Submitted by kerem aytan on Thu, 2009-06-18 18:45

  Since I was a strong supporter of VİTD3 supplementation, I feel responsible to post that report which is very supportive for Marshall protocol. I'ıı try to discuss this issue with Dr. Stratton to decide whether I should go on taking high dose VitD3 supplemantation.  DR. CHENEY: Balance the Immune System (Th1/Th2) Print E-mail Articles - Chronic Fatigue Syndrome Articles      That's MP, you can easily see the similarities. ''In people infected with cell-wall-deficient bacteria, the production of 1,25-D can spiral out of control and rapidly reach damaging levels.  This happens because, as an evolved survival mechanism, cell-wall-deficient bacteria are capable of catalyzing the process by which Vitamin D is converted to 1,25-D.  Instead of a slow, controlled conversion which occurs only in the kidneys, 1,25-D production becomes uncontrolled, occurring throughout the body inside cells infected with cell-wall-deficient bacteria. Specifically, immune system cells harboring cell-wall-deficient bacteria can turn into tiny, unrestrained factories producing excessive amounts of 1,25-D. Bacteria catalyze the 1,25-D conversion process intentionally to cause immune system suppression and create a more favorable living environment in the body.   The result of catalyzed 1,25-D production is a subclinical yet devastating immunosuppression syndrome that allows Lyme Disease (and other types of cell-wall-deficient) bacteria to persist chronically in the body.  When present in appropriately controlled quantities, 1,25-D is a critical nutrient and is important to health, as we have said.  However, when present in excessive quantities, 1,25-D is immunosuppressive and inhibits the immune system from fighting infections. This process is one of the core survival mechanisms of Borrelia Burgdorferi.  The excessive levels of 1,25-D often present in people harboring chronic infections leads to a greatly inhibited host defense system. By accelerating conversion of Vitamin D to 1,25-D, these tiny bacteria are basically able to neutralize the human immune system. ''

  Lousie, I didn't check my heavy methal levels, but I do think I'm intoxicated. Many years ago I had an amlagam filling and 2 years ago ıt leaked into my mouth, I didn't understand what was it, I didn't worry and swallowed it. This leakage lasted for a few months. So I plan to check it soon.

  Norman, don't be sure you are not intoxicated, I advice you go and get a urine test after DMSA chelation.

  pgm, thank you for all this usefull information.


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

  pgm, there's one more thing, do DMSA or ALA also chelates the antibiotics and supplements we are swallowing.


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

Kerem, do you recommend DMSA plus urine test to everyone? Because it's not like I'm searching for causes of health problems, these days; I'm feeling pretty good. If you recommend it to me, you might as well recommend it to most everyone.

As for your amalgam "leaking" into the mouth, I'd get that filling replaced, if you haven't already. Not because it is amalgam, but because it might be hiding an infection under it, which might have been what was really leaking out. (It would have to have been a very poorly done amalgam filling for the amalgam itself to leak. And leakage lasting months is particularly unlikely to be the metal of the filling itself.) Even if it were the amalgam that leaked out, that would leave the filling with a gap under it which could harbor bacteria. For an example of the insidious effect that that can have, see this paper, whose abstract is:

This report describes a remission of rheumatoid arthritis (RA) of 16 years duration, apparently caused by the extraction of endodontically well-treated, healthy looking teeth. The only clue that the teeth were contributing to the disease pathogenesis in this case of RA was that the patient was able to reproducibly induce severe attacks of arthritis after prolonged, heavy pressure on some of his teeth treated with root canal fillings. After extraction, a small pus layer was found to cover the apices of the clinically healthy looking teeth. The rheumatoid factor (RF) became negative and the patient remained symptom free for the next 16 years. The possible connections between micro-organisms in closed dental foci under constant pressure and the chronicity and exacerbations of RA are discussed.

PGM, those mercury/cytokine results have so much noise in them that it's hard to know if they have any meaning, at least as regards the results for doses of mercury too low to interfere with cell vitality. Even some of their control experiments have results varying by a factor of ten.

As regards the NF-kappa B inhibition, just because a molecule inhibits NF-kappa B at really high concentrations doesn't mean it'll do anything at all to it at low concentrations. Activity is not always proportional to concentration; it's often less, especially in a complicated environment like the cells these experiments were conducted in. And even if it were proportional to concentration, the sorts of concentrations one gets from oral supplementation are hundreds of times lower than the concentrations used in the studies you linked to, and would thus yield a decrease of less than 1% in NF-kappa B activity, which isn't likely to be noticeable amidst all the other influences on that pathway. It may do good things as regards apoptosis, in the usual oral doses; but if anything, the studies you linked to show that if it does do those good things, it doesn't work via NF-kappa B, because the concentration would have to be unachievably high for it to work that way. Instead it would have to work via some other mechanism. (Say, by promoting mitochondrial health, in its role as an important mitochondrial cofactor; the mitochondria are heavily involved in apoptosis.)

By the way, I've been trying out alpha lipoic acid, and it does indeed seem to enhance die-off symptoms quite a lot. (I'm taking it with antibiotics). So I have no quarrel with the idea that it might be a very useful supplement. I just don't believe those particular papers show a mechanism of action that's relevant to the sorts of doses I'm taking.

 Norman, yes, I do recommend DMSA+urine test to everyone who have diseases like MS, ALS, AUTİSM,CFS etc. For every condition or disease we accuse CPN or microorganisms there are doctors and peoples accusing heavy methals. This is an example posted by Raven. 

Evenif you may not believe heavy methals having any role on these diseases, there is evidence showing that heavy methals make it very diffucult to fight against infections, by forming biofilms or some other mechanisms making them resistant to antibiotics. That was posted also by Raven I think

 So if you do really well with antibiotics ,you may not need cehatation tests.

 If we talk about the thing leaking into my mouth, you may be right, it might be an infectious fluid also, but in any case it's something related to amalgam filling. And you are right again, I have to go and take it out. I didn't do that; because untill recently I never thought that I may be a patient. I always thought that what all I experience were just reactions to antibiotics, because almost all of them started with NAC test and following CAP treatment. Since I'm a very hardworking doctor, I also didn't have anytime to do that. But recently, after feeling an increase on my symptoms and realizing my partially atrophic forearm, and new level of CPN titers which is 1/1280, I started to afraid of a CPN(and/or lyme) related serious disease even ALS. So I'm waiting for the results of western blot and co-infection tests. After getting them I will go to a big city, to a good medical faculty, I will get my MRI,EMG,DMSA CHELATİON and some other tests (ıts not easy to do all these evenif I'm a cardiologist, because neurologist will not enjoy me when I talk about all these infections and tests, because they are all big doctors, big professors, they know all what to be done) and then I will get my amalgam out.

 If we talk about ALA, how do you differantiate your symptoms as die-off, I also got ALA 200mg daily for a year and after learning that it has a heavymethal chelating property and may cause redistribution of mercury if not used properly, I stopped taking it, because I couldn't be sure of that it was die-off, it could also be redistrubution of mercury.



KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

Kerem, I appluad your continuing afforts to understand in detail these mysteries that have become so difficult to unravel. Its not easy when other microrganisms come into play along with cpn.

Each microrganism has its own behaviors, metabolism, and effects on the immune system so without knowing the exact combination of what is going on in each person, its almost impossible to say what is the right and wrong option for any supplement, alternative treatment or antibiotic. Its really an individual thing and you need to take what is relevant to you and decide what works.

I have proven some things to myself through this scrutiny process that reflect the work of Dr straton, ceratin supplements and the suggestion  to endure a slow die off process for cpn for example, but I also have picked up other perspectives in which for other microrganisms a slow cap may not be the best option.

I personally disagree that this protocol can cure lyme and severe cases of bartonella. It also does not cover babesia.  Lyme requires at least 400 doxy a day, ( to cross the bbb ) where cap for cpn uses doxy 200 per day. Bartonella requires high dose rifampin ( 600 ) per day with doxy or zithro daily where cap suggests 300 per day rifampin with doxy and zithro mwf as part of a combo. The Roxy dose for lyme treatment is also higher than the roxy dose for cap.

Thats about all i disagree with in regards to slow cap. I do think its the correct and only option for treatment of c pneumoniae and i very much appreciate all the information Ive gained here. I also think C poneumonia has to be treated first before tic borne illness. So its seems sensible to me that if you have cpn with other pathogens, start with the CAP for cpn and when your antibodies to c pneumoniae go down and you are pcr negative, .. a few months after that, if you still have symptoms, switch over to high dose treatment in a progression for tic borne illnesses. Bartonella- lyme, then babesia- lyme, then lyme itself. Erlichia would already be taken care of by the cap for cpn. At the very least cap will at least prevent lyme and bartonella from spreading while treating the c pneumoniae infection.

I like your approach kerem, process of elimination through scrutiny... if you keep sorting you will get answers.

I still did not produce a bartonella antibody at 8 months on abx. I am going tomorrow to test again for antibody to lyme and bartonella now at 14 months. I wish i could do the extensive bartonella or Lyme WB testing but right now its not an option financially.

I was pcr positive for c pneumoniae prior to treatment, at 4 months pos in blood, at 6 months pos in tissue and blood and I was officially pcr negative for c pneumoniae at 13 months

Keeping in mind there are many species of bartonella and most labs test for only B hensalae. Please pm me if you would like information on a lab that specializes in bartonella diagnostics with multiple species. I still have not done the tests there, they are about 300.00 but are very extensive

Also the bands on the western blot for lyme disease are also known to change over time with those that were equivocal, converting to positive. Im going to eventually to do a re-test for that as well.

As for vitamin D, its a tough call. Im going with the crowd here on this one and have chosen to up my levels. My concern though, is that the drug companies are behind most of the vitamin d research and Ive leanred that they always have distorted agendas. They seem so obsessed with proving vitamin D to be godsent, it almost makes me wonder if its done with hidden agenda like all the other drugs they tout such as MS meds.

Furthermore I believe based on my own research the benefits of benicar, so I have one vote for marshall on that one, plus i believe that minocin is the most effective drug for all of these diseases which makes it harder to discredit marshalls D hypothisis. However, as i mentioned, Im still going with the crowd here on this one, mostly because Im too tired and frustrated to sort through the mass of variables on this debate. Its alot of work so im just gonna go with my gut- majority rules. I vote for sunshine. I admire that you have the motivation to sort it out, I do think it can be sorted but again I personally just dont have the energy or brainspace right now. If you do sort it out through your own methodologies, please let me know your findings.

My best to you, stay strong and dont stop searching for answers



 clammed_up; thank you for all these appreciating words. I will be strong, because I'm not fighting for myself, before that I'm fighting for my children.

 When we talk about VİTD3, you shouldn't worry about drug firms, they can not make money by VitD3, because it's the cheapest drug in the world, you go out the sun, and you get your VitD3 with no payment. Depleting VitD3 sources looks very unnaturel when we have so much VitD3 receptors in our body, but I think there should be an optimum level that VitD3 helps, I don't believe anymore that higher the VitD3, better the our health, there should be an optimum level and optimum dose of supplementation, and nobody knows this dose.

 When I have enough time I wan to investigate MP in details, but ıt looks me possible that highly evoluted microorganisms like Borrelia and CPN (THEY HAVE UNBELİEVABLE CAPABİLİTİES REALLY) might be using our D VİT receptors for their own benefits (Borrelia forexample can peel B lymphocyte's membrane and wear it for camouflage, can send posts to other microorganisms etc.., CPN can use apoptotic mechanisms in an unbelievable way to replicate freely inside the macrophages for months-I got this article newly, after inspecting it I will post here.)

  While CAP can block borrelial and bartonella infection, it wouldn't be enough for babesiosis which may be the most dangerous one, we should also consider it.   

  And lastly, evenif we don't know which microorganism is the ringleader, Dr. Stratton thinks that it's CPN, and if you can beat it, immüne system will beat the others.



KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

The only real test for whether something is die-off is whether you feel better, after it's over, than you did when you started. (Not just better than you felt in the middle of the reactions, but better than you felt when you started.) Here, by that test, I'm speaking prematurely; I've just started ALA. So I don't really know. But I have a fair bit of experience with what symptoms I get from die-off (as proven by that strict test), and this feels about the same.

As for that article whose abstract you link to, Yilmaz, on cilantro, mercury, and chlamydia, I believe there was an earlier link on these forums to the full article. I glanced through it, and it struck me as complete nonsense. I forget exactly why, except that they hardly did any laboratory measurements (of, for instance, mercury concentration); they just hypothesized that all these things were occurring.

Anyway, why wait to have expensive and difficult tests done, before getting that filling out? One way or another, it needs to get fixed, so just go to a dentist and get it done. You might lose a bit of information as to the precise cause of your ills; but getting better is more important than knowing exactly why you felt bad.

(Sorry, by the way, for calling you Kerem earlier.)

Drug companies if they had a hidden agenda with vitamin D, it would be to change some metabolic process in the body which would lead to a specific chronic illness or disordered state, under some condition eventually leading to dependency on some sort of expensive medication. A bit far fetched and I dont think thats the case here, but that is how they operate. Human welllness is not thier agenda. Money is thier agenda, and that can only come from human illness. So when theres too much hype on something, one needs to be suspicious and consider the motivations, examine the sources of funding of the research etc..





KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

Hey yilmaz,  I felt compelled to do basic D debate research... interesting that the marshall perspective on distorted VDR ( vitamin D receptors ) appears to support my conspiracy thoery. -->

"to change some metabolic process in the body which would lead to a specific chronic illness or disordered state, under some condition eventually leading to dependency on some sort of expensive medication."

The marshall perspective is that D supplementation will not work for us ( the multi and lyme infected )because we have distorted VDR's from the infection ( blocked with lignands and/or unable to be expressed)and the more we try to supplement the more we create distorted ( blocked or unexpressed )VDR which then depresses our inate immune system thus we cannot recover . Benicar because of its abilty to knock out lignands, will prevent distorted VDR and then stimulate our innate immunity.Eventually with increased kill of the offending microrganisms by the immune system, the VDR will regulate itself. Until then, one should not supplement with vitamin D because the receptors are distorted

Totally simplified ofcourse, but Is that the correct idea without getting technical?

Some quotes from marshalls site:

Rising levels of 25D and 1,25D start knocking out other receptors as well as the VDR and, the bacterial load shuts down other receptors as well as the VDR in the case of Bb perhaps the Estrogen beta receptor.

Bacteria that produce a ligand (e.g. capnine)  blocks the VDR.

Benicar is effective at displacing this ligand from the VDR and re-activating it.

Live Borrelia burgdorferi reduced VDR expression in monocytes by 50 times, and lysates ('dead' Borrelia) reduced it by 8 times

Benicar has two roles. It selectively suppresses the immune system to reduce inflammatory symptoms. And it activates the Vitamin D receptor to enable the immune system to kill intracellular bacteria resulting in immunopathology, indirectly increasing symptoms

As we recover and the innate immune system becomes more active, 1,25-D will recommence its role as VDR agonist. At some point the immunosuppressive action of Benicar (and it's ability to reduce symptoms) becomes dominant over its role in activation of the VDR (which is so critically important at the start of treatment).

Benicar is not a "medication." It is a method of turning-on your body's VDR (Vitamin D Receptor). This is a key part of the immune system, and transcribes over 1000 genes which affect body processes from calcium homeostasis to cancer metastasis. We know that the VDR is blocked from operating properly by the intraphagocytic microbiota.

Now how do we decide if this is true or not... nothing really to do except weight out the conflicting research against each other and examine the credibility of all the sources and consider the motivations. Thats a whole lot of work isnt it?

Maybe its as simple as assuming if the drug companies support something, then maybe we should do the opposite. Maybe the drug compnies know that vitamin D supplementation in healthy people = good health but supplementation in infected people = autoimmunity. What if that is the case? Remember these drug companies need people to have autoimmunity to keep thier finances afloat.

I still have no permanent opinion, but i will admit, i am being swayed to a certain degree. What if this info is correct?

I have low BP so the idea of taking benicar is sort of worrysome to me.



This turned out to become a complicated discussion. I have tried to knock the MP theory down as well with the VDR+Benicar, but have been unable to do so. But at least one thing appears to be wrong with the MP theory; vit-D doesnt seem to be immunosuppressive (at least for everyone) like they claim, but rather immunomodulatory, or else you would not get die-off symptoms which are comparable to those which antibiotics cause. Perhaps only more nastier bugs like borrelia causes this dysregulation of VDR, but not Cpn?

But one more thing regarding lipoic acid. Some people feel that their inflammation is reduced sometimes when taking ALA (especially in a frequent-dosing manner); this effect of lipoic acid can't only be explained by mitochondrial effects alone. I realise that there can be other factors than NF-kappa B involved in the die-off, but at the moment it seems the only reasonable explanation, because it is also related to the inflammatory cytokines. Inhibiting NF-kappa B, leads to less inflammation, but also die-off, which is what people report when taking alpha lipoic acid. The effects seem to also be similar to Benicar, which is also said to inhibit NF-kappa B via VDR. Of course, we have no research in this case what amounts of Benicar is necessary to inhibit NF-kappa B. I would also believe you can't accurately say at all what amount of substance is needed for total inhibition of NF-kappa B in various cases, depends a bit on the infection, how strongly the NF-kappa B is activated by the infection. Moreover, ALA inhibits NF-kappa B in a dose-dependent manner; total inhibition is not necessary for all the good effects to occur. The researchers in this paper
suggested that ALA could actually be used as a therapeutic agent to reduce NF-kappa B. I don't pretend to understand everything about NF-kappa B inhibition, but it still seems like the most reasonable explanation for the effects of ALA to me.

"pgm, there's one more thing, do DMSA or ALA also chelates the antibiotics and supplements we are swallowing."

Well ALA is not known to chelate e.g. any minerals, as it is something that cells take up and convert to DHLA. DMSA on the other hand stays in the extracellular fluid where it can pick up various things like mercury or porphyrins, and some have reported that it can chelate minerals away as well. But antibiotics in themselves can also have some chelating properties - I've heard some claims about minocycline being a chelator of some minerals, and it does cause teeth discoloration in some people.

No official diagnosis.

That paper still is looking at millimolar and high micromolar concentrations: for example 33% inhibition of NF-kappa B for 250 umol/liter ALA. To quote Derek Lowe:

By traditional med-chem standards, single-digit nanomolar = good, double-digit nanomolar = not bad, triple-digit nanomolar or low micromolar = starting point to make something better, high micromolar = ignore, and millimolar = can do better with stuff off the bottom of your shoe.

The reason medicinal chemists despise such compounds is that there's no way of getting close to those levels, in human dosing. If I recall correctly, you said, for instance, that you were taking 300 mg doses at a time. That's about 1.5 millimoles, something like 30% of which is absorbed (0.5 millimoles). That's enough to fill up two liters to a level of 250 umol/liter... but human body volume is more like 50 liters, so what you can actually get is 0.01 millimoles/liter. (Actually, less than that, since it isn't all absorbed at once, and it gets eliminated quickly.) If the inhibition scales linearly, that'll give about 1.3% inhibition of NF-kappa B. The activity of the NF-kappa B pathway in any given cell probably varies more than that just from random thermal noise, not to mention all the other influences on it.

(And yes, it is nevertheless true that those researchers suggested ALA could be used as a therapeutic agent to reduce NF-kappa B. One of the dirty little secrets of reading papers is that you always have to check the concentration at which they found an effect, to see what relation it bears to achievable doses. Remember, these people operate in a publish-or-perish environment; and saying that they found a useless effect, which is only measurable at ridiculously high concentrations, is not a good way to get published.)

PGM, They mentioned this VDR issue to be a problem in TB, aids, and lyme thus far, but I dont know if they have looked for the problem beyond those infections yet.



These are quotes from an article which likely explains one reason why D supplementation could be a bad thing

In sarcoidosis, tuberculosis, and several granulomatoses, IFN-γ induces 1,25D synthesis by macrophages and inhibits 1,25D induction of 24-hydroxylase, a key enzyme in 1,25D inactivation, causing high levels of 1,25D in serum and hypercalcemia

The cytokine gamma interferon (IFN-γ) and the calcitropic steroid hormone 1,25-dihydroxyvitamin D (1,25D) are activators of macrophage immune function.

IFN-γ impairs 1,25D control of its own synthesis and catabolism.

This is a "key" quote from an article on c pneumoniae

The levels of circulatory plasma markers (IL-4, IL-8, IL-13, ICAM-1, and VCAM-1) were significantly higher, whereas, levels of IL-10 and IFN-γ were significantly lower in CAD pts compared to healthy controls

* note c pneumoniae does not cause high levels of

IFN-γ !

This is just a random quote from a non relevant article that happens to mention that bartonella is considered a "granulomatous" disease

... was also observed in other granulomatous infections with intracellular bacteria, such as Bartonella henselae.

Other granulomatous diseases

Histoplasmata capsulatum Blastomycosis dermatitidis . Phycomycosis (a.k.a. mucormycosis) Aspergillus fumigatus .Candida albicans, .Rhinosporidium seeberi .Coccidioides immitis and Cryptococcus neoformans Leishmaniasis Toxoplasma gondii Mycobacterium tuberculosis Non-TB mycobacterium are M. kansaii, M. scrofulaceum, M.avium- intracellularis, M. gordonii, and M. fortuitum. Mycobacterium leprae Cat-Scratch Disease (, Rochalimae henselae, or Afipia felis, )Actinomycosis .Syphilis, Klebsiella rhinoscleromatis .Granuloma inguinale, anthrax, brucellosis, and tularemia are other, granulomatous diseases.

Does this in sum say that in granulomatous infections, D supplementation is a problem because 1,25d cant regulate itself due to high INF-y which impairs it. However with c pneumoniae (hypothetically) it would not to be an issue because INF-y is low in c pneumoniae infections. ???


Interferon-gamma is one of the main tools the body uses to suppress Cpn and kill it. That study doesn't show that the body always fails to use this response. What it found was a much narrower result: that coronary artery disease patients (who are losing their battle with Cpn) have less interferon-gamma in their blood than healthy controls (who keep their Cpn well suppressed).


Ok, this seems like a good idea to assume only certain bacteria like borrelia and some CWD bacteria like mycoplasma can cause dysregulation of VDR. The MP was never developed to defeat Cpn infections, but more to diseases that caused dysregulation of VDR. So comparing MP and CAP is a bit like comparing apples and oranges. The MP does also treat Cpn infections to some degree at least, because minocycline and azithromycin is used there on that protocol as well, and clindamycin is some abx directed against anaerobic bacteria, so perhaps it will hit these cryptic forms as well. At least people report a lot of brain fog when using it, if they have central nervous system involvement in their disease.

If the VDR is dysregulated, it seems you need Benicar to activate it again, because VDR is a key component in the NF-kappa B pathway as well, and cells will not be able to self-destruct, if the VDR is too compromised. The results with the ALA/DMSA protocol to treat Lyme disease have been disappointing, and this goes in line with that lipoic acid is not known to affect the VDR.

"If I recall correctly, you said, for instance, that you were taking 300 mg doses at a time. "
No, I'm just taking 100 mg at a time currently. But a single dose won't take you far. You have to keep dosing it e.g. every three hours until you start getting die-off. There are some more efficient forms of ALA, like Na-R-lipoic acid, and even mixtures with dihydrolipoic acid (DHLA), to make ALA more bioavailable. I have not tried these.

Regarding the paper about ALA and NF-kappa B, they mention another paper where they found isolated mononuclear cells from diabetic patients that had 38% reduced activity of NF-kappa B from ALA, after taking 600 mg per day for three days. So, I still wouldn't say that ALA would be a useless therapeutic agent. Perhaps the inhibition status increases for each dose you take, so that the effects will be cumulative, and in the end you can reach a pretty high inhibition level. Anyways, I don't see the use for total inhibition, that would be way too dangerous, if many intracellular bacteria indeed use this mechanism to suppress apoptosis.

No official diagnosis.

You may not want 100% inhibition, but you'll want something more than 1%, because 1% would just be lost in the noise. And alpha lipoic acid is cleared from the body quite fast -- at least the excess over what the body normally uses is. I forge the exact figure, but it only lasts an hour or two. Taking a pill every three hours won't improve the calculation I did, because the stuff doesn't last long enough for the doses to pile up on top of each other. It'll just mean that you'll have frequent spikes in your blood level, instead of infrequent spikes.

But I've never said that ALA would be useless; I've just been questioning the very narrow idea that it acts directly on the NF-kappa B pathway in doses that are achievable. It could well do something else to improve the health of diabetics, in a way that after a couple of days lowers their inflammation levels, among them the level of NF-kappa B activity. Perhaps it does the same for non-diabetics, too. Those studies you linked to were just on isolated cells, but the body has a large number of cells, constantly talking to one another via chemical messages. There are thousands of chemicals in the body; you don't need to single out NF-kappa B in particular as the ones that ALA influences. Personally, I can't keep track of all those chemicals; I couldn't tell you off the top of my head what, say, IL-10 does. That's why I prefer the brute-force approach of killing the bacteria with antibiotics, not the more subtle approach of tinkering with the immune system.

As for the idea of "dysregulation of the VDR", just because you can't knock down a theory that Marshall promulgates doesn't mean you have to accept it. It's up to him to prove his theories, not up to us to disprove them.

  I tried to read MP for 2 times but stopped at half simply because ıt looked me very strange. I will try once more.  Anyway there seems to be a confusion here.

  I wonder whether a properly working D-VİT receptor is a good thing in CPN or other intracellüler infections. Because ıt's certain that DVİT supresses Th1 by working on properly working D receptors, and activates Th2 again by working on properly working D receptors. This effect of VitD3(Th2 supression and Th1 activation) is thought to be it's most beneficial effect on autoimmune diseases like MS.

  What is Th1; it's cellüler immünity , it's the immünity which is effective against all intracellüler infections, it's the immünity which destroy human tissue in autoimmune diseases.

   What's Th2; it's the immünity against extracelluler infections, it doesn't help in intracellüler infection and doesn't cause tissue damage in autoimmune diseases.

  So, if we have an autoimmüne disease, it's good to take Dvit suplements, ıf we have an extracellüler infection it's good to take DVİT suplements, but if we have intracellüler infections; is it good or bad to take D vit suplements? (Remember, Dr. Cheney say that many intracellüler pathogen misdirect immüne system towards Th2 for their own benefits)

  If we have an intracellüler infection the situation is complex. If we are on an effective antibiotic treatment against responsible pathogen, devit would help. But if the pathogen that infect us is a resistant one, or if it's a virus Dvit suplementation may be harmfull. But it has some many other effects which may change the situation.

  Evenif Dr. Stratton promised to give a detailed and thoughtfull answer to my questions about Vitd3, he didn't yet. So he may also be thinking that the issue is complex to give a true answer.(he answers other questions much more easily)



KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

You don't have the Th1 versus Th2 distinction quite right; Th1 is indeed mostly response against intracellular infection, but Th2 is more a matter of allergic response and antibody response than of response against extracellular infection. But the whole Th1/Th2 distinction is a rather fuzzy one, not a well defined one -- as illustrated by the recent discovery of another group of Th cells, called Th17, which has yet another set of responses. If one wants to speak precisely, one has to speak of individual molecules (interferon-gamma, IL-4, or whatever); it's appealing to herd all those molecules into just two groups called Th1 and Th2, since that makes things simpler, but it's easy to confuse oneself that way.


Indeed, the Th1 vs. Th2 immune response is a controversial issue, for example asthma is widely regarded as a Th2 disease, but it is also caused by the same intracellular bacteria as the rest of the so called Th1 diseases.
Here's a review paper on this topic:

Regarding this issue about NF-kappa B and ALA, it is well known that ALA leaves the bloodstream quickly, but it is converted into DHLA in the cells. How long time this substance affects the NF-kappa B within the cell is not known, but I suppose the effect stays longer in the cell than just a few hours. Then the extracellular amount of ALA doesn't directly influence the NF-kappa B status, and it is cumulative up to some degree. I have found no research about this topic, so we can't say anything for sure. But in many experiments, ALA is given in large amounts for several days, so the researchers seem to suspect some cumulative effect.

Anyways while the immune system is complicated, I think NF-kappa B needs to be considered as a very important part, as this is the key part that deals with apoptosis. The VDR is also a part of this system, and independent research supports the idea that at least some CWD bacteria are able to suppress this part of the immune system. It's quite clear, however, that not all infections are CWD dominant.

The right way to determine if CWD bacteria are also a part of your problem in addition to Cpn is to measure the 1,25-D as Marshall suggests. And I think another indicator of a CWD infection is a poor response to abx alone. Unfortunately, Benicar appears to be currently the only known substance to activate the VDR reliably.

No official diagnosis.

 Norman, since there is so many cytokins and chemokins and even more than those which are not known yet but will be known in the future, speaking over these cytokins will make the issue more sensitive but more complicated, I'm not a cytokin expert and ıt does not fit me. I don2t know about Th17 but if you have any report about it please post it, I would be happy to see.

 pgm, If you look at doctors Cheney's report you will see that intracellüler infections misdirect immüne system to give a Th2 response instead of Th1. So in diseases which were caused by intracellüler pathogens, like asthma, we can observe Th2 response so that thay will called as Th2 disease.

 To discuss about NF-kappa B inhibition and apoptosis I would suggest you to read the article posted by NellyP ıf you didn't yet.


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

Measuring your blood level of 1,25-D doesn't tell you squat about cell wall deficient bacteria; that's Marshalloid nonsense. Really that measurement tells you only about your calcium balance. That's because that is what 1,25-D in the blood is used for: regulating blood calcium. If you have a high-calcium diet, your 1,25-D will be low; if you have a low-calcium diet, your 1,25-D will be high. Only in extreme cases, where too much 1,25-D used for other purposes leaks into the blood, is your blood 1,25-D level determined by anything other than the need to control your blood calcium level. And the main way to tell whether you are one of those extreme cases is not to look at the 1,25-D level, but to look at the blood calcium level. Normally, blood calcium is strictly regulated, as lots of biochemistry (like the beating of your heart) depends on it being inside a narrow range. If it's high, then your blood 1,25-D level is too high for you (on your current diet). And that's probably because you are infected, and your immune cells are leaking too much 1,25-D into your blood; you are probably one of the rare people who really does have to avoid sunlight and other sources of vitamin D. But that doesn't mean your infection is some mysterious "cell wall deficient" pathogen; ordinary tuberculosis can do it. Still, even among people who have TB, unless they have a really bad case of it, they probably will be helped rather than hurt by vitamin D. This is because if the immune system leakage of 1,25-D is less than the body's requirements for blood 1,25-D, then it doesn't end up affecting the blood 1,25-D at all, since the kidneys compensate by decreasing their own production of 1,25-D so as to keep blood calcium constant. Only when the kidney production of 1,25-D is zero, because the leakage from other sources is above the requirement, do you get into trouble, because kidney production can't be decreased below zero.

In any case, what matters most about bacteria is what species they are, not whether or not they are "cell wall deficient". There are lots of species of bacteria, and each one does different things. To say that "cell wall deficient bacteria" do something or other, scarcely has any meaning. Different species of bacteria don't all suddenly start behaving the same when they lose their cell walls. Take, for instance, that bit about the vitamin D receptor. For just about any part of the immune system, there is some germ or other that knows how to subvert it for its own purposes. So it's a fair guess that there are indeed some species of bacteria that know how to muck with the vitamin D receptor. But that doesn't mean that all bacteria suddenly learn how to do that, the instant they become cell wall deficient. That'd be ridiculous; it takes a special set of genes to do something like that.

Of course there are a few things that cell wall deficient bacteria have in common, like the inability to survive in harsh environments where having a thick cell wall is important for mechanical reasons. Even pure water is deadly for cell wall deficient bacteria; they swell up from osmosis, and explode.

I don't know much about Th17, and can't point you at any report as being particularly worth reading.

As for "intracellular infections" misdirecting the immune system to give a Th2 response rather than Th1, I'll wager that really only a few of the large number of intracellular germs do that. But Cpn is likely to be one of them. There was a recent paper finding that a certain chlamydia species did exactly that. (They used mice, and a weird sort of mouse chlamydia, so it may not apply to humans and Cpn; but it's likely.)

 Norman, thank you for this interesting article. I also dont heard  anything about 1,25 D3 leakage to blood, do you have detailed information?


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.


But regarding this 1,25D metabolite test, the MP team presented some research about this:
I know this leaves much to be desired (e.g. no comparison to healthy controls), but elevated 1,25D seems to be a rather sensitive test for chronic disease, at least compared to usual tests CRP, ferritin etc. But I do agree that high 1,25D doesn't necessarily tell about CWD bacteria; it's just that TM has put many bacteria under that category (including TB and borrelia) which he all calls CWD bacteria. I just meant CWD bacteria in that sense that TM calls them.

"In any case, what matters most about bacteria is what species they are, not whether or not they are "cell wall deficient". There are lots of species of bacteria, and each one does different things."

This is a bad thing about TM's theories, that he puts many bacteria under the CWD category, without looking at how these bacteria actually operate in detail.

BTW. I found a nice study about ALA, the Na-R-ALA form is highly bioavailable, and in a research it was found that 600 mg taken every 15 minutes three times, increased the plasma concentration of ALA to over 100 µM. This is about the same concentration that 300 mg usual ALA given intravenously in 20 minutes would achieve, and many times higher than what can be achieved with the same dosing of usual ALA.

"To discussabout NF-kappa B inhibition and apoptosis I would suggest you to read the article posted by NellyP if you didn't yet."
This is probably a special case (hiding within a neutrophil granulocyte); if no immune system cell would be able to successfully phagocytize a free EB, then the infection would grow uncontrollably, and this doesn't happen. Surely, these EB's can't be invincible.

No official diagnosis.

pgm, it doesn't look like a special case. Macrophages can succesfully phagosyte free EBs and can stop EBs growth leading persistant infection with CB formation. The problem is living EBs in apoptotic PMN cells which can not be seen by macrophages and can grow uncontrollaby, maybe this why it's so difficult to eradicate CPN. Maybe we should adress CPNs inside the macrophages much prominently to overcome this infection.


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

One talk by a doctor who says that a lot of his 'autoimmune and associated diseases' patients have elevated 1,25-D levels is not a piece of evidence that can even scratch at the toenails of the mainstream research into the sources and effects of blood 1,25-D. What I described is old and well-established stuff; it's the classical role of vitamin D: a messenger molecule in a feedback loop involving the kidneys, the parathyroid glands, and the bones, which keeps blood calcium levels constant by taking calcium out of the bones as needed. What has been added in the last twenty years or so is the knowledge that vitamin D has other roles, too. But a single molecule, in a single place, can't have two roles that contradict each other, or even that have nothing to do with each other. This is why, in just about every overview of the newly-found roles of 1,25-D, the words "paracrine or autocrine" appear. Paracrine means that the hormone is both created and destroyed within a small area, as opposed to "endocrine" where it circulates throughout the whole body. Autocrine means that the effect is within the same cell which creates the hormone. In either case, it doesn't get into the bloodstream (except as a small proportion of leakage), and thus doesn't affect the role of vitamin D in maintaining blood calcium levels. That's how two very different roles for 1,25-D can coexist in the same body: the role depends on where the hormone is located. Except in rare disorders, the two roles don't conflict with each other: the leakage from the use for immune purposes is low enough that the feedback control loop for calcium can handle it.

Of course we are not all properly-functioning humans; some of us have diseases like sarcoidosis, where so many white blood cells gather together that they form a whole tissue type, a "granuloma", consisting almost entirely of white blood cells. In such cases the leakage, even if small from each individual cell, can become overwhelming.

That said, looking into this further, I was being a bit too dogmatic. I'd thought of the situation as being one where there was a single control variable (1,25-D), and a single variable to be controlled (blood calcium); in such a case, if the variable to be controlled needs to be held constant, there can be only one possible value of the control variable. Actually it is a bit more complicated than that: there is also parathyroid hormone involved, and it exerts action not just through 1,25-D but also directly on bones. With two control variables, there is some flexibility for levels of 1,25-D to rise and fall with immune system leakage, even while calcium levels remain under perfect control. But the fact remains that when one measures blood 1,25-D one is measuring a hormone whose principal purpose is to control calcium, and which varies greatly with the amount of calcium in the diet. If you wanted to measure immune use of vitamin D, you'd have to measure the 1,25-D content of a biopsy of the tissue of interest.

It's hard to say about Lyme; but in tuberculosis, few of the bacteria are in a 'cell wall deficient' state. TB bacteria are normally distinguished by their unusually thick and waxy cell walls.

Here is a interesting comment from wiki talk (I do not know, how to insert link on just this part, so I rather copy it, sorry):

I'm an M.D. whose attention was drawn to Trevor Marshall recently. Going to his website, he appears to be an intelligent, somewhat charismatic person who has sold some interesting ideas to a bunch of chronic disease sufferers and in the process has created the usual cult of hopeful pseudoscientists who are drawn to such efforts. There are a few interesting ideas presented there, and in fairness I suspect he may even be onto a few things with respect to sarcoidosis and maybe one or two other conditions that actually are exacerbated by high levels of D/calcium. Otherwise, it's apparent that there's a lot of sloppiness, speculation, and spin, and frankly I find many of their claims with respect to Vitamin D's harmfulness to be not only unsubstantiated but downright scary and having the potential to do great harm--particularly since he/they have a paucity of evidence for their positions and seem to disdain a great many actual clinical research studies that contradict their thesis that Vitamin D supplementation is generally bad. (A greater value is apparently placed on his 'in silico experiments'. That smacks of just a wee bit of hubris in my book.) His topics are deep (seeing as how they deal with biochemistry and molecular biology on a level that's too complex to be properly followed by any who aren't versed in those subjects), but despite the richness of detail of his arguments there are some important errors. For any of his followers who happen to be reading this, one such example would be talking about binding constants and the measured competitive antagonism of calcidiol (aka 25-OHD) on the VDR. Such antagonism may be measurable in vitro, but in vivo it's actually irrelevant. As Marshall's followers all well know, VDRs are NUCLEAR receptors, and as such they aren't directly exposed to circulating (plasma) calcidiol. In the plasma, calcidiol is bound to DBP (D binding protein) and (to a much lesser extent) albumin. Following transport through the plasma, DBP and calcidiol in turn bind to megalin proteins that are expressed on some cell surfaces, which binding in turn triggers clathrin to induce endocytosis. Following endocytosis, calcidiol is released from DBP into the cytoplasm, where it is immediately bound to hsc70 (a constitutively expressed chaperone protein that binds many things, including other D-metabolites such as calcitriol). From there, different metabolites of D appear to be selectively directed to specific intracellular organelles. Most relevantly, hsc70-bound calcitriol (aka 1,25(OH)2D, aka the "active D metabolite") has a higher binding affinity to a nuclear chaperone called BAG-1 than hsc70-bound calcidiol does (see This is important because since BAG-1 guides D-metabolites to the VDR, it means that high calcidiol levels won't significantly interfere with VDR binding of calcitriol--and thus Marshall's "in silico"-supported hypothesis that exogenous Vitamin D supplementation interferes with VDR activation turns out to be erroneous. (For his fans, I also don't know what the significance of this VDR-presenting mechanism might be with regard to Marshall's proposed use of Benicar as an artificial VDR agonist. It might or might not be relevant.) Anyway, history may yet vindicate some of Marshall's other ideas and prove me wrong about him, but for now I see every indication that this guy is well-meaning but dangerously overconfident about the veracity of his theories. If I'm right, then unless/until such theories are thoroughly discredited he will remain an intelligent and articulate person who can convince a lot of other people to join him in his misguided crusade to get the "truth" out about the dangers of Vitamin D. For his fellow co-sufferers of sarcoidosis (and possibly those few other rare conditions exacerbated by high calcium levels) this might be forgivable. For the other 99+% of us, such efforts may have potentially grave consequences. If the thrust of the emerging body of peer-reviewed Vitamin D research is to be believed, a billion people on this planet currently suffer from Vitamin D deficiency, and many of those will enjoy longer and much healthier lives (less cancer, diabetes, hypertension, heart disease, multiple sclerosis, osteoporosis, possibly even asthma and depression) as a result of getting proper Vitamin D3 supplementation. With that at stake, I'd just as soon let people who look up Trevor Marshall know that his ideas are not necessarily as well-respected within the mainstream scientific community as some people here might suggest. He certainly deserves to have a bio, but his claims remain *quite* controversial. Slowgenius (talk) 18:21, 14 August 2008 (UTC)


Stratton/Wheldon protocol 02/2006 - 10/11 for CFS and many problems 30 years

 Lala, thank you this good information. I want to emphesize that, for one more time, I don't believe Trevor Marshall and his theories infact. My major concern is about VitD3 dosing; I do worry about shifting immüne system towards Th2 too much, by overdosing. High levels of Th1 may give harm by collateral damage but we still need some Th1 for fighting against CPN and other intracellüler infections.

 Since Dr. Stratton didn't give an answer to my questions about VitD3 (evenif he promissed for 2 times he didn't, I suppose he doesn't want to make any speculation on this sensitive topic), I get into contact with some doctors on VİTD3 consul. I will post their opinions.


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

This report is about Trevor Marshall and MP. It was sent me by a member of VİTD consul.Marshall ...pdf


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

 That was my question to members of VİTD counsil,

Dr. xxxx ; I'm a cardiologist from Turkey, I'm a strong supporter of VitD3 supplementation for many chronic diseases including autoimmüne diseases. But some reports made me worried about VitD3 supplementation on intracellüler infections such as lyme disease, chlamydia pneumonia infections or viral infections. (recently these infections are claimed to be associated with many autoimmüne or inflammatory diseases including coronary arterial disease) You can see one of them below. Since Th1 immüne response is so important for fighting against intracellüler infections do you think high doses of VitD3 supplementation may give harm? 

and you can see the answers below.


No, Trevor Marshall, who is probably behind the concern, has sarcoidosis.  Those with sarcoidosis, granulomatous diseases in general, and some with lymphoma can develop hypercalcemia due to the body's innate immune system producing more 1,25(OH)2D in the serum.  Marshall should be ignored.  I've tangled with him; he does not like or accept epidemiological studies as they disagree with his ideological position.


The world's expert on high doses of vitamin D is Reinhold Vieth in Toronto. He has written much on the topic.

Please let me know if you are interested in having any of my papers listed at (search Grant WB).

Best regards,

No more than significant sun exposure in the summer would. I do not think so.


I am a Ph.D. and it would be better for you to speak with a MD vitamin D expert. I suggest that you contact Professor Roger Bouillon who is at LEGEND at the Medical School of KU Leuven in Belgium. His email address is included here.

    Tony Norman

In my opinion there should be no concern about vitamin D increasing risk of intracellular infections. From my perspective vitamin D  modulates the immune response rather than completely shutting off the Th1 immune response.

Best Michael

Dear Doctor.
You bring up a good point. The immune system is remarkably complex. Another aspect for which vit D is important is the innate immune system. Production of one of the major natural antibiotics cathelcidin is dependent of adequate vitamin D. Thus, low vit D is bad from this important aspect, irrespective of the Th1/Th2 balance. Although we need to learn more, based on a large body of evidence it seems that vit D levels around 30-40 ng/mL are much more likely to do good than harm from the perspective of infectious and autoimmune disease. However, it is possible in some sub-group some harm is possible. It also makes sense to avoid very very high doses.
Best regards,
Ed G


I am not myself an expert on the immune system and its diseases, so I fear that I cannot give you a very helpful response.  However, I take some comfort in what seems to be a sensible position, namely that human physiology evolved in an environment that would have sustained serum 25(OH)D levels in excess of 80 nmol;/L.  Hence, oral D supplementation that produces such levels ought to be safe.  I hope this perspective helps.RegardsRobert P. Heaney, M.D.John A. Creighton University ProfessorCreighton University601 North 30th St., Suite 4841Omaha, NE 68131Phone: (402) 280-4029Fax: (402) 280-4751Email:



Dear Dr Ayhan:  I checked the web page you mention below, and see nothing on the topic of vitamin D.  However, your mention of lyme disease does remind me of some wierd claims by Trevor Marshall, who refers to those "intracellular infections" and whose bio I attach here.  It speaks for itself.  To answer your question, NO, I do not think that vitamin D supplementation up to 10,000 IU daily can cause harm.Best wishes,Reinhold Vieth


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.


Hmm, interesting. I'm also currently believing (like I said earlier), that vit-D3 is likely to be immunomodulatory rather than immunosuppressive.

Marshall does, however, keep statistics of his over 1000 patient cohort with various diseases (and they have their 25D and 1,25D measured several times during the treatment time), and TM thinks that low levels of 25D is necessary for getting immune system up again (based on the data he collects from his patients). He says most people Herx better with low 25D. TM hasn't done any trials though with patients that don't try to avoid vit-D3.

Some other points: the 1,25D levels seem to stabilize on their own for those who are at their endpoint in the recovery on the MP, that is, the 1,25D come down. TM has not mentioned how calcium affects 1,25D, but he does recommend that patients take calcium while on the treatment. The 1,25D values can also fluctuate rather much on the treatment, but people seem to be able to keep the 25D consistently low, if they avoid vitD3, and this makes me think that 25D doesn't control 1,25D.

On the MP site, they say that cancer is not a problem for anyone in the cohort, even if they avoid vitD3. If anyone has cancer before they started the treatment, it hasnt at least spread. This may be due to the Olmesartan (rather than VitD3 avoidance), as angiotensin blockers have been used in cancer treatments as well.

Another interesting point (from TM's latest conference presentations) is that around 70% of the people who start the MP get no symptoms from starting Benicar every 6-8 hours, while the rest either feels worse or better. Perhaps this tells something about the infection; if VDR is not blocked, you do not really need Benicar to clear the infection, and it won't cause any symptoms either in that case.

But anyways, I think the 1,25D is more important than the 25D in the infections, as the 1,25D level is an order of magnitude less concentration than 25D in blood. The bacteria can't produce stuff in very high quantities anyways (or make other cells to produce it), so if they want to disturb something, the 1,25D levels are much easier to distort. And it must be something that circulates in bloodstream to disable the whole immune system. The link between that high 25D would lead to high 1,25D is also not certain, only TM claims that.

No official diagnosis.

WARNING to newcomers. The previous post quotes comments and unverifiable 'statistics' from another website which are not endorsed or espoused by this website. Trevor Marshall is not associated with this site and his theories are not promoted here.

The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi

Yimaz, After 9 months on VitD310,000IU, my Vit D 25-Hydroxy (25-OH) is now 66.9ng/mL (Reference Range from the LifeExtention National Diagnostics, Inc. Lab 32.-100.0  (self ordered test about $35US and done on serum).  In Oct 08 it was 29ng/mL on 4,000IU/day.  I upped to 10,000 at that time.  In April 09 it was 72.9ng/mL.   I have been very consistent with taking my doses.   At this point it seems that D3 10,000IU is a good dosage to continue with for me, personally since I have been on this dose for 9 months and and still fall well within the mid fererence range   I plan to retest in October and see where my level stands at that time.  I would still like to see my results at the higher end of the range, my doctors original goal for me was 100ng/mL.   Louise

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

  pgm, vitD3 certainly modulates immüne system which means it supresses cellüler immünity(Th1), elevates humoral immünity(Th2) and also increases synthesis and secretion of natural antibiotics like cathelicidines. This is called immüne modulation.

  The net effect of this immüne modulation may be different in different blood values of 25(OH)D3 and also in different intracellüler and extracellüler infections.

  25(OH)D3 levels can not control 1,25(OH)D3 because there is another factor ;parathyroid hormone; which causes increased concersion of 25(OH) to 1,25(OH) resulting in normal or slightly increased levels of 1,25(OH)D3 despite low levels of 25(OH).


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

Lousie; my 25(OH)level is 62ng/ml and I dont want to go higher anymore. There's no evidence showing that these levels are safe for us(people having manykind of intracellüler infections). I stop taking it for now.

When we look at the answers of VİTD counsil members, only two of them talks about blood levels, Dr. Giovannucci and Dr. Heaney, thay say 30-40 ng/ml and 80 nmol/L are safe, these levels are lower than our levels.


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

Yilmaz, I read much of the research that has been collected from reputable websites that are posted here under the Vit D book created by Red to make these studied easy to find.  Dr Veith says up to 10,000IU daily  is safe and I believe this and that I need a high dose to stay even in the mid range.  Personally, I do not have fear about this.  If anything I have fear of developing progressive ostoperosis if I take low dose Vit D as I have for the past 35 years and it did not prevent me from starting the decline of my bones. 

For me I have gotten very well starting with CAP in June 2007.   Adding Iodine supplement in March 2008, adding BHRT in May 2008, Changing to Iodoral Iodine in July and increasing to 25mg in August, adding Methylation supports (Sam-e and others) Aug. 2008,  going to higher Dose Vit D 10,000IU in Oct. 2008, added LDN Feb 17,2009  and finally adding recently in June 2009 5HTP/P5P per my doctor.  

I did several lengthy Pulses the last long pulse was of a months duration in Dec/Jan 2009.

I began intermittent on Feb 4, 2009 because I felt well and because I wanted to take an ABX break for elevated liver enzymes after 20 months on Stratton/Wheldon CAP.  In April they came down but still mildly elevated and I have plateaued since this time (now 3 months no appreciable variation of levels.)  For better or worse I am still on the abx break.  My intention is to restart.   This may demand disregarding my doctor since I have improved in the Liver enzymes but I still am elevated.  My perspective is that this is my baseline.  My AST pre abx is what it was then now but that is slightly elevated to start.  I have no other Enzymes to compare. I have been screened for all the liver viruses and they are negative.  I may lie outside the bell curve and this is my baseline.  

Hard to argue with my provider.  Hard to know what to do.  I feel really rather well, yet I know that without testing intermittent I will not know if there is more that needs treatment.   I expected to take 3 - 5 years so I am not rushing it from my choice. 

I am still looking for unexplained reasons for mildly elevated liver enzymes.  In the meantime the clock keeps ticking and I want to get back on the protocol.   

Worrying about Vit D toxicity is not something that concerns me at this point.     I feel very comfortable with my potential target goal for Vit D and with my current dose of 10,000IU and lab level of Vit D 25-OH of 66.0ng/mL.  But most of all CAP has vastly improved my life!   I agree I will keep a eye on the level every 3 months for the first year and then I will see, maybe twice a year, early spring and late fall might be good times for me.

Thanks for your concern and responding.  I hope you read more of the supportive research articles.   People who put recommendations in writing tend to be a bit more conservative in their guidance.  I have found this with my provider.  I am one person concerned only with myself, he sees many and needs to keep many stories straight.  So I am at an advantage I remember more about what he says and the comments that he makes in passing than he does understandably.   I can say he vasilates when you try to pin him down to something and I actually understand why this happens and do not fault anyone.  But again I have only one concern myself.   So I am more concerned about restarting abx than he is having me restart.  It will have to be at my own volition so that he cannot be held to blame.      Sending you healing thoughts.   Louise

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

  Lousie, I also read many articles supporting VİTD supplementation but don't remember anyone suggesting a level around 100ng/ml, ıf you have, please let me know. The more important thing is the blood level, not the supplementation dose in my opinion, so ıf you wanna you can go upto 100-110, but DVİT counsil members didn't suggested that levels. We all have to give our own decisions, 62 is good for me. Don't forget this is from Dr. Giovanucci, a VİTD expert;  ''Although we need to learn more, based on a large body of evidence it seems that vit D levels around 30-40 ng/mL are much more likely to do good than harm from the perspective of infectious and autoimmune disease. ''

  I'm really very happy for you feeling so well, did you ever check your AST,ALT prior to CAP?

  I also wonder about your methylation strategy and iodoral treatment. If you have time please let me know about them by private message.


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

Yilmaz, only the AST was order before starting any abx.  I don't know why the entire liver enzyme picture or a complete chemistry was not done.  Many test were done including the C.Pn. antibodies which is how I came to be treated for it.

 I was being screened for unrelenting fatigue at a Fibro and Fatigue Clinic in US in May 2007. 

(I have tried to be complete in my blogs about my story).

 In May 2007 prior to abx the AST was 61 (ref range Quest lab at that time was 0 - 33).

Regarding support for upper levels of Vit D, Perhaps Red, who has a mind for these details, can point you in the direction of the articles that mention blood levels in the upper ranges.   

Red has his blood level up to 101 ng/mL (note the scale of expression ng/mL as opposed to scale expressed in nmol/mL, there are two, as you are sure to know.  These two co-existing scales are likely to cause a continued confusion for some readers here).  I hope Red will link you to a few of the best sources supporting high dose Vit D3 and health maintenance.

There have been many topic posts about methylation here, some with good links, I know you want good references.         Also the same is true for Iodoral which is a High PotencyIodine/Potassium Iodide supplement(5mg Iodine and 7.5mg Potassium Iodide combination), there is a book by Dr Brownstein, Iodine Why You Need It, Why You Can't Live Without it, 3rd edition and also information on the web even a talk by him given at a conference, JimK suggests people look into this book before considering it. In the book a self test is described I would not attempt to explain it the author does it better.   I never took the test personally just started slowly. 

Take a browse forum topic Adjuncts             You may well find the topic filed there with input from others here who have used it.   I added magnescent Iodine (google for the website) in March 2008, it is much lower dosing and I changed to Iodoral in July 2007.   The Brownstein book talks about a bromine detox that can be possible but since I have had very little wheat flour products in the past 25+ years I fortunately, had no detox symptoms when I started either form of iodine.

Here is on link I tried to start

I hope that some of this is helpful.   I'll see what I have in my computer files regarding methylation enhancement and iodine. 

It was my doctor that mentioned a target of 100ng/mL for me as a passing comment!

I agree that to keep track of blood levels is important when you get into therapeutic ranges of Vitamin D dosing in  particular, and that this detail should not be lost track of over time.    

Best Regards,  Louise

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

Hi Louise and All,

This article discusses and gives reference to many of the recent studies trialing "pharmacological" doses of Vit D3 to treat existing disease:

Use of Vitamin D in Clinical Practice

Note in particular, Yilmaz, the recent study of high dose Vit D3 for MS (by Vieth, et al) on the right of page 15 where they found reduction in existing (and new) MS lesions.    Again, they used "pharmacological" doses, increasing to as much as 40,000IU a day and blood serum 25(OH)D concentrations reached a mean of 154ng/mL.

The following study, also by Vieth, et al, discusses quite well, the safety of doses of Vit D3 at the 10,000IU level:

Risk assessment for vitamin D






Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-

Yeah, I'm not promoting here the MP, but there is something to learn from the MP as well. Every inventor seems to get at least something right, while nobody gets it all right from the beginning.

While much of the mainstream research says vitamin D supplementation is useful, most people there don't have the whole picture in front of them. I think most of the vit D researchers have no idea that we are fighting intracellular infections the whole time, and anything we throw in that affects the immune system, might be potentially harmful.

This topic still needs some thinking, because if 25D doesn't control the calcium balance, then how can excessive amounts of vit-D3 supplementation still cause hypercalcemia, which has indeed been reported, if it doesn't affect 1,25D? This should mean that at least excessive supplementation with D3 is harmful.

No official diagnosis.

pgm, of course excessive supplementation with almost anything is harmful.  The situation as I see it is that the old level of excess is shifting upward from a very miminal level which at best prevented rickets  to a level that true reflects toxicity. 

Of subject, So what supplements are you just using to treat your condition, I am curious as to what you have committed to doing for your depression and cognitive issues since you started here over a year ago?

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

The amounts of vitamin D3 supplementation required to cause hypercalcemia in normal people are ridiculously large. To repeat a quote from Vieth which I've used before:

"If you really want to see what vitamin D toxicity is like, check the
Feb 23, 2002 issue of the Lancet, in which two people each consumed
over 1 million IU of vit D3, daily, for SEVEN MONTHS! From what you
say, you would have only taken a grand total of 1.5 million units -
what these patients took in just one day. The patients we reported in
the Lancet showed all the classic signs: hypercalcemia,
hypercalciuria, kidney calcium deposits, dehydration, nausea,
vomiting, weight loss."

At such high levels, all sorts of things which one can generally describe by the phrase "that doesn't happen" actually happen. It's like saying that "you can't squeeze solid matter down to half its original size". Well, if you put it in the middle of a nuclear weapon, you can. But generally you can't.

As for Marshall's statistics, I doubt that the not-so-small number of people who have gotten worse on his protocol, hate him, and refuse to have anything to do with him, are represented in those statistics. Mainstream researchers report such people as "lost to followup". Does Marshall have even that level of transparency? Or is he just trying to illustrate once again the merits of the saying that "There are lies, damned lies, and statistics"?

As for

"On the MP site, they say that cancer is not a problem for anyone in the cohort, even if they avoid vitD3. If anyone has cancer before they started the treatment, it hasnt at least spread."

Now that claim I simply don't believe. I think I've actually heard of a case of cancer emerging in someone on the MP, although I don't recall who it was, or even if a name was given. Even aside from that, it'd be quite odd for a cohort of over a thousand people, most quite sick, to have no cases of cancer. More likely most MP patients who get cancer become disillusioned and don't report it to Marshall, and he and his disciples censor the few who do. (Even so, I'm guessing that Trevor himself doesn't make strong claims like that, about cancer; he's too slick for that. Instead he'd make some sort of guarded statement, and let his disciples proclaim it as a certainty.)

By heavily censoring his website, Marshall has cut himself off both from patient feedback and from intellectual feedback. It's okay to make mistakes when innovating; what is not okay is to refuse to admit them. "He that seeketh to be eminent amongst able men, hath a great task; but that is ever good for the public. But he, that plots to be the only figure amongst ciphers, is the decay of a whole age." -- Francis Bacon

Oh, by the way, the 1,25-D concentration in blood is not just one order of magnitude lower than the 25-D concentration; it's three orders of magnitude lower. (For those unfamiliar with the term, "an order of magnitude" means "about a factor of ten"; in this case the difference is about a thousand.) This is why a small leakage from uses of 1,25-D outside the bloodstream can be enough to cause problems.


"Oh, by the way, the 1,25-D concentration in blood is not just one order of magnitude lower than the 25-D concentration; it's three orders of magnitude lower."
Yeah, I know that, I just didn't get it right. Picograms and nanograms. But this demonstrates the problem with 1,25-D, its easy for bacteria to mess up with such a small quantity, I wonder how it is even possible to measure this small quantity. So if you wan't to shoot down all TM's theories, then leave at least this with VDR + Benicar left.

"Of subject, So what supplements are you just using to treat your condition, I am curious as to what you have committed to doing for your depression and cognitive issuessince you started here over a year ago?"
Well I have been using ALA, garlic and iodine + some supplements I feel help with porphyria, like magnesium, molybdenum, glutamine and B12. B5 has helped lots with adrenal fatigue as well. But I'm much better these days, though not entirely healed yet. I would also recommend benfotiamine (not ordinary tiamine) for cognitive issues, it helped enormously at least in the beginning, and it makes your heart beat softer. Tested benfo too on another person with similar problems like I had, and about same response. And arginine is not bad either, it caused chills and flu-like symptoms for me at least in the beginning for several weeks. I also had cardiovascular issues, like chest pain and tachycardia, and high blood pressure (sometimes over 180/115), but these are not a problem any longer either. Since ECG was normal, these problems didn't interest anyone.

You wouldn't believe it, but some of the above mentioned supplements have been /and are still hard for me to tolerate. If you have Cpn in the CNS (all those with depression certainly have) the reactions are not pleasant, and they come each day, when you try to kill the Cpn.

No official diagnosis.

Yilmaz, you might want to consider choosing a dosage lower than your present to test it's effect for your physiology.   If you stop you will doubtlessly drop your level I did when I first loaded at 6000IU and returned to 4,000IU and went down to the 20ng/mL range. That is when I started the 10,000IU.  But you will not have a sense of how much is enough to get to the level that you consider your target goal.

I admit that I seem to have a higher dosage need than some to get up to the below 80ng/mL range that is the conservative upper limit these days.  Perhpas because I am near the 45th parallel so solar manufactured Vit D3 is a rarity only about 8 - 10 weeks to expose arms, legs and back with any possible regularity.

Have you tested at the suggested 4000IU after a three month period?  I am planning to test every three months until I am convinced that I am stable then backing down to 6mos and then after a time maybe a year.  I have not thrown caution to the wind, so to speak!    Louise

  • CAP(TiniOnly): 06/07-02/09 for CFS
  • MethylationProtocolSupplements: Started08/08
  • Intermtnt CAP: 02/09-02/10
  • Full MethylProtocol & LDN 02/09
  • Off CAP: 02/10, cont LDN & MethlyProtocol support

  pgm, eventhough I represent a conservative approach to high VİTD blood levels (in the case of intracellüler infections), I do still think that neither Trevor marshall himself nor his theories are reliable. Marshall's theories have no scientific baseline infect. So I would advice you not to care about MP so much. You can continue to follow up Marshall and enable us from the new devolopments ofcourse and that would be good for us also.

  pgm, when I look at your supplements I can not see VitD3 between them, so I wonder whether you ever took VİTD in the past and what's your blood level of 25(OH)VitD3.  As you know, there are many of reports saying that VİTD is helpfull on depression and cognitive issues.

  Red, the article that you emphesize is the one which inspire me with most hope, but 12 patients is a very small number to make a conclusion.

  Lousie,Red; My drawbacks about high levels of VİTD may be related to my own experiences infect. I may have a very heavy bacterial load(titer is 1280, despite 13 months of CAP)  and go fast on VİTD accordingly(upto 6250 ıu in 3 months), so that I had heavy die-off reactions. After a while stopping VİTD, I'm free from visual symptoms(which might be die-off,porhiric neuropathy, phorphiric photosensitivity, disease progression etc.). But I have musculer atrophy on my left forearm (also a slight atrophy on right arm) now and I realized it after VİTD3 supplementation, ıt's not difficult to see the atrophy(when you put your forearms sidebyside, you can see easily), but I didn't see it before VİTD3 supplementation. What's that atrophy??? I was also asymptomatic before NAC test. These all make me worried about the way I walk on. Anyway, I'm waiting for my lyme test results, then I will go and get my MRI,EMG,CPN titers,VİTD levels again, I will try to get a certain neurologic diagnosis  and make my decision for VİTD supplementation and overall theraphy.


KEREM'S TAKECARER;Suspıcıon of MS (transient nystagmus during conjugated gaze on february 2008, blepharospazms and some optic complaints on february 2009-no plaque on MRI), Vit D3 started 400 IU and elevated to 2000 ıu ın 40 days.

I certainly have to give Marshall credit for being the first one to convince me that vitamin D was a powerful weapon. Now if only he hadn't been telling me to look down the barrel from the wrong end...

As for the vitamin D receptor / Benicar stuff, where exactly does that come from? If it's Marshall's molecular modeling, I'm afraid I don't trust that one bit. Have a look at this article by Derek Lowe, to see how miserable the state of the art is, in that field. (Or if you're actually interested in an explanation of the various techniques used, this MIT course is good.) On the other hand, if this is one of the things Marshall found in the scientific literature and worked into his own theories, I'd be curious to see a citation.