA and UVB light make vitamin D. You can read more about sunscreens and vitamin D production in these articles:

http://bacteriality.com/2008/01/15/sunscreen/

http://bacteriality.com/2007/09/15/vitamind/#5

Also, even the US Department of Agriculture Website agrees that Rickets in not a disease caused by vitamin D deficiency. It is caused by low levels of phosphorous and calcium, a reality recently confirmed by several studies conducted at Harvard. Does it really make sense that the majority of Rickets cases occur in Africa where young children are getting abundant sunlight? The person you know who has “recovered” on vitamin D is simply extremely immunosuppressed by a very powerful steroid and his bacteria are still very much alive. Read more about Rickets here:

http://bacteriality.com/2007/09/15/vitamind/#8

Thirdly, you say Marshall’s work is not viable because his model was generated using molecular technology? That’s absurd when you consider the reality that only molecular data can provide information on the exact affinities and molecular interactions needed to fully understand chronic disease. And then you say that Marshall’s work has not been tested on human subjects? What then is the Marshall Protocol phase II study trial? It’s a trial in which literally thousands of patients are putting Marshall’s model to the test in a clinical setting. Even better they are all human subjects. Read more about the benefits of approaching medicine using molecular technology here:

http://bacteriality.com/2008/02/23/misconceptions/#5

If you insist that Indians can’t get sun because of pollution (something I think most people would consider extremely far-fetched), then there are plenty of other studies showing that people who get abundant sunlight also still often have low levels of 25-D. Take this study titled, “Low levels of vitamin D despite abundant sun exposure”

http://jcem.endojournals.org/cgi/content/full/92/6/2130

The reality is that the chronic disease process itself is downregulates 25-D levels. A low 25-D is NOT a sign of deficiency, it is a sign of chronic infection.

I encourage you to read more of Dr. Marshall’s papers and read more information on the study site in order to more fully understand what Marshall is putting forth.

Best,

Amy

I have read that link before. It is no way a study but an opinion based on interpretations of others studies. Where in this piece is ‘*we* studied…And *we* conclude?’

I do not dispute that some inflammatory diseases are caused by bacteria - and in this instance you have some fascinating points.
However, 1,25D increases the production of an antimicrobial peptide called cathelicidin. That is, a natural antibiotic.

I must stress again that in Europe fortification of foods and supplementation is rare than norm, and there is actually an increase in ill health since food fortification diminished here in the 70’s.
Need I point out Scotland as a good example?

I actually do know one person who has been ‘cured’ long term by vitamin D, though I will concede long term in his case is a child who’s now in his mid 20’s.
While not an autoimmune disease, I personally know this young man who had rickets and seizures corrected by supplementation of vitamin D, alongside surgical intervention on his legs due to the severity of the condition. Calcium alone had made very little impact.
Resultantly, he now doesn’t have osteomalacia, seizures or a recurrence of rickets - confirmed by blood reports.

I have no problems understanding Marshall’s hypothesis, I just believe it is incorrect and is fallible due to being based on software than public made studies on human beings.

There is an article that asserts positive effects of the MP are not proof of it’s theories: http://stuff.mit.edu/people/london/universe.htm

You also misunderstand my comment on India. I didn’t say that people in India don’t get sun anymore, I say they as a polluted country get less UVB.
Please read http://www.blackwell-synergy.com/doi/abs/10.1111/j.1751-1097.1996.tb01839.x
A tan is not indicative of vitamin D production. UVA makes people tan. UVB synthesizes vitamin D.

It is speculation to say that a new young generation don’t cover up the way old generations do. How many Muslims in Muslim countries do you know who dress liberally? Very few you’ll find. That’s why studies in India, Pakistan, Bangladesh, Saudi Arabia, very polluted China and even America are invalid. The Mediterranean is a perfect testing ground.

Whether Bangladeshi women are veiled or not, by and large it is not speculation to say Bangladeshi women don’t go out in sparse dressing.

I hope my tone is not forceful, as I wish to be anything but. I am just not won over by this hypothesis. If anything I have some respect for what you’re doing because it helps create challenges for the view I support.

Wrong. There is peer reviewed evidence that 25-D is immunosuppressive. Apparently you have not read Dr. Marshall’s latest paper on vitamin D metabolism that was recently published in BioEssays? Here’s the link:

http://TrevorMarshall.com/BioEssays-Feb08-Marshall-Preprint.pdf

Not to mention the fact that Dr. Marshall just returned from giving a presentation about vitamin D and the pathogenesis of inflammatory disease at the Days of Molecular Medicine Conference in Karolinska, and that he will be charing an entire session about vitamin D and the VDR at the upcoming 6th Annual Conference on Autoimmunity.

The understanding that inflammatory diseases are caused by bacteria flips the conventional model of vitamin D metabolism on its head. 25-D is a secosteroid, and not surprisingly it works just like other steroids. It slows innate immune function in the short-term, preventing the rise in immunopathology and inflammation that occurs when bacteria are killed. This leads to short-term palliation, but in the long-run bacteria are able to spread with greater ease. When I say long run, I mean decades.

And this hypothesis makes sense - As people in all areas of the world supplement with higher than ever levels of vitamin D the rate of chronic disease continues to soar. Do you know one person who has been cured, long-term by vitamin D? Or do they feel better for a decade or two and then remain ill?

I encourage you to read other articles on this site so that you can understand Marshall’s alternate hypothesis for vitamin D in greater detail. His model is not only based on solid in silico data but is backed by an increasing array of clinical evidence derived from the Marshall Protocol study site itself. At least read this article:

“The truth about vitamin D: 14 reasons why misunderstanding endures”

http://bacteriality.com/2007/09/15/vitamind/

The rest of your comments, in my opinion, are too speculative to influence the discussion. Are you honestly saying that people in India don’t get sun anymore because of pollution? That’s ridiculous. Any visitor to India would come back with a tan. And are you aware that there is a new young generation of Indians who don’t cover up the way the old generations do? I’m quite sure that Indian hospital workers wear clothes comparable to those worn by their European counterparts.

The other study I cited specifically states that it tested the 25-D levels of NON-veiled Bangladeshi women.

So I encourage you to be open-minded and at least read Dr. Marshall’s papers the other literature on this site, and possibly data from the MP study before coming to a conclusion. A lot of assumptions have been made about vitamin D, but the alternate hypotheses must always be put on the table too.

Best,

Amy

You don’t factor in that pollution, of which is abundant and increasing in India, is a factor in inhibiting UVB.

In Europe, fortification of D in foods is either insignificant or trace.
High levels in Europe are seen in those who periodically get UVB exposure, or natural matched levels by supplementation. This could be from tanning beds or the Mediterranean for example (relatively clean compared to India).

Also bare in mind that Bangladeshi women are by and large Muslim, and there is a conservative dress sense. Indeed, India too has a large Muslim community and even the Hindu and Sikh communities employ similar body exposure attitudes.

There is no peer reviewed evidence that 25D is immunosuppressive.
Since 25D is locally converted by tissues - and doesn’t contribute significantly to serum 1,25D - how can you say this when it’s 25D that is optimising local 1,25D? It’s not blocking it but helping it, hence a decrease in symptoms.