IS VİTD3 SO HELPFULL?
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 Immunei System (Th1/Th2) 
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 Di 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 infectionsi. 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. ''
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''What do you make uric
''What do you make uric acid from? You make it from RNA and DNA metabolism and that is produced endogenously [within the body] and exogenously [outside the body]. Endogenous production is by apoptosis [normal, programmed cell deathi.] ''
That's from Dr. Pall's book and may explaine one of the mechanisms that how VİTD helps MS patients who doesn't take antibioticsi. As it's indicated in the book, uric acid is a powerfull scavenger of peroxynitrite which cause oxidative damage in this kind of diseasesi. VitD, may increase urıc acid levels, by increasing apoptosis of infected cells.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
Thank you Norman, I
Thank you Norman, I discussed this with Dr. Straton and that was his answer;
''I agree that going after the infected macrophages make the most sense. I believe that rifampins are the best, particularly 150 mg of rifabutin per day. Take care.''
I couldn't find rifambutin in Turkey, and started rifampin.
Dr. Stratton attached those articles also.
Ct-Rifabu...pdf (228,2 KB), Rifampin ...pdf (198,5 KB)
yılmaz
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
If you're worried about
As for Cpn hiding inside apoptotic neutrophils, the germ definitely inhibits aptoposis; and it wouldn't do that unless it got some survival benefit from it. Anything that hurts it helps us, as a general rule. There can be exceptions to that, and perhaps apoptosisi of neutrophils is one such exception; but that's not necessarily the case: it might still help if those neutrophils committed apoptosis earlier rather than later, and thus left fewer RBs for macrophages to eat.
Lousi, I'm on 2500 i.u
Lousi, I'm on 2500 i.u VİTD3 for just 2 days. I will make a blog about my test results and treatment changes after taking my second borrelia results. The first result was not clear enough and I try to check it in Turkey.
Norman, I totally agree with you on that;
''To really string together a couple of papers like that, and get any reliable conclusions, takes a lot of attention not only to which precise chemicals are involved but also to the concentration that is reported as having activity, the place and time at which that concentration is achieved, and other such details.''
But ıf we can manage to do that truely ıt would help us to understand the diseasesi proceses and treatment models deeply.
I will try to do that again.
That's the page,as you noted, posted by Red which contains the articles showing how CPNi prevents apoptosisi; and how VİTD3 might be helpfull against CPN.
http://www.cpnhelp.org/vitamin_d3_chlamydia_pneu
And that's the page posted by Nellyp which shows how CPN hides inside the apoptotic neutrophils and silently infects macrophages to find itself longliving hosts.(That was the article made me worried about those infected macrophages, then I decided to target these macrophages directly and started Rifampin)
Chlamydia pneumoniae Hides inside Apoptotic Neutrophils to Silently Infect and Propagate in Macrophages
Putting these together I can not be sure that whether apoptosis helps infected people or CPN.
But that's all very theoretical and should be test out experimentally to be sure.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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 way vitamin Di might be
http://www.cpnhelp.org/vitamin_d3_chlamydia_pneu
Cpn inhibits apoptosisi in cells it infects, presumably so that it can finish growing inside the cell before it transforms into EBs and kills the cell to release the EBs. The second paper referenced on that page says that it uses the NF-kappa B pathway in order to do this inhibiting of apoptosis. In particular, it increases the amount of NF-kappa B. Other papers referenced on that page say that Vitamin D decreases NF-kappa B. Putting the two together, it can be guessed that vitamin D might induce apoptosis in Cpn-infected cells, and thus help in fighting a Cpn infection. But that is just conjecture; one would have to test it out experimentally to be sure.
(These things are more complicated than the usual language implies. NF-kappa B isn't even just a single well-defined chemical, but rather a family of five or so similar molecules. Most probably those different variants of NF-kappa B will eventually be found to have subtly different functions, and to behave in different ways. To really string together a couple of papers like that, and get any reliable conclusions, takes a lot of attention not only to which precise chemicals are involved but also to the concentration that is reported as having activity, the place and time at which that concentration is achieved, and other such details. That's why I used so many weasel-words above: this is just a hint that vitamin D could be helpful by this mechanism, nowhere near proof.)
Yilmaz, how long have you
Yilmaz, how long have you been back on VitD3 and in what dosage? And how are you feeling? Are you noticing any die-off in relationship to your restart.
I get my most recent 25-OH D level soon, likely on Thursday in the mail. I will also see what my B12 level is and my current CMP and Genetic testing for Gluten Enteropathy should be in my mail box tomorrow.
I would be interested if you might blog on your current response to your changes in treatment and results of the tests that you were considering having done. I am wondering if you had any response to the Borrelia B. testing results. I will write an update blog after my doctor's visit next week. My intention is to restart Abxi at that time.
So far I am doing OK, perhaps the high dose vit D and the Iodoral are helpful in holding me steady during these past 6 months of CAPi abxi.
But I know that it could be only a matter of time before a relapse could occur. Louise
Mac, you may be right
Mac, you may be right about the term of ''as we all know'', and if you know a way to wipe it off please do that, it would be better. But I don't believe that this term would make so much sense on newbies.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
Mac, I can understand you
Mac, I can understand you and not serious about that feeling, ıf I would serious I would stop making blog.
I don't think that newbies would deal with this kind of theoretical discussions, they will look at the pages like home, getting started, CPNi handbook, patient stories, etc... which make much sense on them. Evenif I'm a doctor, I also did so and started to follow blogs only after reading and understanding all those important pages.
Don't worry; newbies will follow the true way.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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's the problem with the
That's the problem with the printed word, it is at risk to multiple interpertations. Everyone understands what they think they mean to say but how it is heard is up for grabs.
I would think that newbies would be concerning themselves with the information available through the tabs at the top of each page. The real how to of the process. There have always been theoretical discussions, some that have been way above my head yet I would not try to flag them or control them, IMHOi, particularly in a user's blog space.
Louise
My first post was clear
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
Lousie, thank you for
Lousie, thank you for your support, I realy need it. I started to feel that asif everybody in this site are against me:)).
I am a kind of person who like the discuss all possibilities and if I have a questionmark on my mind I don't afraid to look for the answer. I don't want to be religious about anything if it's not proved especially.
People in this site need encouragement so much and there are many encouraging people here. I'm gratefull to all of them.
We also need people who ask questions and criticize to get closer the truth. Norman is one of them forinstance and evenif I get crazy about him sometimes I like him so much. I learned much from his critiques, he force me to investigate deeply.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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 hope you are not
Yilmaz, I hope you are not serious in feeling everyone is against you. Mentioning (for the benefit of non-science minded readers) that this level of technical discussion is not required reading for those who are simply interested in learning about cpni and in implementing the antibiotic protocol, is not a personal attack on anyone.
The comment you have a right to post whatever you choose is entirely correct and no one here has said you do not have that right. However, the assumption should not be made that 'as we all know' something. A handful of participants here might be very engaged in the minutiae of a specific scientific/medical point, but most here simply do not have the expertise to follow such a discussion. I know, for a certainty, that if I had come to a site such as this for help with my MSi investigation four years ago, and people 'just assumed' I could understand this thread and participate in it as if this were routine and part of my everyday understanding of medicine and science, I would have left the site.
My post was simply a reminder to newbies and to posters that this is very advanced stuff and not what 'we all know', or pretend to know, or need to know, in order to pursue a CAPi. Newbies who are overwhelmed and brain-fogged might not recognize the difference and be intimidated into abandoning this resource before understanding they walked into the doctoral-level discussion when they really wanted abxi 101.
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
"Sarah,there is no
"Sarah,there is no relation of PGM with this."
Sorry, Yilmaz, I should have said "pgm" uncapitalised, who has posted Marshallite views on Vit D both in your blog and in other places.............Sarah
An Itinerary in Light and Shadow
I would like to point out
I would like to point out that this thread and conversation is not a forum topic, it is Blog Space that is listed under Yilmaz's user name. From my perspective he is entitled to host whatever discussion, (within the boundaries of non-offensive contentl) that he may so choose to discuss, in whatever language he wants even if many of us may not understand or agree with the content.
The beauty of Blog space is that the user gets to talk about whatever is of interest to themselves, they can even wipe out the entire blog at their own volition should the user chose to do so.
Yilmaz I am glad that you have decided to take VitD3 again! Louise
I think there is a
I think there is a misunderstanding here. There is nothing against VİTD use in my comment, but you can see just the opposite;
''So VİTD would be helpfull in this situation to break down the vicious cycle at the cost of decreased immünity against CPNi. If you are on a good antibiotic protocol that would make no problem. But ıf VİTD helps to patients taking no antibiotic we should find some other mechanisms.''
As far as I know almost all people here are under antibiotic treatment, so there is no problem. But we should find the mechanism how vit D3 helps to MS patients who doesn't take antibioticsi. After reading all these Dr. Pall's work I did decided to restart VİTD3 again, and thinking to restart it for my son to decrease peroxynitrite damage.
Sarah,there is no relation of PGM with this.
yılmaz.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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 agree with MacKintosh
I agree with MacKintosh that newbie would have have difficulty on understanding this discussion. But this site is a very scientific site and there are many other scientific discussions here. Newbies will have difficulty on understanding some other important issues like secondary porphiria, co-infectionsi, cytokin reactions, endotoxini reactions etc. also.
I also know that there are many other scientific and knowlegable people in this site. Even I am a medical doctor I leaned many thing from them. I'm thankfull to them. I believe many people in this site can follow this discussion ıf they want.
There are many articles saying that NF-KappaB is an important contributor to CPNi infections and autoimmüne diseasesi like MSi. We can find some of them at that link posted by Red.
http://www.cpnhelp.org/vitamin_d_1
That is another one and a very good one showing interactions between NF-KappaB, vitD3, curcumin etc.
NephroPal: Inflammation and NF-kB -
In this site there are some discussions which are builded up on personal experiences which is much more unscientific but we still get benefit from them.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
Yes, continue with Vit D -
Yes, continue with Vit D - thanks to Red, we know the deficienty is rampant. For me, it is like not realizing that my right arm was not working. Though I am left-handed, I did not even notice - how can that be? Only years later did I understand that brain-fog is also rampant - and can be deadly, causing you not to notice that your foundation is beyond crumbling.
I received word this weekend that a dear friend has just been diagnosed with stage 3 ovarian cancer. Her Vit D level is 23.
Rica
3/9 Symptoms returning. Began 5 abxi protocol 5/9 Rifampin 600, Amox 1000, Doxyi 200, MWF Azith 250, flagyli 1000 daily. Began Sept 04 PPMSi EDSSi 6.7 Now good days EDSS 1 Mind, like parachute, work only when open. Charlie Chan In for the duration.
Quote from the indomitable
Quote from the indomitable Mackintosh:"I was struck by Yilmaz' comment, "As we all know..." and felt the need to jump in here. No, we do not "all know". I'm finding this conversation has become increasingly detailed and technical. After four years here, I find I cannot follow it, so I assume some others can't, either"
I might have known that PGM would be behind this somewhere! Carry on taking your vitamin Di, everyone because you need it, especially those with MSi who tend to be deficient. I can't be doing with all the techno-speak, I have better things to do and I am doing them well after taking a minimum of 4000iu of the stuff even before I started CAPi...........Sarah
An Itinerary in Light and Shadow
As we all know VİTD
As we all know VİTD decreases NF-Kappa B activity. We can also see at the Dr. Martin Pall's work that, NF-Kappa B causes increased secretion of IL-1B, IL-6, IL-8, TNF-alfa, IFN-gamma, all of which causes increased synthesis of NO by immüne cells. NO is protective against CPNi infection but also give harm to healty tissue. If you get into a vicious cycle of NO/ONOO it may result in big harm. So VİTD would be helpfull in this situation to break down the vicious cycle at the cost of decreased immünity against CPN. If you are on a good antibiotic protocol that would make no problem. But ıf VİTD helps to patients taking no antibiotic we should find some other mechanisms.
yılmaz
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
NEWBIE ALERT: I was struck
NEWBIE ALERT: I was struck by Yilmaz' comment, "As we all know..." and felt the need to jump in here. No, we do not "all know". I'm finding this conversation has become increasingly detailed and technical. After four years here, I find I cannot follow it, so I assume some others can't, either.
Now, while this is wonderful for those who are 'into it' and who understand medical and techno-speak, it CAN be very intimidating to newcomers. (While a few of us are doctors, most of us aren't medical professionals.) The protocol was designed to be simple and clear enough for even the most brain-fogged among us to be able to use it and (hopefully) still function in our lives.
NEWBIES,
please be aware that you don't have to understand or follow this very detailed conversation on chemistry to go ahead and get on the cpni protocol!!! (I really do think, if I'd been exposed to this type of post when - totally brainfogged - I first searched for information on curing MSi, I'd have taken a pass on this protocol.) Newbies should know this stuff goes WAY beyond the basics you need to know in order to do this treatment.
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
For what it's worth, I don't
pgm, I really don't know
pgm, I really don't know that, whether olmesartan (benicar) has any effect on VİTD recerptors, I didin't read any scientific report about that. We use olmesartan for antihypertansive purposes, thus I asked to the represants of olmesartan about this issue and wanted them to bring report about this issue if they have any. I'm still waiting, for 20 days.
Lets assume that Marshall is right and benicar corrects VDR dysfunction. Please explaine me what happens after that. We have functioning VDRs and little amount of D3 in our bodies. Then what happens?
yılmaz
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
Thanks indeed for this
Thanks indeed for this posting, Yilmaz. I've made up my mind now what follows from this. I seem to have been fooled by the idea that immunosuppressive stuff never causes die-off. This isn't true of course, depends a bit on how your immune system is working. For those whose immune system works, I assume that luring out the Cpni from cryptic form to replicating form is enough to cause die-off, as this reveals the Cpn to the immune system.
The reason why I say that it's a bad thing to not get die-off from immunosuppressive stuff or abxi is that the immune system doesn't seem to recognize the problem, and you are still left with the bugs. In this case, I would say that driving the immune system even more away from Th1 with vit-D would be a bad idea at least in the long term. Marshall's idea of avoiding vit D and taking Benicar for this problem seems to work well for this *subset* of people. It's just that this is not necessary for most(?) people. I'm of course open to other ideas of getting the immune system up and running for this subset of people. Perhaps supplement with interferon-gamma? :). And what are the causes of this problem? I'm betting for some other co-infection involved.
That is the discussion
That is the discussion with Dr. Stratton about DVİT3.(Q:QUESTİON, A:ANSWER)
Q-Dr. Stratton; does Cpni has any effect on CD57 count?
A-NK cells are important in the development of immunity against Cpn. Therefore, if there were a deficiency of NM function, immunity to Cpn would not develop. The Japanese believe that Chronic Fatigue Syndromei is a genetically related functional deficit of NK cells. What I don’t know is whether Cpn directly infects NK cells and thus may lead to poor functioning of these cells. I suspect this is the case, but I haven’t seen anything in the medical literature about Cpn infection NK cells.
Q-Dr. Stratton, so you say that NK cells are very important for body to fight against cpn by the activation of type 1 cellüler immünity which seems to me just the opposite of immünomodülatuar effect of VİTD3. So do you think that VİTD3 intake might be harmfull for cpn infected people and also for MS (at least after a certain dose)? What's the optimal levels of VİTD3 in cpn infected or MS people? Do you think more the vit D3, better the the effect on otoimmüne disease (unless intocsication)?
A-I don’t think anyone knows the correct amount of Vit D3. Remember, an afternoon in the sun is 20,000 International Units. So, 1000 IU twice a day is not very much.
Q-Do you think much of VİTD3 may give harm by supressing Th1 cells? I take 5000 ıu myself and give myson 2000 ıu daily
A-I don’t think so. These doses (5,000 and 2,000) are quite small compared to being out in the sun. Take care.
Q- Dr. Stratton; which kind of immüne response, Th1 or Th2 type, would you prefer in a chronic CPN infection and which kind would you prefer in MS?
A-I would want a Th1 for an intracellulari infection. See attached.
Q-So would you want a powerfull Th1 response in MS also?,
As far as I know VitD3 strengthens Th2 response decreasing inflammationi at the cost of decreased power against intracellüler infectionsi.
A-Yes I would if it were caused by Cpn (see attached) and the patient was on antichlamydial antibioticsi. Take care.
Q-Do you think VİT D3 may be harmfull after a certain dose(while still in nontoxic levels), by supressing Th1 too much. Do you believe VİTD3 is helpfull in MS infact?
A-I think that vitamin D3 is useful in MS and isn’t toxic. I don’t think suppressing the TH1 is a problem as antibodies are not important in MS.
Q- Even if we talked about vit D, even if you send me some articles and even if I read may be hundreds of articles suggesting benefits of Vit D in MS, since these articles assume MS as an autoimmüne disease( rather than an intracellüler infection) and the effect of Vit d3 is different on intracellüler infections I want to be sure and confident while giving my children Vit D. I know VitD3 supreses Th1 response but do you think that may also be true?
''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, immunei 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.''
They also make a hint that Dr. James Shaller thinks similar and put some sentences from Dr.Bryan Bosner's book suggesting same thoughts.
A-Don’t worry about asking questions. I’ve been out of town and haven’t been getting my E-mails. I’ll get to your questions this weekend, but remember, I don’t have all the answers. I will go back and answer each question tomorrow. Take care.
Q-Dr. Stratton, you forgot me:((
A-I haven’t forgotten you. It’s just that June is the end of our academic year. I have been doing exit interviews and just haven’t had the time for thoughtful answers. I will do this as soon as I’m less busy. Take care.
Q-Dr. Stratton, there is some evidence showing that chlamydia sp. may misdirect immüne system towards Th2 for their own benefits. So there seems to be a potential, on high dose Vit D supplementation, for helping these organism. As you said before the true dose important.
A-I think that if you are treating Cpn with antimicrobial agents, the vitamin D supplementation is a non-issue. In fact, if it were “helping” them, as steroids may do (see attached), it would actually make the Cpn more susceptible to the antimicrobial agents. Take care.
Q-Dr. Stratton; this was your answer about vitD.
''I think that if you are treating Cpn with antimicrobial agents, the vitamin D supplementation is a non-issue. In fact, if it were “helping” them, as steroids may do (see attached), it would actually make the Cpn more susceptible to the antimicrobial agents. Take care. ''
Would you advice an MS patient to get VİTD supplementation if he/she is not taking antibioyics?
A-I suspect that most people are not getting enough Vitamin D simply because we all avoid the sun. I think everyone should be taking extra Vitamin D.
A-
KEREM'S TAKECARER;
Suspıcıon of MSi (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, Thank you for
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
pgm, thanks for good
pgm, thanks for good interpretation. I'm at hospital now and when turn back to home I'll try to post detailed discussion.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
MacKintosh, Stratton seems
pgm, I was asking
pgm, I was asking Yilmaz what specific question was asked of Dr. Stratton. I could post the answer "the rabbit was found on the road" and we could imagine any number of questions that might have been asked to receive that answer. Only, one, however, would be the true question that was asked.
What I was asking is what was the original question posed to the doctor.
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
Could you tell us what the
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
Those are Dr. Stratton's
Those are Dr. Stratton's thoughts about VİTD;
''I think that if you are treating Cpni with antimicrobial agents, the vitamin Di supplementation is a non-issue. In fact, if it were “helping” them, as steroids may do (see attached), it would actually make the Cpn more susceptible to the antimicrobial agents. Take care. ''
''I suspect that most people are not getting enough Vitamin D simply because we all avoid the sun. I think everyone should be taking extra Vitamin D.''
KEREM'S TAKECARER;
Suspıcıon of MSi (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, VİTD3 really seems
pgm, VİTD3 really seems to be ,immünsuppressive in some aspects, but it still can be beneficial for certain doses (we don't know what the true dose is yet) If MS is an intracellüler infection, we expect to see an overactivated Th1 response which will result in a heavy tissue damage inturn. So by supplementing VİTD3 we can balance the overactivated TH1, in certain doses ofcourse, and we can prevent the collateral tissue damage. It would be best for an MS patient to be on an appropriate antibiotic portocol also.
What would happen to people who are not on an antimicrobial protocol. Normally I would expect them to have an increased risk of exacerbation of their MS in long term. But epidemiologic studies say just the opposite. People get benefit from VİTD3 supplementation. So how can we explain this situtation?
1-these studies are unreliable?
2-MS is not a CPNi infection, it's autoimmüne infact?
3-VitD3 has some unknown antiCPN or antiinfective effects which neutrolizes or overcome it's immünesuppressive effects?
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
Well, while we covered the
http://bloodjournal.hematologylibrary.org/cgi/content/full/106/13/4351
http://www.fasebj.org/cgi/content/full/21/12/3208
This all means that high 1,25D has some immunosuppressive properties. And if 25D is high, you'll get a high 1,25D in the immunei system response as well (not necessarily visible in circulating blood levels). But as you can see in the above discussion about the MP, no one except for Marshall has his patients to measure also 1,25D in addition to 25D in blood levels. Although this idea was rejected earlier here, people with chronic disease appears to have high 1,25D and low 25D. What this really means remains to be inspected in more detail.
What this really leads to appears to vary according to what infection you have. An excessive supplementation of VitD3 is at least harmful in sarcoidosis, because it can lead to granuloma formation. In other diseasesi like MS, it can lead to immunosuppression, because of the interferon-gamma suppression that is important against viral infectionsi. For the rest, more die-off of D3 supplementation can result. So what I said above about the Sun causing more die-off may not hold in all cases. And while i said previously that 25D doesnt seem to be immunosuppressive, this time we are discussing the effects of 1,25D, and this can unfortunately change the whole issue again. As long as we don't exactly know what 1,25D does, we can't say whether supplementing with 25D is useful or not.
The second of those journal
With the immune system being a complicated mass of interactions, it's hard to tell what the implications are of the sorts of cell-culture experiments done in the remainder of those two papers. Did they use the right dose of vitamin D? (40 nM sounds a bit high for 1,25-OH-D). Does turning one part of the immune system down turn another part up, which maybe they didn't include in their experiment? But when they study a whole infection, as in those mouse footpads, it's at least clear for those mice, for that infection, what the overall effect is (presuming they did the experiment correctly).
In any case, for just about any part of the immune system (or the body in general), there is some medical situation in which it is better to suppress its function. But generally that isn't the way to bet.
"" Those who get die-off
"" Those who get die-off appear to be in a better shape to be begin with." (quoting pgm) Where is the evidence for this?"
That's just my anecdotal findings. I have some, but ignore this for the moment.
I think we can finally reach an agreement here on this topic if we abandon just a part of Marshall's theories (namely that 25D is immunosuppressive, which appears to be incorrect) and add the other part from the mainstream research.
The part that appears to be right in the MPi is that Benicar is useful for some people. Because many people on the MP start to get sunlight sensitive after starting Benicar; that means they start getting die-off again from vitamin D. If you don't take Benicar, vitD will have no or little effect.
So what you need actually is Benicar + VitD3, and not necessarily any antibiotics to start with. Just take the Benicar, get out in the sun and as much as you can tolerate it and there you go.. use appropriate moppers for porphyrins, like DMSA, and there you have e.g. the Benicar - Sun - DMSA protocol :). Definitely worth a try if you dont get a proper response on abxi alone. The die-off can be rather strong from Benicar alone some say.
But as you know, not all infections are like this.. I don't yet know what kind of species you need to have to get VDR blocked, or whatever makes the Benicar useful. I just go by die-off reactions, they are the most reliable indicators that something useful is happening.
"I couldn't get the whole article you posted. When I read abot MP I see only what TM says; 25D is an immünesuppressive secosteroid, I can not see any scientific evidence and good explanations about the mechanisms for these claims (there may be but I didn't see anyone). TM also seems to be changing his mind about VITD, he was advicing people to run away from sun previously, but nowadays I see him saying that supplementation of 25Dacts differently than VITD synthesized byskin with the help of sun, this supplemented form of vitD is harmfull. So he seems to be twisting.(If I misunderstood please let me know)."
I dont know about this that he had changed his mind, but there we at least caught him; he is inconsistent in saying that people should avoid sunlight when it causes die-off, that's just what he wants people to have anyway, as it is a sign that the body is actively killing pathogens. It's cheaper to kill them with VitD3 anyways, as long as it works this way.
pgm, I know there may be
pgm, I know there may be some different explanations, forexample I read one saying that the lower incedence of MSi in equatorial region is due to differences in magnetic forces not due to VİTD (it was in Turkish so I didn't post it).
I couldn't get the whole article you posted. When I read abot MP I see only what TM says; 25D is an immünesuppressive secosteroidi, I can not see any scientific evidence and good explanations about the mechanisms for these claims (there may be but I didn't see anyone). TM also seems to be changing his mind about VİTD, he was advicing people to run away from sun previously, but nowadays I see him saying that supplementation of 25D acts differently than VİTD synthesized by skin with the help of sun, this supplemented form of vitD is harmfull. So he seems to be twisting.(If I misunderstood please let me know).
In my thought, there seem to be a confusion about MS-CPNi infection-VİTD relationship. I will try to summarize how it looks from my point of view; these are what the people here believe or know.
1)MS is an intracellüler infection caused by CPN
2)Vit D is very helpfull against MS
3)Main way of body for elimination of intracellüler pathogens and CPN is Th1 immüne response.( cellüler immünity)
4)overactive Th1 is responsible for the collateral neurological damage which is the major form of damage seen in MS.
5)VİTD helps by balancing immüne system towards Th2, so it decreases collateral damage.
And this is the questionmark on my mind;
If MS is an intracellüler infection caused by CPN, how decreased Th1 may be helpfull, especially in big majority of patients who doesn't take antibioticsi, ıt may help; at the beginning; by preventing immüne damage but since decreased Th1 would result in an increased infection I would expect it to give harm in long term.
There may be many different answers, some of which are below.
1)MS is not an infection, it's an autoimmüne disease caused by Th1 and VİTD is helpfull.
2)MS is an CPN infection and VİTD gives harm in long term infact.
3)MS is an CPN infection and VİTD helps by decraising Th1, it also doesn't cause infection to get stronger, VitD may have some powerfull antiinfective properties against CPN which we don't know yet, so while decreasing immüne damage it also fights with CPN and beat it. (Since there's no evidence that cathelicidins is effective against CPN, I don't think that cathelicidines help, I also don't believe that apoptosisi would help, because it may result in phagocytosis of apoptotic cell by macrophages which in turn would make CPN very happy, since macrophages will work as a CPN factory and CPN will feel itself at home)
4)MS is an infection but not an CPN infection, it's caused by another pathogen against which VİTD, defensins, cathelicidines and apoptosis would be effective.
We can lengthen the list; what I want to believe is number 3, since we have some pistol against CPN and VİTD would be a powerfull one.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
" Those who get die-off
" Those who get die-off appear to be in a better shape to be begin with." (quoting pgm)
Where is the evidence for this?
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
"pgm, it is not a good
"pgm, it is not a good explanation; if you try to explain lower incidence ofautoimmune diseasesin equatorial places with the any effect of sunlight, how can you believe a man who advice to people, with outoimmune diseases, to run away from the sun?"
I didn't say I believe him, but there seems to always be some alternative explanation for something, so it's a bit hard to say anything definitive at this point. At this point I assume that Vit D3 can be useful to some people. And I'm still puzzled that some people get symptom palliation from large doses of D3, while others get just more die-off. Those who get die-off appear to be in a better shape to be begin with.
Since MSi can also have
Since MSi can also have a viral component in it, sunlight (and therefore UV light) kills viruses or makes them inactive, and makes their spreading more difficult when there is more sunlight.
pgm, it is not a good explanation; if you try to explain lower incidence of autoimmune diseases in equatorial places with the any effect of sunlight, how can you believe a man who advice to people, with outoimmune diseases, to run away from the sun? It doesn't matter how sunlight helps, whether by killing viruses or in some other ways.
If TM claims that 25D is harmfull in autoimmüne diseases he should find a reliable explanation for this issue, orelse he must stop talking.
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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, I read the abstract
"pgm, I read the abstract and didn't see anything related to PXR nucleer receptors. If you have the complete article please post it here."
Just google for the paper name, TM keeps preprints of all of his papers on his website. I suppose you dont want links here to TM's site.
"pgm, you know, the incidence of MSii and some other autoimmune diseasesii are lower in equatorial places, how does TM explain this issue?"
He doesn't explain it, but it can be explained in some other ways too. Since MS can also have a viral component in it, sunlight (and therefore UV light) kills viruses or makes them inactive, and makes their spreading more difficult when there is more sunlight.
" The 1,25-D blood level is the thing that is three orders of magnitude lower than the 25-D blood level. Levels of 1,25-D outside the blood can be much greater than blood levels -- indeed, they have to be, for leakage into the blood to be an issue."
Good point - you'll have to dig into the issue more to find this explained. The wikipedia entry on vit D is just crap.. hahhaa. And I don't have the energy to dig through tons of papers on vit D. Thanks for this clarification.
Norman, how do you think
Norman, how do you think VitD kill CPNi, by apoptosisi of infected cells and/or some other mechanisms?
yılmaz
KEREM'S TAKECARER;
Suspıcıon of MSi (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 have no idea. (I don't
By the way, there are
The 1,25-D blood level is
The reason this doesn't apply to 1,25-D blood levels is that those levels are part of a feedback control loop. The kidneys dump however much 1,25-D into the blood is needed to regulate calcium; they stop dumping in 1,25-D when calcium is high enough. A lower 25-D concentration just means that the dumping happens slower, not that the final result is much different.
pgm, I read the abstract
pgm, I read the abstract and didn't see anything related to PXR nucleer receptors. If you have the complete article please post it here.
''The 1,25D has a magnitude of three orders smaller than 25D, you'll always have enough of it, regardless what your 25D status is, and the 25D and 1,25D are not directly coupled even.''
I'm not sure whether this statement is true or false. Because, as far as I know, the measured 1,25D is the 1,25 D which is synthesized by kidney and regulates Ca homeostasis. But the 1,25D which act on nucleer VDR are recieved from circulation into the cell of anykind and then converted to 1,25D within the cell, and the blood levels are important for internalization of 25D by cells. If the blood level of 25D is low, then it would be difficult for many cell to find a 25D and take it inside.
pgm, you know, the incidence of MSi and some other autoimmune diseasesi are lower in equatorial places, how does TM explain this issue?
yılmaz.
KEREM'S TAKECARER;
Suspıcıon of MSi (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 think the vitamin Di issue
http://www.ncbi.nlm.nih.gov/pubmed/18200565
Namely, while the 25D metabolite is often said to be the inactive form, that just floats around bound in the plasma with little other effects, it does affect e.g. the PXR nuclear receptor, which further transcribe some CYPs that further transcribe the VDR. In TM's paper, he clearly states that 25D does not bind to VDR nuclear receptor, so this is not the issue, but the 25D can and does bind to PXR.
But the 1,25D is still the active hormone that does all the important job, e.g. antimicrobial peptides etc, so why do we want to have high 25D, when this is not the active form of the vitD hormone. The 1,25D has a magnitude of three orders smaller than 25D, you'll always have enough of it, regardless what your 25D status is, and the 25D and 1,25D are not directly coupled even.
To do molecular dynamics,
As for not believing that lack of vitamin Di can cause depression, all I can say is: give it a try.
"Vitamin Di cause
"Vitamin Di cause depression? Quite the opposite, I would have thought."
Well I didn't say that, just that I don't believe that lack of VitD causes depression.
"With great difficulty! The basic equation to be solved is the Schroedinger equation; and the Schroedinger equation for N electrons is a 3N-dimensional partial differential equation."
To be more accurate it was molecular dynamics (MD) simulations, where clusters were bombarded on a surface. The simulations TM used are of the same type (MD). You can forget about more accurate simulations anyways, if you want more than hundreds of atoms. With MD you can probably come up to millions of atoms at a time. Simulation times are limited though, and accuracy too (only applicable to some situations). What TM studied was docking of a molecule into a receptor or something like that. You can do many things with MD anyways.
Vitamin Di for depression
As regards: I have done some atomistic simulations in physics, but I don't know about how you can apply it to biological systems. With great difficulty! The basic equation to be solved is the Schroedinger equation; and the Schroedinger equation for N electrons is a 3N-dimensional partial differential equation. It's most difficult even to solve it for a single atom; even with just two electrons, you're dealing with a six-dimensional equation. If each of those dimensions is discretized using a hundred points, it yields a trillion-variable problem -- just within the reach of today's computers, and that's just the helium atom. Go up to lithium, and you've added another three dimensions to the problem, and another factor of a million in the number of variables. Carbon? Forget it.
What they do in practice, to get a problem small enough for computers to handle, is to pile approximation on top of approximation on top of approximation, until it becomes very uncertain as to what relationship to reality the results have. Still, I wasn't surprised to see Professor Ceder's name on the list of authors of a recent breakthrough in lithium battery charge/discharge speed; he seemed like the more practical of the two teachers of that MIT course.
I agree with Sarah, when I
I agree with Sarah, when I take vitD I feel happy also. May be this s due to it's taste, I take it as drops on my bread, I like it's taste.
YILMAZ.
KEREM'S TAKECARER;
Suspıcıon of MSi (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.
Sarah, I would be jealous if
Stratton/Wheldon protocol 02/2006 - 10/11 for CFSi and many problems 30 years