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Prof Trevor Marshall
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Well, it is early Saturday morning here in Stockholm, and the DMM2006 conference at the Karolinska Institut is winding down into its final sessions. A half day today, and I suspect many of the International participants will be leaving early, flying home for the weekend. I am staying until tomorrow, to make sure I get the chance to talk with everybody I can.

With the help of several MP members we managed to get our key messages condensed down to just a few words on a 30 inch x 40inch poster board. There are copies of that poster available for download from URL
http://autoimmunityResearch.org/karolinska.jpg

The actual text has been re-arranged into a more easily printed form at
http://autoimmunityResearch.org/karolinska-handout.pdf

Please print them out, discuss the core points, and make sure your physicians and friends get to understand the message that we presented to the experts gathered here.

This conference is the sixth in the series “Days of Molecular Medicine” with the theme “Inflammation in Chronic Disease.” There are about 300 scientists here, with another 150 graduates, interns, and students from this most excellent University and Hospital complex. The ‘locals’ are watching the proceedings on a video link in an adjacent conference room, as the main lecture hall is full.

The conference is being held in the same lecture hall where Nobel Laureates deliver their orations after the yearly prize has been announced. It is quite an experience to realize how influential this one location has become to the advance of medical knowledge.

The keynote was delivered by 1997 Nobel Laureate, Prof Rolf Zinkernagel, from the University Hospital of Zurich. Rolf must have been reading our presentation right before his lecture, as he told the delegates that signs that ‘autoimmune’ inflammation was linked to bacteria were becoming unmistakable, and that maybe 30% of diseases could be linked to “intra-cytoplasmic” infection. Further, he emphasized that ‘immuno-pathology’ (what we call herx) was the key to attainable recovery rate. I was just sitting there dumbfounded, while most of this went straight over the heads of those seated around me:):) Still, now that the conference has wound down, I am starting to get some really good questions and comments. The bacterial pathogenesis will become accepted sooner, rather than later, IMO.

I hate to tinge this optimistic scientific note with reality, but there was also a presentation about Sarcoidosis from a Pulmonologist-led study group. I took photos of their poster, and will make it available for discussion when I get a few spare moments (probably Monday). In summary, however, it was striking that the first few lines of both posters emphasized TLR2 and TLR4 as key to Sarcoid inflammation, with the primary difference being that our poster explained that they were transcribed by VDR, with the pulmonologists still content to merely observe their presence. I was told that they need to be thorough and methodical’ as they move forward. Which I guess explains why there is this constant pressure upon us to slow down the rate of change.. gotta be more ‘thorough’ –LOL

Anyway, I have to get some more sleep and prepare for the morning sessions. Take a look at the material, try and understand why we are focusing the emphasis on ‘VDR Competence’ and away from “which species of bacteria is it?” (still the most common question I get) and help people focus on plasmids, with horizontal transfer of DNA between multiple species accumulated during a lifetime.

Indeed, it was Rolf's opening lecture that had emphasized these same polymicrobial concepts, and sent me scurrying for the library to incorporate some of his excellent references into my upcoming presentation(s) for LAX:X

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Trevor, it sounds like a brilliant conference and a breakthrough for you (and us). 

I really want to understand this science but I am having trouble with bits of it.  In the spirit of discussing the core points:

From the Karolinska handout:

During Th1 immune challenge, the VDR is activated by the endogenous secosteroid 1,25 dihydroxyvitaminD.'Vitamin D' is actually a seco-steroid, disables VDR, and strongly supresses Th1 innate immunity.
...25-D (which is commonly tested in clinical trials), 24,25-D; 25,26-D; and even cholecalciferol itself will displace the activating metabolite 1,25-D from the VDR, thus inactivating innate immunity.
The 1st quote seems to say or might say that an activated VDR is bad.  2nd quote seems to say that an inactivated VDR is bad.  Third quote seems to say that docked 1,25D is good.  In fact the 3rd quote might argue for having lots of 1,25D in the body.  Maybe I need to stick to physical science because I find this to be terribly confusing.


  1. Does an activated VDR fight bacteria or suppress the fight?
  2. Do we actually want 1,25-D docked to the VDR?  If so, wouldn't we like to have more of it rather than less of it?
  3. I believe the 2nd quote above argues for staying out of sunlight (cholicalciferol) and avoiding dietary D.  That seems familiar and reassuring.
  4. I believe that the 3rd quote above would argue that having high measured levels of 1,25-D is a good thing.
  5. What exactly does Olmesartin do to the VDR?  I can't quite make it out, but I get the idea that it stablizes the 1,25-D that is docked to the VDR and prevents the other 'D's from dislodging it.
Help!

Last edited on Fri May 26th, 2006 20:17 by John McDonald

Morris W. Milnes
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John,

      Your question got me curious and I went looking. 

I went to our post of the importance of avoiding Vitamin D

http://www.marshallprotocol.com/forum2/4062.html

and I think it in combination with the parts you quoted clarify the matter a little better.  It's different than I had thought I understood it.  It appears that 1,25 D does activate the vdr but needs to be dampend by olmesarten to keep us from killing ourselves with herx.  You also don't want excess 1,25 D because of the other bad things it does to our system such as dissolve bones and redeposit calcium in soft tissue and organs.  Excess 25- D  competes with 1,25 D and stops the immunes system like prednisone by displacing the 1,25 D on the receptor.  If I have  overstepped myself, staff, or misinterpreted please feel free to delete this.  I really don't like to say stupid things.

Morris

Last edited on Fri May 26th, 2006 22:33 by Morris W. Milnes

Prof Trevor Marshall
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John, Morris,
The conference is over now, and I can focus on returning to reality:):)

First, Olmesartan has an effect on many receptors in the human body, and probably also some receptors expressed from bacterial genomes (see the MRSA model in my Karolinska presentation).

1,25-D, and the other Vitamins-D, have a high affinity for a number of receptors. Generally, 1,25-D activates VDR, but it also has a high affinity for the Glucocorticoid Receptor and for the Alpha and Beta Thyroid receptors. So, as the concentration of 1,25-D in the body rises, it displaces Cortisol out of the GCR, T3 and T4 out of the Thyroid receptors. Some of us have had practical experience of this:):)

As the level of Vitamin D itself, or its metabolite 25-D, rises in the bloodstream some of them will enter the phagocytes, and, if the concentration of cholecalciferol or 25-D is high enough, they will displace 1,25-D from the VDR and inactivate it.

This means that they have disabled the body's last line of defense against intracellular pathogens. Which is not good. I think that a level of 25-D above 20ng/ml is totally suppressive of VDR activation, and therefore of innate immunity, and that levels of 25-D below 12 ng/ml seem to allow it to function moderately well. Olmesartan should be handy in this transition region. Once somebody has their 25-D into the single digits, and is not ingesting cholecalciferol, the VDR should be sufficiently active without needing any more Olmesartan intervention to activate innate immunity.

But Olmesartan also acts on other receptors- producing a palliative action in addition to the antibacterial effects it has when it interacts with VDR. I have identified one of these receptors, and over the next few days I think I will be able to track down another (based on a presentation I just saw...). These palliative actions include anti-anxiolytic and anti-panic effects, as well as pain palliation.

Hmm... John... I haven't really directly answered your questions exactly as they were asked. But have I clarified what is happening?

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Very nice conference and poster.
I got lost like John, the VDR science starts to be more and more complicated for me too

Last edited on Sat May 27th, 2006 03:29 by wrotek

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Trevor,

Congratulations on the conference.  Things are hotting up! :)

Once somebody has their 25-D into the single digits, and is not ingesting cholecalciferol, the VDR should be sufficiently active without needing any more Olmesartan intervention to activate innate immunity. But Olmesartan also acts on other receptors- producing a palliative action in addition to the antibacterial effects it has when it interacts with VDR.In the light of this, would it be a good idea to experiment with continuing the abx regime without olmesartan, for someone like me who has done over two years of MP (25D 8.8)?  Presumably if the herx got too bad, one could always start up the olmesartan again.  Can you foresee any possible drawbacks to this experiment?

Julia 

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Julia,
Try to stretch out the dosing intervals. That will tell you whether it is worth saving the money on Olmesartan. Its palliative effects are excellent, and will last as long as you get herx from the abx. If cost is not a factor, the organ-protective effects of Olmesartan are pretty convincing, and I would keep a blockade in place...

As for the complexity of the science - yes, the science is becoming more precise all the time, and the depth of knowledge is increasing by leaps and bounds. I sometimes shudder to read a lot of what I wrote just 12 months ago:X:X

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But Olmesartan also acts on other receptors- producing a palliative action in addition to the antibacterial effects it has when it interacts with VDR. I have identified one of these receptors, and over the next few days I think I will be able to track down another (based on a presentation I just saw...). These palliative actions include anti-anxiolytic and anti-panic effects, as well as pain palliation.
Bolding is my emphasis :)

Recently I have been going through the anxiety of waiting for test results for a serious condition. I can attest to being much less anxious, in this waiting period, than I would have been pre-MP. I assumed this is because I have improved enough on the MP to cause the "less anxious" effect, but perhaps it is a combination of improvement *and* the beneficial effects of the Olmesartan.

Thanks for the excellent new handout, Dr. Marshall. :cool:

Catlady

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There are too many kinds of D and the web sources aren't consistent about which D is which. Also for the moment, the role of the Olmesartin is confusing. I scrambled too many questions into my previous post so I am going to be a reductionist. Leaving aside Olmesartin only for the moment:

  • Do I want my VDR activated or not? I do, right? It is embarrasing to ask this but I am trying to be crystal clear about whether an active VDR or inactive VDR supports bacterial destruction.
  • I think you responded that 1,25 D activates the VDR (good?) but does bad things elsewhere.
  • Previously I believed that the bacteria synthesize 1,25 D for their own prosperity. Do we still think that?
  • I think I get the ingested 25-D. It deactivates the VDR (bad?).
Please bear with me, once I get this I will retain it. ::::::::::::john

P.S. I have had a heck of a time this week reaclimating to my home time zone. Jet lag can be as bad as a herx and I often think of the day after a long flight as a time of convalesence. You have gone equally far in the opposite direction. I hope you recover quickly. ::::::::::j

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Congratulations, Trevor, for the excellent poster presentation and on the well-deserved accolades from the distinguished attendees!  Yes, I also predict that it will be sooner than later for the overdue respect and appreciation of your efforts!  :D

We all THANK YOU! . . . Carole

Prof Trevor Marshall
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John,
Jet lag is easier to manage when you have your health back. I did arrive on Tuesday morning and the first conference event was Wed evening, but I missed nothing due to zone problems. Which is a nice warm feeling after all these years of struggling with travel...

So, question 1 - yes, the VDR must be activated as part of innate immunity.

Q2 - The Vitamins-D have a high affinity for the Glucocorticoid receptor, and the thyroid receptors, where presumably they do immunosuppressive, feedback, or other yet-to-be defined things. These apparently occur at higher concentrations of 1,25-D - after the VDR has been activated.

Q3 - I am not sure what the bacterial defense mechanism is, although it is clearly based in the properties of those biofilms we keep photgraphing in the blood under darkfield.

I did show the world expert on cell apoptosis (Dr Kristoff Binder) the video I had from Andy Wright, and Kristoff assured me that the filaments we were imaging were like nothing associated with apoptosis, where the cell memberane breaks into much larger 'blebs' as the cell disintegrates.

Q4 - both Vitamin D (cholecalciferol) and its hydroxylated metabolite 25-D displace 1,25-D from the VDR in a concentration-dependent manner, and deactivate the VDR.

..Trevor..

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John,

I can empathize with you on the VDR and D questions and although Trevor's answers are just above this post and may be clear to you, I'd like to add my nickel's worth. :cool:

It took me a little while to get that (I hope this is right ;)) it's not as simple as yes or no in regards to 1,25-D and VDR, but also HOW MUCH. 

In other words, we need some 1,25-D but more is not better.  That's when we run into problems and why ingesting D foods, (especially supplements and foods that add D) create problems in those of us with Th1 illnesses that can't regulate the proper amounts necessary of all of the Ds for proper functioning, especially once the CWD have entered our immune cells causing havoc. 

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Excellent.  Now I know in which direction to throw the VDR light switch.  I want it activated.  Now again from the handout:

During Th1 immune challenge, the VDR is activated by the endogenous secosteroid 1,25 dihydroxyvitaminD.

So a bit of 1,25D seems to be good, to activate the VDR.  But from this:

Q2 - The Vitamins-D have a high affinity for the Glucocorticoid receptor, and the thyroid receptors, where presumably they do immunosuppressive, feedback, or other yet-to-be defined things. These apparently occur at higher concentrations of 1,25-D - after the VDR has been activated.

Too much 1,25-D is not a good thing, probably immunosuppresive.  Presumably if we have Th1 symptoms then we have too much 1,25-D, though some small fraction of it is doing us good and may be essential.

Do you know if anything else switches on the VDR?  Is it just 1,25-D?

thanks,        john

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The VDR is unique among the Nuclear Receptors in having only one known activator, 1,25-dihydroxyvitamin-D. But, as the years go by, other endogenous receptor activators may well be identified, just as there are with the other nuclear receptors.

I can tell you that 1,25-D and the VDR are totally below the radar of everybody here. Nobody laughed at the Vitamin D connection, as many physicians do back home, but I guess 'bewilderment' and 'consternation' were the best description of reactions here.

Milk is not routinely supplemented here (Sweden is one of the countries with the least sunshine in the world) but butter is, only a little, about 9% RDA per serving. You can buy enriched milk, and they are just starting to put it in infant formulas. One of the pediatricians confided that she had wondered why the recent surge in Autism, so I suspect her patients' kids will no longer be supplemented:):)

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but I guess 'bewilderment' and 'consternation' were the best description of reactions here.

Years ago I got a valuable lesson in self psychology.  I was taking my modern physics survey course and I found Relativity Theory and Quantum Mechanics to be outrageously counter-intuitive, maybe preposterous.  I wondered how anybody could believe that stuff no matter how solid the mathematical evidence.  Then a few weeks later I noticed that I no longer felt that way.  It seemed intuitively reasonable.  Nothing changed except I had a few weeks to habituate to the ideas.  So this "common sense" or intuition in my case simply required adjustment to "feel" true.  So my intuition was and is pretty suspect.  I reckon that is true for all of us.  Please use small words and speak slowly to your colleagues (and to me).  They have a lot of "common sense" and antiquated intuition to overcome.

There must be 4 or 5 vitamins-D.  How many in the conference, do you suppose, can tell them apart?

john

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I am at the conference in spirit feeling your awesome progress Dr. Marshall. Keep up the great work you are doing and sleep to keep going! Much happiness comes from reading your enthusiasm about finally figuring this all out and fine tuning.

10,000 Thankyous

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Milk is not routinely supplemented here (one of the countries with the least sunshine in the world) but butter is, only a little, about 9% RDA per serving. You can buy enriched milk, and they are just starting to put it in infant formulas. One of the pediatricians confided that she had wondered why the recent surge in Autism, so I suspect her patients' kids will no longer be supplemented:):)

Here neither, except butter is enriched. Do other european MPers know or their countries are enriching things other then butter? When I saw the "Foods to Avoid" list, where could be putten Vitamin D in, I realised that the US situation is really different then the European. I cannot find a normal food wich lists added Vitamin D, except butter.

Bw,
Jeroen

GC
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Dr Trevor Marshall wrote:

As the level of Vitamin D itself, or its metabolite 25-D, rises in the bloodstream some of them will enter the phagocytes, and, if the concentration of cholecalciferol or 25-D is high enough, they will displace 1,25-D from the VDR and inactivate it.

This means that they have disabled the body's last line of defense against intracellular pathogens. Which is not good. I think that a level of 25-D above 20ng/ml is totally suppressive of VDR activation, and therefore of innate immunity, and that levels of 25-D below 12 ng/ml seem to allow it to function moderately well. Olmesartan should be


I have some problems with this interpretation. Do you have any references to show that 25OHD3 is capable of displacing 1,25D3 from the VDR? My understanding is that 1,25D3 binds over 400x more strongly to the VDR than 25D3.

In Prof. R Veith's chaper 61, page 5, of the book "Vitamin D" he explains that

There are
two ways to improve capacity for 1,25(OH)2D production
at kidney, and at peripheral tissues: provide more
substrate, or increase 1-hydroxylase content of the tissue.
This is fundamentally different from the situation relevant
to every other part of the endocrine system. No other
hormone is so dependent on the arbitrary, external supply
of its structural raw material. The concept of a mass action
relationship for 1,25(OH)2D production is the basis
of the argument that operation of paracrine control
systems dependent on vitamin D supply can be improved
by improving vitamin D nutrition."

So, increasing 25D3 nutrition will lead to increased synthesis of 1,25D3 in the paracrine system, and therefore improved function of the innate immune system.

Prof Trevor Marshall
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GC,
If you are representing his position accurately, then Veith is totally incorrect (again).

I have given my receptor affinity data at Karolinska. I will be happy to share it with Reinhold, if he requests it. There is less than a factor of 3 difference in affinity for the VDR between 1,25-D and 25-D. This difference is easily swamped by the higher available concentration of (exogenous) 25-D (untethered by DBP). Take a look at the figure on my poster which shows all the metabolites docked into the VDR. There is no significant difference in conformation between all of them. Neither are there any significznt differences between the binding affinities.

But only endogenous 1,25-D has the hydroxylated 1-alpha position. Only 1,25-D can activate the VDR.

I will not joust at phantoms when discussing scientific issues. If you wish to challenge the scientific integrity of my work, then you will need to identify yourself, and come out from behind the nom-de-plume. Because of the proliferation of your 'hostile' posts over the last several hours, you have been banned from further such comments until you comply with this professional courtesy.

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MPers, welcome to the wild,wild west of molecular genomics:) Sam

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Sam,
Actually molecular genomics is a precise mathematical science. Unfortunately it brings a newfound precision to the world of medical epidemiology, where the actions of drugs could merely be observed (in clinical studies), and/or guessed at.

With molecular genomics one can be pretty certain of at least the precise actions you are examining.

Back in 2003 I wrote some letters to the British Medical Journal suggesting that Vitamin D's actions may not be all good. Prof. Veith was one of my correspondents at the time, and he made it quite clear that he, and his academic colleagues, would follow each and every paper I might write about Vitamin D, telling the Editors that I was wrong, and that they, the experts, knew that I was wrong, and that my papers shouldn't be published.

So for the last 3 years I haven't written much about the actions of this steroid, except when it was necessary to help you folks recover your lives.

Now I have the molecular genomics data, and it confirms my 2003 view of the Vitamins D. So now I am beginning to publish, and the Vitamin D lobby is apparently taking notice:):)

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5:25AM Stockholm - You certainly are being productive.:cool:

Prof Trevor Marshall
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Trying to get back onto hometime PST, so that I can sleep during the flight and hit the ground running:):)

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Bouquets of roses and congratulations to you. It looks like all your hard work is starting to make sense to some people, the right people.

Good luck and please rest

Morris W. Milnes
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Makes me a little nervous to think something as big and powerful as the vitamin D lobby would be out to get us:shock:.

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Trevor, the hormone D fight may be the toughest battle yet; there is so much liability with linking chronic disease to D.
Sounds like this latest conference was wildly successful :) Sam

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About Prof. Veit anti attitude story- it is fortunate that writing an article about that someone is wrong is not much worth without scientific data presented behing the statement. I also have met funny attitude from science people in high rank of medical community argumenting that "this is wrong and that is it..." saying it without any scientific argumentation. How can anyone argue with such "powerfull " arguments. ;)

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Now I have the molecular genomics data, and it confirms my 2003 view of the Vitamins D. So now I am beginning to publish, and the Vitamin D lobby is apparently taking notice:):)

If the science is irrefutable, isn't it likely other scientists will eventually jump on-board, enough to silence TPTB?

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TPTB are making big waves so that other scientist did not swim to island occupied by them and the patients interest is always secondary. I wonder don`t they feel guilt for patients
that ended up in terrible conditions (or died) during the last years when they supressed bringing science to the eyes of the world.

Last edited on Sun May 28th, 2006 06:56 by wrotek

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Eurico, sorry to sound cynical, but that depends who's paying the other scientists :shock:

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Trevor, I didn't mean to insinuate that molecular genomics wasn't accurate, but that it is very fluid right now, with discoveries being made left and right.It's very encouraging to hear that others are coming to the same conclusions that you have too. Sam

wrotek
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I have noticed on karolinska poster that there is no Borrelia patients in Phase 2 "Cohort/Recovery Stats by diagnosis" table.

Last edited on Sun May 28th, 2006 12:18 by wrotek

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Wrotek,

Many Chronic Lyme (Borrelia) patients are also diagnosed with FMS and/or CFS/CFIDS.  I think you can also note that all of the patient groups on that poster are recovering at about the same rate (more or less) regardless of their diagnosis.

Last edited on Sun May 28th, 2006 13:47 by Reenie

wrotek
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Well if it was a criterium in Poland like CFS or CFIDS i would fit :) Also FMS.

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I just wanted to mention with regard to questions raised earlier in this thread on the relation of our view of vitamin D to previous research, that we do address most of those questions in detail in the book chapter (many are also addressed in other links on this site, but in less detail).

We have been told that the book is coming out soon, but there may still be time to order it with the 40% prepub. discount, Nova Sciences Publisher: Novascience@earthlink.net . And the rest of the questions should be addressed in my conference presentation on June 18 in L.A.

The book:  Vitamin D: New Research, Editor Veronica D. Stoltz, Nova Science Publishers, ISBN: 1-60021-000-7, see: http://novapublishers.com/catalog/product_info.php?products_id=4130

We know our view differs from previous notions in a number of ways, but besides the scientific information, responses to treatment are so much better with reduced D and Benicar than minocycline alone, as shown by many experiences posted on this web site, that it provides strong support for the Marshall Protocol.

Joyce Waterhouse, Ph.D.

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Dr. Marshall, re: your comment about Autism, is it assumed that once the damage has been done to a child in their formative years and they are diagnosed with Autism, that the Autism is irreversible? Has there been any experience in treating Autistic children with the MP? What effects were there, or, would you expect?

Many thanks for "fighting the good fight" for all of us who are suffering!

Prof Trevor Marshall
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Barbara,
With the exception of fibrotic tissue deposited in the organs by years of disease, we have seen the body exhibit a miraculous ability to heal itself.

The adults have recovered their brains, their memories, their cognition, decades of their lives. I don't see why we shouldn't expect the same phenomena of neuro-regeneration in children. There is one child, Matt, who has indeed exhibited such a recovery.

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Trevor,

In regards to fibrotic tissue, I have an area of excess fibrotic tissue just below the skin that's visible on my left side due to a surgery which hurts at times when herxing and appears to be decreasing since I progressed thru Phase 2.  It's making my left and right sides look more symmetrical and although I don't know how much of it will go away the MP is definitely helping some, IMO. :cool: 

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Reeenie, I would expect fibrosis to slowly remodel, but progress with that will be very slow, I think.

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Dr. Marshall,

My MP doctor has a 3 year old boy with autism.  I passed along your conversation with the Pediatrician in Sweden who has noticed higher autism rates. 

I suspect this MP doctor will call you for advice on her own son.

Sherry

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Trevor,

If I look at the Karolinska handout I see that Olmesartan is an agonist of the VDR. However, it says 'low'.

If I am not mistaken, that means that low levels activate VDR, whereas high levels don't.

Can you explain why?

Reason I ask is I am trying to convince Ellen that she should start with beni 40mg/8 hrs, but she is scared to death. That stems from last year, when she tried beni at about 10/20MG per 24 hours. She herxed like crazy then and leads her to now fear the beni. Especially at higher doses.

She doesn't react normally to any medicin. Higher mino leads to more pain, even at doses of 200MG/day. She is probably just infected to heavily.

TIA

Sincerely, Frans

PS  Maybe this info is in the upcoming paper, but since I don't know when that comes out of peer review I decided to ask this question now

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Frans,
Olmesartan is an agonist of the VDR. It activates the recptor by exerting forces on both the active helices which are similar to those of 1,25-D. If the patient has high levels of 25-D then you would need a higher dose of Olmesartan to displace the 25-D from the VDR, as 25-D has a higher affinity for the receptor than does Olmesartan.

But, in general, unless the person is taking D supplements, Olmesartan activates the VDR at typical hypotensive doses. To get the palliative action of Benicar you have to use the higher doses (40mg every 6-8 hours), as different receptors are involved in the palliative actions.

The moderators now have a means to help Doc manage runaway herx, so you no longer need to fear that.

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Frans, I had a similar experience to Ellen. Prior to my official start of a full dose of Benicar, I was only able to get 30 Benicar. I was eager to begin the MP and not understanding exactly what Dr Marshall just explained, I did about the same as Ellen did and took 20mg 3x a day. I was hoping that would get me by while I found a doctor that would prescribe the full recommended amount, but thought I'd just get started on a lower dose with what I had. Silly me! 

That low dose was enough to start me on my way to a magnificent neuro Herx, but not enough to protect me from the worst of it. With the good advice of Lottie and Dr Marshall the next day, I stopped the Benicar until I could get on the full 40mg 3x to 4x a day.

Like Ellen, when it came time to start the Benicar at the full recommended dose, I had some real concerns because I had experienced this horrid Herx on less. I wondered how more could be safe. But I took the leap of faith and in the time I've been on the approved MP dose for Benicar, all Herxing has been tolerable. Methods to control a runaway Herx are available now, too.

Also Frans, I thought how great it was to see you at the conference just for me. But maybe it was for Ellen too. You can tell her I am a real person that had a similar experience to hers on a sub-optimal dose, but I have been able to regain much of my health at the recommended Benicar dose.

I wish you both the best--Janet

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Thank you Trevor and Janet,

And yes, it has given Ellen a very good feeling to know she is not the only one having symptoms and problems and that others have had the same experiences.

 

Trevor, I have another question that concerns the Karolinska handout. I have shown it to some people, amongst those was our doc, and they ask me what the numbers behind the diseases mean.

Is that the number of people responding or is it the number of people who have shown progress/recovery/full recovery?  Eg for ME/CFIDS it states:  77/40.

Thank you, Frans

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The larger number is the number of patients reporting in phase 2/3 who have that definitive diagnosis, along with the number who are reporting positive results already.

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Thank you Trevor, that is exactly what I wanted to hear/read  :cool:

Frans

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Ok, now what I have done is make someone sleep a little less easy than before  :cool:

Why? Well, we have an authority on vit. D in our little country, a certain Professor P. Lips.

To check, go to pubmed.com and type in: "lips p"[Author]  including the quotes.

I thought it only prudent to inform him about dr Marshall's findings, so I sent him the Karolinska handout  :D   I have received a notification that he read the e-mail.

I have also ent him the link to book coming up from Novascience.

Now let's see what happens...  this will blow his believe system about vit. D apart I guess  :D:D

Sincerely, Frans

PS  I also informed JJ Kragt MD about this (also in The Netherlands). She is working on a paper about levels of 1,25D in Multiple Sclerosis, see:

- http://tinyurl.com/p4akz

 

Last edited on Sun Jul 30th, 2006 05:04 by Frans

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Don't bother about Dr Marjolein Drent, the chief sarcoidosis 'expert' in The Netherlands. She canned our first paper (in 2003) and wouldn't even speak with Meg and Belinda at the WASOG conference in Denver last year. Your Crown Prince is out of luck, I guess (I have heard he suffers from Sarcoidosis):X

ps: actually, I guess that familial aggregation might be a particular problem in this case:X

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Trevor, I know, I have been in contact with dr D. in the past :D

Maybe it would be nice to rattle her cage a little more by sending a link to the new book :cool:

About our Crown Prince, you told me once. If and when my energylevels permit it, I will try to contact our Prince and bring him up-to-date, but it takes a lot of time getting all the info together to explain. They don't use email, so all has to be printed out...

Sincerely, Frans

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Don't his aides use the telephone?
I would tell them about the conference you attended where the International experts (Canada, Japan, USA) all agreed on the bacterial pathogensis for Sarcoidosis, and how you have been unable to get Marjolein interested in the past... And how she didn't even bother to attend the conference... Nor even talk about the new discoveries when she had the chance at the Denver Conference last year.

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Telephone? They should, shouldn't they? Some of the most simple things keep eluding me...

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I think that I have a decent understanding of how 25D, 125D and Benicar affect the VDR and other receptors.

However I would like to be able to explain to people how our bacteria fit into the picture. I think you said you are not sure exactly how they disregulate our D metabolism...but perhaps you have some idea.

Does it still hold true that our bacteria convert 25D more rapidly to 1,25D (hence the altered ratio of the two D's seen in Th1 patients?)

If bacteria do cause levels of 1,25D to rise I understand how this would be detrimental to the thyriod, glutocorticoid receptors etc. However how would an increased level of 1,25D negatively affect the ability of the VDR to funtion? It seems that less 25D and more 1,25D would actually help the VDR stay more active.

Any help appreciated!

Amy

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High levels of 1,25-D make sure the VDR continues to function fully activated. Innate immunity will mostly work fine. But higher levels will affect the Glucocortocoid receptor, which affects other immune functions, mostly in adaptive immunity.

In the last year there have been discoveries about the enzyme which makes 1,25-D from 25-D; called CYP27A1, and also experiments showing that CYP27A1 is active in macrophages, and not just CYP27B1. Another study showed that CYP24, the enzyme which breaks down 1,25-D; is expressed (controlled) by VDR activation.

D-Binding Protein (DBP) releases 25-D dependent on the presence of 1,25-D

So it is clear that the level of 25-D follows not just the simple over-usage model of years past, but is much more complex. IMO it is likely that the availability of 25-D is directly controlled by the immune system's need for that precursor.

Ingested vitamin D would upset that homeostasis.

The Bacteria feed the inflammation. They may interfer with the D metabolism directly, but I suspect that thye just feed the inflammatory reponse, and that is enough to cause the immune system to hyper-produce 1,25-D

Hope this helps

ps: here is one of the papers describing the enzyme actions:
"Metabolism of vitamin D3 by cytochromes P450"
http://tinyurl.com/lgady

Last edited on Sun Aug 6th, 2006 08:47 by Prof Trevor Marshall

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Very helpful..thanks!

Wait..actually...

It seems that the presence of bacteria leads to lower levels of 25D and higher levels of 1,25D. But if this is the case I feel Th1 patients should have a very strong innate immunity response..

Can that be right?

Last edited on Sun Aug 6th, 2006 10:14 by Ames

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I'm glad this topic is being discussed. I took this from Cell Wall Deficient Bacteria and the Marshall Protocol:

"High levels of 1,25-D allow the bacteria to colonize the phagocytes, avoiding the lysosomal phagocytosis."

It does seem that the bacteria don't necessarily have to directly control 1,25D. Bacteria just signal cytokine release, cytokines inflame, inflamation stimulates 1,25D, 1,25D allows bacteria to colonize and avoid lysosomal phagocytosis. How the bacteria avoid lysosomal phagocytosis I would like to know.

Perhaps CYP24 is being manipulated by the bacteria. Maybe CYP24 isn't expressed mainly by the VDR. It could be suppressed via another receptor in more strength.

~Greg

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Greg,
I think that the way the Th1 inflammation initially overpowers the immune system, is that the level of infection gets to a critical value, and then an incident occurs (eg, sun-holiday, pregnancy, acute infection) which causes extra 1,25-D production, leading to a breakdown of the negative-feedback mechanisms which normally control the 1,25-D production in the phagocytes. From that point onwards those control mechanisms are not able to reliably maintain control. The patient enters a "relapsing-remitting" phase of the disease process.

Additionally, the TACO membrane protein, through which Mycobacteria infect the phagocyte (and possibly L-forms too), is down-regulated by VDR. So the actual entry of the bacteria into the phagocyte may be facilitated by excess ingested 25-D or Vitamin D causing the VDR to shut down.
http://tinyurl.com/nkb7x

Cholesterol is also involved in the expression of TACO:
http://tinyurl.com/l8rzj

Last edited on Sun Aug 6th, 2006 12:17 by Prof Trevor Marshall

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I had intially thought there was a threshold that 1,25 could be regulated to and then anything over that the feedback get's fuzzy.

In essence I take it that up to a specific threshold 1,25D keeps the VDR activated but down regulates the GCR, adaptive immunity if 1,25D is above that threshold.

Hyper-produced 1,25D keeps the negative feedback from expressing CYP24 that causes breakdown of 1,25D. On top of that, ingesting 25D inactivates the VDR causing CYP24 to not be expressed. That's how 25D (and cholesterol) facilitates the process by which the TACO membrane protein is down regulated and colonization takes place along with avoiding lysosomal phagocytosis. That is, if L-Forms use the TACO membrane protein. Is there anyone looking to find it? Are we talking about the protein shell around the colony or larger form or cyst? Why do we call it "biofilm"? I thought the term biofilm represented a group of larger Prokaryotes in colony extracellularly. Is it correct to say that intracellular bacterial colonies have a biofilm?

Sorry if it's all jumbled or wrong :) I'm just trying to learn. 

~Greg

Last edited on Sun Aug 6th, 2006 15:35 by tickbite

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Nevermind :) I'm jumbled. I figure I need to finish reading Lida and Alan's books amongst everything else. I'm intrigued that Alan mentions Edgar Cayce in his book "The Cancer Microbe". Bizarre how his name keeps coming up. I'm so happy to be reading the history of filterable forms and mycobacteria.

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Greg,
Let me explain it this way. When every VDR receptor is occupied by a 1,25-D molecule you have a saturated VDR subsystem. At that point CYP24 would be up-regulated to maximum (assuming VDR is the primary regulation of CYPR24, which is currently believed) and that would tend to catalyze any unbound 1,25-D to oxidize to inactive 24,25-D 25,26-D and 25-D.

If the 1,25-D keeps being hyper-expressed beyond this level, maybe by excessive solar exposure, pregnancy, or by a bacteria-induced catalysis, then the higher 1,25-D concentrations will progressively affect GCR and Thyroid receptors. Perhaps by ths point those receptors are already heavily occupied with 1,25-D it would depend on their native metabolite, and factors we can't yet quantify.

I hope this helps

..Trevor..

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This fits with my experience.  In July 2002 I took a sun holiday up in Alaska for 1 week.  After coming home I had an operation (partial hyster) some 10 days later.  Although I thought I recovered nicely from that surgery (my first and only) my overall energy level decreased as my brain fog increased.  I took another Alaskan vacation in August 2004.    Sarcoidosis was diagnosed in December 2004.

Possibly it is coincidence, but it fits the pattern. 

Sherry

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This fits my experience too. My first significant symptoms started in my first year of teaching (stress!), and then my next set of significant symptoms (neurological) came after my 2nd child's pregnancy. Then toward the end of my third pregnancy, I started having frequent arrhythmias. For the last 10 years since then it's gone downhill steadily.

:shock: Jill

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Dr. M,

You wrote:

1,25-D, and the other Vitamins-D, have a high affinity for a number of receptors. Generally, 1,25-D activates VDR, but it also has a high affinity for the Glucocorticoid Receptor and for the Alpha and Beta Thyroid receptors. So, as the concentration of 1,25-D in the body rises, it displaces Cortisol out of the GCR, T3 and T4 out of the Thyroid receptors.

What does this mean regarding any assumptions (if any) that can be made about cortisol or free T3/T4 levels with regard to high 1,25-D levels?

Thanks,

Alison

Last edited on Mon Aug 28th, 2006 10:26 by Alison

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Alison,
We are now looking much more closely at the 25-D levels, and have developed a better understanding of how to use that data intelligently. Joyce covered much of this in her presentation at our 2006 Conference (the DVDs will be available in a few weeks).

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HI ALL

This is Fred in WV.  I hope I am reading about the vit-D correctly.  Here is my live story about the vit-D in just a few words.

I was born Sept 1, 1939.  I had rickets at that time.  The doctor said it was a vit-D shortage and mothers milk was not strong enough so I was put on can milk. So now a new born getting more vit-D and the weak immune system I did not have a chance.  A few years later I was diagnosed with iron diffent anemia. So I took several meds for this including getting liver extract shots every other day for some time. I was in about the 2nd or 3th grade at that time.

So I think this all caused the sarc.  I hope this is not off the subject.

Remember, we are all in this together and I am pulling for us.

Your friend in sarcoidosis

Freddie

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Freddie,
Joyce (and the rest of the team) have been looking into the new discoveries about Rickets. It is now certain that Rickets is not caused by a lack of Vitamin D, but by a lack of dietary Calcium and Phosphorus.

Just this morning I found this study on mice
http://tinyurl.com/z7k2s
which confirmed this big Government study
http://tinyurl.com/l63hk
which concluded: Rickets "is not due to vitamin D deficiency but is caused by not having enough calcium in the diet"

Not only is Rickets is not caused by a lack of Vitamin D, but you don't need to supplement Vitamin D in order to cure it.

I would rate that as the second biggest mistake in medical history - the first was calling 'vitamin D' a 'vitamin':X

You might also be interested in looking over a paper from 1857, a paper which pointed away from Vitamin D as the cause of Rickets.
http://ije.oxfordjournals.org/cgi/content/full/32/3/336

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Freddie,

I have been looking at a lot of studies on Rickets and so far I have not come across any reports of Rickets in newborns. Are you sure you were actually diagnosed with it at birth? There may be cases, but I just haven't found them reported.

Most case seem to occur after weaning when the parents give them very low calcium diets for various reasons.

Joyce Waterhouse

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HI JOYCE

This is Fred in WV.  First thanks Trevor for all the info.  Second, Joyce the story I was told all my life by my parents was that I had problems and mothers milk was not strong enough. This happened just a little while after I was born.  So they put me on can milk.  That it caused the rickets.  Thanks for your interest in this.  If I can answer any othe questions please let me know. 

Remember, we are all in this together and I am pulling for us.

Your friend in sarcoidosis

Freddie

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Fred, Joyce,
In years past it has been thought that Mothers milk was not "strong enough" because of its "appearance" as compared to the stronger *appearance*/coloration of cows milk, and many babies were weaned from their Mothers onto cows milk for this reason.
Thanks, Barb .... 

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HI ALL

This is Fred in WV.  I forget to tell you also I was so knocked kneed that when I ran I would lay down and cry because I hurt me knees so bad and they would be blue.  But I did out grow the knocked kneed problems.

Thanks

Your friend in sarcoidosis

Freddie

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Dr. M,

Thanks for the info. I look forward to seeing Joyce's presentation (and every other presentation) when the DVD's are available.

Presumably this new insight into 25-D (vs 1,25-D) will eventually lead to the "advanced diagnostics" that you have spoken of before. You probably noticed my question in the General forum regarding these new diagnositcs. I'll assume by the lack of answer (though I hate to assume) that the info isn't really available to "publish" yet. Admittedly I am anxious to see it.

For my case in particular, I'm seeing some confusing data in some of my own recent pre-MP test results (which I plan to post as soon as they are all in). This is wrt 25-D, 1,25-D and T4, amoung other things. Nothing seems to make sense from the "old school medicine" perspective. That's why the some new diagnostic "tools" are so intriguing to me.

I'd also like to echo previous member comments regarding your willingness and ability to adapt your theory and approach to follow the actual science, instead of the other way around. Too many scientists don't have that (the ability or the willingness). Bravo, Dr. M.

In much appreciation,

Alison

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Alison
Dr Marshall has replied to you here in this thread: see above..

and you will be replied re your own D tests when you are able to post them.
Please see What to include in your preliminary test result reports.

Thanks, all best, Barb ...

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I had rickets after birth. I don`t know if i was put on vitamin D but probably yes, why should not I considering current medical thinking in those years. Maybe this could explain some of my constant health problems during life, like allergies and beginnings of asthma.

So Vitamin D abnormalities does not affect absorption of calcium ,is not that a great breakthrough? Most people thinks that rickets is caused by reduced calcium absorption due to vitamin d deficiency. I remember that 1,25-D high levels causes bones resorption into the blood and in case of Th1 inflammation, consuming more vitamin D only weakens bones more. In this case could not we suplement some minerals, calcium to normalize levels that are beeing depressed ? Would it help in healing ,herxing,symptoms or better functioning of immune system, anything ?

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Wrotek,
The ARF team has been looking into Rickets over the last few weeks, and what we have found will interest you, I am sure. I will start a new thread on Rickets in my 'perspective' thread. Please post anything you can find out about your own joust with Rickets into that thread.

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Yes i am curious what effect on the future disease story may have this disease, or vitamin d youngsters suplementation. I suppose, like in the mice with diabetes studies, that what happens to young persons in their first months of life is crucial for immune system functioning in the future



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